Indian Journal of Dermatology
  Publication of IADVL, WB
  Official organ of AADV
Indexed with Science Citation Index (E) , Web of Science and PubMed
 
Users online: 329  
Home About  Editorial Board  Current Issue Archives Online Early Coming Soon Guidelines Subscriptions  e-Alerts    Login  
    Small font sizeDefault font sizeIncrease font size Print this page Email this page


 
Table of Contents 
CME ARTICLE
Year : 2014  |  Volume : 59  |  Issue : 1  |  Page : 3-14
Reticulate dermatoses


Department of Dermatology, Venereology and Leprosy, SBMP Medical College, Hospital and Research Center, BLDE University, Bijapur, Karnataka, India

Date of Web Publication23-Dec-2013

Correspondence Address:
Arun C Inamadar
Department of Dermatology, Venereology and Leprosy, SBMP Medical College, Hospital and Research Center, BLDE University, Bijapur, Karnataka - 586 103
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-5154.123480

Rights and Permissions

   Abstract 

The term "reticulate" is used for clinical description of skin lesions that are configured in a net-like pattern. Many primary and secondary dermatoses present in such patterns involving specific body sites. Certain cutaneous manifestations of systemic diseases or genodermatoses also present in such manner. This review classifies and describes such conditions with reticulate lesions and briefly, their associated features.


Keywords: Mottling, net-like, reticulate, retiform


How to cite this article:
Adya KA, Inamadar AC, Palit A. Reticulate dermatoses. Indian J Dermatol 2014;59:3-14

How to cite this URL:
Adya KA, Inamadar AC, Palit A. Reticulate dermatoses. Indian J Dermatol [serial online] 2014 [cited 2018 Sep 18];59:3-14. Available from: http://www.e-ijd.org/text.asp?2014/59/1/3/123480

What was known?
Reticulate configuration of lesions is seen in many primary dermatoses and also as cutaneous reaction patterns consequent to internal pathology.



   Reticulate Dermatoses Top


The term "reticulate" is commonly used for clinical description of "net-like", "sieve-like," or "chicken wire" configuration of the skin lesions. Various congenital and acquired dermatoses present with this pattern of skin lesions. Many systemic diseases also present with such cutaneous manifestations providing useful clues to diagnosis.

Classification

  1. Vascular
    1. Cutis marmorata
    2. Cutis marmorata telangiectatica congenita (CMTC)
    3. Livedo reticularis (LR)
    4. Livedo racemosa
    5. Livedoid vasculopathy
    6. Reticulate purpura
  2. Pigmentary
    1. Dowling-Degos disease (DDD)
    2. Galli-Galli disease
    3. Dermatopathia pigmentosa reticularis
    4. Dyschromatosis universalis hereditaria (DUH)
    5. Reticulate acropigmentation
      • Reticulate acropigmentation of Dohi
      • Reticulate acropigmentation of Kitamura
    6. Syndromes associated with reticulate pigmentation
      • Naegeli-Franceschetti-Jadassohn syndrome
      • Mendes da Costa-van der Valk syndrome
      • Hoyeraal-Hreidarrson syndrome
      • Partington syndrome
    7. Atopic dirty neck
    8. Epidermolysis bullosa with mottled pigmentation
    9. Systemic sclerosis
  3. Poikilodermatous
    1. Inherited
      •  Rothmund-Thomson syndrome More Details
      • Dyskeratosis congenita
      • Xeroderma pigmentosum
      • Cockayne syndrome
      • Fanconi anemia
      • Mendes da Costa syndrome
      • Kindler syndrome
      • Degos-Touraine syndrome
      • Hereditary sclerosing poikiloderma of Weary
      • Hereditary acrokeratotic poikiloderma of Weary
      • Werner's syndrome (adult progeria)
      • Chanarin-Dorfman syndrome
      • Diffuse and macular atrophic dermatosis
    2. Acquired
      • Poikiloderma of Civatte
      • Injury by cold, heat, or ionizing radiation
      • Chronic graft-versus-host disease (cGVHD)
    3. Others
      • Dermatomyositis
      • Lupus erythematosus
      • Parapsoriasis
      • Mycosis fungoides
      • Poikiloderma-like cutaneous amyloidosis
  4. Infectious
    1. Confluent and reticulate papillomatosis (CRP)
    2. Erythema infectiosum
    3. Erythema marginatum (EM)
    4. Congenital rubella syndrome
  5. Metabolic
    1. Macular amyloidosis
    2. Amyloidosis cutis dyschromica
    3. Reticular erythematous mucinosis
    4. Hunter's syndrome
  6. Others
    1. Erythema ab igne
    2. Prurigo pigmentosa
    3. Mucosal lichen planus
    4. Leukoplakia
    5. Neonatal lupus erythematosus (LE)
    6. Hereditary angioedema
    7. Extensive congenital erosions and vesicles healing with reticulate scarring
    8. Atrophodermia vermiculata
    9. Nekam's disease



   Vascular Causes of Reticulate Lesions Top


Cutis marmorata

Cutis marmorata is a physiological response to cold exposure seen in neonates that readily disappears on re-warming. It is characterized by marbling of the skin in the form of a reticulate bluish vascular pattern due to dilatation of capillaries and small venules. [1],[2] It involves the limbs and trunk in a symmetrical manner [Figure 1]. This physiological mottling disappears by 6 months of age. [3] Persistent cutis marmorata, or the one which recurs until early childhood, is associated with cretinism and forms a part of various inherited syndromes [Table 1]. In some infants, due to transient constriction of the deep vasculature, a white negative pattern of cutis marmorata (cutis marmorata alba) may occur. [2]
Figure 1: Cutis marmorata

Click here to view
Table 1: Syndromes associated with persistent cutis marmorata

Click here to view


CMTC (congenital phlebectasia, van Lohuizen syndrome)

CMTC is a distinct condition characterized by reticular vascular mottling, predominantly involving the trunk and limbs, that resembles the physiological cutis marmorata. However, it is distinguished from the latter by the persistent nature (even after re-warming), deep livid-purple color, and association with cutaneous atrophy or ulceration. [4] Distribution may be localized, segmental, or widespread. [5] The mottling gets accentuated by cold temperature, crying, or vigorous activity. More than half of the cases are associated with other anomalies. CMTC forms a part of various syndromes also [6] [Table 2].
Table 2: Associations of CMTC


