Journal Article Kikuchi's disease, skin and systemic lupus erythematosus Get access British Journal of Dermatology, Volume 146, Issue 1, 1 January 2002, Pages 167–168, https://doi.org/10.1046/j.1365-2133.2002.4513_4.x Published: 01 January 2002
Subacute cutaneous lupus erythematosus (SCLE) manifests with erythematous, nonscarring, annular, or papulosquamous plaques. Proton pump inhibitors (PPIs) are increasingly being incriminated in its causation, but reports of similar nature from India are lacking.To describe the characteristics of seven patients with SCLE induced by PPIs and to review the published cases in order to provide a better perspective of the association.We describe seven patients of PPI-induced SCLE, seen over a period of 6 years. We also review the literature for additional data on PPI-induced SCLE. The selected publications were reviewed, and relevant clinical and laboratory data were extracted.Of the total seven cases, there were four males and three females with a mean age of 60.2 ± 5.5 years (range 53-70 years). Nine episodes of PPI-induced SCLE were recorded in the seven patients. Of the initial episodes, esomeprazole was implicated in four, pantoprazole in two, and rabeprazole in one patient. Latency period ranged from 2 weeks to 1 year (mean 11.4 ± 16.2 weeks). Morphology was described as annular scaly plaques in six and papulosquamous in one. Antinuclear antibodies and anti-Ro antibodies were positive in all patients. Naranjo probability scale was used in all patients; two were categorized as definite and five as probable. Treatments included drug withdrawal in six patients, topical steroids in one, systemic corticosteroids in all seven, and hydroxychloroquine in one patient, used alone or in combinations. Complete remission was achieved in six cases, while one had partial remission.Retrospective nature of this study and limited number of patients.PPIs can trigger SCLE.
Dermatopathia pigmentosa reticularis is a rare ectodermal dysplasia characterized by a triad of generalized reticulate hyperpigmentation, noncicatricial alopecia, and onychodystrophy. We report a case of a 22-year-old male with characteristic features of the diagnostic triad and adermatoglyphia of palm and soles. On dermoscopic examination reticulated hyperpigmented spots, reticulated pigmented spots, monotonous pigmented spots, reticulated hypopigmented spots, with perifollicular hypopigmentation were observed. Dermoscopic findings of palm and soles showed hyperpigmented reticular pattern with dots and adermatoglyphia. Onychoscopy and trichoscopy are also discussed. Histopathology revealed orthokeratosis, epidermal atrophy, increase in melanin pigment in basal layers with vacuolization, and dermal pigmentary incontinence. Other inherited reticulate dermatoses such as Naegeli–Franceschetti–Jadassohn syndrome, dyschromatosis symmetrica hereditaria, and dyskeratosis congenita were considered in differential diagnosis and are discussed.
Kikuchi's disease is a rare, benign, self-limited disorder, characterised clinically by fever and tender regional lymphadenopathy. It has been reported worldwide and is particularly common in people of Asian descent. The cause of Kikuchi's disease is unknown. It predominantly affects young females and can closely mimic several infectious and immunological conditions. Histopathologic features of lymph nodes in Kikuchi's disease are characteristic and permit differentiation of this benign condition from lymphomas, systemic lupus erythematosus and infectious lymphadenopathies. We report a female patient presenting with fever and tender cervical lymphadenopathy. She was being treated for tubercular lymphadenitis and was referred after she developed a transient hepatitis and a skin rash following treatment with anti-tubercular drugs. An excisional biopsy of the lymph node revealed histiocytic necrotising lymphadenitis, consistent with Kikuchi's disease. A brief review of the pathogenesis and differential diagnosis of Kikuchi's disease is presented.
Abstract A 27 year old man presented with multiple papules, nodules, and hyperpigmented spots on the body, which he had had since early childhood. In addition, he had a deformity of the right forearm. Examination revealed multiple large sized café-au-lait macules, axillary freckling, and soft cutaneous neurofibromas (mollusca fibrosa). The right forearm was grossly shortened with a length of only 12 cm (fig 1). It presented a globular appearance and on palpation the forearm bones had a break in their continuity. There was hypermobility at the wrist and elbow joints in addition to abnormal movements through the forearm. The left forearm was 28 cm in length and bones were normal. Radiological examination revealed pseudoarthrosis in the mid-part of right forearm involving both the radius and ulna, dislocation of humeroulnar joint, radioulnar diastasis, and a decrease in the bone density (fig 2). On ophthalmological examination, there were multiple bilateral Lisch nodules. A diagnosis of neurofibromatosis type-1 and pseudoarthrosis as a complication was thus established.
