scholarly journals Carbamazepine-Induced Toxic Epidermal Necrolysis Managed by Mobile Teledermatology in COVID-19 Pandemic in Rural Nepal

2020 ◽  
Vol 2020 ◽  
pp. 1-3
Author(s):  
Vikash Paudel ◽  
Deepa Chudal
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Community Health Center ◽  
Smart Phone ◽  
Skin Lesions ◽  
Clinical Findings ◽  
Clinical Impression ◽  
Symptomatic Management ◽  
Life Threatening ◽  
History Of ◽  
Rural Nepal

Toxic epidermal necrolysis is a life-threatening dermatological emergency with high mortality if not treated in time. Here we report a case of toxic epidermal necrolysis due to carbamazepine in rural Nepal in COVID-19 pandemic who was successfully treated with the help of mobile teledermatology. The clinical impression of toxic epidermal necrolysis was made from “WhatsApp” video calls using a smart phone. The supportive features were the history of starting of carbamazepine 2 weeks prior for seizure disorder, clinical findings in serial photographs of skin with 40 percent body surface area involvement of necrotic skin lesions and bulla, and involvement of oral mucosa and eyes. The patient was immediately asked to stop carbamazepine and was treated with intravenous fluids and systemic steroids along with symptomatic management. As the whole world was suffering from lockdown due to COVID-19 crisis, it was impossible for the rural area patient to visit a dermatologist. Thus, with the help of paramedics staff in a community health center and mobile teledermatology, the patient was diagnosed as carbamazepine-induced toxic epidermal necrolysis and treated successfully with good outcome.

scholarly journals Apoptosis as a Mechanism for Keratinocyte Death in Canine Toxic Epidermal Necrolysis

2016 ◽  
Vol 54 (2) ◽  
pp. 249-253 ◽  
Author(s):  
F. Banovic ◽  
S. Dunston ◽  
K. E. Linder ◽  
P. Rakich ◽  
T. Olivry
Keyword(s):  
Cell Death ◽  
Toxic Epidermal Necrolysis ◽  
Caspase 3 ◽  
Skin Lesions ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Epidermal Keratinocytes ◽  
Biopsy Specimens ◽  
Significant Difference ◽  
Keratinocyte Cell ◽  
Life Threatening

In humans and dogs, toxic epidermal necrolysis (TEN) is a life-threatening dermatosis characterized by sudden epidermal death resulting in extensive skin detachment. There is little information on the pathogenesis of keratinocyte cell death in canine TEN. We studied the occurrence of apoptosis in skin lesions of dogs with TEN to determine if apoptosis contributes to the pathogenesis of this disease. Immunostaining with antibodies to activated caspase-3 and the terminal deoxynucleotidyl-transferase (TdT)–mediated deoxyuridine triphosphate (dUTP) nick-end labeling technique revealed positive apoptotic keratinocytes in basal and suprabasal epidermal compartments in 17 biopsy specimens collected from 3 dogs with TEN and 16 from 3 dogs with erythema multiforme (EM). There was no significant difference in the number of positively stained epidermal cells between TEN and EM. These results suggest that apoptosis of epidermal keratinocytes and lymphocytic satellitosis represent one of the early steps in the pathogenesis of canine TEN, as in the human disease counterpart.

scholarly journals Meropenem-induced Stevens-Johnson syndrome/toxic epidermal necrolysis in a patient with known type IV penicillin hypersensitivity

2019 ◽  
Vol 12 (8) ◽  
pp. e230144 ◽  
Author(s):  
Muhammad Sameed ◽  
Christine Nwaiser ◽  
Prashant Bhandari ◽  
Sarah A Schmalzle
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Cross Reactivity ◽  
Delayed Hypersensitivity ◽  
Stevens Johnson Syndrome ◽  
Hypersensitivity Reactions ◽  
Beta Lactam ◽  
Type Iv ◽  
Johnson Syndrome ◽  
Life Threatening ◽  
History Of