Click here to view


LR and livedo racemosa

LR is perhaps the prototype among the reticulate dermatoses. It is characterized by bluish-red discoloration of the skin in a typical net-like pattern due to decreased blood flow through and decreased oxygen tension in the cutaneous venous plexuses. [12] Lower temperature accentuate the mottling. The anatomical organization of the cutaneous vasculature is the basis of this particular pattern of mottling. Lower extremities are predominantly involved. The net-like pattern is usually complete in LR as opposed to livedo racemosa which has a branching pattern (broken livedo). Other differences between LR and livedo racemosa [12],[13],[14] are listed in [Table 3].
Table 3: Differences between LR and livedo racemosa

Click here to view


LR may be physiological (cutis marmorata), idiopathic (usually benign), or may be associated with other conditions [9],[15],[16],[17] [Table 4]. If the mottling is associated with necrosis or purpura, the terms necrotizing livedo or retiform purpura (see below), respectively, are used. Livedo racemosa and livedo with purpura or necrosis are almost always associated with systemic diseases. [12]
Table 4: Conditions associated with LR

Click here to view


Livedoid vasculopathy (livedoid vasculitis, segmental hyalinizing vasculitis, LR with summer/winter ulceration)

One of the synonyms for this condition is "painful purpuric ulcers with reticular pattern of the lower extremities (PURPLE)," which precisely describes the clinical features of this entity. Livedoid vasculitis, usually a disease of middle aged women, [18] presents in two stages; initial manifestations are painful purpuric lesions involving predominantly the gaiter region of the lower extremities (usually bilateral) that evolve into painful shallow ulcers. Later the ulcers heal with stellate ivory-white scars, which have a reticulate pattern (atrophie blanche).

The pathogenesis of this condition is attributed to hyper-coagulable states resulting in microvascular thrombosis and consequently cutaneous ischemia and necrosis. The term livedoid vasculitis could be misleading as histopathological evaluation shows more of intravascular changes like fibrin thrombi, and sparse peri-vascular lymphocytic infiltrate without true vessel wall infiltration. [19],[20]

Livedoid vasculopathy may be idiopathic or associated with other conditions [Table 5]. One of the common associations is chronic venous hypertension. Unlike the typical evolution, atrophie blanche associated with chronic venous hypertension is not preceded by painful purpura or ulcers. [15]
Table 5: Associations of livedoid vasculopathy

Click here to view


Reticulate purpura

Reticulate or retiform purpuric lesions are usually associated with disorders causing cutaneous microvascular occlusion. This pattern of purpura forms a useful clinical indicator for this group of disorders and helps in differentiating from other causes of purpura. Other clinical features that suggest this category of diseases [Table 6] as the underlying cause are purpura without erythema, eschar without erythema, and branching extension of the lesional margins. [15]
Table 6: Microvascular occlusive disorders associated with reticulate purpura

Click here to view



   Reticulate Pigmentary Disorders Top


DDD (reticular pigmented anomaly of the flexures)

DDD is an autosomal dominant disorder that manifests after puberty and is characterized by asymptomatic symmetrical reticulate hyperpigmentation involving the neck, axillae [Figure 2], groins, and other flexures like the inframammary folds in females. [36],[37] It occurs due to mutation in the keratin 5 gene, [38] which is also the genetic anomaly seen in a variant of epidermolysis bullosa simplex associated with reticulate pigmentation (see below). Lesions may also involve the vulva. Other associated cutaneous findings include comedo-like lesions and pitted perioral scars. [39] It has been reported to be associated with hidradenitis supurrativa. [40],[41],[42] Typical histopathological features include irregular elongated thin rete ridges with heavily pigmented tips. [39]
Figure 2: Dowling- Degos disease

Click here to view


Galli-Galli disease is a variant of DDD [43] with identical inheritance and clinical features. The differentiating histopathological features are presence of a suprabasal cleft [44] and suprapapillary thinning of the epidermis in addition to digitate down-growth of rete ridges.

Dermatopathia pigmentosa reticularis

Dermatopathia pigmentosa reticularis is an autosomal dominant condition characterized by reticulate hyperpigmentation, nail dystrophy, adermatoglyphia, hypohidrosis, and non-cicatricial alopecia. [45],[46] It shares the same genetic defect (nonsense or frameshift mutations in the KRT 14 gene) [47],[48] with Naegeli-Franceschetti-Jadassohn syndrome (see below). The reticulate hyperpigmentation begins in early childhood, or may be present since birth, and predominantly involves the trunk. Other reported findings include palmoplantar keratoderma, [46] hair shaft defects, [49] oral mucosal pigmentation, and atraumatic non-scarring blisters over the extremities. [50]

Dyschromatosis universalis hereditaria

DUH is an autosomal dominant disorder characterized by an early onset of multiple reticulate hyper- and hypopigmented macules scattered allover the body. [51] The condition is more common among Japanese and Chinese. The dyschromia initially appears on the trunk and later becomes generalized, which may include the palms and soles. The general health of the affected individuals is otherwise normal. However, ocular and auditory anomalies, photosensitivity, developmental delay, and short stature are uncommonly reported, [50] so has been the autosomal recessive mode of inheritance. [52]

Reticulate acropigmentation

Reticulate acropigmentation of Dohi (dyschromatosis symmetrica hereditaria (DSH)) and reticulate acropigmentation of Kitamura are the two classical disorders of this group. Both have autosomal dominant inheritance and were initially described among the Japanese population.

Reticulate acropigmentation of Dohi is characterized by reticulate hyper- and hypopigmented macules on the extensor aspect of the extremities, especially on the dorsum of hands [Figure 3] and feet. [53] Mutations affecting the ADAR1 gene [54] have been ascertained as the cause of DSH. There may be associated freckle-like macules on the face. The lesions appear early in life and become non-progressive by adolescence. [50]
Figure 3: Reticulate acropigmentation of Dohi

Click here to view


Reticulate acropigmentation of Kitamura is characterized by reticular freckle-like pigmentation involving the dorsum of hands and feet that begins in early childhood or adolescence, and may eventually become generalized. The distinguishing feature of this disease is the presence of fine palmar pits and interruptions in dermatoglyphics. [55]

Atopic dirty neck

In the childhood phase of atopic dermatitis, along with flexural localization of the dermatitis, some patients may develop a conspicuous reticulate hyperpigmentation of the neck that bears quite a resemblance with macular amyloidosis. [56],[57] Interestingly, amyloid has been demonstrated in some of these cases at the ultrastructural level, but not on light microscopy. [58]

Systemic sclerosis

The typical "salt and pepper" pigmentation, which is characterized by hypopigmented to depigmented patches with perifollicular retained pigmentation, giving a reticulate pattern, is the most common cutaneous pigmentary change seen in systemic sclerosis. It predominantly involves the face, back, lower abdomen, and less commonly, the legs. Other pigmentary changes include diffuse Addisonian pigmentation, flexural hyperpigmentation resembling acanthosis nigricans, and diffuse mottled pigmentation.

