|Year : 2014 | Volume
| Issue : 5 | Page : 425-441
|Biologics in dermatology: An integrated review
Virendra N Sehgal1, Deepika Pandhi2, Ananta Khurana2
1 Dermato Venereology (Skin/VD) Center, Sehgal Nursing Home, Delhi, India
2 Department of Dermatology and STD, University College of Medical Sciences and Associated Guru Teg Bahadur Hospital, Delhi, India
|Date of Web Publication||1-Sep-2014|
Virendra N Sehgal
Dermato Venerology (Skin/VD) Center, Sehgal Nursing Home, A/6 Panchwati, Delhi 110 033
Source of Support: None, Conflict of Interest: None
| Abstract|| |
The advent of biologics in dermatologic treatment armentarium has added refreshing dimensions, for it is a major breakthrough. Several agents are now available for use. It is therefore imperative to succinctly comprehend their pharmacokinetics for their apt use. A concerted endeavor has been made to delve on this subject. The major groups of biologics have been covered and include: Drugs acting against TNF-α, Alefacept, Ustekinumab, Rituximab, IVIG and Omalizumab. The relevant pharmacokinetic characteristics have been detailed. Their respective label (approved) and off-label (unapproved) indications have been defined, highlighting their dosage protocol, availability and mode of administration. The evidence level of each indication has also been discussed to apprise the clinician of their current and prospective uses. Individual anti-TNF drugs are not identical in their actions and often one is superior to the other in a particular disease. Hence, the section on anti-TNF agents mentions the literature on each drug separately, and not as a group. The limitations for their use have also been clearly brought out.
Keywords: Biologics in dermatology, intravenous immuno-globulin, level of evidence, tumor necrosis factor - alpha
|How to cite this article:|
Sehgal VN, Pandhi D, Khurana A. Biologics in dermatology: An integrated review. Indian J Dermatol 2014;59:425-41
What was known?
Biologics have been used for various dermatological conditions with some good and some equivocal results. Their use in psoriasis spearheaded trials for use in other dermatoses. However, level of evidence for majority of these unapproved conditions is low..
| Introduction|| |
The term 'biologic' refers to agents synthesized from the products of living organism.  The target-specific mediators of inflammation have become an important and useful part of the dermatologists' treatment armamentarium. They modulate the immune system through stimulatory or inhibitory actions, acting at only specific parts of the immune system; hence, their safety profile is generally considered to be more favorable than that of traditional systemic immuno-suppressive agents.  Nevertheless, they are not devoid of adverse reactions, a few of which are associated with significant morbidity. The initial over enthusiasm though has been replaced by a guarded and cautious approach now, with increasing years of experience with these drugs. The following account focuses attention to the biologics, which are/or may become useful in dermatological diseases. Broadly, these include agents acting against tumor necrosis factor-α (TNF-α), those acting on cell surface receptors, fuspion proteins and intravenous immunoglobulins (IVIG).
Biological Agents Acting Against Tumor Necrosis Factor-Alpha
Tumor Necrosis Factor-Alpha (TNF-α) is produced by multiple cell lines in the skin, including keratinocytes, langerhans cells and cutaneous mast cells.  It is released as a soluble cytokine (sTNF) following cleavage from its cell surface-bound precursor (tmTNF). Both sTNF and tmTNF are biologically active, and bind to either of two distinct receptors: TNF receptor 1 (TNFR1, p55) and TNF receptor 2 (TNFR2, p75).  This leads to NF-κB activation, promoting inflammation and/or cell apoptosis.  TNF receptors are primarily located on the surface of keratinocytes, neutrophils, endothelial cells and fibroblasts.  Soluble forms of the TNF receptors also exist and by binding and neutralizing sTNF may act as natural TNF antagonists.
TNF-α is involved in the recruitment of immune cells to the cutaneous micro-environment.  TNF also induces secretion of metalloproteinases and release of pro-inflammatory cytokines IL-1, IL-6, IL-8 and GM-CSF.  TNF-α also induces interferon γ, which in turn augments IL-12 secretion and ultimately causes a strong type 1 response. Thus, it plays a key role in the host response against inflammation, infection and tumor defense. 
TNF-α antagonists block its binding to the receptor, interrupting the subsequent signaling and inflammatory pathways. These are the most widely used biological agents and include infliximab, etanercept and adalimumab.
Infliximab is a 149 KDa chimeric antibody composed of murine variable (Fab) region and human constant (Fc) region which binds and neutralizes both sTNF and tmTNF. In addition, it can fix complement and cause cell apoptosis.  The second action of Infliximab probably explains its effect in granulomatous diseases. Infliximab binds TNF quickly and irreversibly. It was approved for the use in Crohn's disease in 1999, and a year later for rheumatoid arthritis. 
It is administered as an intravenous infusion in the doses of 5 mg/kg.  The commonly followed protocol is of administering at 0, 2 and 6 weeks, and subsequently every 8 weeks for maintenance. No systemic accumulation of Infliximab occurs upon continued repeated treatment. 
No major differences in clearance or volume of distribution occur with age, weight, gender, hepatic or renal function. A subgroup analysis of three randomized placebo-controlled trials showed that PASI-75 response rates at 10 weeks were similar regardless of body mass index (BMI). 
The pharmacokinerics are similar in the pediatric age group as well. Infliximab produces prompt effects in many responsive conditions.
Adalimumab is the first fully human monoclonal anti-TNF-α antibody. It is a highly specific TNF-α inhibitor. The drug exerts its pharmacological effect by binding to sTNF-α and preventing its interaction with TNFR1 and TNFR2 receptors. 
Adalimumab is administered subcutaneously. It is absorbed slowly, with peak serum concentrations being achieved in 5 days.  It is used in the doses of 80 mg subcutaneously initially, followed by 40 mg every other week (EOW), starting a minimum of 1 week after the first dose. Adalimumab is available as single-use pre-filled glass syringes, and also in vials as a sterile, preservative-free solution. 
Therapy should be reconsidered in case of no response within 16 weeks of treatment.  Safety and efficacy has not been established in children.
A weight-dependent decrease of treatment efficacy has been reported in REVEAL, BELIEVE and CHAMPION trials. ,,,
Etanercept is a fusion protein consisting of the extracellular domain of the p75 TNF receptor and the Fc portion of human IgG1. , It binds sTNF-α preventing its interaction with the receptor, and changes the cytokine pattern from type 1 to type 2. 
No formal pharmacokinetic studies have been conducted to examine the effects of renal or hepatic impairment on etanercept disposition. 
It is available as pre-filled syringes, and multiple use vials. In psoriasis, a starting dose of 50 mg. twice weekly is given for 3 months, followed by 50 mg once weekly.
For psoriatic arthritis, the dose is just 50 mg SC weekly.  For pediatric psoriasis a dose of 0.8 mg/kg, up to 50 mg weekly has been used, and is considered safe and effective. 
For etanercept as well, the effect of weight and BMI on therapeutic efficacy has been examined. , In the study by Strobe et al. superior response (defined as PASI 90 response at 3 or more postbaseline visits) was achieved by 40.57% of normal-weight patients, and 28.57%, 18.29% and 15.25% of overweight, obese and extremely obese individuals, respectively. Sub-optimal response was noted in only 9.43% of normal-weight individuals, but noted in 20.73% and 27.12% of obese patients and extremely obese patients, respectively. 
Golimumab and certolizumab
Golimumab is a human monoclonal antibody to TNF-α, while certolizumab is a PEGylated Fab fragment of humanized monoclonal TNF-α antibody. Both of these were approved for RA in 2009. Efficacy has also been reported in psoriatic arthritis. 
Certolizumab differs from other TNF inhibitors in not having the Fc portion of the antibody and the PEGylation of the Fab fragment. This results in less immunogenicity and longer half life, respectively. It practically relates to less frequent dosing requirement. It is administered subcutaneously in a dose of 400 mg, which is repeated 2 and 4 weeks after the first dose and subsequently a maintenance dose of 400 mg every 4 weeks. 
The major advantage of Golimumab is the one monthly dosing schedule. It is administered in the dose of 50 mg subcutaneously. 
Ustekinumab is a human IgG1κ monoclonal antibody that specifically binds to the p40 protein subunit of the interleukins IL-12 and IL-23. 
It prevents IL-12 and IL-23 from binding to their IL-12Rβ1 receptor protein expressed on the surface of immune cells.  The two cytokines participate in the immune response by activation of natural killer (NK) cells and CD4+ T-cell differentiation. IL-12 induces differentiation towards a Th-1 type of response with expression of TNF-α, and interferon. , IL-23, on the other hand, induces differentiation toward a T-helper 17 (Th17) phenotype, expression of IL-17, and an increase keratinocyte expression of inducible nitric oxide synthase, also implicated in the pathophysiology of psoriasis. ,, In addition IL-20 and IL-22 are also released, which contribute to keratinocyte hyperproliferation in psoriasis. ,
It is available as 45 mg and 90 mg pre-filled syringes, and 45 mg vials.
It is administered subcutaneously, in the dose of 45 mg, in those weighing <100 kg, at weeks 0 and 4, and thereafter every 12 weeks. A dose of 90 mg is recommended in patients with a body weight greater than 100 kg. 
In case of an inadequate response, consideration may be given to treating every 8 weeks, and increasing dose to 90 mg, with the initial dosing regimen used was 45 mg. , Should there be no response after 28 weeks,  it should be discontinued.
The apparent clearance of Ustekinumab is 55% higher for patients weighing more than 100 kg, compared with those 100 kg or less.  A decrease in serum Ustekinumab concentration with increasing weight was seen for both the 45 mg and the 90 mg doses in the PHOENIX 1 and PHOENIX 2 studies. ,, Also, for patients weighing more than 100 kg, the PASI 75 response rate was about 20% higher in the 90-mg group than in the 45-mg group. By contrast, for lighter patients (≤100 kg), PASI 75 response rates were similar between the 90-mg and 45-mg groups.
Alefacept was the first biologic agent approved for the treatment of moderate to severe chronic plaque psoriasis (2003). It is a recombinant dimeric fusion protein that consists of the extra-cellular CD2-binding portion of the human leukocyte function antigen-3 (LFA-3) linked to the Fc portion of the human IgG  Activation of T lymphocytes involves interaction between LFA-3 on the antigen-presenting cells and CD2 on T lymphocytes. Alefacept binds to CD2 on lymphocytes, thereby inhibiting the LFA-3/CD2 interaction. Thus, it interferes with the activation and proliferation of memory T lymphocytes.  In addition, alefacept interacts with the immunoglobulin receptors FcγRIII on accessory cells, such as NK cells and macrophages, to induce selective CD45RO+ T-cell apoptosis. These effects produce a selective reduction in memory-effector T cells, the source of the clonal precursors that emigrate from the blood, and drive the disease in the skin, while having relatively no effect on naive T-cell populations. 
Alefacept is produced by recombinant DNA technology in a Chinese hamster ovary (CHO) mammalian cell expression system and possesses a molecular weight of 91.4 kilodaltons. ,
The standard treatment course consists of twelve 15 mg weekly injections.  Repeat courses are considered for patients only after a 12-week drug holiday provided that CD4+ T lymphocyte counts are within the normal range.  Various modifications of this regimen have been tried including using a higher doses in the initial or later part of the course or extended duration of treatment extending to 16 to 24 weeks.  Although it has the distinct advantage of safety, yet one of the longest durations of therapeutic effect. It is the least used biologic due to its erratic efficacy and slow onset of action, maximal efficacy is seen approximately 6 weeks following a full 12-week course of the medication. However, it has been reported in a small pilot study that, whether a systemic course would achieve a satisfactory response or not, may be assessed by the response achieved with a single intralesional injection into a target plaque.  But, further studies are required to confirm these findings.
Efalizumab is a recombinant, humanized, monoclonal immunoglobulin G1 antibody that binds to CD11a, the α-subunit of the T-cell marker leukocyte function-associated antigen (LFA)-1, preventing LFA-1 from binding to intercellular adhesion molecule 1. , As a result, multiple LFA-1-mediated T-cell interactions that are critical to the pathogenesis of psoriasis and the maintenance of psoriatic plaques are inhibited. 
Multiple placebo-controlled Phase III clinical studies have assessed the safety and efficacy of efalizumab therapy in patients with moderate to severe chronic plaque psoriasis. ,,,,,,
However, following reports of development of progressive, multifocal, leukoencephalopathy (PML) during treatment it has been pulled from the market by European and Canadian regulatory agencies. Later, the manufacturer voluntarily withdrew efalizumab from the United States market. 
Rituximab is a chimeric murine-human monoclonal antibody to CD20 which induces depletion of B cells in vivo.  CD20 is a B-cell-specific antigen expressed on the surface of B lymphocytes throughout differentiation from the pre-B-cell to the mature B-cell stage, but not on plasma cells or stem cells. , Because plasma cells and hematopoetic precursors are spared, immunoglobulin levels do not fall dramatically and B cells typically begin to return to the circulation within 6 months of therapy. , The Fab regions of Rituximab binds to the CD20 antigen on B lymphocytes, while the Fc domain recruits antibodies and complements to mediate cell lysis.  Thus, Rituximab's cytotoxicity is mediated by three mechanisms including antibody-dependent cellular cytotoxicity, complement-mediated lysis, and direct disruption of signaling pathways and triggering of apoptosis. The contribution of each mechanism in vivo remains unclear, and different mechanisms may predominate in the treatment of different diseases. ,,
It has a half life of 8 hours and is most likely removed from the system by opsonization via the reticuloendothelial system when bound to B lymphocytes, or by human antimurine antibody production. 
The initial approved dosing regiment was four weekly infusions of 375 mg/m 2 .  However, modifications of this have been used in many studies.
