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Paradoxical reaction manifesting as worsening of inflammation: 2 case reports In a report, two men aged 34 years and 48 years were described, of whom the 34-year-old man developed paradoxical reaction manifesting as worsening of inflammation during treatment with ethambutol, isoniazid, moxifloxacin, pyrazinamide and rifampicin for pulmonary tuberculosis, and the 48-year-old man developed paradoxical reaction manifesting as worsening of inflammation during treatment with ethambutol, isoniazid, pyrazinamide and rifampicin for pulmonary tuberculosis [dosages, routes and duration of treatments to reactions onsets not stated]. Case A: The 34-year-old man, who had a history of substance abuse and diabetes, admitted with cough, weight loss and night sweats. His sputum culture showed Mycobacterium tuberculosis. He was anemic. Ling tissue cytology specimens and bronchoscopic mediastinal lymph node revealed the presence of polynuclear giant cells in the lymph nodes consistent with granulomatous necrotizing inflammation. He started receiving rifampicin, isoniazid, pyrazinamide and ethambutol. After 10 days, drug susceptibility testing showed isoniazid mono-resistance. Hence, isoniazid therapy was replaced with moxifloxacin. One month after initiation of therapy, he developed night sweats, failure to gain weight and pyrexia after initial clinical improvement. Two months after initiation of therapy, culture negativity was achieved after reduction in the bacterial load in the sputum. The signs and symptoms of increased inflammation and deterioration of the chest radiograph were consistent with paradoxical inflammation. Subsequently, he was treated with prednisolone while he continued receiving rifampicin, moxifloxacin, pyrazinamide and ethambutol. Following treatment, his body temperature decreased and dyspnoea resolved. Two weeks later, prednisolone dose was tapered when his symptoms started to subside. Then, the prednisolone dose was further reduced and stopped after 37 days. Case B: The 48-year-old man, who had a history of chronic alcohol abuse, presented with dyspnoea, cough, fever and chest pain at another facility. He was anemic and had elevated CRP level of 195 mg/L. His sputum culture revealed Mycobacterium tuberculosis. He started receiving isoniazid, rifampicin, ethambutol and pyrazinamide. He also received thiamine and pyridoxine for alcohol-related nutritional deficiencies. Then, he was hospitalised and the radiographic imaging showed bilateral extensive pulmonary infiltrates. He had diarrhoea and vomiting initially and suspected to have intestinal, or peritoneal or CNS involvement of tuberculosis. A brain MRI showed no abnormalities; hence, brain involvement was excluded. After one week, his condition deteriorated with tachycardia (145 beats per minute) and hypotensive shock (80/50mm Hg). In spite of reduction in CRP and dyspnoea during the first week, the tachycardia and hypotension persisted. However, a reversal of these clinical improvements was observed in the same time frame that followed. An intercurrent