Many inherited syndromes are associated with reticulate cutaneous pigmentation [Table 7]. The reticulate pigmentary anomaly may be congenital in some while it develops at a later date in others.
Table 7: Syndromes associated with reticulate pigmentation

Click here to view


Poikilodermatous disorders

The term poikiloderma refers to a triad of cutaneous atrophy, telangiectasia, and reticulated dyspigmentation, which is hyper- or hypopigmentation [Figure 4]. Poikiloderma is a feature of various inherited genodermatoses [Table 8], acquired, or associated with other disorders. Histopathology of poikiloderma shows variable areas of epidermal hyperkeratosis and atrophy, interface reaction (vacuolar degeneration of the basal layer with band-like mononuclear infiltrate), and dermal melanophages with perivascular lymphocytic infiltrate.
Figure 4: Poikiloderma

Click here to view
Table 8: Genodermatoses associated with poikiloderma

Click here to view


Acquired causes of poikiloderma include poikiloderma of Civatte, cGVHD, and poikiloderma due to injury by cold, heat, or ionizing radiation. Poikiloderma of Civatte is seen in middle-aged fair-skinned women and is characterized by poikilodermatous involvement of the front and sides of the neck, the V-area of the upper chest, with conspicuous sparing of the submental and submandibular region. This distribution is suggestive of ultraviolet (UV) exposure as the underlying cause. [73] cGVHD occurs in 60%-70% of stem cell transplant recipients, which is usually seen beyond the 100 th post-transplant day. The most commonly affected organs are the skin, eyes, mouth, and liver. The common skin manifestations include lichenoid papules, poikiloderma, and sclerodermatous changes. Oral involvement is characterized by oral lichen planus (OLP)-like lesions. Xerosis affects both the oral cavity and eyes. Hepatic involvement is characterized by cholestasis with consequent elevated alkaline phosphatase and bilirubin. [74] Other conditions associated with poikiloderma are listed in [Table 9].
Table 9: Other conditions associated with poikiloderma

Click here to view



   Reticulate Lesions in Infectious Conditions Top


CRP (of Gougerot and Carteaud)

CRP is a disorder of adolescent males and females characterized by development of dry hyperpigmented papules with minimal scaling that later become confluent in the center, with gradual peripheral extension, where these form a reticulate pattern [Figure 5]. Most commonly, and classically, the inter-mammary region is affected. The neck, upper back, and lateral chest are other commonly involved sites. Dietzia papillomatosis, a novel actinomycete, has been isolated from the lesions. [81] Pityrosporum orbiculare has also been implicated in the pathogenesis, [82] but it has not been isolated from the lesions in many. Response to topical antifungals is disappointing also. Minocycline, azithromycin, and topical mupirocin have been found to be effective, which further supports the role of bacterial pathogens in the disease pathogenesis.
Figure 5: Confluent and reticulate papillomatosis

Click here to view


Erythema infectiosum (5 th disease)

A reticulate pattern of erythematous rash develops in the second stage of the disease that begins in 1-4 days of the appearance of the "slapped-cheek" rash. The rash begins as a confluent erythema, which later develops central clearing at places, producing a reticulate pattern. The rash predominantly involves the limbs and trunk, and may be pruritic. It fades over 2-3 weeks, but may episodically recur following UV exposure, hot bath, etc. [83],[84]

Erythema marginatum

EM and subcutaneous nodules are the two dermatological manifestations of rheumatic fever that are included in the revised Jones diagnostic criteria. EM appears as evanescent patchy erythema, predominantly over the trunk that develops central clearing and peripheral extension. Adjacent lesions may coalesce to produce a reticulate pattern. Successive crops may occur over few weeks and they tend to be more prominent in the afternoon. EM has to be differentiated from acute urticaria, erythema multiforme, and other reactive erythemas.

Congenital rubella syndrome

The distinct cutaneous lesions of congenital rubella syndrome are the initial "cranberry muffin" lesions (raised red spongy papules), which develop intralesional hemorrhage, producing the conspicuous "blueberry muffin" lesions [85] that are indicative of persistent dermal erythropoiesis. However, a reticulate erythema involving the face and limbs in association with lymphadenopathy is also seen. [2],[86]


   Reticulate Lesions in Metabolic Disorders Top


Primary cutaneous amyloidosis

The more common macular amyloidosis and the rare amyloidosis cutis dyschromica are the types of primary cutaneous amyloidosis that have reticulate morphological patterns, apart from the poikiloderma-like cutaneous amyloidosis (PCA) as described in [Table 9].

Macular amyloidosis presents as hyperpigmented macules configured in a typical "rippled" pattern giving a tight net-like appearance. Lesions are mostly asymptomatic. Classical sites involved are the interscapular region and outer arms. Exact etiology has not been ascertained but chronic rubbing has been implicated as one. Amyloidosis cutis dyschromica is a rare form of primary cutaneous amyloidosis that is characterized by reticulate hyper- and hypopigmented macules scattered all over the body, which are mostly asymptomatic and begin before puberty. [80] This rare entity was first described by Eng et al. [87] and thereafter several familial clusters have been described by others. [88],[89]

Reticular erythematous mucinosis

Reticular erythematous mucinosis is one of the primary cutaneous mucinoses characterized by reticulate erythema classically involving the inter-mammary region [Figure 6]. [90] Involvement of face, abdomen, and groins has also been reported, so has been exacerbation with oral contraceptive use and during pregnancy. [91] The condition is asymptomatic, although photosensitivity is a feature. It most commonly affects middle-aged women and is generally not associated with systemic diseases. Histopathology shows deposition of mucin in the dermis with a round cell infiltrate. [92]
Figure 6: Reticular erythematous mucinosis

Click here to view


Hunter syndrome (mucopolysaccharidosis II, MPS II)

Hunter syndrome is an X-linked recessive lysosomal storage disorder due to deficiency of the enzyme iduronate-2-sulfatase. The clinical manifestations include short stature, large head, short neck, coarse facies, thickened tongue and lips, and mental retardation which is generally mild. Frequent upper and lower respiratory tract infections are attributed to enlarged adenoids and tonsils. Distinct cutaneous eruption consists of fleshy, ivory-white papules and nodules ("pebbling") in a ridging or reticular pattern, involving symmetrically the area between the angle of the scapula and the anterior axillary line. [93] The nape of the neck, the pectoral ridges, and the buttocks are the other sites affected. [94] They begin before the age of 10 years and disappear spontaneously. [95] Such pebbling is noted mainly in Hunter syndrome and serves a clinical marker for differentiating it from other MPS.


