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Year : 2022  |  Volume : 67  |  Issue : 6  |  Page : 772-773
Skin Lesion in Haematological Malignancy—How Dermatology Can Save the Life of a Patient

1 From the Department of Dermatology, Apollo Multispeciality Hospitals, Kolkata, West Bengal, India
2 Department of Dermatology, Venereology and Leprosy, Silchar Medical College and Hospital, Silchar, Assam, India
3 Department of Oncology, Apollo Multispeciality Hospitals, Kolkata, West Bengal, India
4 Department of Dermatology, Apollo Multispeciality Hospitals, Kolkata, West Bengal, India

Date of Web Publication23-Feb-2023

Correspondence Address:
Kinnor Das
Department of Dermatology, Venereology and Leprosy, Silchar Medical College and Hospital, Silchar, Assam
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijd.ijd_52_21

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How to cite this article:
Gorai S, Das K, Chakrapani A, Lahiri K, Bhattacharyya S. Skin Lesion in Haematological Malignancy—How Dermatology Can Save the Life of a Patient. Indian J Dermatol 2022;67:772-3

How to cite this URL:
Gorai S, Das K, Chakrapani A, Lahiri K, Bhattacharyya S. Skin Lesion in Haematological Malignancy—How Dermatology Can Save the Life of a Patient. Indian J Dermatol [serial online] 2022 [cited 2023 Mar 23];67:772-3. Available from:


A 61-year-old female from Ranchi, Jharkhand, India presented with myelodysplastic syndrome and multiple comorbidities including left bundle branch block and hypertension. The myelodysplastic syndrome presents with a myeloblast of 20%–29% and is the predecessor of acute myeloid leukaemia where the myeloblast count is more than 30%.[1] The patient was started on azacytidine 112 mg daily for 7 days cycle, to be repeated every 28 days. After 12 days of the first cycle, the patient got admitted to a bone marrow transplant unit with complaints of persistent fever for 5–6 days, cough and severe weakness accompanied by skin lesions. In the light of the pandemic era, the chances of coronavirus disease 2019 (COVID-19) were fancied and a computed tomography (CT) scan of the thorax, real-time polymerase chain reaction (RT-PCR) GeneXpart was done alongside other routine investigations. The investigation results on the first day of admission were as follows: erythrocyte sedimentation rate (ESR) >140, heamoglobin (Hb%): 7.4, total leucocyte count (TLC): 1400/cumm, platelet: 26,000/cumm, neutrophils (N): 46%, lymphocyte (L): 39%, atypical/blast cells: 3 and metamyelocyte: 2, random plasma glucose: 166, total bilirubin: 1.1(direct 0.4), aspartate deaminase (AST): 49, sodium: 135, potassium: 3.1, calcium: 8.1, magnesium: 1.6 and on chest X-ray ill-defined nodular centrilobular/ground glass densities involving both lungs were seen. COVID-19 RT-PCR by GeneXpart (Food and Drug Administration [FDA]-approved machine) was negative. Pancytopenia picture propelled the oncologist to start Inj Meropenem: 1g IV OD, Inj Teicoplanin: 400 mg IV OD, Inj Colistin: 150 mg/day, Inj Caspofungin: 50 mg IV OD and Inj Acyclovir: 10 mg/kg; along with other supportive therapies according to pancytopenia protocol. Even though high-end antimicrobials were started, the condition of the patient was worsening. After a week of admission and 14 days from the onset of fever the author was called for expert opinion with no improvement of fever, no improvement in skin lesions and very sick such that he was barely able to speak. The investigations on day 7 of admission showed Hb% 7.1, TLC 460/cumm, platelet 14,000/cumm, 25 DC, N 08 L15 M2. The blood culture, wound swab culture, throat swab culture and urine culture were all negative after 3 days of incubation. Procalcitonin (PCT) level was 0.65 (0.10–0.49 ng/dL) and C-reactive protein (CRP) was 58 mg/L; which was out of track for systemic bacteremia. The patient was not responding well to verbal stimuli. The patient was very pale with a high respiratory rate, heart rate of 126/min and blood pressure of 112/64 mmHg. Icterus, clubbing, cyanosis, oedema and organomegaly was absent. The skin lesions showed multiple well-defined, round to oval plaques of different sizes according to their evolution with central haemorrhagic necrosis. Few black crusted lesions were present with eschar formation in a few. There was ulceration with pigmented border. Few lesions had a discharge of serous fluid. The lesions were distributed mainly on limbs, back, neck and a few on the chest. Lesions were indurated and tender. Many possibilities in skin lesions of haematological malignancies like neutrophilic dermatosis, leukaemia cutis, opportunistic infections by bacteria, viruses and fungi and leukemic vasculitis. The situation was complicated, lacked time and intervention was not possible. To confirm the diagnosis, a skin biopsy could not be done as platelet levels were diminishing and the oncologist denied permission. Time was scanty and the circumstances needed immediate action. This confusion can prove to be fatal in the bargain. With perplexity, the author took a perch bedside for going through the literature. After a couple of hours of reading, the author swapped from Caspofungin to Liposomal-amphotericin B (AMB) at 150 mg/day considering Fusarium infection as a diagnosis of exclusion. The patient responded exorbitantly after starting liposomal AMB. Liposomal AMB was continued for the next 10 days and the patient was released from the hospital in stable condition. After 3 weeks, 2nd cycle of Azacytidine was given. No, opportunistic infections were seen after the second cycle of chemotherapy. While dealing with such cases, we should keep in mind that we may deal with a pathogen that may not be susceptible to all these brilliant drugs. Fusarium infection presents with persistent fever, and early onset skin lesions >80% of cases.[2] The skin lesions include erythematous macules, papules, plaque and nodules that ulcerate with central infarction.[3] Fusarium infection may prove to be fatal if not treated early. Fusarium does not respond to Caspofungin. Invasive fungal disease is one of the major causes of mortality and morbidity in immunocompromised individuals in haematological malignancies. The introduction of fluconazole significantly decreased invasive candidiasis but the incidence of mould fungus is on the rise now. Aspergillosis and fusariosis, two common mould fungi are on rising nowadays.[4],[5] Fusarium spp are soil pathogen and cause plant or animal disease. Disseminated fusariosis occurs exclusively in an immunocompromised state.[6] Mainly associated with prolonged and profound neutropenia. F. saloni was found in 50% of cases. Others are Oxysporum, Moniliforme and Verticilloides. Fusarium is inherently resistant to many antifungal agents but AMB remained the drug of choice. Voriconazole was approved for the treatment of fusariosis in May 2002 by FDA.[7] Among 84 cases of Fusarium spp infection with haematological malignancies, only 21% were alive 90 days after diagnosis.[8] Cutaneous appearance may be red or gray macules or papules with central necrosis or eschar. Purpuric papules, pustules and subcutaneous nodules may be present. The same patient may have all the lesions as our patient had, it indicates lesions under evolution. Cutaneous necrosis happens due to blockage of dermal blood vessels with Fusarium hyphae.[3] Lung involvement is very common. Diagnosis is usually by biopsy and blood culture. Other than AMB, supportive therapy for pancytopenia and surgical debridement may be done for necrotic tissue.[9] After handling such a convoluted case, the author has some take-home messages for the readers. Interdepartmental collaboration and personal communication are very important. During a time of crisis, investigations and the best drugs cannot be banked upon. In a plot like this bedside reading can extricate us from confusion. Moreover, invasive fusariosis should always be kept in mind in an immunocompromised case like this and coverage with AMB is better for a few Fusarium spp.