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are considered variants of a disease continuum that results in a life-threatening exfoliative mucocutaneous disease. These are categorised as type IV cell-mediated delayed hypersensitivity reactions, and antibiotics are often implicated as a cause. Penicillins and other beta-lactam antibiotics are known to cause both immediate and delayed hypersensitivity reactions. While immediate IgE-mediated cross-reactivity between penicillins and carbapenems is well studied, less information on the risk of type IV delayed cell-mediated cross-reactivity between the two is available. We present a case of meropenem-induced SJS in a patient with documented history of SJS from amoxicillin. There are few cases of cross-reactivity with carbapenems reported in the literature, but based on the potential for life-threatening reaction, it is likely prudent to avoid the use of any beta-lactams in a patient with a history of SJS, TEN or any other severe cutaneous adverse reactions to another beta-lactam antibiotic.

scholarly journals Atypical clinical presentation of distal renal tubular acidosis: a case report registered in Amazonas, Brazil

2020 ◽  
Vol 42 (3) ◽  
pp. 380-383
Author(s):  
Daniel Monteiro Queiroz ◽  
Rolando Guillermo Vermehren Valenzuela ◽  
Ana Wanda Guerra Barreto Marinho ◽  
Samanta Samara Bicharra dos Santos ◽  
Danielle Ochoa da Silva ◽  
...  
Keyword(s):  
Renal Tubular Acidosis ◽  
Skin Lesions ◽  
Clinical Findings ◽  
Distal Renal Tubular Acidosis ◽  
Lower Limbs ◽  
Hypokalemic Paralysis ◽  
Immunological Tests ◽  
History Of ◽  
Similar Report ◽  
Renal Tubular

ABSTRACT We report an unusual case of a 24-year-old girl with a history of recurrent hypokalemic paralysis episodes and skin lesions on the lower limbs and buttocks, both of which had an acute evolution. In subsequent investigations, the patient also had nephrocalcinosis, nephrolithiasis, hyperchloremic metabolic acidosis and persistent alkaline urinary pH. The findings were consistent with distal renal tubular acidosis as the cause of hypokalemic paralysis. Clinical findings, immunological tests and the result of skin biopsy suggested primary Sjögren's syndrome as an underlying cause. The patient developed azotemia due to obstructive nephrolithiasis. All the features presented in this case are an unusual manifestation of distal renal tubular acidosis; so far, we are not aware of a similar report in the literature.

scholarly journals Natural history of transient myeloproliferative disorder clinically diagnosed in Down syndrome neonates: a report from the Children's Oncology Group Study A2971

Blood ◽  
2011 ◽  
Vol 118 (26) ◽  
pp. 6752-6759 ◽  
Author(s):  
Alan S. Gamis ◽  
Todd A. Alonzo ◽  
Robert B. Gerbing ◽  
Joanne M. Hilden ◽  
April D. Sorrell ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Natural History ◽  
Trisomy 21 ◽  
Myeloid Leukemia ◽  
Clinical Findings ◽  
Myeloproliferative Disorder ◽  
Spontaneous Resolution ◽  
Transient Myeloproliferative Disorder ◽  
Life Threatening ◽  
History Of

Abstract Transient myeloproliferative disorder (TMD), restricted to newborns with trisomy 21, is a megakaryocytic leukemia that although lethal in some is distinguished by its spontaneous resolution. Later development of acute myeloid leukemia (AML) occurs in some. Prospective enrollment (n = 135) elucidated the natural history in Down syndrome (DS) patients diagnosed with TMD via the use of uniform monitoring and intervention guidelines. Prevalent at diagnosis were leukocytosis, peripheral blast exceeding marrow blast percentage, and hepatomegaly. Among those with life-threatening symptoms, most (n = 29/38; 76%) received intervention therapy until symptoms abated and then were monitored similarly. Organomegaly with cardiopulmonary compromise most frequently led to intervention (43%). Death occurred in 21% but only 10% were attributable to TMD (intervention vs observation patients: 13/14 vs 1/15 because of TMD). Among those solely observed, peripheral blasts and all other TMD symptoms cleared at a median of 36 and 49 days from diagnosis, respectively. On the basis of the diagnostic clinical findings of hepatomegaly with or without life-threatening symptoms, 3 groups were identified with differing survival: low risk with neither finding (38%), intermediate risk with hepatomegaly alone (40%), and high risk with both (21%; overall survival: 92% ± 8%, 77% ± 12%, and 51% ± 19%, respectively; P ≤ .001). Among all, AML subsequently occurred in 16% at a median of 441 days (range, 118-1085 days). The trial is registered at http://www.clinicaltrials.gov as NCT00003593.