   Other Reticulate Dermatoses Top


Erythema ab igne

Erythema ab igne is a condition that occurs due to repeated or prolonged exposure to infrared radiation of sub-threshold intensity (43 o C-47 o C) that is insufficient to cause burn. It begins as a reticulate erythema due to local hemostasis that becomes persistent over time. Later pigmentation develops [Figure 7], and telangiectasia and atrophy may also ensue. [96] It may occur at any age and affect either sex [97] in whom there is a history of repeatedly or habitually being exposed to heat, as in heating pads, fireplace, laptops, [98] or occupationally as in cooks, goldsmiths, and silversmiths. Histopathology is reminiscent of chronic actinic damage. Development of squamous cell carcinoma has been reported, [96] which tends to be aggressive.
Figure 7: Erythema ab igne

Click here to view


Prurigo pigmentosa

Prurigo pigmentosa is a condition characterized by development of pruritic reticulate erythematous papules that leave behind hyperpigmentation in the same pattern. It is mostly seen among the Japanese. It predominantly affects middle-aged females and involves the trunk and neck more commonly. Associations with diabetes and anorexia have been reported, so has been aggravation during menses and pregnancy. [99],[100]

Reticulate lesions affecting the oral mucosa

Among this group, the classical examples include OLP and leukoplakia. A reticulate lacy pattern of white streaks (Wickham's striae) involving the buccal mucosa [Figure 8] is the most common form of OLP. Similar lesions may also affect the vaginal mucosa. Other morphological variants of OLP are atrophic, hypertrophic, erosive, and ulcerative patterns. Leukoplakia of the oral cavity presents as a whitish thickened plaque or reticulate streaks involving the buccal mucosa, soft palate, and tongue. The plaques are adherent and forceful removal causes bleeding. The condition is most often considered benign and is associated with chronic irritation (e.g., ill-fitting dentures), chronic smoking, tobacco chewing, etc., Transformation into invasive carcinoma is associated with high-risk factors like old age, female gender, soft palate involvement, non-homogenous morphology, and erythroplakia. [101],[102]
Figure 8: Oral lichen planus

Click here to view


Neonatal lupus erythematosus

The most common cutaneous manifestation of neonatal lupus erythematosus (NLE) resembles lesions of sub-acute cutaneous lupus erythematosus of adults. NLE presenting as extensive reticulate erythema with atrophy, resembling cutis marmorata telangiectatica congenita, has also been reported. [103],[104],[105]

Hereditary angioedema

Hereditary angioedema is an autosomal condition characterized by recurrent episodes of angioedema associated with gastrointestinal symptoms. It occurs due to inherited deficiency of C1 esterase inhibitor. A reticulate erythematous rash resembling EM may occur prodromally in some familial cases. [106],[107]

Extensive congenital erosions and vesicles healing with reticulate scarring

This condition is characterized by presence of extensive superficial erosions all over the body at birth, which heals in a few days, leaving behind a rather conspicuous reticulate hyperpigmentation. It is a rare condition whose exact etiology is not known. However, it may indicate intrauterine insults. [108]

Atrophodermia vermiculata

It is also known as "atrophoderma reticulatum", "folliculitis ulerythematosa reticulata," and "honeycomb atrophy". It is characterized by symmetric reticulate or honeycomb atrophy of the cheeks that may extend to the ears and forehead. It is thought to be due to defective keratinization of pilosebaceous follicles. [109],[110]

Nekam's disease (keratosis lichenoides chronica)

It is a rare condition affecting the skin and mucous membranes characterized by reticulate or linearly arranged violaceous, keratotic papules, and nodules predominantly over the extremities and buttocks associated with a seborrheic dermatitis-like or rosacea-like eruption on the face. Its exact etiology is not known. Young adolescent males are commonly affected. Other associated features are recurrent oral aphthae, nail dystrophy, palmoplantar keratoderma, keratotic papules over the scrotum, and ocular manifestation. Treatment is difficult. [111],[112]

 
   References Top

1.Paige DG, Gennery AR, Cant AJ. The neonate. In: Burns T, Breathnach S, Cox N, Griffiths C, editors. Rook's Textbook of Dermatology. 8 th ed. Oxford: Wiley-Blackwell; 2010. p. 17.1-85.  Back to cited text no. 1
    
2.Paller AS, Mancini A. Cutaneous disorders of the newborn. In: Paller AS, Mancini A, editors. Hurwitz Clinical Pediatric Dermatology. 4 th ed. Edinburgh: Elsevier Saunders; 2011. p. 10-36.  Back to cited text no. 2
    
3.Chang MW, Orlow SJ. Neonatal, pediatric and adolescent dermatology. In: Wolff K, Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, editors. Fitzpatrick's Dermatology in General Medicine. 7 th ed. New York: McGraw-Hill; 2008. p. 935-55.  Back to cited text no. 3
    
4.Picascia DD, Esterly NB. Cutis marmorata telangiectatica congenita: Report of 22 cases. J Am Acad Dermatol 1989;20:1098-104.  Back to cited text no. 4
[PUBMED]    
5.Cohen BA. Neonatal dermatology. In: Cohen BA, editor. Pediatric Dermatology. 3 rd ed. Philadelphia: Elsevier Mosby; 2005. p. 15-66.  Back to cited text no. 5
    
6.James WD, Berger TG, Elston DM. Dermal and subcutaneous tumors. In: James WD, Berger TG, Elston DM, editors. Andrews' Diseases of the Skin Clinical Dermatology. 11 th ed. Philadelphia: Elsevier Saunders; 2011. p. 574-619.  Back to cited text no. 6
    
7.Pehr K, Moroz B. Cutis marmorata telangiectatica congenita: Long-term follow up, review of the literature and report of a case in conjunction with congenital hypothyroidism. Pediatr Dermatol 1993;10:6-11.  Back to cited text no. 7
[PUBMED]    
8.Devillers AC, de Waard-van der Spek FB, Oranje AP. Cutis marmorata telangiectatica congenita: Clinical features in 35 cases. Arch Dermatol 1999;135:34-8.  Back to cited text no. 8
[PUBMED]    
9.Paller AS, Mancini A. Vascular disorders of infancy and childhood. In: Paller AS, Mancini A, editors. Hurwitz Clinical Pediatric Dermatology. 4 th ed. Edinburgh: Elsevier Saunders; 2011. p. 268-302.  Back to cited text no. 9
    
