Immune-Mediated Adverse Drug Reactions (IM-ARDs) in the Form of Drug-Induced Immune Thrombocytopenia and Cutaneous Adverse Drug Reactions (CARD) Due to Clindamycin in an Human Immunodeficieny Virus (HIV) Patient.

BACKGROUND Many drugs have been reported to cause immune-mediated adverse drug reactions (IM-ADRs) in human immunodeficiency virus (HIV) patients; the most common is cutaneous adverse drug reaction (CADR). Immune thrombocytopenia purpura (ITP) is frequent in HIV patients, and it can be caused HIV, opportunistic infections, or drugs. Although drugs can cause immune thrombocytopenia, termed drug-induced immune thrombocytopenia (DIIT), there has been no study on DIIT in HIV patients. CASE REPORT A 33-year-old male patient was admitted to our hospital with pruritic skin lesion over the entire body, which started 7 days before. He was diagnosed with HIV infection, brain toxoplasmosis, and pulmonary tuberculosis 2 weeks before admission, and was given trimethoprim sulphamethoxazole, isoniazid, rifampicin, pyrazinamide, and ethambutol. Clindamycin was added 10 days before admission. Skin examination revealed generalized erythematous macules with palpable petechiae and purpura. The platelet count was 141 000/µL when he was diagnosed with HIV, and it was 2000/µL at the time of admission. Clindamycin was discontinued and he was given steroids and platelet transfusion. The skin lesions improved along with an increased platelet count. He was discharged on the 10th day of admission, with platelet count of 42 000/µL. When he returned to the outpatient clinic on the 15th day, his platelet was 54 000/µL. The skin lesions had resolved completely and become hyperpigmented, and no purpura or petechiae were seen. CONCLUSIONS We present a case of an HIV patient with IM-ADR in the form of DIIT in conjunction with CADR that might have been caused by clindamycin.

Double atypical co-infection in ecthyma gangrenosum: a peculiar case report.

Introduction: Ecthyma gangrenosum (EG) is a rare cutaneous manifestation commonly associated with Pseudomonas aeruginosa infection in immunocompromised individuals. Additionally, different bacterial and fungal pathogens have also been identified. However, co-infection on EG lesions has never been reported before. Case report: We present the case of a seven-year-old female Asian patient who initially was diagnosed with febrile neutropenia. Initially, on the sixth day of admission, dermatological status revealed multiple painless erythematous macules on the face and arms together with persistent fever followed by evolution to multiple black, deep-seated, and large central eschars and early identification of Pseudomonas aeruginosa in the blood culture. Further evaluation revealed the development of EG with XDR Acinetobacter baumannii and Aspergillus spp. isolated from the samples harvested intraoperatively. Conclusions: Specific identification of etiological agents will serve its importance for early diagnosis, aggressive antibiotic treatment, and/or surgical intervention to improve the prognosis.