Background Baboon syndrome is a rare, type IV hypersensitivity reaction causing a maculopapular rash. Tamoxifen is an antineoplastic agent, working as an estrogen receptor antagonist, also called a selective estrogen receptor modulator. A variety of rashes were reported with Tamoxifen use to‐date except baboon syndrome. The Tamoxifen‐induced baboon syndrome seems to be reversible, as discontinuation of the drug improves clinical outcomes. Aim Herein, we present the first case of Tamoxifen‐induced baboon syndrome which occurred 8 years after initiation of Tamoxifen use. Patients A 44‐year‐old woman presented with papulovesicular eruption on her body and erythema on her face for a duration of 6 months. There was no evidence of ocular or mucosal involvement. She was diagnosed with breast cancer and treated with tamoxifen 10 mg twice daily over the past 8 years. She was not taking other medications or over‐the‐counter supplements at the time of presentation. The patient underwent urgent skin biopsies of two lesions on her buttock and thigh. No organisms were seen on Gram stain. The patient's skin biopsy revealed extensive hyperorthokeratosis, minimal parakeratosis, hypergranulosis, and lichenoid interface dermatitis in the irregularly acanthotic epidermis supporting diagnosis of fixed drug eruption. Following a multidisciplinary discussion, the patient was diagnosed with baboon syndrome or symmetrical drug‐related intertriginous and flexural exanthema (SDRIFE) associated with Tamoxifen. Results Hence, Tamoxifen was immediately discontinued and treated with oral steroid along with topical agents. She showed improvement of clinical abnormalities within days after discontinuation of Tamoxifen. Conclusions Given the widespread use of Tamoxifen in the management of patients with breast cancer, it is important that healthcare professionals monitor for rare, however clinically significant, and potentially life‐threatening dermatological manifestations of Tamoxifen use, such as baboon syndrome.
We report a 26-year-old male with a 4 mm diameter, asymmetric, irregularly pigmented and bordered, brown maculopapular lesion on the right nipple present since childhood with enlargement of the lesion within the last 3 months. Dermoscopy revealed a global globular pattern with the presence of focally light brown globules and irregular black globules in its centre. In vivo reflectance confocal microscopy (RCM) revealed dense junctional and dermal melanocytic nests of different sizes and shapes that appeared as sharply demarcated round to oval reflective structures; cellular outlines of single melanocytes were not always detected. In the centre of the lesion within the upper dermis, irregularly shaped, homogeneously reflecting structures were observed. As a clear differentiation between clusters of melanophages and melanocytic nests could not be made with certainty, an excisional biopsy was performed to establish the diagnosis of compound nevus with features of congenital nevus. Therefore, to prove that dermoscopic globules correlated with melanophages, the correlation between dermoscopic RCM and histopathology was necessary.
Our finding revealed that resistance against amphotericin B, itraconazole, ketoconazole, posaconazole, and fluconazole can be observed in C. albicans.
Background: Fixed Drug Eruption (FDE) is a drug reaction involving the skin and less commonly the mucosal membranes. Tamsulosin is an alpha-1 adrenergic receptor blocker used to treat benign prostatic hyperplasia. Dizziness and headache are among its most common side effects (Singapore Med J, 2018;59:336). Although cutaneous drug eruption has been reported with other alpha-1 adrenergic receptor blockers.Aims: Drug rash due to Tamsulosin is relatively uncommon (Singapore Med J, 2018; 59:336). In this case we report an incidence of fixed drug eruption due to Tamsulosin.
EditorThe diagnosis and treatment of livedoid vasculopathy is a challenge to the clinician. 1 A 47-year-old patient presented with livid reticular discoloration and ulceration on both legs, aggravated by exposure to cold since the age of 26 years. Clinical examination revealed painful focal purpuric ulcerating lesions, atrophic scarring, teleangiectasia, hemosiderin deposits and hyperpigmentation (Fig. 1a). Laboratory parameters such as coagulation factors, phospholipid antibodies, ANA, ENA, ANCA, C3, C4, immunocomplexes, C-reactive protein, cryoglobulins, cold agglutinins, erythrocyte sedimentation rate, serum protein electrophoresis, and urine were normal or negative. Repeated MRIs of the brain, X-rays of the chest and ultrasound investigations of the abdomen were normal. A skin biopsy specimen revealed dermal thickened vessel walls and fibrin deposits with occasional obliteration. Since 1983
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