10.Weilepp AE, Eichenfeld LF. Association of glaucoma with cutis marmorata telangiectatica congenita: A localized anatomic malformation. J Am Acad Dermatol 1996;35:276-8.  Back to cited text no. 10
    
11.Van Lohuizen CH. Uber eine seltene angeborene Hautanomalie (Cutis marmorata telangiectatica congenita). Acta Dermatol Venereol (Stockh) 1922;3:202-11.  Back to cited text no. 11
    
12.James WD, Berger TG, Elston DM. Cutaneous vascular diseases. In: James WD, Berger TG, Elston DM, editors. Andrews' Diseases of the Skin Clinical Dermatology. 11 th ed. Philadelphia: Elsevier Saunders; 2011. p. 801-62.  Back to cited text no. 12
    
13.Fleischer AB Jr, Resnick SD. Livedo reticularis. Dermatol Clin 1990;8:347-54.  Back to cited text no. 13
[PUBMED]    
14.Picascia DD, Pellegrini JR. Livedo reticularis. Cutis 1987;39:429-32.  Back to cited text no. 14
[PUBMED]    
15.Cox DG, Piette WW. Purpura and microvascular occlusion. In: Burns T, Breathnach S, Cox N, Griffiths C, editors. Rook's Textbook of Dermatology. 8 th ed. Oxford: Wiley-Blackwell; 2010. p. 49.1-51.  Back to cited text no. 15
    
16.Richards KA, Paller AS. Livedo reticularis in association with Moyamoya disease. Pediatr Dermatol 2003;20:124-8.  Back to cited text no. 16
[PUBMED]    
17.Sladden MJ, Nicolaou N, Johnston GA, Hutchinson PE. Livedo reticularis induced by amantadine. Br J Dermatol 2003;149:656-8.  Back to cited text no. 17
[PUBMED]    
18.Maessen-Visch M, Koedam M, Hamulyak K, Neumann H. Atrophie blanche. Int J Dermatol 1999;38:161-72.  Back to cited text no. 18
    
19.Robson K, Piette W. The presentation and differential diagnosis of cutaneous vascular occlusion syndromes. Adv Dermatol 1999;15:153-82.  Back to cited text no. 19
    
20.McCalmont CS, McCalmont TH, Jorizzo JC, White WL, Leshin B, Rothberger H. Livedo vasculitis: Vasculitis or thrombotic vasculopathy? Clin Exp Dermatol 1992;17:4-8.  Back to cited text no. 20
    
21.Acland K, Darvay A, Wakelin S, Russell-Jones R. Livedoid vasculitis: A manifestation of the antiphospholipid syndrome? Br J Dermatol 1999;140:131-5.  Back to cited text no. 21
    
22.Calamia K, Balabanova M, Perniciaro C, Walsh J. Livedo (livedoid) vasculitis and the factor V Leiden mutation: Additional evidence for abnormal coagulation. J Am Acad Dermatol 2002;46:133-7.  Back to cited text no. 22
    
23.Boyvat A, Kundakci N, Babikir MO, Gurgey E. Livedoid vasculopathy associated with heterozygous protein C deficiency. Br J Dermatol 2000;143:840-2.  Back to cited text no. 23
    
24.Anavekar NS, Kelly R. Heterozygous prothrombin gene mutation associated with livedoid vasculopathy. Australas J Dermatol 2007;48:120-5.  Back to cited text no. 24
[PUBMED]    
25.Browning CE, Callen JP. Warfarin therapy for livedoid vasculopathy associated with cryofibrinogenemia and hyperhomocysteinemia. Arch Dermatol 2006;142:75-8.  Back to cited text no. 25
[PUBMED]    
26.Deng A, Gocke CD, Hess J, Heyman M, Paltiel M, Gaspari A. Livedoid vasculopathy associated with plasminogen activator inhibitor-1 promoter homozygosity (4G/4G) treated successfully with tissue plasminogen activator. Arch Dermatol 2006;142:1466-9.  Back to cited text no. 26
[PUBMED]    
27.Cardoso R, Goncalo M, Tellechea O, Maia R, Bores C, Silva JA, et al. Livedoid vasculopathy and hypercoagulability in a patient with primary Sjögren's syndrome. Int J Dermatol 2007;46:431-4.  Back to cited text no. 27
    
28.Amdo TD, Welkar JA. An approach to the diagnosis and treatment of cryofibrinogenemia. Am J Med 2004;116:332-7.  Back to cited text no. 28
    
29.Smith A, Arkin C. Cryofibrinogenemia: Incidence, clinical correlations, and a review of the literature. Am J Clin Pathol 1972;58:524-30.  Back to cited text no. 29
    
30.Bessler M, Hiken J. The pathophysiology of disease in patients with paroxysmal nocturnal hemoglobinuria. Hematology Am Soc Hematol Educ Program 2008; 2008:104-10.  Back to cited text no. 30
    
31.Arepally GM, Ortel TL. Heparin-induced thrombocytopenia. N Engl J Med 2006;355;809-17.  Back to cited text no. 31
    
32.Allford S, Hunt B, Rose P, Machin S. Guidelines on the diagnosis and management of the thrombotic microangiopathic haemolytic anaemias. Br J Haematol 2003;120:556-73.  Back to cited text no. 32
    
33.McLaughlin ER, Morris R, Weiss SW, Arbiser JL. Diffuse dermal angiomatosis of the breast: Response to isotretinoin. J Am Acad Dermatol 2001;45:462-5.  Back to cited text no. 33
[PUBMED]    
34.Yang H, Ahmed I, Verghese M, Schroeter AL. Diffuse dermal angiomatosis of the breast. Arch Dermatol 2006;142:343-7.  Back to cited text no. 34
    
35.Culpeper KS, Nousari HC. Purpura fulminans. Lancet 2003;361:384.  Back to cited text no. 35
[PUBMED]    
36.Dowling GB, Freudenthal W. A case of acanthosis nigricans. Br J Dermatol 1938;50:467-71.  Back to cited text no. 36
    
37.Degos R, Ossipowski B. Dermatose pigmentaire réticulée de plis (discussion de l'acanthosis nigricans). Ann Dermatol Syphiligr 1954;81:147-51.  Back to cited text no. 37
    
38.Betz RC, Planko L, Eigelshoven S, Hanneken S, Pasternack SM, Bussow H, et al. Loss-of-function mutations in the keratin 5 gene lead to Dowling-Degos disease. Am J Hum Genet 2006;78:510-9.  Back to cited text no. 38
[PUBMED]    
39.Irvine AD, Mellerio JE. Genetics and genodermatoses. In: Burns T, Breathnach S, Cox N, Griffiths C, editors. Rook's Textbook of Dermatology. 8 th ed. Oxford: Wiley-Blackwell; 2010. p. 15.1-97.  Back to cited text no. 39
    