scholarly journals Toxic Epidermal Necrolysis and Graft-versus-Host Reaction: Revisiting a Puzzling Similarity

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
G. E. Piérard ◽  
T. Hermanns-Lê ◽  
P. Paquet ◽  
A. F. Rousseau ◽  
P. Delvenne ◽  
...  
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Inflammatory Cell ◽  
Skin Lesions ◽  
Graft Versus Host Reaction ◽  
Host Reaction ◽  
Drug Induced ◽  
Effector Cells ◽  
Graft Versus Host ◽  
Life Threatening ◽  
Skin Biopsies

Drug-induced toxic epidermal necrolysis (TEN) and acute cutaneous graft-versus-host reaction (GVHR) under immunopreventive therapy share some histopathological resemblance. So far, there are no serum biomarkers and no immunohistochemical criteria distinguishing with confidence and specificity the skin lesions of TEN and GVHR. Both diseases present as an inflammatory cell-poor necrotic reaction of the epidermis. This report compares three sets of 15 immunostaining patterns found in TEN, GVHR, and partial thickness thermal burns (PTTB), respectively. Three series of 17 skin biopsies were scrutinized. Irrespective of the distinct causal pathobiology of TEN and GVHR, similar secondary effector cells were recruited in lesional skin. Burns were less enriched in cells of the monocyte-macrophage disease. These cells likely exert deleterious effects in TEN and GVHR and cannot be simply regarded as passive bystanders. These life-threatening conditions are probably nursed, at least in part, by macrophages.

scholarly journals Stevens-Johnson Syndrome in a Child on Phenytoin, Exacerbated with Cefixime

2019 ◽  
Vol 39 (3) ◽  
pp. 193-196 ◽  
Author(s):  
Yam Bahadur Roka ◽  
Sabrina Shrestha ◽  
Narayani Roka ◽  
Mohan Karki
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Whole Body ◽  
Stevens Johnson Syndrome ◽  
Intravenous Fluids ◽  
Oral Ulceration ◽  
Topical Antibiotics ◽  
Johnson Syndrome ◽  
Life Threatening ◽  
History Of ◽  
Steven Johnson Syndrome

Steven Johnson syndrome and toxic epidermal necrolysis are rare but potentially life threatening muco-cutaneous disorders. Their incidence ranges from 1.2 to six per million patient-years for Steven Johnson syndrome and 0.4 to 1.2 per million patient-years for toxic epidermal necrolysis. Drugs are the primary cause for these syndromes in majority cases. They might also be due to infections with Mycoplasma Pneumoniae or Herpes Simplex. The mortality ranges from five to 40% in these cases. We report a 10-year old girl who presented with history of multiple skin eruptions involving whole body and oral ulceration for five days. She was a known case of seizure disorder on phenytoin and had been prescribed Cefexime for fever. She was managed with intravenous fluids, corticosteroids, opiates, antacids and topical antibiotics. We want to highlight the possibility of Steven Johnson syndrome following the combination of these two drugs.

scholarly journals Skin-limited Langerhans cell histiocytosis in an adult: a case report

2021 ◽  
Author(s):  
Neringa Guobytė ◽  
Emilija Šerpytienė ◽  
Monika Macejevska ◽  
Milda Krivickaitė ◽  
Jūratė Grigaitienė
Keyword(s):  
Langerhans Cell Histiocytosis ◽  
Skin Lesions ◽  
Langerhans Cell ◽  
Braf V600e ◽  
Multisystem Disease ◽  
Small Nodule ◽  
Systemic Spread ◽  
Life Threatening ◽  
History Of ◽  
Skin Surgery

Langerhans cell histiocytosis (LCH) is an idiopathic group of disorders characterized histologically by proliferation and infiltration of tissue by Langerhans cell-type histiocytes. This disease can affect various organs. Patients with single system lesion should be followed carefully. Detection of somatic BRAF-V600E mutation in circulating blood cells or in lesional biopsies has been associated with high-risk clinical characteristics. A 38-year old male presented to our Dermatology Centre with a 3 months history of small nodule on his right leg skin. Surgery to remove the lesion was performed. The diagnosis of skin-limited Langerhans cell histiocytosis was established. Due to possible systemic spread the patient was referred to a haematologist for further evaluation. Full body CT scan did not show any infiltrates in other organs. Bone marrow aspirate and biopsy was performed, no Langerhans cells were detected. Sometimes skin lesions may represent the most clinically evident manifestation of potentially life-threatening multisystem disease.