Sir, A 62-year-old male presented with fever, skin rash, and oral erosions of one-week duration. He was a known case of metastatic carcinoma urinary bladder with bilateral DJ stent in situ, on regular oncology follow-up. He received injection enfortumab 1.25 mg/kg on days 1 and 8 of the first cycle. Skin rashes started 3 days after the first infusion of enfortumab given on October 19, 2020; no dose modification was required as these were of grade 1. However, skin rashes worsened after the second infusion which was given a week later. Past treatments included four cycles of gemcitabine and cisplatin and eight cycles of pembrolizumab. His medical history was significant for hypertension, coronary artery bypass grafting in 2006, and chronic liver disease. On examination, the patient was febrile, drowsy, with tender, macular, reticulate erythematous rash over neck, axillae, forearms, flanks [Figure 1a and b], groin folds, proximal thighs, lower trunk, and feet [Figure 2a-c]. Erosions over lips and palate, multiple scattered follicular pustules over scalp, and crusting over nasolabial folds were also observed [Figure 3a-c]. Conjunctival redness, discharge from eyes, and erythema over palms and soles without target lesions or blisters were present.Figure 1: Erythematous macules and patches in reticular pattern over forearm (a) and flank (b)Figure 2: Reticular erythematous macules and patches over lower trunk (a), thighs (b), and feet (c)Figure 3: Erosions over lips and palate (a), multiple scattered follicular pustules over the scalp (b), and crusting over nasolabial folds (c)Investigations revealed hemoglobin 8.8 g/dL, total leucocyte count 2.3 × 109/L, with 58.9% neutrophils, 29.9% lymphocytes, 10.2% monocytes, and 0.8% eosinophils and platelet count 90 × 103/L. Serum creatinine was 2.9 mg/dL and total and direct bilirubin level were 3.1 and 2.3 mg/dL, respectively. Serum albumin was 2.5 mg/dL, and serum transaminases were normal. Urine routine, chest X-ray, ECG, and thyroid profile were normal. A diagnosis of enfortumab-induced symmetrical flexural and intertriginous exanthem (grade 4 skin rash, Common Terminology Criteria for Adverse Events) was considered. Patient was treated with antibiotics, systemic and topical corticosteroids, and other supportive care. Gradually over the next 2 days, he remained febrile with extreme difficulty in swallowing and the erythema persisted with development of erosions over trunk. His urine output decreased; serum creatinine increased to 4.9 mg/dL with worsening leucopenia (total leucocyte count 100 × 109/L, absolute neutrophil count 1 × 109/L) and thrombocytopenia, platelet count of 26 × 103/mm3. Total and direct bilirubin increased to 5.9 and 5.1 mg/dL. Blood and urine cultures showed no growth. Chest X-ray and ultrasound abdomen were normal. Arterial blood gas analysis showed lactic acidosis. Continuous renal replacement therapy was planned after nephrology review, while transfusion of fresh frozen plasma and platelets was continued. On day 5, peeling of skin occurred at sites of removal of micropore tape, corresponding to positive pseudo-nikolsky sign [Figure 4]. Also, the skin over the back and axilla started peeling off forming sheets of erosions [Figure 5a and b]. Toxic epidermal necrolysis (TEN) induced by enfortumab vedotin was considered and he was shifted to the intensive care unit. SCORTEN score was 5. Consent for skin biopsy was not given. The condition of patient remained critical, and on day 6, he developed hypotension, multi-organ failure, and septic shock and subsequently he expired.Figure 4: Peeling of skin at sites of removal of micropore tapeFigure 5: Sheets of erosions over axilla (a) and back (b)Enfortumab vedotin is antimitotic antibody–drug conjugate which is directed against Nectin-4 present on calcium-dependent immunoglobulin adhesion molecules located at adherens junctions, thus inhibiting microtubule assembly.[1] The drug binds with high affinity to nectin-4, expressed on tumor cells, which induces internalization of monomethyl auristatin E, a microtubule-disrupting agent which leads to cell apoptosis and impaired cell division. It has a role in cell–cell adhesion, and a functional disturbance could lead to impaired cell–cell attachment, which could explain the epidermal detachment observed in TEN.