40.Weber LA, Kantor GR, Bergfeld WF. Reticulate pigmented anomaly of the flexures (Dowling-Degos disease): A case report associated with hidradenitis suppurativa and squamous cell carcinoma. Cutis 1990;45:446-50.  Back to cited text no. 40
[PUBMED]    
41.Fenske NA, Groover CE, Lober CW, Espinoza CG. Dowling-Degos disease, hidradenitis suppurativa, and multiple keratoacanthomas. A disorder that may be caused by a single underlying defect in pilosebaceous epithelial proliferation. J Am Acad Dermatol 1991;24:888-92.  Back to cited text no. 41
    
42.Loo WJ, Rytina E, Todd PM. Hidradenitis suppurativa, Dowling-Degos and multiple epidermal cysts: A new follicular occlusion triad. Clin Exp Dermatol 2004;29:622-4.  Back to cited text no. 42
[PUBMED]    
43.Sprecher E, Indelmam M, Khamaysi Z, Lugassy J, Petronius D, Bergman R. Galli-Galli disease is an acantholytic variant of Dowling-Degos disease. Br J Dermatol 2007;156:572-4.  Back to cited text no. 43
    
44.Gilchrist H, Jakson S, Morse L, Nicotri T, Nesbitt LT. Galli-Galli disease: A case report with review of the literature. J Am Acad Dermatol 2008;58:299-302.  Back to cited text no. 44
    
45.Brar BK, Mehta V, Kubba A. Dermatopathia pigmentosa reticularis. Pediatr Dermatol 2007;24:566-70.  Back to cited text no. 45
[PUBMED]    
46.Kelsell DP, Leigh IM. Inherited keratodermas of palms and soles. In: Wolff K, Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, editors. Fitzpatrick's Dermatology in General Medicine. 7 th ed. New York: McGraw-Hill; 2008. p. 424-31.  Back to cited text no. 46
    
47.Paller AS, Mancini A. Disorders of pigmentation. In: Paller AS, Mancini A, editors. Hurwitz Clinical Pediatric Dermatology. 4 th ed. Edinburgh: Elsevier Saunders; 2011. p. 234-67.  Back to cited text no. 47
    
48.Lugassy J, Itin P, Ishida-Yamamoto A, Holland K, Huson S, Geiger D, et al. Naegeli-Franceschetti-Jadassohn syndrome and dermatopathia pigmentosa reticularis: Two allelic ectodermal dysplasias caused by dominant mutations in KRT14. Am J Hum Genet 2006;79:724-30.  Back to cited text no. 48
[PUBMED]    
49.Goh BK, Common JE, Gan WH, Kumarasinghe P. A case of dermatopathia pigmentosa reticularis with wiry scalp hair and digital fibromatosis resulting from a recurrent KRT14 mutation. Clin Exp Dermatol 2009;34:340-3.  Back to cited text no. 49
[PUBMED]    
50.James WD, Berger TG, Elston DM. Disturbances of pigmentation. In: James WD, Berger TG, Elston DM, editors. Andrews' Diseases of the Skin Clinical Dermatology. 11 th ed. Philadelphia: Elsevier Saunders; 2011. p. 846-62.  Back to cited text no. 50
    
51.Nuber UA, Tinschert S, Mundlos S, Hausser I. Dyschromatosis universalis hereditaria: Familial case and ultrastructural skin investigation. Am J Med Genet 2004;125A: 261-6.  Back to cited text no. 51
    
52.Bukhari IA, El-Harith EA, Stuhrmann M. Dyschromatosis universalis hereditaria as an autosomal recessive disease in five members of one family. J Eur Acad Dermatol Venereol 2006;20:628-9.  Back to cited text no. 52
[PUBMED]    
53.Oyama M, Shimizu H, Ohata Y, Tajima S, Nishikawa T. Dyschromatosis symmetrica hereditaria (reticulate acropigmentation of Dohi): Report of a Japanese family with the condition and a literature review of 185 cases. Br J Dermatol 1999;140:491-6.  Back to cited text no. 53
[PUBMED]    
54.Kondo T, Suzuki T, Mitsuhashi Y, Ito S, Kono M, Komine M, et al. Six novel mutations of the ADAR1 gene in patients with dyschromatosis symmetrica hereditaria: Histological observation and comparison of genotypes and clinical phenotypes. J Dermatol 2008;35:395-406.  Back to cited text no. 54
[PUBMED]    
55.Kocaturk E, Kavala M, Zindanci I, Zemheri E, Koc MK, Sarigul S. Reticulate acropigmentation of Kitamura: Report of a familial case. Dermatol Online J 2008;14:7.  Back to cited text no. 55
    
56.Colver GB, Mortimer PS, Millard PR, Dawber RP, Ryan TJ. The 'dirty neck'-reticulate pigmentation in atopics. Clin Exp Dermatol 1987;12:1-4.  Back to cited text no. 56
[PUBMED]    
57.Hughes BR, Cunliffe WJ. Rippled hyperpigmentation resembling macular amyloidosis-a feature of atopic eczema. Clin Exp Dermatol 1990;15:380-1.  Back to cited text no. 57
[PUBMED]    
58.Sarkany RP, Breathnach SM, Morris AA, Weismann K, Flynn PD. Metabolic and nutritional disorders. In: Burns T, Breathnach S, Cox N, Griffiths C, editors. Rook's Textbook of Dermatology. 8 th ed. Oxford: Wiley-Blackwell; 2010. p. 59.1-103.  Back to cited text no. 58
    
59.Hassing JH, Doeglas HM. Dystrophia bullosa hereditaria, typus maculates (Mendes da Costa-van der Valk): A rare genodermatosis. Br J Dermatol 1980;102:474-6.  Back to cited text no. 59
[PUBMED]    
60.James WD, Berger TG, Elston DM. Genodermatoses and congenital anomalies. In: James WD, Berger TG, Elston DM, editors. Andrews' Diseases of the Skin Clinical Dermatology. 11 th ed. Philadelphia: Elsevier Saunders; 2011. p. 538-73.  Back to cited text no. 60
    
61.Bruckner-Tuderman L, Vogel A, Ruegger S, Vogel A, Ruegger S, Odermatt B, et al. Epidermolysis bullosa simplex with mottled pigmentation. J Am Acad Dermatol 1989;21:425-32.  Back to cited text no. 61
    
