Background-A study was undertaken to evaluate the diagnostic value of pleural fluid concentrations of interferon gamma (IFN-) as a marker of tuberculosis. Methods-Patients admitted to King Chulalongkorn Memorial Hospital between April 1997 and January 1998 with a lymphocytic exudative pleural eVusion were enrolled into the study. The pleural fluids were examined for cytology, staining for acid fast bacilli, and mycobacterial culture. Pathological examination and mycobacterial culture were performed on each pleural biopsy specimen. The diagnosis of tuberculosis was made when one of the following criteria was met: (1) Mycobacterium tuberculosis was isolated from either the pleural fluid or pleural tissue; (2) granulomas were demonstrated in the pleural tissue which stained positive for acid fast bacilli (AFB); or (3) in the presence of granulomas negative on staining for AFB in pleural tissue there was a response to antituberculous treatment on follow up. All pleural fluid samples were stored at -70°C and the IFN-level was measured by immunoassay. Analysis was made using sensitivity, specificity, and likelihood ratio for a positive test result. The best cut oV point was determined by the highest likelihood ratio and receiver operating characteristic curve. Results-A total of 66 patients were enrolled and tuberculosis was confirmed in 39 of them. The diagnoses in the nontuberculous group included malignancy (15), paramalignancy (11), and chronic pleuritis secondary to infective endocarditis (1). The mean (SE) IFN-level in the pleural fluid was significantly higher in the tuberculous group than in the nontuberculous group (1493.3 (131.3) pg/ml versus 80.1 (50.4) pg/ml, p<0.001). The overlap between the two groups was minimal. At the cut oV value of 240 pg/ml the sensitivity was 94.9% (95% CI 86.6 to 100), the specificity was 96.3% (95% CI 89.2 to 100), and the likelihood ratio for a positive test result was 25.6. Conclusions-The pleural fluid concentration of IFN-is a good and useful diagnostic marker of tuberculosis presenting as a lymphocytic exudative pleural eVusion. (Thorax 1999;54:921-924)
Between January 1981 and December 1991, 68 adults were treated at Chulalongkorn University for cobra bites. Respiratory failure developed in the bite victims even when an adequate genus-specific antivenin was administered at the onset of neuromuscular paralysis. The duration of time spent on a respirator was, however, significantly less in patients treated with an intravenous 100-ml antivenin bolus given at the onset of neurotoxic signs. We found that a bolus of 100 ml of purified equine antivenin produced by the Queen Saovabha Memorial Institute, Bangkok, from Naja kauthia venom was adequate and that increasing the dose did not lead to added benefits. Time spent on a respirator was approximately 10 h in antivenin-treated groups and 40 h if no antivenin or an inadequate dose was used. Competent respiratory and nursing care alone without antivenin will lead to eventual recovery and prevent death. Local bite site tissue necrosis and duration of hospitalization were not related to the dose of antivenin given. Hospitalization was prolonged in subjects who developed sepsis or who had severe tissue necrosis or other surgical or medical complications.
A patient bitten by Bungarus candidus (Malayan krait) developed nausea, vomiting, weakness, and myalgia 30 minutes after being bitten. One hour later, ptosis and occulomotor palsies as well as tightness of his chest were noted. Respiratory failure requiring mechanical respiration appeared 8 hours after the bite and lasted for nearly 96 hours. The two bite sites were virtually painless and resulted in slight transient erythema and edema. No specific antivenin was available, and treatment consisted of respiratory support and management of aspiration pneumonitis. Recovery was complete.
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