Intravenous immunoglobulin (IVIG)
It is composed of human plasma derived from pools of 1000 to 15,000 donors.  It is derived from healthy human plasma via Cohn fractionation. The purification processes to remove pathogenic organisms include cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography.  Caprylate and nanofiltration may also remove prions.  Newer viral inactivation techniques include incubation at pH 4 and solvent detergent treatment.  The purified immunoglobulin is stabilized with glucose, maltose, sucrose, mannitol, sorbitol, glycine, or albumin.
IVIG is made up of more than 90% IgG and small amounts of IgM and IgA. IgG subclasses are represented as approximately 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4.  The total amount of immunoglobulins that are infused with a 2-g/kg dose is enormous leading to approximately five-fold increase in serum IgG concentrations. 
It has varied mechanisms by which it acts in different group of disorders. In the dermatologic setting, the major mechanisms include: Reducing levels of deleterious antibodies, via the contained anti-idiotypic antibodies , accelerating the catabolism of pathogenic IgG by saturating FcRn receptors with exogenous IgG, , anti cytokine effect  inhibiting T-cell activation, , inhibiting complement-mediated damage,  interfering with the production, release, and function of inflammatory cytokines, including interleukins 2, 3, 4, 5, 6, and 10, tumor necrosis factor-alpha, and granulocyte-macrophage colony-stimulating factor, ,,,, inhibiting the differentiation and maturation of dendritic cells,  inhibition of thromboxane A2 and endothelin, and increased prostacyclin secretion. 
The most commonly used dosing schedule in dermatological disorders is 2 g/kg/cycle, with cycles being repeated every 3-4 weeks. The interval between cycles may be prolonged as the disease comes under control. 
Omalizumab is a humanized recombinant monoclonal antibody that blocks the high-affinity.
Fc receptor of immunoglobulin E (IgE) reduces serum levels of IgE and blocks the attachment of IgE to mast cells, and other immune cells, thereby preventing IgE-mediated inflammatory changes. Dosing is based on weight and pretreatment serum IgE levels and is administered via subcutaneous injection every 2 to 4 weeks.
| Indications and Uses|| |
Biologics have been used in many dermatological conditions. However, indications approved by various drug authorities are only a few.
The sections beneath first list the approved uses of these drugs followed by brief descriptions and available evidence for the off label uses.
TNF-alpha inhibitors amongst dermatological diseases, Infliximab, Adalimumab and Etanercept are all approved by the US-FDA for the treatment of moderate to severe plaque psoriasis and psoriatic arthritis.
Off-label dermatologic uses of anti-TNF-a therapies
The efficacy of Infliximab has been demonstrated in a randomized controlled trial and many case series and case reports (LOE1B). ,,, The reports include patients both with/without underlying inflammatory bowel disease. In the trial by Brooklyn et al., there was no difference in the response to Infliximab with or without coexistence of IBD. 
Case reports of a good response to Adalimumab are also reported in the literature (LOE5). ,, Hubbard et al. published a case, who responded well to but had a severe systemic reaction to Infliximab at the second dose. The disease did not respond to etanercept given subsequently. However, with treatment with Adalimumab, initially in combination with prednisone 20 mg, the PG resolved within 5 months.
On the other hand, Etanercept has also been shown to be beneficial in PG in few case reports and small patient series (LOE4). ,,,
Autoimmune bullous diseases
A case of aggressive IgA pemphigus of the subcorneal pustular dermatosis (SCPD) subtype treated with Adalimumab, 40 mg subcutaneously eow, and myco-phenolate mophetil (1 g daily) gives direction to the use of TNF inhibitors in this group of disorders (LOE5). 
There are three reports ,, of efficacy of Infliximab in subcorneal pustular dermatoses, one of which reports a patient with concomitant SLE (LOE5). However, the response was found to be only transient.  Etanercept , has also been successfully tried in SCPD on two occasions (LOE5).
There are two case reports of efficacy of Infliximab, and one report of its failure in the management of pemphigus vulgaris. Hence, further studies to validate the role in pemphigus are warranted. ,, Adalimumab has been used with success, in a patient of pemphigus vulgaris who developed severe side effects with combined immunosuppressive therapy.  Etanercept has been used in pemphigus vulgaris, vegetans and foliaceus in occasional reports. ,, However, there is also a report  of induction of pemphigus vulgaris with etanercept, which was used for psoriasis in this case. Hence, so far the level of evidence for all these three drugs is low.
There is one report  of concomitant bullous pemphigoid and psoriasis treated with etanercept, which allowed successful tapering of the systemic steroids without inducing a flare (LOE5). Four treatment refractory patients of mucous membrane pemphigoid have been treated with etanercept and achieved clinical remission (LOE5). ,
Though these drugs may prove useful in a few recalcitrant cases, further data is needed to confirm their benefits. But, the reports of induction of autoimmune bullous disorders (pemphigus vulgaris/foliaceus and bullous pemphigoid) with TNF-α inhibitors raise a grave safety concern in the use in TNF-α inhibitor  in these conditions.
Hidradenitis suppurativa (HS) is a recurrent suppurative disease with a prolonged and indolent course. None of the available therapies are wholly satisfactory or uniformly effective. 
Infliximab has been assessed in HS in a few prospective observational studies, retrospective analyses, case series and case reports (LOE4). ,,,,,,, Although a significant benefit has been shown in most, confounding factors in terms of concomitant medications and diseases (Crohns) are present in many.
Satisfactory evidence for this drug comes from a double-blind placebo-controlled randomized trial (LOE1B).  Twenty-one patients were included, of whom 15 received Adalimumab and 6 received placebo. A significant reduction was seen in Sartorius score after 6 weeks and an almost significant reduction after 12 weeks of active treatment when compared with placebo. However, no long-term curative effect was uniformly seen.
Another parallel randomized, placebo controlled, blinded trial  involving 154 patients across 26 centers compared treatment with weekly Adalimumab injections, EOW injections and placebo. At week 16, 3.9% of placebo patients, 9.6% of EOW patients, and 17.6% of weekly patients, achieved clinical response.  Significantly, greater improvements in patient-reported outcomes and pain were seen in the weekly dosing group than in the placebo group. A decrease in response was seen after the switch from weekly to EOW dosing.
label trials and case report ,, related to use of etanercept in HS are available (LOE4). Some have reported good efficacy, while others have achieved minimal to no response.
Efalizumab  has been tried in five patients, only two of whom completed the study and none showed improvement in disease severity (LOE4).
| Connective Issue Disorders|| |
Although TNF-α is proposed to have a pathogenetic role in connective tissue disorders, the utility of TNF-α inhibitors is marred by the reports of development of anti-nuclear antibodies with the use of these agents.
There are occasional report  of treatment of scleroderma with etanercept. It has been shown, in a mouse model of bleomycin-induced scleroderma, to significantly reduce the dermal sclerosis, collagen accumulation and the number of infiltrating myofibroblastic cells.
In a trial  of 10 patients of systemic sclerosis, treated with etanercept (LOE4) for 6 months, 4 had improvement of skin scores and 3 of 4 patients with digital ulcers reported improvement. Other measures like pulmonary function tests, oral aperture and hand extension remained stable. 
In a retrospective trial  of 18 patients with joint involvement, treated with etanercept, it was found that 15 of 18 patients experienced a significant decrease in signs of inflammation and synovitis. There was no worsening of skin involvement during the treatment.
However, there are two reports , of development of multifocal and localized morphea with the use of etanercept for psoriasis vulgaris and rheumatoid arthritis, respectively.
An open-label trial  reported 16 cases of diffuse cutaneous systemic sclerosis who received five infusions of Infliximab. Although there was no clear benefit at 26 weeks but clinical stabilization and a fall in two laboratory markers of collagen synthesis was observed (LOE4).
Another report  mentions the efficacy of Infliximab treatment in a patient with lung fibrosis and pulmonary hypertension associated with advanced systemic sclerosis, refractory to conventional therapies. The patient was treated with Infliximab, 5 mg/kg, and methotrexate 10 mg/week for 1 year, with which there was improvement in patient's quality of life and laboratory and radiological parameters remained stable. The condition worsened on stopping Infliximab. 
However, there are reports , of severe adverse effects like pancytopenia and pulmonary actinomycosis in patients of scleroderma treated with Infliximab.
Also, there is a case reported,  of development of scleredema-like skin induration after treatment with Infliximab skin induration occurred within a few weeks of initiation of Infliximab, resolved with discontinuation of the drug, and recurred with rechallenge with the drug, implicating Infliximab as the offending agent. Interestingly, it did not recur with the use of etanercept. 
There are conflicting results on the use of Infliximab in dermatomyositis (DM), with few reports demonstrating benefit while others demonstrate a failure (LOE5). ,,,, The treatment has been beneficial in some patients, whether treatment resistant or naive, but it is difficult to predict which patients would respond. A report of development of non-Hodgkin lymphoma 4 months after Infliximab infusions raises concern in the use of TNF blockers in syndromes known to have paraneoplastic associations (like DM). 
There is a single report of successful treatment of recalcitrant dermatomyositis with efalizumab. 
Systemic lupus erythematosus (SLE)
TNF-α is implicated as a key player in the SLE disease process. However, its treatment with TNF inhibitors remains controversial. There are numerous reports of increased production of autoantibodies and of drug-induced lupus with this group of drugs.  Most of these reports are of patients with rheumatoid arthritis and Crohn's disease. 
However, there are also reports of beneficial outcomes (LOE5). Improvement of arthritis and proteinuria has been reported in six patients treated with Infliximab.  Aringer et al.  reported improvement in lupus nephritis in patients receiving Infliximab along with immunosuppressive therapy.
Report , of improvement of subacute Cutaneous LE treated with etanercept can also be found in the literature (LOE5).
There are two reports of improvement in Sweet's syndrome with etanercept, wherein two of the patients (Yamauchi et al.) had co-existing rheumatoid arthritis (LOE5). ,
There are two reports of Crohn's-associated Sweet's syndrome, and one of polychondritis associated disease responding to Infliximab infusions (LOE5). ,,
Another report  mentions successful treatment of highly refractory Sweet's syndrome with underlying myelodysplastic disorder, with Infliximab, which was subsequently changed to Adalimumab for sustained remission. The disease did not recur with this therapy.
Among the biologic agents which inhibit TNF, Infliximab (LOE1B) has been studied ,, most extensively in sarcoidosis with fewer reports available for Adalimumab and etanercept.
Infliximab has been used with success in cutaneous, ocular, neuro, pulmonary and musculoskeletal manifestations. ,,,, Rosen et al. have reported long-term control (>3 years) with 8-10 weekly maintenance infusions.
However, there are also concerns of development of sarcoidosis, mainly pulmonary and lymph node involvement with TNF inhibitors. 
Granuloma annulare (GA) generally resolves itself within 2 years in 50% of cases, but there is a 40% recurrence rate. 
There are a few case reports , of success of Infliximab therapy in disseminated GA (LOE5). The response was maintained even after stopping the drug. There is also a report  of beneficial response with efalizumab in a patient of disseminated GA, who also had plaque psoriasis.
However, there are also numerous cases of GA, mostly generalized induced by TNF inhibitors (Infliximab, Adalimumab and etanercept) in patients of rheumatoid arthritis treated with these drugs. 
Toxic epidermal necrolysis (TEN)
The role of TNF α in TEN is well known, hence the enthusiasm of using anti-TNF agents in this disease. There are many reports ,,,,, of successful use of Infliximab, and a few of etanercept (LOE5). It has been used alone, as well as in combination with IVIG and steroids, producing rapid response. However, the risk of infection is a major limiting factor.
Pityriasis rubra pilaris
Anti-TNF agents, primarily Infliximab and etanercept, have been used in adult and juvenile forms of Pityriasis rubra pilaris (PRP) (types 1, II and III) with good responses (LOE5). In a report of seven patients, only one patient, who had type II PRP, developed disease in the 12 month post treatment discontinuation period. Muller et al. also reported a persistent response following Infliximab in their patient. ,,
A recent systematic literature review  concluded that a complete response occurs in 80% of patients with a mean time to maximal response being 5 months.
A large number of publications suggest that inhibition of TNF, mainly using Infliximab, is a promising therapeutic approach for this disease. However, the current evidence of therapeutic efficacy is low grade, and there is only one randomized trial available, which assessed the effects of the soluble TNF receptor etanercept in muco-cutaneous manifestations and found it to be very effective (LOEIB). ,
There are numerous reports ,,,,,,,, of rapid and marked response with Infliximab in refractory disease, either alone or in combination with other immunosuppressives. Case series and case reports suggest that patients with severe mucocutaneous lesions exhibit rapid and good responses to 5 mg/kg or 3 mg/kg of Infliximab (LOE4). Some patients with orogenital ulcers being unresponsive  and/or intolerant  to conventional treatments remained disease-free for the first time in years. Almost all patients were resistant to conventional treatments and were treated with Infliximab alone , or as an add-on therapy. ,,,
In addition, Infliximab has been extensively studied in ocular Behcets with rapid and gratifying results. 
Cases of efficacy in gastro-intestinal,  vascular  and neurological  manifestations are also reported.
Etanercept has been evaluated in a double-blind, placebo-controlled study  of 40 male patients with Behcet's disease (LOE2B). Etanercept 25 mg twice a week for 4 weeks was effective in suppressing most muco-cutaneous lesions. The drug had a clear effect on oral ulcers, and nodular lesions, and the response was evident as early as the 1 st week.  Almost half of the patients receiving etanercept were free of oral ulcers at the end of the study, compared with 5% of the placebo group, whereas the absence of nodular lesions was evident in 85% and 25% of patients receiving the drug and placebo, respectively.  Although the drug decreased the number of genital ulcers and arthritis episodes during the treatment period, the difference was not significant. Recurrences developed in some patients 3 months after etanercept was discontinued. 
