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Methylprednisolone/prednisolone/ruxolitinib Various toxicities: case report

An approximately 79-year-old man [exact age at the time of reaction onset not stated] developed pneumocystis pneumonia (PCP) and pulmonary Mycobacterium avium complex (MAC) infection secondary to pulmonary alveolar proteinosis (PAP) following treatment with ruxolitinib for primary myelofibrosis (PMF). He also experienced worsening of MAC infection following treatment with methylprednisolone and prednisolone for presumed eosinophilic pneumonia [routes not stated; not all dosages and outcomes stated]. The man, at the age of 70 years, presented with general malaise and appetite loss. Based on investigational findings, he was diagnosed with PMF. Seven years after the diagnosis of PMF, he started receiving ruxolitinib. However, two years after the initiation of ruxolitinib therapy, he developed high fever and respiratory failure. The man was treated with unspecified antibiotics to which the fever did not respond. Thereafter, he was hospitalised. CT scan revealed diffuse ground grass opacity in the bilateral lungs (crazy-paving pattern). Laboratory investigation at the time of admission revealed elevated levels of lactate dehydrogenase, β-D-glucan, C-reactive protein (CRP) and Krebs von den Lungen-6. His haemoglobin, haematocrit and platelet counts were decreased. Bronchoscopy demonstrated milky bronchoalveolar lavage fluid (BALF), which revealed foamy macrophages with a background of amorphous materials by Papanicolaou stain. Elevation in the eosinophil proportion was observed. Polymerase chain reaction for Pneumocystis jirovecii in the BALF was found to be positive. He was diagnosed with secondary PAP. He was also diagnosed with complication of PCP. The secondary PAP was suspected to be due to ruxolitinib therapy. He was treated with cotrimoxazole and cefepime. Ruxolitinib was discontinued. Thereafter, his body temperature normalised and levels of CRP and β- D-glucan decreased. However, three weeks after admission, he developed a second fever and his CRP level increased. Due to increased eosinophil proportion in the BALF, eosinophilic pneumonia was presumed. Therefore, he started receiving methylprednisolone 1 mg/kg and prednisolone [routes not stated; not all dosages stated]. His body temperature decreased again, and the CRP levels recovering. However, four weeks after admission, his body temperature and CRP level exacerbated again. Mycobacterium intracellulae was detect in the sputum and BALF collected at the admission. The serum samples were found positive for MAC antibody. He was diagnosed with complication of pulmonary MAC infection. Methylprednisolone dose was decreased to 0.5 mg/kg followed by 0.3 mg/kg. He was treated with clarithromycin and ethambutol. However, his respiratory failure progressed. He died 65 days after admission. Autopsy was performed which revealed that both the lungs were filled with eosinophilic material. This eosinophilic material in the alveoli was positive for Periodic acid-Schiff and surfactant A stains. Zi