62.Wang LL, Plon SE. Rothmund-Thomson syndrome. In: Pagon RA, Bird TD, Dolan CR, Stephens K, Adam MP, editors. GeneReviews™. Seattle, WA: University of Washington; 1993-1999 Oct 06 [Last updated 2009 Apr 07].  Back to cited text no. 62
    
63.Paller AS, Mancini A. Disorders of hair and nails. In: Paller AS, Mancini A, editors. Hurwitz Clinical Pediatric Dermatology. 4 th ed. Edinburgh: Elsevier Saunders; 2011. p. 130-66.  Back to cited text no. 63
    
64.Roth A, Baerlocher GM. Dyskeratosis congenita. Br J Haematol 2008;141:412.  Back to cited text no. 64
    
65.Lehmann AR, McGibbon D, Stefanini M. Xeroderma pigmentosum. Orphanet J Rare Dis 2011;6:70.  Back to cited text no. 65
[PUBMED]    
66.Soulier J. Fanconi anemia. Hematology Am Soc Hematol Educ Program 2011;2011:492-7.  Back to cited text no. 66
[PUBMED]    
67.Kaviarasan PK, Prasad PV, Shradda, Viswanathan P. Kindler syndrome. Indian J Dermatol Venereol Leprol 2005;71:348-50.  Back to cited text no. 67
[PUBMED]  Medknow Journal  
68.Wiebe CB, Petricca G, Häkkinen L, Jiang G, Wu C, Larjava HS. Kindler syndrome and periodontal disease: Review of the literature and a 12-year follow-up case. J Periodontol 2008;79:961-6.  Back to cited text no. 68
    
69.Burrows NP, Lovell CR. Disorders of connective tissue. In: Burns T, Breathnach S, Cox N, Griffiths C, editors. Rook's Textbook of Dermatology. 8 th ed. Oxford: Wiley-Blackwell; 2010. p. 45.1-70.  Back to cited text no. 69
    
70.Grau Salvat C, Pont V, Cors JR, Aliaga A. Hereditary sclerosing poikiloderma of Weary: Report of a new case. Br J Dermatol 1999;140:366-8.  Back to cited text no. 70
[PUBMED]    
71.Paller AS, Mancini A. Hereditary disorders of the dermis. In: Paller AS, Mancini A, editors. Hurwitz Clinical Pediatric Dermatology. 4 th ed. Edinburgh: Elsevier Saunders; 2011. p. 115-29.  Back to cited text no. 71
    
72.Goto M, Miller RW, Ishikawa Y, Sugano H. Excess of rare cancers in Werner syndrome (adult progeria). Cancer Epidermiol Biomarkers Prev 1996;5:239-46.  Back to cited text no. 72
    
73.James WD, Berger TG, Elston DM. Dermatoses resulting from physical factors. In: James WD, Berger TG, Elston DM, editors. Andrews' Diseases of the Skin Clinical Dermatology. 11 th ed. Philadelphia: Elsevier Saunders; 2011. p. 18-44.  Back to cited text no. 73
    
74.Pidala J. Graft-vs-host disease following allogeneic hematopoietic cell transplantation. Cancer Control 2011;18:268-76.  Back to cited text no. 74
[PUBMED]    
75.Sontheimer RD, Costner MI. Dermatomyositis. In: Wolff K, Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, editors. Fitzpatrick's Dermatology in General Medicine. 7 th ed. New York: McGraw-Hill; 2008.p. 1536-53.  Back to cited text no. 75
    
76.Das S, Giri PP. Poikilodermatous parapsoriasis: 2 cases with review of literature. Indian J Dermatol 2009;54:S32-6.  Back to cited text no. 76
    
77.Whittaker SJ. Cutaneous lymphomas and lymphocytic infiltrates. In: Burns T, Breathnach S, Cox N, Griffiths C, editors. Rook's Textbook of Dermatology. 8 th ed. Oxford: Wiley-Blackwell; 2010. p. 57.1-57.64.  Back to cited text no. 77
    
78.Keehn CA, Belongie IP, Shistik G, Fenske NA, Glass FL. The diagnosis, staging, and treatment options for mycosis fungoides. Cancer Control 2007;14:102-11.  Back to cited text no. 78
    
79.Sayal SK, Gupta CM, Malik AK. Lichen planus induced poikiloderma. Indian J Dermatol 2001;46:178-9.  Back to cited text no. 79
  Medknow Journal  
80.Yang W, Lin Y, Yang J, Lin W. Amyloidosis cutis dyschromica in two female siblings: Cases report. BMC Dermatol 2011;11:4.  Back to cited text no. 80
[PUBMED]    
81.Jones AL, Koerner RJ, Natarajan S, Perry JD, Goodfellow M. Dietzia papillomatosis sp. nov., a novel actinomycete isolated from the skin of an immunocompetent patient with confluent and reticulated papillomatosis. Int J Syst Evol Microbiol 2008;58:68-72.  Back to cited text no. 81
    
82.Roberts SO, Lachapelle JM. Confluent and reticulate papillomatosis (Gougerot-Carteaud) and Pityrosporum orbiculare. Br J Dermatol 1969;81:841-5.  Back to cited text no. 82
[PUBMED]    
83.Paller AS, Mancini A. Exanthematous diseases of childhood. In: Paller AS, Mancini A, editors. Hurwitz Clinical Pediatric Dermatology. 4 th ed. Edinburgh: Elsevier Saunders; 2011. p. 370-89.  Back to cited text no. 83
    
84.Bard JW, Perry HO. Erythema infectiosum. Arch Dermatol 1966;93:49-53.  Back to cited text no. 84
[PUBMED]    
85.Friedlander SF, Bradley JS. Viral infections. In: Eichenfield LF, Frieden IJ, Esterly NB, editors. Neonatal Dermatology. 2 nd ed. Philadelphia: Saunders Elsevier; 2001. p. 193-212.  Back to cited text no. 85
    
86.James WD, Berger TG, Elston DM. Viral diseases. In: James WD, Berger TG, Elston DM, editors. Andrews' Diseases of the Skin Clinical Dermatology. 11 th ed. Philadelphia: Elsevier Saunders; 2011. p. 360-413.  Back to cited text no. 86
    