In other report ,, rapid resolution of severe mucocutaneous manifestations and arthritis  were noted following etanercept treatment, while another patient who failed to respond to etanercept, responded dramatically to Infliximab treatment with rapid resolution of orogenital ulcers and erythema nodosum and marked improvement in arthralgia and iritis.  Etanercept was also given to two children with BD-associated uveitis. A favorable response was noted in the first, but not in the second patient. The latter patient achieved a moderate response following subsequent treatment with Infliximab. 
Adalimumab has also been tried in a few reports (LOE5). In a retrospective analysis of 19 patients treated with Adalimumab, 17 achieved clinical improvements of note, ocular manifestations panuveitis and retinal vasculitis responded rapidly in all cases. 
Calvo Catalα et al.  also reported their experience of using Adalimumab in six cases with a good clinical response in all patients. Good disease control was achieved after a mean follow-up of 26.8 months with no adverse effects. Olivieri et al.  reported response to Adalimumab in patients who had failed Infliximab previously (LOE5).
| Synovitis Acne Pustulosis Hyperostosis Osteitis Syndrome (SAPHO)|| |
Cases of response with Infliximab have been reported. Iqbal et al. used Infliximab in a patient with the SAPHO syndrome with acne fulminans. Ten months after initiating therapy with Infliximab, the area of the patient's ulcerative lesions was reduced by 70%. In another two cases,  only four infusions of Infliximab achieved remission of both skin and bone involvement, which was maintained over a period of 18 months (LOE5). However, in the report by Massara et al.  although the osteoarticular complaints improved, palmoplantar pustulosis relapsed in two of four patients.
Necrobiosis lipoidica diabeticorum
A few cases of the use of Infliximab and etanercept in ulcerated (and one in pre-ulcerative stage) can be found in the literature with reported good efficacy (LOE5). ,,,
There is one report of intralesional Infliximab (three cycles of weekly injections of intralesional Infliximab for 3 weeks followed by a 1-week treatment interruption) which produced complete remission for up to 18 months in two of the three patients treated. 
| Others|| |
Anecdotal reports of efficacy of TNF inhibitors in multicentric reticulohistiocytosis, atopic dermatitis, erythema annulare centrifugum, cutaneous vasculitis, erosive oral lichen planus and alopecia areata can also be found in the literature. ,,213],,,,,
| Omalizumab|| |
Omalizumab has been used off label in the management of severe atopic dermatitis (one prospective stud; case series and reports), (LOE2B) and chronic urticaria (case series and reports) (LOE4). ,,,,
| Rituximab|| |
Rituximab is approved for the treatment of B-lymphocyte malignancies and rheumatoid arthritis. 
Although there have been only occasional randomized trials of Rituximab in dermatologic diseases, case reports describe its use in treatment of pemphigus vulgaris (PV), paraneoplastic pemphigus (PNP), epidermolysis bullosa acquisita, cutaneous B-cell lymphoma, DM, and Graft-versus-host disease (GVHD).
In pemphigus (LOE4), two dosing regimens  for Rituximab have been used-the lymphoma protocol, consisting of four weekly infusions of 375 mg/m 2 , and the rheumatoid arthritis (RA) protocol consisting of two infusions of 1000 mg each 15 days apart.
A recent review  on the use of Rituximab in pemphigus vulgaris stated that a complete remission occurred in 66.66% of patients in the lymphoma protocol and 75% in the RA protocol.
The authors also noted that the use of the lymphoma protocol produces a lower response rate, a lower rate of recurrences and serious infections, but a higher mortality rate,  whereas patients treated by the RA protocol had higher response rates, a larger number of infections, but a lower mortality rate.  This could be partly due to the fact that more patients were on corticosteroids and immunosuppressive agents as concomitant therapy in the lymphoma protocol, thus adding to the degree and duration of prolonged immune suppression. Of significant interest is the fact that there were no non-responders in patients treated with the RA protocol compared to 3.9% in the lymphoma protocol (LOE4). 
Studies  have shown that patients with severe disease often have high levels of anti-dsg3 IgG-producing B cells in the peripheral blood, which may explain the therapeutic effect of Rituximab.
Rituximab has also been tried in bullous pemphigoid with 69% patients showing a complete response, 6% having a partial response, and another 6% showing no response. 14 of the 16 patients were treated with the lymphoma protocol, and two with RA protocol. 
Paraneoplastic pemphigus (PNP)
Case reports ,, of both success and failure of Rituximab included regimens, for PNP associated with B-cell lymphoma, can be found in the literature (LOE5).
Ishigami et al.  have suggested that since almost all patients with NHL and PNP succumb within 3 months to 2 years after diagnosis, except for a couple of individual reports of long-time survivors by classical immunosuppressive treatments, the regime including Rituximab may be more effective for PNP than the classical treatments.
Rituximab has also shown efficacy in epidermolysis bullosa acquisita (EBA) in a few case reports , either alone or with other modalities (LOE5).
There are also a few reports and case series  of efficacy in mucous membrane pemphigoid (LOE4). Recently, a critical analysis was published,  where in 20 of 28 patients had a complete response, 3 had a partial response, 2 were nonresponders, and 1 had stabilization of disease. However, they noted that long-term follow-up data after Rituximab therapy is lacking.
Rituximab has been evaluated in DM in a randomized trial, a prospective multicenter study and case reports (LOE1B). ,,, It has been reported to reduce steroid requirement, and allow for tapering of steroid doses and avoid use of other imnunosuppressives. In the study by Bader-Meunier et al.  complete clinical response was achieved in three patients treated with Rituximab for muscle involvement. In these responders steroid therapy was stopped or tapered to <15% of the baseline dosage, with no relapse, with a follow up ranging from 1.3 to 3 years. But, calcinosis did not improve in the six affected patients.  Rituximab has also been used in systemic lupus erythematosus and lupus nephritis. Systematic review and meta-analysis by Lan et al. ,, noted that the observational studies indicate that Rituximab is effective in severe and refractory SLE patients, with decreased Systemic Lupus Erythematosus Disease Activity Index (SLEDAI), British Isles Lupus Assessment Group Index (BILAG), urine protein levels, prednisolone dosage and also complete or partial remission in some lupus nephritis patients. But, a randomized controlled trial did not achieve primary and second endpoints, which makes the true effect attributed to Rituximab questionable.
Other conditions ,,, where Rituximab has been tried with variable success include Graft-versus-host disease (GvHD), atopic dermatitis and vasculitis (LOE5).
| Intravenous Immunoglobulin (IVIG)|| |
Approved indications for IVIG include hypogammaglobulinemia, chronic lymphocytic leukemia, HIV in children, allogeneic bone-marrow transplantation, idiopathic thrombocytopenic purpura, and Kawasaki syndrome.  However, it has been used in numerous dermatological disorders, mainly autoimmune bullous disorders, connective tissue diseases, toxic epidermal necrolysis, vasculitides, urticarias, pyoderma gangrenosum (PG), scleromyxedema, pretibial myxedema, nephrogenic fibrosing dermopathy, Kaposi's sarcoma, mixed connective tissue disease, anticonvulsant syndrome and Polymorphous light eruption. , Here, we shall be reviewing the literature on most important of these disorders.
Autoimmune bullous disorders
IVIG has been shown to have good efficacy in a variety of autoimmune bullous disorders especially pemphigus (LOE1B). It can rapidly lower serum levels of auto-antibodies in patients with pemphigus. Coadministration of a cytotoxic drug  may improve its efficacy.
IVIG is usually employed when conventional therapy fails, causes side effects or is contraindicated. Beneficial clinical effects have been demonstrated in the treatment of pemphigus vulgaris, pemphigus foliaceus, bullous pemphigoid, mucous membrane pemphigoid and epidermolysis bullosa acquisita. 
A 'Consensus Statement' on the use of IVIG in these diseases recommended a dose of 2 g/kg/cycle, given monthly until clinical control, with a progressive increase of the intervals between the cycles thereafter.  The last cycle is given after a 16-week interval and is considered as the end point of therapy. 
156 patients treated with IVIG using this protocol demonstrated successful clinical outcomes.  In these patients IVIGg could be used as monotherapy, once concomitant prednisone and immunosuppressive agents were gradually discontinued.  These included 42 patients with pemphigus vulgaris, 26 with pemphigus foliaceus, 32 with bullous pemphigoid, 68 with mucous membrane pemphigoid and 9 with epidermolysis bullosa acquisita.  IVIG produced long-term, sustained remission for at least 2 years of follow-up, after discontinuation. The patients were in serological remission, and enjoyed a high quality of life. 
Evidence for efficacy comes from case reports and small case series (LOE4). Patients treated include those with and without other underlying disorders, like inflammatory bowel disease RA, and myelodysplastic syndromes. ;252],,,
Stevens-Johnson syndrome More Details (SJS) and toxic epidermal necrolysis (TEN)
The evidence for and against IVIG in the treatment of SJS and TEN consists of a few prospective, retrospective studies, case series and case reports (LOE2B).
In a retrospective multicenter-study, 48 patients treated with IVIG had a survival rate of 88%, much higher than expected. 
In a review of published literature by Mydlarski et al., 11 out of 14 studies demonstrated IVIG's effectiveness.  European Dermatology Forum Guidelines Subcommitte, recommends starting IVIG treatment early after confirmation of TEN diagnosis (LOE IIIb). 
However, there is evidence pointing to lack of efficacy also, with 2 prospective studies with 3  and 16 patients  and showing no benefit.
Although a high dose of >2 g/kg is generally recommended, a few reports , have reported shown efficacy with much lower doses, thus bringing down the cost significantly.
Connective tissue disorders
IVIG is generally not the first-line therapy for DM/polymyositis (PM), but is used in conjunction with other drugs. The beneficial effect of IVIG in refractory, flared-up, rapidly progressive, or severe PM/DM has been documented in many open-label trials and reports (LOE2). ,,
In a recent systematic literature review, Wang et al. evaluated the literature on the use of IVIG in DM/PM from 1985 to 2011, which included two randomized controlled trials, nine prospective open studies, and three retrospective studies with a total of 308 adult patients.  They concluded that IVIG has been used successfully in the treatment of PM/DM (LOE1B).The standard dose is 2 g/kg,  its course is usually 3 to 6 months. In some patients, IVIG can lower the corticosteroid dose required for maintenance, demonstrating the most effective steroid-sparing effect. 
Another retrospective study, on the long-term effects of IVIG, concluded that patients on drug combinations, which included IVIG, had lesser muscular and cutaneous involvement, as well as lower percentages of muscular relapses. The total number of muscular relapses was inversely associated with the number of pulses of IVIG. 
Many reports and open label trials had documented the efficacy of IVIG in treatment of cutaneous manifestations of lupus erythematosus (LE), including facial rash, photo-sensitivity, vasculitis, urticaria, discoid lesions and subacute cutaneous LE lesions. ,,, However, there are also reports of failure/limited response. 
IVIG has shown efficacy in experimental murine models of bleomycin (BLM)-induced scleroderma. It has been tried in systemic sclerosis, with success being assessed by improvement in skin scores and joint involvement (LOE4). ,,
There are three reports ,, of the beneficial effect of IVIG in mixed connective tissue disease (MCTD), especially with severe cutaneous involvement (LOE5).
IVIG has also shown efficacy in different forms of cutaneous vasculitis, Behçet's disease, leukocytoclastic vasculitis, livedoid vasculitis and cutaneous polyarteritis nodosa. ,,,
| Contemporary Prospective Innovations|| |
Interleukin-17A (IL-17 or IL-17A) has now emerged as a major factor in the pathogenesis of psoriasis vulgaris. , It is produced by Th17 cells, a class of T helper cells that act outside the established Th1/Th2 paradigm for regulation of innate and adaptive immunity. Hence, drugs targeting this cytokine are being widely researched. Currently, there are three different IL-17 antagonists under clinical evaluation for psoriasis. The monoclonal antibodies ixekizumab and secukinumab both target IL-17A, while brodalumab blocks the IL-17 receptor IL-17RA.1. All three drugs have completed phase 2 trials and have entered into phase 3. ,,
In phase 2 trials with ixekizumab, at 12 weeks, the percentage of patients with a reduction in the PASI score by at least 75% was significantly greater with ixekizumab-with 82.1% participants in the 150 mg group, 82.8% in the 75 mg group, and 76.7% in the 25 mg group achieving this figure. 
With Brodalumab, 77% patients receiving 140 mg dose and 82% patients receiving 210 mg dose achieved PASI 75 after 12 weeks of treatment. PASI 90 was achieved by 72% in the first group and 75% in the second group. 
Similar results have also been reported with secukinumab with 82% patients achieving PASI 75 at 12 weeks. 