[2] In 2019, the United States Food and Drug Administration approved the drug as a third-line treatment for patients who had failed in previous trials of programed cell death protein 1 and platinum-based chemotherapeutic agents in patients of metastatic urothelial carcinoma.[1] The drug has demonstrated to have a significant response rate in early phase trials and is known for its tolerable side-effect profile.[3] The most common adverse reactions include fatigue, peripheral neuropathy, decreased appetite, nausea, dysgeusia, diarrhea, dry eyes, rash, alopecia, pruritus, and dry skin.[3] Cutaneous adverse reactions can be observed with enfortumab vedotin and are generally low grade and manageable, often demonstrating a maculopapular and diffuse appearance.[1] Skin rashes have been reported in 54% of patients given enfortumab, of which 26% presented with maculopapular rash while 30% had pruritus.[3] Grades 3–4 skin reactions occurred in 10% patients and included symmetrical drug-related intertriginous and flexural exanthem (SDRIFE), bullous dermatitis, exfoliative dermatitis, and palmo-plantar erythrodysesthesia.[3] Enfortumab vedotin is a new drug on the horizon for metastatic urothelial carcinoma. We are reporting this case from India to highlight the risk of severe cutaneous adverse reactions from this drug. Skin biopsy helps in differentiating from other possible entities though TEN is mainly a clinical diagnosis. Consent for skin biopsy was refused in our patient by his family because of his critical condition. On initial evaluation, in our patient, morphology of rash resembled SDRIFE; however, rapidly progressing erosions and worsening mucosal involvement occurred. In the absence of skin biopsy, it remains inconclusive whether the rash of SDRIFE progressed to TEN or it was a case of atypical presentation of TEN. Physicians using this molecule should remain extremely vigilant since most of the patients are elderly, have comorbidities, and on multiple other drugs. Two patients of enfortumab-induced TEN with fatal outcome have been reported previously[45] and our would be third such patient. Abbreviations SDRIFE: Symmetrical drug-related intertriginous and flexural exanthem. TEN: Toxic epidermal necrolysis. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.
Anti-epileptic drugs can be associated with a wide spectrum of cutaneous adverse reactions ranging from simple maculopapular rashes to more severe and life threatening reactions like Stevens-Johnson syndrome and toxic epidermal necrolysis. These rashes are well documented with older antiepileptic drugs like phenytoin, phenobarbitone and carbamazapine. Lamotrigine is a newer, unrelated antiepileptic drug that causes skin rashes in 3-10% of new users. Higher starting dose or rapid escalation, concurrent treatment with valproic acid, and a previous history of a rash with other antiepileptic drugs are well recognized risk factors for lamotrigine related serious rashes. We report two patients with toxic epidermal necrolysis, resulting from concomitant use of lamotrigine and valproic acid. It is emphasized that clinicians adhere to the recommended dosage guidelines and adopt a slow dose titration when initiating treatment with lamotrigine.
Abstract A man whose psoriasis was well controlled on methotrexate treatment developed pellagra-like photosensitive dermatitis when he started taking haloperidol. Reactivation of his dermatitis was observed with methotrexate as a recall photosensitivity phenomenon. This false photosensitivity reaction of methotrexate is an important but rarely encountered adverse effect. A possible interaction between methotrexate and haloperidol is emphasised.
Acantholytic squamous cell carcinoma is a rare and aggressive histological variant of squamous cell carcinoma, characterized by tubular and alveolar patterns as a consequence of the acantholysis. We report a case of acantholytic squamous cell carcinoma in a 70-year-old woman, who was admitted to our institution for the progressively enlarging exophytic and ulcerated lesion. We report this interesting lesion due to the rarity of acantholytic variant of squamous cell carcinoma and the literature is briefly reviewed.
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