87.Eng AM, Cogan L, Gunnar RM, Blekys I. Familial generalized dyschromic amyloidosis cutis. J Cutan Pathol 1976;3:102-8.  Back to cited text no. 87
[PUBMED]    
88.Choonhakarn C, Wittayachanyapong S. Familial amyloidosis cutis dyschromica: Six cases from three families. J Dermatol 2002;29:439-42.  Back to cited text no. 88
[PUBMED]    
89.Vijaikumar M, Thappa DM. Amyloidosis cutis dyschromica in two siblings. Clin Exp Dermatol 2001;26:674-6.  Back to cited text no. 89
[PUBMED]    
90.Meewes C, Henrich A, Kreig T, Hunzelmann N. Treatment of reticular erythematous mucinosis with UV-A1 radiation. Arch Dermatol 2004;140:660-2.  Back to cited text no. 90
    
91.James WD, Berger TG, Elston DM. Mucinosis. In: James WD, Berger TG, Elston DM, editors. Andrews' Diseases of the Skin Clinical Dermatology. 11 th ed. Philadelphia: Elsevier Saunders; 2011. p. 182-7.  Back to cited text no. 91
    
92.Steigleder GK, Gartmann H, Linker V. REM syndrome: Reticular erythematous mucinosis (round-cell erythematosis): A new entity? Br J Dermatol 1974;91:191-9.  Back to cited text no. 92
    
93.Gajula P, Ramalingam K, Dinesh Bhadrashetty D. A rare case of mucopolysaccharidosis: Hunter syndrome. J Nat Sci Biol Med 2012;3:97-100.  Back to cited text no. 93
    
94.Prystowsky SD, Maumenee IH, Freeman RG, Herndon JH Jr, Harrod MJ. A cutaneous marker in the Hunter syndrome. Arch Dermatol 1977;113:602-5.  Back to cited text no. 94
[PUBMED]    
95.Paller AS, Mancini A. Inborn errors of metabolism. In: Paller AS, Mancini A, editors. Hurwitz Clinical Pediatric Dermatology. 4 th ed. Edinburgh: Elsevier Saunders; 2011. p. 546-61.  Back to cited text no. 95
    
96.Miller K, Hunt R, Chu J, Meehan S, Stein J. Erythema ab igne. Dermatol Online J 2011;17:28.  Back to cited text no. 96
[PUBMED]    
97.Wilson NJE, Sharpe GR. Erythema ab igne in a child with atopic eczema. Clin Exp Dermatol 1999;24:336-9.  Back to cited text no. 97
    
98.Giraldi S, Diettrich F, Abbage KT, Carvalho Vde O, Marinoni LP. Erythema ab igne induced by a laptop computer in an adolescent. An Bras Dermatol 2011;86:128-30.  Back to cited text no. 98
[PUBMED]    
99.Lin SH, Ho JC, Cheng YW, Huang PH, Wang CY. Prurigo pigmentosa: A clinical and histopathologic study of 11 cases. Chang Gung Med J 2010;33:157-63.  Back to cited text no. 99
[PUBMED]    
100.Nakada T, Sueki H, Iijima M. Prurigo pigmentosa (Nagashima) associated with anorexia. Clin Exp Dermatol 1998;23:25-7.  Back to cited text no. 100
[PUBMED]    
101.Mishra M, Mohanty J, Sengupta S, Tripathy S. Epidemiological and clinicopathological study of oral leukoplakia. Indian J Dermatol Venereol Leprol 2005;71:161-5.  Back to cited text no. 101
[PUBMED]  Medknow Journal  
102.Liu W, Wang YF, Zhou HW, Shi P, Zhou ZT, Tang GY. Malignant transformation of oral leukoplakia: A retrospective cohort study of 218 Chinese patients. BMC Cancer 2010;10:685.  Back to cited text no. 102
[PUBMED]    
103.Sawant S, Amladi ST, Wadhawa SL, Nayak CS, Nikam BP. Cutaneous neonatal lupus erythematosus with unusual features. Indian J Dermatol Venereol Leprol 2007;73:250-2.  Back to cited text no. 103
[PUBMED]  Medknow Journal  
104.Carrascosa JM, Ribera M, Bielsa I, Coroleu W, Ferrándiz C. Cutis marmorata telangiectatica congenita or neonatal lupus? Pediatr Dermatol 1996;13:230-2.  Back to cited text no. 104
    
105.Greist MC, Probst E. Cutis marmorata telangiectatica congenita or neonatal lupus. Arch Dermatol 1980;116:1102-3.  Back to cited text no. 105
[PUBMED]    
106.Williamson DM. Reticulate erythema: A prodrome in hereditary angio-oedema. Br J Dermatol 1979;101:549-52.  Back to cited text no. 106
[PUBMED]    
107.Starr JC, Brasher GW. Erythema marginatum preceding hereditary angioedema. J Allergy Clin Immunol 1974;53:352-5.  Back to cited text no. 107
[PUBMED]    
108.Stein S, Stone S, Paller AS. Ongoing blistering in a boy with congenital erosive and vesicular dermatosis healing with reticulated supple scarring. J Am Acad Dermatol 2001;45:946-8.  Back to cited text no. 108
[PUBMED]    
109.Hsu S, Nikko A. Unilateral atrophic skin lesion with features of atrophoderma vermiculatum: A variant of the epidermal nevus syndrome? J Am Acad Dermatol 2000;43:310-2.  Back to cited text no. 109
[PUBMED]    
110.Weightman W. A case of atrophoderma vermiculatum responding to isotretinoin. Clin Exp Dermatol 1998;23:89-91.  Back to cited text no. 110
[PUBMED]    
111.Martins LC, Horne M, Moreira DN Jr, Follador I, Almeida VR. Keratosis lichenoides chronica: Case report. An Bras Dermatol 2011;86:148-5.  Back to cited text no. 111
    
112.Wozniacka A, Schwartz RA, Omulecki A, Lesiak A, Sysa-Jedrzejowska A. Keratosis lichenoides chronica: A diagnostic and therapeutic challenge. Clin Exp Dermatol 2006;31:48-50.  Back to cited text no. 112
[PUBMED]    

What is new?
This review is an attempt to compile various reticulate dermatoses and categorize them based on the clinical features and underlying pathogenesis which would be helpful for diagnosis and management of such conditions.


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9]



 

Top
Print this article  Email this article
 
 
  Search
 
  
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Article in PDF (2,370 KB)
    Citation Manager
    Access Statistics
    Reader Comments
    Email Alert *
    Add to My List *
* Registration required (free)  


    Abstract
    Reticulate Derma...
    Vascular Causes ...
    Reticulate Pigme...
    Reticulate Lesio...
    Reticulate Lesio...
    Other Reticulate...
    References
    Article Figures
    Article Tables

 Article Access Statistics
    Viewed9885    
    Printed108    
    Emailed3    
    PDF Downloaded641    
    Comments [Add]    

Recommend this journal