However, the safety profile of these drugs is not well known so far, and hence it will be some time before they get incorporated into routine practice.
| References|| |
|1.||Graves JE, Nunley K, Heffernan MP. Off label uses of biologics in dermatology: Rituximab, omalizumab, infliximab, etanercept, adalimumab, efalizumab, and alefacept (part 2 of 2). J Am Acad Dermatol 2007;56:e55-79. |
|2.||LaDuca JR, Gaspari AA. Targeting tumor necrosis factor alpha. New drugs used to modulate inflammatory diseases. Dermatol Clin 2001;19:617-35. |
|3.||Breathnach SM, Smith CH, Chalmers RJ, Hay RJ. Systemic therapy. In: Burns T, Breathnach S, Cox N, Griffiths C, editors. Rook's Textbook of Dermatology. 8 th ed. UK: Blackwell Publishing Ltd; 2010. p. 74.4-74.14. |
|4.||Springer TA. Adhesion receptors of the immune system. Nature 1990;346:425-34. |
|5.||Lebwohl MG. Use of etanercept in the dermatology setting: A review. Am J Clin Dermatol 2005;6:49-59. |
|6.||Chaudhari U, Romano P, Mulcahy LD, Dooley LT, Baker DG, Gottlieb AB. Efficacy and safety of infliximab monotherapy for plaque-type psoriasis: A randomised trial. Lancet 2001;357:1842-7. |
|7.||Rott S, Mrowietz U. The use of infliximab in dermatology. J Dtsch Dermatol Ges 2007;5:655-60. |
|8.||DrugBank: Infliximab (DB00065). Available from: http://www.drugbank.ca/drugs/DB00065. [Last accessed on 2013 Jul 23]. |
|9.||Prescribing Information of Infliximab. Available from: http://www.accessdata.fda.gov/drugsatfda_docs/label/2011/ 103772s5281lbl.pdf. [Last accessed on 2013 Jul 23]. |
|10.||Reich K, Menter A, Plotnick M, Guzzo C, Li S, Gottlieb A. Consistency of infliximab response across subgroups of patients with psoriasis: Integrated results from randomized clinical trials. Psoriasis Forum 2007;13:21-7. |
|11.||Shukla R, Vender RB. Pharmacology of TNF inhibitors. In: Weinberg JM, Buholtz R. editors. TNF-alpha Inhibitors. Basel: Birkhäuser Verlag; 2006. p. 23-43. |
|12.||European Medicines Agency. Summary of Product Characteristics. Available from: http://www.emea.europa.eu/humandocs/PDFs/EPAR/humira/H-481-PI-en.pdf. [Last accessed on 2008 Apr 3]. |
|13.||Humira (Adalimumab). Available from: http://www.fda.gov/downloads/Drugs/DevelopmentApprovalProcess/HowDrugsareDeveloped andApproved/ApprovalApplications/TherapeuticBiologic Applications/ucm092762.pdf. [Last accessed on 2013 Jul 7]. |
|14.||Menter A, Gordon K, Goldblum O, Gu Y. Efficacy and safety of adalimumab are consistent across weight quartiles in patients with moderate to severe psoriasis: Subanalysis of REVEAL. J Am Acad Dermatol 2009;60 Suppl 1:AB173. |
|15.||Menter A, Gordon KB, Leonardi CL, Gu Y, Goldblum OM. Efficacy and safety of adalimumab across subgroups of patients with moderate to severe psoriasis. J Am Acad Dermatol 2010;63:448-56. |
|16.||Kragballe K, Sygehus Å, Thaci D, Unnebrink K, Goldblum O. Adalimumab plus topical treatment (calcipotriol ⁄ betamethasone) in the treatment of moderate to severe psoriasis: Response across subgroups in BELIEVE. J Am Acad Dermatol 2010; 62 Suppl 1:AB133. |
|17.||Saurat J-H, Unnebrink K, Goldblum O, Bissonnette R. Adalimumab response is consistent across subgroups of patients with moderate to severe psoriasis: Subanalysis of the CHAMPION study. J Am Acad Dermatol 2010;62 Suppl 1:AB124. |
|18.||Feldmann M, Charles P, Taylor P, Maini RN. Biological insights from clinical trials with anti-TNF therapy. Springer Semin Immunopathol 1998;20:211-28. |
|19.||DrugBank: Etanercept (DB00005). Available from: http://www.drugbank.ca/drugs/DB00005. [Last accessed on 2013 Jul 7]. |
|20.||Becher B, Blain M, Giacomini PS, Antel JP. Inhibition of Th1 polarization by soluble TNF receptor is dependent on antigen-presenting cell-derived IL-12. J Immunol 1999;162:684-8. |
|21.||Enbrel prescribing information. Available from http://pi.amgen.com/united_states/enbrel/derm/enbrel_pi.pdf (last accessed on 2014 May 15). [Last accessed on 2013 Jul 7]. |
|22.||Ortleb M, Levitt JO. Practical use of biologic therapy in dermatology: Some considerations and checklists. Dermatol Online J 2012;18:2. |
|23.||Strober B, Gottlieb A, Leonardi C, Papp K, Dunn M, Peloso P, et al. Levels of response of psoriasis patients with different baseline characteristics treated with etanercept. J Am Acad Dermatol 2006;54:AB220. |
|24.||Gordon K, Korman N, Frankel E, Wang H, Jahreis A, Zitnik R, et al. Efficacy of etanercept in an integrated multistudy database of patients with psoriasis. J Am Acad Dermatol 2006;54 3 Suppl 2:S101-11. |
|25.||Mittal M, Raychaudhuri SP. Golimumab and certolizumab: The two new anti-tumor necrosis factor kids on the block. Indian J Dermatol Venereol Leprol 2010;76:602-9. |
|26.||Stelara Datasheet. Available from: http://www.medsafe.govt.nz/profs/datasheet/s/stelarainj.pdf. [Last accessed on 2013 Jul 7]. |
|27.||Leonardi CL, Kimball AB, Papp KA, Yeilding N, Guzzo C, Wang Y, et al. PHOENIX 1 study investigators. Efficacy and safety of ustekinumab, a human interleukin-12/23 monoclonal antibody, in patients with psoriasis: 76-week results from a randomised, double-blind, placebo-controlled trial (PHOENIX 1). Lancet 2008;371:1665-74. |
|28.||Trinchieri G. Interleukin-12 and the regulation of innate resistance and adaptive immunity. Nat Rev Immunol 2003;3:133-46. |
|29.||Krueger JG. The immunologic basis for the treatment of psoriasis with new biologic agents. J Am Acad Dermatol 2002;46:1-26. |
|30.||Wilson NJ, Boniface K, Chan JR, McKenzie BS, Blumenschein WM, Mattson JD, et al. Development, cytokine profile and function of human interleukin 17-producing helper T cells. Nat Immunol 2007;8:950-7. |
|31.||Bruch-Gerharz D, Fehsel K, Suschek C, Michel G, Ruzicka T, Kolb-Bachofen V. A proinflammatory activity of interleukin 8 in human skin: Expression of the inducible nitric oxide synthase in psoriatic lesions and cultured keratinocytes. J Exp Med 1996;184:2007-12. |
|32.||Nickoloff BJ. Cracking the cytokine code in psoriasis. Nat Med 2007;13:242-4. |
|33.||Vanden Eijnden S, Goriely S, De Wit D, Willems F, Goldman M. IL-23 up-regulates IL-10 and induces IL-17 synthesis by polyclonally activated naïve T cells in human. Eur J Immunol 2005;35:469-75. |
|34.||Zheng Y, Danilenko DM, Valdez P, Kasman I, Eastham-Anderson J, Wu J, et al. Interleukin-22, a T (H) 17 cytokine, mediates IL-23-induced dermal inflammation and acanthosis. Nature 2007;445:648-51. |
|35.||Reich K, Papp KA, Griffiths CE, Szapary PO, Yeilding N, Wasfi Y, et al. PHOENIX 1, PHOENIX 2, and ACCEPT investigators. An update on the long-term safety experience of ustekinumab: Results from the psoriasis clinical development program with up to four years of follow-up. J Drugs Dermatol 2012;11:300-12. |
|36.||Zhu Y, Hu C, Lu M, Liao S, Marini JC, Yohrling J, et al. Population pharmacokinetic modeling of ustekinumab, a human monoclonal antibody targeting IL-12 ⁄ 23p40, in patients with moderate to severe plaque psoriasis. J Clin Pharmacol 2009;49:162-75. |
|37.||Lebwohl M, Yeilding N, Szapary P, Wang Y, Li S, Zhu Y, et al. Impact of weight on the efficacy and safety of ustekinumab in patients with moderate to severe psoriasis: Rationale for dosing recommendations. J Am Acad Dermatol 2010;63:571-9. |
|38.||Amevive (Alefacept) [package insert]. Available from: http://www.fda.gov/downloads/Drugs/DevelopmentApprovalProcess/HowDrugsareDevelopedandApproved/ApprovalApplications/TherapeuticBiologicApplications/ucm086009.pdf [last accessed 2014 May 15]. |
|39.||Alefacept Ref 1 Package Insert AMEVIVEH (alefacept). Biogen Inc. Available from: http://www.fda.gov/cder/foi/label/2003/alefbio013003LB.htm. [Last accessed on 2005 Aug 1]. |
|40.||Wong VK, Lebwohl M. The use of alefacept in the treatment of psoriasis. Skin Therapy Lett 2003;8:1-7. |
|41.||Perlmutter A, Cather J, Franks B, Jaracz E, Menter A. Alefacept revisited: Our 3-year clinical experience in 200 patients with chronic plaque psoriasis. J Am Acad Dermatol 2008;58:116-24. |
|42.||Gattu S, Busse K, Bhutani T, Chiang C, Nguyen T, Becker E, et al. Psoriasis responds to intralesional injections of alefacept and may predict systemic response to intramuscular alefacept: Interim results of a single-arm, open-label study. J Dermatolog Treat 2012;23:103-8. |
|43.||Jullien D, Prinz JC, Langley RG, Caro I, Dummer W, Joshi A, et al. T-cell modulation for the treatment of chronic plaque psoriasis with efalizumab (Raptiva): Mechanisms of action. Dermatology 2004;208:297-306. |
|44.||Werther WA, Gonzalez TN, O'Connor SJ, McCabe S, Chan B, Hotaling T, et al. Humanization of an anti-lymphocyte function-associated antigen (LFA)-1 monoclonal antibody and reengineering of the humanized antibody for binding to rhesus LFA-1. J Immunol 1996;157:4986-95. |
|45.||Gordon KB, Papp KA, Hamilton TK, Walicke PA, Dummer W, Li N, et al. Efalizumab Study Group. Efalizumab for patients with moderate to severe plaque psoriasis: A randomized controlled trial. JAMA 2003;290:3073-80. |
|46.||Lebwohl M, Tyring SK, Hamilton TK, Toth D, Glazer S, Tawfik NH, et al. Efalizumab Study Group. A novel targeted T-cell modulator, efalizumab, for plaque psoriasis. N Engl J Med 2003;349:2004-13. |
|47.||Leonardi CL, Papp KA, Gordon KB, Menter A, Feldman SR, Caro I, et al. Efalizumab Study Group. Extended efalizumab therapy improves chronic plaque psoriasis: Results from a randomized phase III trial. J Am Acad Dermatol 2005;52:425-33. |
|48.||Menter A, Gordon K, Carey W, Hamilton T, Glazer S, Caro I, et al. Efficacy and safety observed during 24 weeks of efalizumab therapy in patients with moderate to severe plaque psoriasis. Arch Dermatol 2005;141:31-8. |
|49.||Gottlieb AB, Gordon KB, Lebwohl MG, Caro I, Walicke PA, Li N, et al. Efalizumab Study Group. Extended efalizumab therapy sustains efficacy without increasing toxicity in patients with moderate to severe chronic plaque psoriasis. J Drugs Dermatol 2004;3:614-24. |
|50.||Papp KA, Bressinck R, Fretzin S, Goffe B, Kempers S, Gordon KB, et al. Efalizumab Study Group. Safety of efalizumab in adults with chronic moderate to severe plaque psoriasis: A phase IIIb, randomized, controlled trial. Int J Dermatol 2006;45:605-14. |
|51.||Ortonne JP, Shear N, Shumack S, Henninger E; CLEAR Multinational Study Group. Impact of efalizumab on patient-reported outcomes in high-need psoriasis patients: Results of the international, randomized, placebo-controlled Phase III clinical experience acquired with raptiva (CLEAR) trial [NCT00256139]. BMC Dermatol 2005;5:13. |
|52.||Pugashetti R, Koo J. Efalizumab discontinuation: A practical strategy. J Dermatolog Treat 2009;20:132-6. |
|53.||Reff ME, Carner K, Chambers KS, Chinn PC, Leonard JE, Raab R, et al. Depletion of B cells in vivo by a chimeric mouse human monoclonal antibody to CD20. Blood 1994;83:435-45. |
|54.||Stashenko P, Nadler LM, Hardy R, Schlossman SF. Characterization of a human B lymphocyte-specific antigen. J Immunol 1980;125:1678-85. |
|55.||Maloney DG, Grillo-López AJ, White CA, Bodkin D, Schilder RJ, Neidhart JA, et al. IDEC-C2B8 (Rituximab) anti-CD20 monoclonal antibody therapy in patients with relapsed low-grade non-Hodgkin's lymphoma. Blood 1997;90:2188-95. |
|56.||Maloney DG, Liles TM, Czerwinski DK, Waldichuk C, Rosenberg J, Grillo-Lopez A, et al. Phase I clinical trial using escalating single-dose infusion of chimeric anti-CD20 monoclonal antibody (IDEC-C2B8) in patients with recurrent B-cell lymphoma. Blood 1994;84:2457-66. |