scholarly journals Satu kasus nekrolisis epidermal toksik yang diduga disebabkan oleh kotrimoksasol

2017 ◽  
Vol 9 (1) ◽  
Author(s):  
Ellen Gunawan ◽  
Anthony S. Wibawa ◽  
Pieter L. Suling ◽  
Nurdjannah J. Niode
Keyword(s):  
Toxic Epidermal Necrolysis ◽  
Specific Treatment ◽  
Polymyxin B ◽  
Electrolyte Balance ◽  
Eye Drops ◽  
Conjunctival Hyperemia ◽  
The Face ◽  
Life Threatening ◽  
History Of ◽  
Extensive Necrosis

Abstract: Toxic epidermal necrolysis (TEN) is an acute life-threatening muco-cutaneous reaction, characterized by extensive necrosis and detachment of the epidermis (>30% BSA). Drugs are often suspected as the main cause, one of which is trimethoprim- sulfamethoxazole (TMP-SMX). Management includes immediate termination of alleged drugs, supportive treatment such as maintenance of electrolyte balance, nutrition, analgesics, antibiotics and specific treatment of immunosuppressants with dexamethasone injection. We reported a female 36 yo who complained of dark red spots and flaky skin on the face, chest, abdomen, back, arms, and genitals associated with fever, dysphagia, and sore eyes. There was a history of cotrimoxazole consumption prior to the rashes. Skin examination revealed multiple, well defined, erythematous macula, numular to plaque-sized, multiple bullae, purpura, erosion, crusts, and epidermolysis on the face, chest, abdomen, back, and upper extremities. Patient also had vulval erosion and conjunctival hyperemia. Laboratory tests showed total protein 6.5 g/dL and albumin 3.2 g/dL. Patient was treated with intravenous RL:D 5%:NaCl 0.9% = 1:1:1 20 gtt/min, ranitidine injection 2x25 mg IV, ceftriaxone injection 1x2 gr IV, NaCl 0.9% moist dressing 3x30 minutes on erosions, polymyxin B sulphate, neomycin sulphate and dexamethasone eye drops 4x1gtt, artificial tears 6x1gtt, and tapered dexamethasone injection 4x10 mg IV. Diagnosis of TEN was established through anamnesis, physical examination, and laboratory examination. Patient showed clinical improvement within 2 weeks after the discontinuation of cotrimoxazole, and administration of supportive and specific treatment.Keywords: toxic epidermal necrolysis, cotrimoxazoleAbstrak: Nekrolisis epidermal toksik (NET) merupakan reaksi mukokutan akut yang mengancam jiwa, ditandai nekrosis dan pelepasan epidermis yang luas (>30% LPB). Obat diduga sebagai penyebab utama, salah satunya ialah golongan trimetoprim-sulfametoksazol (TMP-SMX). Penatalaksanaan meliputi penghentian segera obat yang diduga penyebab, penanganan suportif (keseimbangan elektrolit, nutrisi, analgetik, antibiotik) dan pengobatan spesifik (imunosupresan deksametason injeksi). Kami melaporkan kasus seorang perempuan 36 tahun dengan bercak merah kehitaman dan kulit terkelupas di wajah, dada, perut, punggung, kedua lengan, dan kelamin disertai demam, nyeri menelan, dan kemerahan pada mata. Riwayat konsumsi kotrimoksazol sebelum timbul ruam. Status dermatologikus: pada wajah, dada, perut, punggung, kedua lengan atas dan bawah terdapat makula eritematosa, batas tegas, multipel, ukuran numular-plakat; bula, purpura, erosi, krusta, dan epidermolisis. Terdapat erosi vulva erosi dan konjungtiva hiperemis bilateral. Pemeriksaan laboratorium: protein total 6,5 g/dL dan albumin 3,2 g/dL. Penanganan berupa IVFD RL:D 5%:NaCl 0.9% = 1:1:1 20 tetes/menit, injeksi ranitidin 2x25 mg IV, injeksi seftriakson 1x2 gr IV, kompres terbuka NaCl 0,9% 3x30 menit (luka), obat tetes mata (polimiksin B sulfat, neomisin sulfat dan deksametason) 4x1 tetes, airGunawan, Wibawa, Suling, Niode: Satu kasus nekrolisis epidermal toksis ... mata buatan 6x1 tetes dan injeksi deksametason 4x10 mg IV yang diturunkan secara bertahap sesuai perbaikan klinis. Diagnosis NET pada kasus ini ditegakkan berdasarkan anamnesis, pemeriksaan fisik, dan pemeriksaan penunjang. Keadaan umum pasien membaik dalam 2 minggu setelah dilakukan penghentian obat yang diduga penyebab, penanganan suportif, dan pengobatan spesifik.Kata kunci: nekrolisis epidermal toksik, kotrimoksazol