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There are no conflicts of interest.

   References Top

Hofmann W-K, Koeffler HP. Myelodysplastic syndrome. Annu Rev Med 2005;56:1-16.  Back to cited text no. 1
Dignani MC, Anaissie E. Human fusariosis. Clin Microbiol Infect 2004;10:67-75.  Back to cited text no. 2
Bodey GP, Boktour M, Mays S, Duvic M, Kontoyiannis D, Hachem R, et al. Skin lesions associated with Fusarium infection. J Am Acad Dermatol 2002;47:659-66.  Back to cited text no. 3
Walsh TJ, Groll AH. Emerging fungal pathogens: Evolving challenges to immunocompromised patients for the twenty-first century. Transpl Infect Dis 1999;1:247-61.  Back to cited text no. 4
Nucci M, Anaissie E. Cutaneous infection by Fusarium species in healthy and immunocompromised hosts: Implications for diagnosis and management. Clin Infect Dis 2002;35:909-20.  Back to cited text no. 5
Vartivarian SE, Anaissie EJ, Bodey GP. Emerging fungal pathogens in immunocompromised patients: Classification, diagnosis, and management. Clin Infect Dis 1993;17(Suppl 2):S487-91.  Back to cited text no. 6
Ho DY, Lee JD, Rosso F, Montoya JG. Treating disseminated fusariosis: amphotericin B, voriconazole or both? Mycoses 2007;50:227-31.  Back to cited text no. 7
Nucci M, Anaissie EJ, Queiroz-Telles F, Martins CA, Trabasso P, Solza C, et al. Outcome predictors of 84 patients with hematologic malignancies and Fusarium infection. Cancer 2003;98:315-9.  Back to cited text no. 8
Muhammed M, Carneiro H, Coleman J, Mylonakis E. The challenge of managing fusariosis. Virulence 2011;2:91-6.  Back to cited text no. 9


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