|57.||Rituximab. Available from: http://www.drugbank.ca/drugs/DB00073. [Last accessed on 2013 Jul 23]. |
|58.||Johnson PW, Glennie MJ. Rituximab: Mechanisms and applications. Br J Cancer 2001;85:1619-23. |
|59.||Olszewski AJ, Grossbard ML. Empowering targeted therapy: Lessons from rituximab. Sci STKE 2004;2004:pe30. |
|60.||Cartron G, Watier H, Golay J, Solal-Celigny P. From the bench to the bedside: Ways to improve rituximab efficacy. Blood 2004;104:2635-42. |
|61.||Grillo-López AJ. Rituximab: An insider's historical perspective. Semin Oncol 2000l; 27 6 Suppl 12:9-16. |
|62.||Jolles S. High-dose intravenous immunoglobulin (hdIVIg) in the treatment of autoimmune blistering disorders. Clin Exp Immunol 2002;129:385-9. |
|63.||IVIG. Available from: http://www.drugbank.ca/drugs/DB00028. [Last accessed on 2013 Jul 23]. |
|64.||Roifman CM, Schroeder H, Berger M, Sorensen R, Ballow M, Buckley RH, et al. Comparison of the efficacy of IGIV-C, 10% (caprylate/chromatography) and IGIV-SD, 10% as replacement therapy in primary immune deficiency: A randomized double-blind trial. Int Immunopharmacol 2003;3:1325-33. |
|65.||Yap PL. The viral safety of intravenous immune globulin. Clin Exp Immunol 1996;104:35-42. |
|66.||Dalakas MC. The use of intravenous immunoglobulin in the treatment of autoimmune neuromuscular diseases: Evidence-based indications and safety profile. Pharmacol Ther 2004;102:177-93. |
|67.||Rossi F, Kazatchkine MD. Antiidiotypes against autoantibodies in pooled normal human polyspecifinc Ig. J Immunol 1989;143:4104-9. |
|68.||Dwyer JM. Manipulating the immune system with immune globulin. N Engl J Med 1992;326:107-16. |
|69.||Yu Z, Lennon VA. Mechanism of intravenous immune globulin therapy in antibody-mediated autoimmune diseases. N Engl J Med 1999;340:227-8. |
|70.||Masson PL. Elimination of infectious antigens and increase of IgG catabolism as possible modes of action of IVIg. J Autoimmun 1993;6:683-9. |
|71.||Abe Y, Horiuchi A, Miyake M, Kimura S. Anti-cytokine nature of natural human immunoglobulin: One possible mechanism of the clinical effect of intravenous immunoglobulin therapy. Immunol Rev 1994;139:5-19. |
|72.||Hurez V, Kaveri SV, Mouhoub A, Dietrich G, Mani JC, Klatzmann D, et al. Anti-CD4 activity of normal human immunoglobulin G for therapeutic use (Intravenous Immunoglobulin, IVIg). Ther Immunol 1994;1:269-77. |
|73.||Toyoda M, Zhang XM, Petrosian A, Wachs K, Moudgil A, Jordan SC. Inhibition of allospecific responses in the mixed lymphocyte reaction by pooled human gamma-globulin. Transpl Immunol 1994;2:337-41. |
|74.||Basta M, Fries LF, Frank MM. High doses of intravenous immunoglobulin do not affect the recognition phase of the classical complement pathway. Blood 1991;78:700-2. |
|75.||Toyoda M, Zhang X, Petrosian A, Galera OA, Wang SJ, Jordan SC. Modulation of immunoglobulin production and cytokine mRNA expression in peripheral blood mononuclear cells by intravenous immunoglobulin. J Clin Immunol 1994;14:178-89. |
|76.||Abe Y, Horiuchi A, Miyake M, Kimura S. Anti-cytokine nature of natural human immunoglobulin: One possible mechanism of the clinical effect of intravenous immunoglobulin therapy. Immunol Rev 1994;139:5-19. |
|77.||Andersson UG, Björk L, Skansén-Saphir U, Andersson JP. Down-regulation of cytokine production and interleukin-2 receptor expression by pooled human IgG. Immunology 1993;79:211-6. |
|78.||Amran D, Renz H, Lack G, Bradley K, Gelfand EW. Suppression of cytokine-dependent human T-cell proliferation by intravenous immunoglobulin. Clin Immunol Immunopathol 1994;73:180-6. |
|79.||Ross C, Svenson M, Hansen MB, Vejlsgaard GL, Bendtzen K. High avidity IFN-neutralizing antibodies in pharmacutically prepared IgG. J Clin Invest 1995;95:1974-8. |
|80.||Bayry J, Lacroix-Desmazes S, Carbonneil C, Misra N, Donkova V, Pashov A, et al. Inhibition of maturation and function of dendritic cells by intravenous immunoglobulin. Blood 2003;101:758-65. |
|81.||Oravec S, Ronda N, Carayon A, Milliez J, Kazatchkine MD, Hornych A. Normal human polyspecific immunoglobulin G (intravenous immunoglobulin) modulates endothelial cell function in vitro. Nephrol Dial Transplant 1995;10:796-800. |
|82.||Smith DI, Swamy PM, Heffernan MP. Off-label uses of biologics in dermatology: Interferon and intravenous immunoglobulin (part 1 of 2). J Am Acad Dermatol 2007;56:e1-54. |
|83.||Kouklakis G, Moschos J, Leontiadis GI, Kadis S, Mpoumponaris A, Molyvas E, et al. Infliximab for treatment of pyoderma gangrenosum associated with clinically inactive Crohn's disease. A case report. Rom J Gastroenterol 2005;14:401-3. |
|84.||Kaur MR, Lewis HM. Severe recalcitrant pyoderma gangrenosum treated with infliximab. Br J Dermatol 2005;153:689-91. |
|85.||Brooklyn TN, Dunnill MG, Shetty A, Bowden JJ, Williams JD, Griffiths CE, et al. Infliximab for the treatment of pyoderma gangrenosum: A randomised, double blind, placebo controlled trial. Gut 2006;55:505-9. |
|86.||Regueiro M, Valentine J, Plevy S, Fleisher MR, Lichtenstein GR. Infliximab for treatment of pyoderma gangrenosum associated with inflammatory bowel disease. Am J Gastroenterol 2003;98:1821-6. |
|87.||Hinterberger L, Müller CS, Vogt T, Pföhler C. Adalimumab: A treatment option for pyoderma gangrenosum after failure of systemic standard therapies. Dermatol Ther (Heidelb) 2012;2:6. |
|88.||Cariñanos I, Acosta MB, Domènech E. Adalimumab for pyoderma gangrenosum associated with inflammatory bowel disease. Inflamm Bowel Dis 2011;17:E153-4. |
|89.||Reddick CL, Singh MN, Chalmers RJ. Successful treatment of superficial pyoderma gangrenosum associated with hidradenitis suppurativa with adalimumab. Dermatol Online J 2010;16:15. |
|90.||Hubbard VG, Friedmann AC, Goldsmith P. Systemic pyoderma gangrenosum responding to infliximab and adalimumab. Br J Dermatol2005;152:1059-61. |
|91.||McGowan JW 4 th , Johnson CA, Lynn A. Treatment of pyoderma gangrenosum with etanercept. J Drugs Dermatol 2004;3:441-4. |
|92.||Pastor N, Betlloch I, Pascual JC, Blanes M, Bañuls J, Silvestre JF. Pyoderma gangrenosum treated with anti-TNF alpha therapy (etanercept). Clin Exp Dermatol 2006;31:152-3. |
|93.||Roy DB, Conte ET, Cohen DJ. The treatment of pyoderma gangrenosum using etanercept. J Am Acad Dermatol 2006;54 3 Suppl 2:S128-34. |
|94.||Disla E, Quayum B, Cuppari GG, Pancorbo R. Successful use of etanercept in a patient with pyoderma gangrenosum complicating rheumatoid arthritis. J Clin Rheumatol 2004;10:50-2. |
|95.||Howell SM, Bessinger GT, Altman CE, Belnap C. Rapid response of IgA pemphigus of the subcorneal pustular dermatosis subtype to treatment with adalimumab and mycophenolate mofetil. J Am Acad Dermatol 2005;53:541-3. |
|96.||Voigtländer C, Lüftl M, Schuler G, Hertl M. Infliximab (anti-tumor necrosis factor alpha antibody): A novel, highly effective treatment of recalcitrant subcorneal pustular dermatosis (Sneddon-Wilkinson disease). Arch Dermatol 2001;137:1571-4. |
|97.||Naretto C, Baldovino S, Rossi E, Spriano M, Roccatello D. The case of SLE associated Sneddon-Wilkinson pustular disease successfully and safely treated with infliximab. Lupus 2009;18:856-7. |
|98.||Bonifati C, Trento E, Cordiali Fei P, Muscardin L, Amantea A, Carducci M. Early but not lasting improvement of recalcitrant subcorneal pustular dermatosis (Sneddon-Wilkinson disease) after infliximab therapy: Relationships with variations in cytokine levels in suction blister fluids. Clin Exp Dermatol 2005;30:662-5. |
|99.||Berk DR, Hurt MA, Mann C, Sheinbein D. Sneddon-Wilkinson disease treated with etanercept: Report of two cases. Clin Exp Dermatol 2009;34:347-51. |
|100.||Iobst W, Ingraham K. Sneddon-Wilkinson disease in a patient with rheumatoid arthritis. Arthritis Rheum 2005;52:3771. |
|101.||Jacobi A, Shuler G, Hertl M. Rapid control of therapy-refractory pemphigus vulgaris by treatment with the tumour necrosis factor-alpha inhibitor infliximab. Br J Dermatol 2005;153:448-9. |
|102.||Pardo J, Mercader P, Mahiques L, Sanchez-Carazo JL, Oliver V, Fortea JM. Infliximab in the management of severe pemphigus vulgaris. Br J Dermatol 2005;153:222-3. |
|103.||García-Rabasco A, Alsina-Gibert M, Pau-Charles I, Iranzo P. Infliximab therapy failure in two patients with pemphigus vulgaris. J Am Acad Dermatol 2012;67:e196-7. |
|104.||Vojáèková N, Fialová J, Vaòousová D, Hercogová J. Pemphigus vulgaris treated with adalimumab: Case study. Dermatol Ther 2012;25:95-7. |
|105.||Shetty A, Marcum CB, Glass LF, Carter JD. Successful treatment of pemphigus vulgaris with etanercept in four patients. J Drugs Dermatol 2009;8:940-3. |
|106.||Gubinelli E, Bergamo F, Didona B, Annessi G, Atzori F, Raskovic D. Pemphigus foliaceus treated with etanercept. J Am Acad Dermatol 2006;55:1107-8. |
|107.||Lin MH, Hsu CK, Lee JY. Successful treatment of recalcitrant pemphigus vulgaris and pemphigus vegetans with etanercept and carbon dioxide laser. Arch Dermatol 2005;141:680-2. |
|108.||Daulat S, Detweiler JG, Pandya AG. Development of pemphigus vulgaris in a patient with psoriasis treated with etanercept. J Eur Acad Dermatol Venereol 2009;23:483-4. |
|109.||Yamauchi PS, Lowe NJ, Gindi V. Treatment of coexisting bullous pemphigoid and psoriasis with the tumor necrosis factor antagonist etanercept. J Am Acad Dermatol 2006;54 3 Suppl 2:S121-2. |
|110.||Sacher C, Rubbert A, König C, Scharffetter-Kochanek K, Krieg T, Hunzelmann N. Treatment of recalcitrant cicatricial pemphigoid with the tumor necrosis factor alpha antagonist etanercept. J Am Acad Dermatol 2002;46:113-5. |
|111.||Canizares MJ, Smith DI, Conners MS, Maverick KJ, Heffernan MP. Successful treatment of mucous membrane pemphigoid with etanercept in 3 patients. Arch Dermatol 2006;142:1457-61. |
|112.||Boussemart L, Jacobelli S, Batteux F, Goulvestre C, Grange P, Carlotti A, et al. Autoimmune bullous skin diseases occurring under anti-tumor necrosis factor therapy: Two case reports. Dermatology 2010;221:201-5. |
|113.||Shuja F, Chan CS, Rosen T. Biologic drugs for the treatment of hidradenitis suppurativa: An evidence-based review. Dermatol Clin 2010;28:511-21. |
|114.||Adams DR, Gordon KB, Devenyi AG, Ioffreda MD. Severe hidradenitis suppurativa treated with infliximab infusion. Arch Dermatol 2003;139:1540-2. |
|115.||Goertz RS, Konturek PC, Naegel A, Janka R, Amann K, Maennlein G, et al. Experiences with a long-term treatment of a massive gluteal acne inversa with infliximab in Crohn's disease. Med Sci Monit 2009;15:CS14-8. |
|116.||Katsanos KH, Christodoulou DK, Tsianos EV. Axillary hidradenitis suppurativa successfully treated with infliximab in a Crohn's disease patient. Am J Gastroenterol 2002;97:2155-6. |
|117.||Lebwohl B, Sapadin AN. Infliximab for the treatment of hidradenitis suppurativa. J Am Acad Dermatol 2003;49 Suppl 5:S275-6. |
|118.||Martínez F, Nos P, Benlloch S, Ponce J. Hidradenitis suppurativa and Crohn's disease: Response to treatment with infliximab. Inflamm Bowel Dis 2001;7:323-6. |
|119.||Moschella SL. Is there a role for infliximab in the current therapy of hidradenitis suppurativa? A report of three treated cases. Int J Dermatol 2007;46:1287-91. |
|120.||Antonucci A, Negosanti M, Negosanti L, Iozzo I, Varotti C. Acne inversa treated with infliximab: Different outcomes in 2 patients. Acta Derm Venereol 2008;88:274-5. |