scholarly journals A Novel and Severe Clinical Picture Related to COVID-19: Multi-Inflammatory Syndrome in Children

2021 ◽  
Author(s):  
Fatih Haşlak ◽  
Mehmet Yıldız ◽  
Sezgin Şahin ◽  
Amra Adrovic Yıldız ◽  
Kenan Barut ◽  
...  
Keyword(s):  
Macrophage Activation ◽  
Clinical Findings ◽  
Disease Course ◽  
Toxic Shock ◽  
Active Infection ◽  
Severe Clinical Picture ◽  
Life Threatening ◽  
History Of ◽  
Distinct Features ◽  
Inflammatory Syndrome

Preliminary data have suggested that children have milder COVID-19 disease course compared to adults. However, pediatric cases with severe clinical findings caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) are being reported since April 2020. These children have been presented with significant hyperinflammatory states resembling Kawasaki disease, toxic shock syndrome, and macrophage activation syndrome. However, they had several distinct features, as well. Therefore, this novel condition was considered a unique disease and named Multi-inflammatory syndrome in children (MIS-C). Thus, new concerns have been raised regarding the vulnerability of the children. However, it has been realized that this condition is extremely rare. Nonetheless, considering that it is a life-threatening disease and may cause devastating consequences, clinicians should be aware of MIS-C while evaluating children with persistent fever and history of COVID-19 contact or active infection.

scholarly journals Hemophagocytic Lymphohistiocytosis as the Initial Presentation of Subcutaneous Panniculitis-Like T-Cell Lymphoma: A Rare Case Responding to Cyclosporine A and Steroids

2020 ◽  
Vol 8 ◽  
pp. 232470962098153
Author(s):  
Caitlin Sullivan ◽  
Arya Loghmani ◽  
Katharine Thomas ◽  
Rachna Jetly-Shridhar ◽  
Rajasree Pia Chowdry
Keyword(s):  
T Cell ◽  
Cyclosporine A ◽  
Hemophagocytic Lymphohistiocytosis ◽  
Cell Lymphoma ◽  
Skin Lesions ◽  
T Cell Lymphoma ◽  
Cytotoxic T Cell ◽  
Life Threatening ◽  
History Of ◽  
Rare Malignancy

Subcutaneous panniculitis-like T-cell lymphoma (SPTCL) is a rare peripheral cytotoxic T-cell lymphoma, clinically resembling panniculitis. Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening syndrome of immune overactivation, triggered by underlying conditions. SPTCL presenting with HLH may represent a severe and rapidly progressive disease course. Currently, there is no standardized approach to treatment of HLH secondary to underlying SPTCL. A 34-year-old Asian male presented with a several months history of high fevers, weight loss, and nonpruritic purple discoloration of the skin. He had a skin biopsy showing atypical lymphohistiocytic panniculitis with dermal mucinosis and erythrophagocytosis consistent with SPTCL. The patient was initiated on treatment with dexamethasone and cyclosporine A. Almost immediate improvement of his skin lesions was noted and laboratory abnormalities trended toward baseline within 2 weeks. He noted complete symptom resolution after 3 months on therapy. SPTCL may be treated effectively with cyclosporine A and steroids to achieve rapid clinical and symptom management of this rare malignancy.

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