Prednisolone
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Disseminated cutaneous mycobacterial co-infection and bacterial sepsis: case report A 56-year-old woman developed disseminated cutaneous mycobacterial co-infection due to Mycobacterium tuberculosis (MTB) and Mycobacterium abscessus (MAB) and fatal sepsis due to Acinetobacter baumannii and Klebsiella pneumoniae following intermittent self-administration of prednisolone for polyarthralgia. The woman, who was diagnosed with lupus nephritis in 2008, presented with a 10-week history of multiple painless ulcers over her abdomen. She reported intermittent selfadministration of oral prednisolone 20mg [frequency not stated] since 8 years for polyarthralgia. Her medical history was significant for iatrogenic hypothalamic pituitary adrenal axis suppression, uncontrolled diabetes mellitus and hypothyroidism. At presentation, physical examination showed protuberant abdomen, cushingoid facies with round face and seven large, ill-defined, erythematous, painless, indurated plaques with central ulceration on the abdomen and both the thighs. Laboratory investigations were positive for anti-nuclear antibody with no presence of anti-doublestranded DNA antibody and hypocomplementaemia suggestive of quiescent lupus. Her morning serum cortisol was low along with elevated thyroid-stimulating hormone and HbA1C levels. Contrast-enhanced CT scan of the chest and abdomen revealed marked hepatosplenomegaly. Histopathology of skin biopsy showed well-formed epithelioid cell granulomas containing mixed inflammatory cell infiltrates and acid-fast bacilli. After 8 weeks of incubation, mycobacterial culture from skin biopsy and pus discharge was negative for both MTB and nontuberculous mycobacterium (NTM). However, multiplex PCR for DNA extracted from the skin biopsy and pus samples identified MTB. The woman was treated with standard anti-tubercular therapy comprising rifampicin, isoniazid, pyrazinamide, ethambutol and pyridoxine. Within 3 weeks of the treatment, new lesions stopped appearing. The ulcers on the right thigh improved significantly but the size of three ulcers (two adjacent ulcers on the abdomen and one on the left thigh) continued to increase. Therefore, the possibility of drugresistant MTB and NTM was suspected, and pus sample was collected from the ulcers and analysed by nucleic acid amplification test (NAAT) and by NTM PCR. NAAT was positive for MTB complex and rifampicin resistance mutations were not observed. NTM PCR was also positive for MAB from both the biopsy and the pus samples using specific primer for the MAB-chelonae complex. Subsequently, MAB was confirmed by hsp65 sequencing using an ABI 3130 sequencer. Finally, she was diagnosed with disseminated cutaneous co-infection with MTB and MAB. Therefore, clarithromycin and amikacin were added, and repeated debridement of ulcers was performed. The lesions improved and their progression stopped. Three weeks later, she developed fatal hospitalacquired sepsis due to Acinetobacter baumannii and Klebsiella pneumoniae. Author comment: "Unsupervised use of oral steroids by our
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