|121.||Sullivan TP, Welsh E, Kerdel FA, Burdick AE, Kirsner RS. Infliximab for hidradenitis suppurativa. Br J Dermatol 2003;149:1046-9. |
|122.||Miller I, Lynggaard CD, Lophaven S, Zachariae C, Dufour DN, Jemec GB. A double-blind placebo-controlled randomized trial of adalimumab in the treatment of hidradenitis suppurativa. Br J Dermatol 2011;165:391-8. |
|123.||Kimball AB, Kerdel F, Adams D, Mrowietz U, Gelfand JM, Gniadecki R, et al. Adalimumab for the treatment of moderate to severe Hidradenitis suppurativa: A parallel randomized trial. Ann Intern Med 2012;157:846-55. |
|124.||Giamarellos-Bourboulis EJ, Pelekanou E, Antonopoulou A, Petropoulou H, Baziaka F, Karagianni V, et al. An open-label phase II study of the safety and efficacy of etanercept for the therapy of hidradenitis suppurativa. Br J Dermatol 2008;158:567-72. |
|125.||Adams DR, Yankura JA, Fogelberg AC, Anderson BE. Treatment of hidradenitis suppurativa with etanercept injection. Arch Dermatol 2010;146:501-4. |
|126.||Lee RA, Dommasch E, Treat J, Sciacca-Kirby J, Chachkin S, Williams J, et al. A prospective clinical trial of open-label etanercept for the treatment of hidradenitis suppurativa. J Am Acad Dermatol 2009;60:565-73. |
|127.||Strober BE, Kim C, Siu K. Efalizumab for the treatment of refractory hidradenitis suppurativa. J Am Acad Dermatol 2007;57:1090-1. |
|128.||Koca SS, Isik A, Ozercan IH, Ustundag B, Evren B, Metin K. Effectiveness of etanercept in bleomycin-induced experimental scleroderma. Rheumatology (Oxford) 2008;47:172-5. |
|129.||Ellman MH, MacDonald PA, Hayes FA. Etanercept as treatment for diffuse scleroderma: A pilot study. Arthritis Rheum 2000;43 Suppl:S392. |
|130.||Lam GK, Hummers LK, Woods A, Wigley FM. Efficacy and safety of etanercept in the treatment of scleroderma-associated joint disease. J Rheumatol 2007;34:1636-7. |
|131.||Stewart FA, Gavino AC, Elewski BE. New side effect of TNF-alpha inhibitors: Morphea. Skinmed 2013;11:59-60. |
|132.||Chimenti MS, Teoli M, Di Stefani A, Giunta A, Esposito M, Perricone R. Resolution with rituximab of localized scleroderma occurring during etanercept treatment in a patient with rheumatoid arthritis. Eur J Dermatol 2013;23:273-4. |
|133.||Denton CP, Engelhart M, Tvede N, Wilson H, Khan K, Shiwen X, et al. An open-label pilot study of infliximab therapy in diffuse cutaneous systemic sclerosis. Ann Rheum Dis 2009;68:1433-9. |
|134.||Bargagli E, Galeazzi M, Bellisai F, Volterrani L, Rottoli P. Infliximab treatment in a patient with systemic sclerosis associated with lung fibrosis and pulmonary hypertension. Respiration 2008;75:346-9. |
|135.||Marie I, Lahaxe L, Levesque H, Heliot P. Pulmonary actinomycosis in a patient with diffuse systemic sclerosis treated with infliximab. QJM 2008;101:419-21. |
|136.||Menon Y, Cucurull E, Espinoza LR. Pancytopenia in a patient with scleroderma treated with infliximab. Rheumatology (Oxford) 2003;42:1273-4. |
|137.||Ranganathan P. Infliximab-induced scleredema in a patient with rheumatoid arthritis. J Clin Rheumatol 2005;11:319-22. |
|138.||Riley P, McCann LJ, Maillard SM, Woo P, Murray KJ, Pilkington CA. Effectiveness of infliximab in the treatment of refractory juvenile dermatomyositis with calcinosis. Rheumatology (Oxford) 2008;47:877-80. |
|139.||Dold S, Justiniano ME, Marquez J, Espinoza LR. Treatment of early and refractory dermatomyositis with infliximab: A report of two cases. Clin Rheumatol 2007;26:1186-8. |
|140.||Efthimiou P, Schwartzman S, Kagen LJ. Possible role for tumour necrosis factor inhibitors in the treatment of resistant dermatomyositis and polymyositis: A retrospective study of eight patients. Ann Rheum Dis 2006;65:1233-6. |
|141.||Hengstman GJ, De Bleecker JL, Feist E, Feist E, Vissing J, Denton CP, et al. Open-label trial of anti-TNF-alpha in dermato- and polymyositis treated concomitantly with methotrexate. Eur Neurol 2008;59:159-63. |
|142.||Dastmalchi M, Grundtman C, Alexanderson H, Mavragani CP, Einarsdottir H, Helmers SB, et al. A high incidence of disease flares in an open pilot study of infliximab in patients with refractory inflammatory myopathies. Ann Rheum Dis 2008;67:1670-7. |
|143.||Roddy E, Courtney PA, Morris A. Non-Hodgkin's lymphoma in a patient with refractory dermatomyositis which had been treated with infliximab. Rheumatology (Oxford) 2002;41:1194-5. |
|144.||Huber A, Gaffal E, Bieber T, Tüting T, Wenzel J. Treatment of recalcitrant dermatomyositis with efalizumab. Acta Derm Venereol 2006;86:254-5. |
|145.||Mazza J, Rossi A, Weinberg JM. Innovative uses of tumor necrosis factor alpha inhibitors. Dermatol Clin 2010;28:559-75. |
|146.||Aringer M, Graninger WB, Steiner G, Smolen JS. Safety and efficacy of tumor necrosis factor alpha blockade in systemic lupus erythematosus: An open-label study. Arthritis Rheum 2004;50:3161-9. |
|147.||Aringer M, Houssiau F, Gordon C, Graninger WB, Voll RE, Rath E, et al. Adverse events and efficacy of TNF-alpha blockade with infliximab in patients with systemic lupus erythematosus: Long-term follow-up of 13 patients. Rheumatology (Oxford) 2009;48:1451-4. |
|148.||Fautrel B, Foltz V, Frances C, Bourgeois P, Rozenberg S. Regression of subacute cutaneous lupus erythematosus in a patient with rheumatoid arthritis treated with a biologic tumor necrosis factor alpha-blocking agent: Comment on the article by Pisetsky and the letter from Aringer et al. Arthritis Rheum 2002;46:1408-9. |
|149.||Norman R, Greenberg RG, Jackson JM. Case reports of etanercept in inflammatory dermatoses. J Am Acad Dermatol 2006;54 3 Suppl 2:S139-42. |
|150.||Ambrose NL, Tobin AM, Howard D. Etanercept treatment in Sweet's syndrome with inflammatory arthritis. J Rheumatol 2009;36:1348-9. |
|151.||Yamauchi PS, Turner L, Lowe NJ, Gindi V, Jackson JM. Treatment of recurrent Sweet's syndrome with coexisting rheumatoid arthritis with the tumor necrosis factor antagonist etanercept. J Am Acad Dermatol 2006;54 3 Suppl 2:S122-6. |
|152.||Foster EN, Nguyen KK, Sheikh RA, Prindiville TP. Crohn's disease associated with Sweet's syndrome and Sjögren's syndrome treated with infliximab. Clin Dev Immunol 2005;12:145-9. |
|153.||Matzkies FG, Manger B, Schmitt-Haendle M, Nagel T, Kraetsch HG, Kalden JR, et al. Severe septicaemia in a patient with polychondritis and Sweet's syndrome after initiation of treatment with infliximab. Ann Rheum Dis 2003;62:81-2. |
|154.||Vanbiervliet G, Anty R, Schneider S, Arab K, Rampal P, Hebuterne X. Sweet's syndrome and erythema nodosum associated with Crohn's disease treated by infliximab. Gastroenterol Clin Biol 2002;26:295-7. |
|155.||Karamlou K, Gorn AH. Refractory sweet syndrome with autoimmune organizing pneumonia treated with monoclonal antibodies to tumor necrosis factor. J Clin Rheumatol 2004;10:331-5. |
|156.||Field S, Regan AO, Sheahan K, Collins P. Recalcitrant cutaneous sarcoidosis responding to adalimumab but not to etanercept. Clin Exp Dermatol 2010;35:795-6. |
|157.||Khanna D, Liebling MR, Louie JS. Etanercept ameliorates sarcoidosis arthritis and skin disease. J Rheumatol 2003;30:1864-7. |
|158.||Baughman RP, Lower EE. Infliximab for refractory sarcoidosis. Sarcoidosis Vasc Diffuse Lung Dis 2001;18:70-4. |
|159.||Mallbris L, Ljungberg A, Hedblad MA, Larsson P, Ståhle-Bäckdahl M. Progressive cutaneous sarcoidosis responding to anti-tumor necrosis factor-alpha therapy. J Am Acad Dermatol 2003;48:290-3. |
|160.||Roberts SD, Wilkes DS, Burgett RA, Knox KS. Refractory sarcoidosis responding to infliximab. Chest 2003;124:2028-31. |
|161.||Haley H, Cantrell W, Smith K. Infliximab therapy for sarcoidosis (lupus pernio). Br J Dermatol 2004;150:146-9. |
|162.||Heffernan MP, Anadkat MJ. Recalcitrant cutaneous sarcoidosis responding to Infliximab. Arch Dermatol 2005;141:910-1. |
|163.||Rosen T, Doherty C. Successful long-term management of refractory cutaneous and upper airway sarcoidosis with periodic infliximabinfusion. Dermatol Online J 2007;13:14. |
|164.||Cathcart S, Sami N, Elewski B. Sarcoidosis as an adverse effect of tumor necrosis factor inhibitors. J Drugs Dermatol 2012;11:609-12. |
|165.||Murdaca G, Colombo BM, Barabino G, Caiti M, Cagnati P, Puppo F. Anti-tumor necrosis factor-α treatment with infliximab for disseminated granuloma annulare. Am J Clin Dermatol 2010;11:437-9. |
|166.||Hertl MS, Haendle I, Schuler G, Hertl M. Rapid improvement of recalcitrant disseminated granuloma annulare upon treatment with the tumour necrosis factor-alpha inhibitor, infliximab. Br J Dermatol 2005;152:552-5. |
|167.||Goffe BS. Disseminated granuloma annulare resolved with the T-cell modulator efalizumab. Arch Dermatol 2004;140:1287-8. |
|168.||Voulgari PV, Markatseli TE, Exarchou SA, Zioga A, Drosos AA. Granuloma annulare induced by anti-tumour necrosis factor therapy. Ann Rheum Dis 2008;67:567-70. |
|169.||Patmanidis K, Sidiras A, Dolianitis K, Simelidis D, Solomonidis C, Gaitanis G, et al. Combination of infliximab and high-dose intravenous immunoglobulin for toxic epidermal necrolysis: Successful treatment of an elderly patient. Case Rep Dermatol Med 2012;2012:915314. |
|170.||Scott-Lang V, Tidman M, McKay D. Toxic epidermal necrolysis in a child successfully treated with infliximab. Pediatr Dermatol 2012. [Epub ahead of print]. |
|171.||Gaitanis G, Spyridonos P, Patmanidis K, Koulouras V, Nakos G, Tzaphlidou M, et al. Treatment of toxic epidermal necrolysis with the combination of infliximab and high-dose intravenous immunoglobulin. Dermatology 2012;224:134-9. |
|172.||Wojtkiewicz A, Wysocki M, Fortuna J, Chrupek M, Matczuk M, Koltan A. Beneficial and rapid effect of infliximab on the course of toxic epidermal necrolysis. Acta Derm Venereol 2008;88:420-1. |
|173.||Gubinelli E, Canzona F, Tonanzi T, Raskovic D, Didona B. Toxic epidermal necrolysis successfully treated with etanercept. J Dermatol 2009;36:150-3. |
|174.||Famularo G, Di Dona B, Canzona F, Girardelli CR, Cruciani G. Etanercept for toxic epidermal necrolysis. Ann Pharmacother 2007;41:1083-4. |
|175.||Dessinioti C, Vergou T, Moustou E, Katsambas A, Antoniou C. Long-term infliximab treatment for refractory type III juvenile pityriasis rubra pilaris. Eur J Dermatol 2011;21:599-600. |
|176.||Garcovich S, Di Giampetruzzi AR, Antonelli G, Garcovich A, Didona B. Treatment of refractory adult-onset pityriasis rubra pilaris with TNF-alpha antagonists: A case series. J Eur Acad Dermatol Venereol 2010;24:881-4. |
|177.||Müller H, Gattringer C, Zelger B, Höpfl R, Eisendle K. Infliximab monotherapy as first-line treatment for adult-onset pityriasis rubra pilaris: Case report and review of the literature on biologic therapy. J Am Acad Dermatol 2008;59 Suppl 5:S65-70. |
|178.||Petrof G, Almaani N, Archer CB, Griffiths WA, Smith CH. A systematic review of the literature on the treatment of pityriasis rubra pilaris type 1 with TNF-antagonists. J Eur Acad Dermatol Venereol 2013;27:e131-5. |
|179.||Sfikakis PP, Markomichelakis N, Alpsoy E, Assaad-Khalil S, Bodaghi B, Gul A, et al. Anti-TNF therapy in the management of Behcet's disease: Review and basis for recommendations. Rheumatology (Oxford) 2007;46:736-41. |
|180.||Melikoglu M, Fresko I, Mat C, Ozyazgan Y, Gogus F, Yurdakul S, et al. Short-term trial of etanercept in Behçet's disease: A double blind, placebo controlled study. J Rheumatol 2005;32:98-105. |
|181.||Gulli S, Arrigo C, Bocchino L, Morgante L, Sangari D, Castagna I, et al. Remission of Behcet's disease with anti-tumour necrosis factor monoclonal antibody therapy: A case report. BMC Musculoskelet Disord 2003;4:19. |
