• PDF / 186,542 Bytes
• 1 Pages / 595.245 x 841.846 pts (A4) Page_size
• 48 Downloads / 164 Views

DOWNLOAD

REPORT

---

1 S

Amphotericin-B liposomal/immunosuppressants/voriconazole Aggravation of aspergillosis due to Aspergillus fumigatus, nephrotoxicity and paraesthesia: case report

A 61-year-old man developed aggravation of aspergillosis due to Aspergillus fumigatus following treatment with methylprednisolone and prednisone for suspected pseudotumoural disease, nephrotoxicity during empiric treatment with amphotericin-B liposomal and paraesthesia during treatment with voriconazole for aspergillosis [not all routes stated; durations of treatment to reactions onset not stated]. The man, whose history was notable for well-controlled diabetes, arterial hypertension and gout, presented in January 2016 with a reduction in right visual acuity along with painless diplopia. MRI was consistent with a provisional diagnosis of right orbital myositis. Pseudotumoural disease was suspected. He started receiving five boluses of methylprednisolone 750–1000mg daily for 3 days, followed by oral prednisone 20–70mg daily for 6 months for suspected tumoural aetiology. However, his symptoms subsequently aggravated, resulting in quasi-blindness and a defect in cranial nerves III, IV and VI. Repeat MRI in July showed development of right sphenoid-ethmoid osteolytic lesions, and a fungal origin was suspected. Investigations showed a β-(1, 3)-Dglucan level of 99 pg/mL and decreased anti-Aspergillus IgG. Giemsa staining revealed the presence of septate mycelia evocative of moulds. Gomori Grocott stain confirmed host tissue invasion by numerous regular, septate filaments with branching at 45°. Culture tests on Sabouraud’s agar isolated and identified multi-sensitive Aspergillus fumigatus with minimum inhibitory concentration of 0.094 mg/L to voriconazole and 0.125 mg/L to amphotericin-B liposomal. Quantitative PCR for Aspergillus DNA targeting the mitocondrial tRNA gene was found to be positive. Ethmoid biopsy by conventional PCR targeting confirmed the presence of Aspergillus fumigatus strain. Therefore, he was diagnosed with rhino-orbital-aspergillosis, and the aggravation of his initial symptoms (i.e. aggravation of aspergillosis due to Aspergillus fumigatus-rhino-orbital-cerebral aspergillosis) was attributed to corticosteroid therapy with methylprednisolone and prednisone. The man received treatment with IV voriconazole 12 mg/kg daily on the first day (loading dose) followed by 8 mg/kg daily for 4 days. The therapy was further continued with oral voriconazole 400 mg daily for 3 months. Therapeutic drug monitoring revealed plasma voriconazole concentration of 6.18 mg/L for loading dose and ranged from 1.78 to 3.95 mg/L between July and October. In October 2016, β-(1, 3)-D-glucan was 75 pg/mL and tests for galactomannan showed an index of 0.05. His blindness persisted and a right frontal lobe lesion was noted on cerebral MRI. Direct examination, histological analysis, culture and quantitative PCR for Aspergillus DNA from the frontal lobe lesion sample also confirmed Aspergillus fumigatus. He underwent a surgical excision, which required hospitalisation.