|182.||Goossens PH, Verburg RJ, Breedveld FC. Remission of Behçet's syndrome with tumour necrosis factor alpha blocking therapy. Ann Rheum Dis 2001;60:637. |
|183.||Robertson LP, Hickling P. Treatment of recalcitrant orogenital ulceration of Behçet's syndrome with infliximab. Rheumatology (Oxford) 2001;40:473-4. |
|184.||Estrach C, Mpofu S, Moots RJ. Behcet's syndrome: Response to infliximab after failure of etanercept. Rheumatology 2002;41:1213-4. |
|185.||Rozenbaum M, Rosner I, Portnoy E. Remission of Behcet's syndrome with TNFalpha blocking treatment. Ann Rheum Dis 2002;61:283-4. |
|186.||Katsiari CG, Theodossiadis PG, Kaklamanis PG, Markomichelakis NN, Sfikakis PP. Successful long-term treatment of refractory Adamantiades-Behcet's disease (ABD) with Infliximab: Report of two patients. Adv Exp Med Biol 2003;528:551-5. |
|187.||Haugeberg G, Velken M, Johnsen V. Successful treatment of genital ulcers with infliximab in Behcet's disease. Ann Rheum Dis 2004;63:744-5. |
|188.||Connolly M, Armstrong JS, Buckley DA. Infliximab treatment for severe orogenital ulceration in Behçet's disease. Br J Dermatol 2005;153:1073-5. |
|189.||Sommer A, Altmeyer P, Kreuter A. A case of mucocutaneous Behçet's disease responding to etanercept. J Am Acad Dermatol 2005;52:717-9. |
|190.||Handa T, Tsunekawa H, Yoneda M, Watanabe D, Mukai T, Yamamura M, et al. Long-term remission of ocular and extraocular manifestations in Behçet's disease using infliximab. Clin Exp Rheumatol 2011;29 4 Suppl 67:S58-63. |
|191.||Adler S, Baumgartner I, Villiger PM. Behçet's disease: Successful treatment with infliximab in 7 patients with severe vascular manifestations. A retrospective analysis. Arthritis Care Res (Hoboken) 2012;64:607-11. |
|192.||Borhani Haghighi A, Safari A, Nazarinia MA, Habibagahi Z, Shenavandeh S. Infliximab for patients with neuro- Behçet's disease: Case series and literature review. Clin Rheumatol 2011;30:1007-12. |
|193.||Naganuma M, Sakuraba A, Hisamatsu T, Ochiai H, Hasegawa H, Ogata H, et al. Efficacy of infliximab for induction and maintenance of remission in intestinal Behçet's disease. Inflamm Bowel Dis 2008;14:1259-64. |
|194.||Melikoglu M, Fresko I, Mat C, Ozyazgan Y, Gogus F, Yurdakul S, et al. Short-term trial of etanercept in Behçet's disease: A double blind, placebo controlled study. J Rheumatol 2005;32:98-105. |
|195.||Sommer A, Altmeyer P, Kreuter A. A case of mucocutaneous Behçet's disease responding to etanercept. J Am Acad Dermatol 2005;52:717-9. |
|196.||Atzeni F, Sarzi-Puttini P, Capsoni F, Mecchia M, Marrazza MG, Carrabba M. Successful treatment of resistant Behçet's disease with etanercept. Clin Exp Rheumatol 2005;23:729. |
|197.||Scheinberg MA. Treatment of recurrent oral aphthous ulcers with etanercept. Clin Exp Rheumatol 2002;20:733-4. |
|198.||Estrach C, Mpofu S, Moots RJ. Behçet's syndrome: Response to infliximab after failure of etanercept. Rheumatology (Oxford) 2002;41:1213-4. |
|199.||Saurenmann RK, Levin AV, Rose JB, Parker S, Rabinovitch T, Tyrrell PN, et al. Tumour necrosis factor alpha inhibitors in the treatment of childhood uveitis. Rheumatology (Oxford) 2006;45:982-9. |
|200.||Perra D, Alba MA, Callejas JL, Mesquida M, Ríos-Fernández R, Adán A, et al. Adalimumab for the treatment of Behçet's disease: Experience in 19 patients. Rheumatology (Oxford) 2012;51:1825-31. |
|201.||Calvo Catalá J, Campos Fernández C, Rueda Cid A, González-Cruz Cervellera MI, Baixauli Rubio A, Pastor Cubillo MD. Efficacy of adalimumab in Behçet's disease. Description of 6 cases. Reumatol Clin 2011;7:258-61. |
|202.||Olivieri I, Leccese P, D'Angelo S, Padula A, Nigro A, Palazzi C, et al. Efficacy of adalimumab in patients with Behçet's disease unsuccessfully treated with infliximab. Clin Exp Rheumatol 2011;29 4 Suppl 67:S54-7. |
|203.||Iqbal M, Kolodney MS. Acne fulminans with synovitis- acne-pustulosis-hyperostosis-osteitis (SAPHO) syndrome treated with infliximab. J Am Acad Dermatol 2005;525 Suppl 1:S118-20. |
|204.||Olivieri I, Padula A, Ciancio G, Salvarani C, Niccoli L, Cantini F. Successful treatment of SAPHO syndrome with infliximab: Report of two cases. Ann Rheum Dis 2002;61:375-6. |
|205.||Massara A, Cavazzini PL, Trotta F. In SAPHO syndrome anti-TNF-alpha therapy may induce persistent amelioration of osteoarticular complaints, but may exacerbate cutaneous manifestations. Rheumatology (Oxford) 2006;45:730-3. |
|206.||Hu SW, Bevona C, Winterfield L, Qureshi AA, Li VW. Treatment of refractory ulcerative necrobiosis lipoidica diabeticorum with infliximab: Report of a case. Arch Dermatol 2009;145:437-9. |
|207.||Suárez-Amor O, Pérez-Bustillo A, Ruiz-González I, Rodríguez-Prieto MA. Necrobiosis lipoidica therapy with biologicals: An ulcerated case responding to etanercept and a review of the literature. Dermatology 2010;221:117-21. |
|208.||Conte H, Milpied B, Kaloga M, Lalanne N, Belin E, Jouary T, et al. Treatment of pre-ulcerative necrobiosis lipoidica with infliximab. Acta Derm Venereol 2011;91:587-8. |
|209.||Kolde G, Muche JM, Schulze P, Fischer P, Lichey J. Infliximab: A promising new treatment option for ulcerated necrobiosis lipoidica. Dermatology 2003;206:180-1. |
|210.||Barde C, Laffitte E, Campanelli A, Saurat JH, Thielen AM. Intralesional infliximab in noninfectious cutaneous granulomas: Three cases of necrobiosis lipoidica. Dermatology 2011;222:212-6. |
|211.||Shannon SE, Schumacher HR, Self S, Brown AN. Multicentric reticulohistiocytosis responding to tumor necrosis factor-alpha inhibition in a renal transplant patient. J Rheumatol 2005;32:565-7. |
|212.||Jacobi A, Antoni C, Manger B, Schuler G, Hertl M. Infliximab in the treatment of moderate to severe atopic dermatitis. J Am Acad Dermatol. 2005;52:522-6. |
|213.||Weinberg JM, Siegfried EC. Successful treatment of severe atopic dermatitis in a child and an adult with the T-cell modulator efalizumab. Arch Dermatol 2006;142:555-8. |
|214.||Minni J, Sarro R. A novel therapeutic approach to erythema annulare centrifugum. J Am Acad Dermatol 2006;54 3 Suppl 2:S134-5. |
|215.||Uthman IW, Touma Z, Sayyad J, Salman S. Response of deep cutaneous vasculitis to infliximab. J Am Acad Dermatol 2005;53:353-4. |
|216.||Cheng A, Mann C. Oral erosive lichen planus treated with efalizumab. Arch Dermatol 2006;142:680-2. |
|217.||Heffernan MP, Hurley MY, Martin KS, Smith DI, Anadkat MJ. Alefacept for alopecia areata. Arch Dermatol 2005;141:1513-6. |
|218.||Sheinkopf LE, Rafi AW, Do LT, Katz RM, Klaustermeyer WB. Efficacy of omalizumab in the treatment of atopic dermatitis: A pilot study. Allergy Asthma Proc 2008;29:530-7. |
|219.||Fernández-Antón Martínez MC, Leis-Dosil V, Alfageme-Roldán F, Paravisini A, Sánchez-Ramón S, Suárez Fernández R. Omalizumab for the treatment of atopic dermatitis. Actas Dermosifiliogr 2012;103:624-8. |
|220.||Lane JE, Cheyney JM, Lane TN, Kent DE, Cohen DJ. Treatment of recalcitrant atopic dermatitis with omalizumab. J Am Acad Dermatol 2006;54:68-72. |
|221.||Armengot-Carbo M, Velasco-Pastor M, Rodrigo-Nicolas B, Pont-Sanjuan V, Quecedo-Estebanez E, Gimeno-Carpio E. Omalizumab in chronic urticaria: A retrospective series of 15 cases. Dermatol Ther 2013;26:257-9. |
|222.||Mankad VS, Burks AW. Omalizumab: Other indications and unanswered questions. Clin Rev Allergy Immunol 2005;29:17-30. |
|223.||Emer JJ, Claire W. Rituximab: A review of dermatological applications. J Clin Aesthet Dermatol 2009;2:29-37. |
|224.||Zakka LR, Shetty SS, Ahmed AR. Rituximab in the treatment of pemphigus vulgaris. Dermatol Ther (Heidelb) 2012;2:17. |
|225.||Kitajima Y. Current and prospective understanding of clinical classification, pathomechanisms and treatment in pemphigus. Arch Dermatol Res 2003;295 Suppl 1:S17-23 |
|226.||Shetty S, Ahmed AR. Treatment of bullous pemphigoid with rituximab: Critical analysis of the current literature. J Drugs Dermatol 2013;12:672-7. |
|227.||Heizmann M, Itin P, Wernli M, Borradori L, Bargetzi MJ. Successful treatment of paraneoplastic pemphigus in follicular NHL with rituximab: Report of a case and review of treatment for paraneoplastic pemphigus in NHL and CLL. Am J Hematol 2001;66:142-4. |
|228.||Rossum MM, Verhaegen NT, Jonkman MF, Mackenzie MA, Koster A, Van Der Valk PG, et al. Follicular non-Hodgkin's lymphoma with refractory paraneoplastic pemphigus: Case report with review of novel treatment modalities. Leuk Lymphoma 2004;45:2327-32. |
|229.||McLaughlin P, Grillo-López AJ, Link BK, Link BK, Levy R, Czuczman MS, et al. Rituximab chimeric anti-CD20 monoclonal antibody therapy for relapsed indolent lymphoma: Half of patients respond to a four-dose treatment program. J Clin Oncol 1998;16:2825-33. |
|230.||Ishigami T, Kubo Y, Matsudate Y, Ansai S, Arase S, Ohyama B, et al. Paraneoplastic pemphigus associated with non-Hodgkin's lymphoma. Eur J Dermatol 2011;21:122-4. |
|231.||Crichlow SM, Mortimer NJ, Harman KE. A successful therapeutic trial of rituximab in the treatment of a patient with recalcitrant, high-titre epidermolysis bullosa acquisita. Br J Dermatol 2007;156:194-6. |
|232.||Cavailhes A, Balme B, Gilbert D, Skowron F. Successful use of combined corticosteroids and rituximab in the treatment of recalcitrant epidermolysis bullosa acquisita. Ann Dermatol Venereol 2009;136:795-9. |
|233.||Kasperkiewicz M, Shimanovich I, Ludwig RJ, Rose C, Zillikens D, Schmidt E. Rituximab for treatment-refractory pemphigus and pemphigoid: A case series of 17 patients. J Am Acad Dermatol 2011;65:552-8. |
|234.||Shetty S, Ahmed AR. Critical analysis of the use of rituximab in mucous membrane pemphigoid: A review of the literature. J Am Acad Dermatol 2013;68:499-506. |
|235.||Oddis CV, Reed AM, Aggarwal R, Rider LG, Ascherman DP, Levesque MC, et al. RIM Study Group. Rituximab in the treatment of refractory adult and juvenile dermatomyositis and adult polymyositis: A randomized, placebo-phase trial. Arthritis Rheum 2013;65:314-24. |
|236.||Bader-Meunier B, Decaluwe H, Barnerias C, Gherardi R, Quartier P, Faye A, et al. Safety and efficacy of rituximab in severe juvenile dermatomyositis: Results from 9 patients from the French Autoimmunity and Rituximab registry. J Rheumatol 2011;38:1436-40. |
|237.||Sánchez-Fernández SÁ, Carrasco Fernández JA, Rojas Vargas LM. Efficacy of rituximab in dermatomyositis and polymyositis refractory to conventional therapy. Reumatol Clin 2013;9:117-9. |
|238.||Haroon M, Devlin J. Rituximab as a first-line agent for the treatment of dermatomyositis. Rheumatol Int 2012;32:1783-4. |
|239.||Lan L, Han F, Chen JH. Efficacy and safety of rituximab therapy for systemic lupus erythematosus: A systematic review and meta-analysis. J Zhejiang Univ Sci B 2012;13:731-44. |
|240.||Furie R, Looney RJ, Rovin B, Latinis Kevin M, Appel G, Sanchez-Guerrero J. Efficacy and safety of rituximab in subjects with active proliferative lupus nephritis (LN): Results from the randomized, double-blind phase III LUNAR study. Arthritis Rheum 2009;60:1149. |
|241.||Merrill JT, Buyon JP, Furie R, Latinis K, Gordon C, Hsieh HJ, et al. Assessment of flares in lupus patients enrolled in a phase II/III study of rituximab (EXPLORER). Lupus 2011;20:709-16. |
|242.||Zaja F, Bacigalupo A, Patriarca F, Stanzani M, Van Lint MT, Filì C, et al. Treatment of refractory chronic GVHD with rituximab: A GITMO study. Bone Marrow Transplant 2007;40:273-7. |
|243.||Wong CF. Rituximab in refractory antineutrophil cytoplasmic antibody-associated vasculitis: What is the current evidence? Nephrol Dial Transplant 2007;22:32-6. |
|244.||Belloni B, Andres C, Ollert M, Ring J, Mempel M. Novel immunological approaches in the treatment of atopic eczema. Curr Opin Allergy Clin Immunol 2008;8:423-7. |
|245.||Sedivá A, Kayserová J, Vernerová E, Poloucková A, Capková S, Spísek R, et al. Anti-CD20 (rituximab) treatment for atopic eczema. J Allergy Clin Immunol 2008;121:1515-7. |
|246.||Jolles S, Hughes J. Use of IGIV in the treatment of atopic dermatitis, urticaria, scleromyxedema, pyoderma gangrenosum, psoriasis, and pretibial myxedema. Int Immunopharmacol 2006;6:579-91. |
|247.||Lolis M, Toosi S, Czernik A, Bystryn JC. Effect of intravenous immunoglobulin with or without cytotoxic drugs on pemphigus intercellular antibodies. J Am Acad Dermatol 2011;64:484-9. |
|248.||Hartung HP, Mouthon L, Ahmed R, Jordan S, Laupland KB, Jolles S. Clinical applications of intravenous immunoglobulins (IVIg)-beyond immunodeficiencies and neurology. Clin Exp Immunol 2009;158 Suppl 1:23-33. |
|249.||Ahmed AR, Dahl MV. Consensus statement on the use of intravenous immunoglobulin therapy in the treatment of autoimmune mucocutaneous blistering diseases. Arch Dermatol 2003;139:1051-9. |
|250.||Ahmed AR. Use of intravenous immunoglobulin therapy in autoimmune blistering diseases. Int Immunopharmacol 2006;6:557-78. |
|251.||Cummins DL, Anhalt GJ, Monahan T, Meyerle JH. Treatment of pyoderma gangrenosum with intravenous immunoglobulin. Br J Dermatol 2007;157:1235-9. |
|252.||Richetta AG, Maiani E, Carboni V, Carlomagno V, Cimillo M, Mattozzi C, et al. Pyoderma gangrenosum: Case series. Clin Ter 2007;158:325-9. |
|253.||Sinnya S, Hamza S. Pyoderma gangrenosum of the breast treated with intravenous immunoglobulin. J Dermatol Case Rep 2013;7:64-8. |
|254.||Tamaki K, Nakazawa T, Mamehara A, Tsuji G, Saigo K, Kawano S, et al. Successful treatment of pyoderma gangrenosum associated with myelodysplastic syndrome using high-dose intravenous immunoglobulin. Intern Med 2008;47:2077-81. |
|255.||de Zwaan SE, Iland HJ, Damian DL. Treatment of refractory pyoderma gangrenosum with intravenous immunoglobulin. Australas J Dermatol 2009;50:56-9. |
|256.||Prins C, Kerdel FA, Padilla RS, Hunziker T, Chimenti S, Viard I, et al. TEN-IVIG Study Group. Toxic epidermal necrolysis-intravenous immunoglobulin. Treatment of toxic epidermal necrolysis with high-dose intravenous immunoglobulins: Multicenter retrospective analysis of 48 consecutive cases. Arch Dermatol 2003;139:26-32. |
|257.||Mydlarski PR, Ho V, Shear NH. Canadian consensus statement on the use of intravenous immunoglobulin therapy in dermatology. J Cutan Med Surg 2006;10:205-21. |
|258.||Enk A. European Dermatology Forum Guideline Subcommitte. Guidelines on the use of high-dose intravenous immunoglobulin in dermatology. Eur J Dermatol 2009;19:90-8. |
|259.||Bachot N, Revuz J, Roujeau JC. Intravenous immunoglobulin treatment for Stevens-Johnson syndrome and toxic epidermal necrolysis: A prospective noncomparative study showing no benefit on mortality or progression. Arch Dermatol 2003;139:33-6. |
|260.||Shortt R, Gomez M, Mittman N, Cartotto R. Intravenous immunoglobulin does not improve outcome in toxic epidermal necrolysis. J Burn Care Rehabil 200;25:246-55. |
|261.||Mangla K, Rastogi S, Goyal P, Solanki RB, Rawal RC. Efficacy of low dose intravenous immunoglobulins in children with toxic epidermal necrolysis: An open uncontrolled study. Indian J Dermatol Venereol Leprol 2005;71:398-400. |
|262.||Viard I, Wehrli P, Bullani R, Schneider P, Holler N, Salomon D, et al. Inhibition of toxic epidermal necrolysis by blockade of CD95 with human intravenous immunoglobulin. Science 1998;282:490-3. |
|263.||Lam CG, Manlhiot C, Pullenayegum EM, Feldman BM. Efficacy of intravenous Ig therapy in juvenile dermatomyositis. Ann Rheum Dis 2011;70:2089-94. |
|264.||Shahani L. Refractory calcinosis in a patient with dermatomyositis: Response to intravenous immune globulin. BMJ Case Rep 2012;2012. pii: bcr2012006629. |
|265.||Peñate Y, Guillermo N, Melwani P, Martel R, Hernández-Machín B, Borrego L. Calcinosis cutis associated with amyopathic dermatomyositis: Response to intravenous immunoglobulin. J Am Acad Dermatol 2009;60:1076-7. |
|266.||Wang DX, Shu XM, Tian XL, Chen F, Zu N, Ma L, et al. Intravenous immunoglobulin therapy in adult patients with polymyositis/dermatomyositis: A systematic literature review. Clin Rheumatol 2012;31:801-6. |
|267.||Kampylafka EI, Kosmidis ML, Panagiotakos DB, Dalakas M, Moutsopoulos HM, Tzioufas AG. The effect of intravenous immunoglobulin (IVIG) treatment on patients with dermatomyositis: A 4-year follow-up study. Clin Exp Rheumatol 2012;30:397-401. |
|268.||Goodfield M, Davison K, Bowden K. Intravenous immunoglobulin (IVIg) for therapy-resistant cutaneous lupus erythematosus (LE). J Dermatolog Treat 2004;15:46-50. |
|269.||Schroeder JO, Zeuner RA, Euler HH, Löffler H. High dose intravenous immunoglobulins in systemic lupus erythematosus: Clinical and serological results of a pilot study. J Rheumatol 1996;23:71-5. |
|270.||Généreau T, Chosidow O, Danel C, Chérin P, Herson S. High-dose intravenous immunoglobulin in cutaneous lupus erythematosus. Arch Dermatol 1999;135:1124-5. |
|271.||Krueter A, Hyun J, Altmeyer P, Gambichler T. Intravenous immunoglobulin for recalcitrant subacute cutaneous lupus erythematosus. Acta Derm Venereol 2005;85:545-7. |
|272.||De Pità O, Bellucci AM, Ruffelli M, Girardelli CR, Puddu P. Intravenous immunoglobulin therapy is not able to efficiently control cutaneous manifestations in patients with lupus erythematosus. Lupus 1997;6:415-7. |
|273.||Kajii M, Suzuki C, Kashihara J, Kobayashi F, Kubo Y, Miyamoto H, et al. Prevention of excessive collagen accumulation by human intravenous immunoglobulin treatment in a murine model of bleomycin-induced scleroderma. Clin Exp Immunol 2011;163:235-41. |
|274.||Nacci F, Righi A, Conforti ML, Miniati I, Fiori G, Martinovic D, et al. Intravenous immunoglobulins improve the function and ameliorate joint involvement in systemic sclerosis: A pilot study. Ann Rheum Dis 2007;66:977-9. |
|275.||Levy Y, Amital H, Langevitz P, Nacci F, Righi A, Conforti L, et al. Intravenous immunoglobulin modulate cutaneous involvement and reduce skin fibrosis in systemic sclerosis: An open-label study. Arthritis Rheum 2004;50:1005-7. |
|276.||Matsuda M, Miki J, Oguchi K, Tabata K, Ikeda S. Fasciitis in mixed connective tissue disease successfully treated with high-dose intravenous immunoglobulin. Intern Med 2003;42:910-1. |
|277.||Ulmer A, Kötter I, Pfaff A, Fierlbeck G. Efficacy of pulsed intravenous immunoglobulin therapy in mixed connective tissue disease. J Am Acad Dermatol 2002;46:123-7. |
|278.||Wetter DA, Davis MD, Yiannias JA, Gibson LE, Dahl MV, el-Azhary RA, et al. Effectiveness of intravenous immunoglobulin therapy for skin disease other than toxic epidermal necrolysis: A retrospective review of Mayo Clinic experience. Mayo Clin Proc 2005;80:41-7. |
|279.||Kreuter A, Gambichler T, Breuckmann F, Bechara FG, Rotterdam S, Stücker M, et al. Pulsed intravenous immunoglobulin therapy in livedoid vasculitis: An open trial evaluating 9 consecutive patients. J Am Acad Dermatol 2004;51:574-9. |
|280.||Kroiss M, Hohenleutner U, Gruss C, Glaessl A, Landthaler M, Stolz W. Transient and partial effect of high-dose intravenous immunoglobulin in polyarteritis nodosa. Dermatology 2001;203:188-9. |
|281.||Gedalia A, Sorensen R. Intravenous immunoglobulin in childhood cutaneous polyarteritis nodosa. Clin Exp Rheumatol 1998;16:767. |
|282.||Asano Y, Ihn H, Maekawa T, Kadono T, Tamaki K. High-dose intravenous immunoglobulin infusion infusion polyarteritis nodosa: Report on one case and review of the literature. Clin Rheumatol 2006;25:396-8. |
|283.||Raychaudhuri SP. Role of IL-17 in psoriasis and psoriatic arthritis. Clin Rev Allergy Immunol 2013;44:183-93. |
|284.||Belge K, Brück J, Ghoreschi K. Advances in treating psoriasis. F1000Prime Rep 2014;6:4. eCollection 2014. |
|285.||Leonardi C, Matheson R, Zachariae C, Cameron G, Li L, Edson-Heredia E, et al. Anti-interleukin-17 monoclonal antibody ixekizumab in chronic plaque psoriasis. N Engl J Med 2012;366:1190-9. |
|286.||Papp KA, Leonardi C, Menter A, Ortonne JP, Krueger JG, Kricorian G, et al. Brodalumab, an anti-interleukin-17-receptor antibody for psoriasis. N Engl J Med 2012;366:1181-9. |
|287.||Papp KA, Langley RG, Sigurgeirsson B, Abe M, Baker DR, Konno P, et al. Efficacy and safety of secukinumab in the treatment of moderate-to severe plaque psoriasis: A randomized, double-blind, placebo-controlled phase II dose-ranging study. Br J Dermatol 2013;168:412-21. |
What is new?
Newer molecules and newer indications of older molecules are emerging in
the field of biological drugs. Drugs against IL-17 cytokine are the latest to join
this ever enlarging group. Longer experience with the older drugs has paved
the way for their judicious and safer use.
|This article has been cited by|
||A Systematic Review and Meta-Analysis of Injection Site Reactions in Randomized-Controlled Trials of Biologic Injections
| ||Patrick J. Kim, Rafael Paolo Lansang, Ron Vender |
| ||Journal of Cutaneous Medicine and Surgery. 2023; |
|[Pubmed] | [DOI]|
||Impact of gut microbiome on skin health: gut-skin axis observed through the lenses of therapeutics and skin diseases
| ||Md. Rayhan Mahmud, Sharmin Akter, Sanjida Khanam Tamanna, Lincon Mazumder, Israt Zahan Esti, Sanchita Banerjee, Sumona Akter, Md. Rakibul Hasan, Mrityunjoy Acharjee, Md. Sajjad Hossain, Anna Maria Pirttilä |
| ||Gut Microbes. 2022; 14(1) |
|[Pubmed] | [DOI]|
||Dermatological aspects of SARS-CoV-2 infection: mechanisms and manifestations
| ||Myriam Garduño-Soto, Jose Alberto Choreño-Parra, Jorge Cazarin-Barrientos |
| ||Archives of Dermatological Research. 2021; 313(8): 611 |
|[Pubmed] | [DOI]|
||Alternative uses of ustekinumab for non-indicated dermatological conditions: a systematic review
| ||Sahil Rawal, Sara Kianian, William Guo, Jocellie Marquez, Marissa Ayasse, Katherine A. Siamas, Yoojin Lee, Joann Salvemini |
| ||Archives of Dermatological Research. 2021; |
|[Pubmed] | [DOI]|
||Hypersensitivity reactions to biologics (part I): allergy as an important differential diagnosis in complex immune-derived adverse events*
| ||Askin Gülsen, Bettina Wedi, Uta Jappe |
| ||Allergo Journal. 2020; 29(4): 32 |
|[Pubmed] | [DOI]|
||Hypersensitivity reactions to biologics (part I): allergy as an important differential diagnosis in complex immune-derived adverse events
| ||Askin Gülsen, Bettina Wedi, Uta Jappe |
| ||Allergo Journal International. 2020; 29(4): 97 |
|[Pubmed] | [DOI]|
||Gene Co-expression Networks Identifies Common Hub Genes Between Cutaneous Sarcoidosis and Discoid Lupus Erythematosus
| ||Melissa A. Nickles, Kai Huang, Yi-Shin Chang, Maria M. Tsoukas, Nadera J. Sweiss, David L. Perkins, Patricia W. Finn |
| ||Frontiers in Medicine. 2020; 7 |
|[Pubmed] | [DOI]|
||Aspects concerning patient adherence to anti-TNFa therapy in psoriasis: A decade of clinical experience
| ||Madalina Mocanu, Mihaela-Paula Toader, Elena Rezus, Tatiana Taranu |
| ||Experimental and Therapeutic Medicine. 2019; |
|[Pubmed] | [DOI]|