Background:Dengue infections may present with neurological complications. Whether these are due to neuromuscular disease or electrolyte imbalance is unclear.Materials and Methods:Eighty-eight patients of dengue fever required hospitalization during epidemic in year 2010. Twelve of them presented with acute neuromuscular weakness. We enrolled them for study. Diagnosis of dengue infection based on clinical profile of patients, positive serum IgM ELISA, NS1 antigen, and sero-typing. Complete hemogram, kidney and liver functions, serum electrolytes, and creatine phosphokinase (CPK) were tested. In addition, two patients underwent nerve conduction velocity (NCV) test and electromyography.Results:Twelve patients were included in the present study. Their age was between 18 and 34 years. Fever, myalgia, and motor weakness of limbs were most common presenting symptoms. Motor weakness developed on 2nd to 4th day of illness in 11 of 12 patients. In one patient, it developed on 10th day of illness. Ten of 12 showed hypokalemia. One was of Guillain-Barré syndrome and other suffered from myositis; they underwent NCV and electromyography. Serum CPK and SGOT raised in 8 out of 12 patients. CPK of patient of myositis was 5098 IU. All of 12 patients had thrombocytopenia. WBC was in normal range. Dengue virus was isolated in three patients, and it was of serotype 1. CSF was normal in all. Within 24 hours, those with hypokalemia recovered by potassium correction.Conclusions:It was concluded that the dengue virus infection led to acute neuromuscular weakness because of hypokalemia, myositis, and Guillain-Barré syndrome. It was suggested to look for presence of hypokalemia in such patients.

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BACKGROUND AND OBJECTIVESTissue hypoxia due to repeated apneas among patients of obstructive sleep apnea syndrome (OSAS) leads to cumulative oxidative stress. It is established that an increased plasma level of hypoxanthine/xanthine may serve as a criterion of tissue hypoxia. We presumed that plasma levels of hypoxanthine/xanthine might be high among patients of OSAS due to oxidative stress. Nobody studied this relationship earlier. The aim of this study was to estimate their plasma levels as markers of hypoxia.DESIGN AND SETTINGSThis case-control study was performed for a period of 1-year including patients referred to a tertiary care hospital, New Delhi, India.MATERIALS AND METHODSIt was a case-control study. A total of 43 patients of OSAS, diagnosed by overnight polysomnography (PSG), were included in the study. Age- and sex-matched 43 subjects in whom the presence of OSAS was not confirmed by overnight PSG were enrolled as healthy controls. The severity of disease was classified on the basis of apnea-hypopnea index (AHI). Out of 43 patients, 9 were moderate and 14 were severe. None was with mild OSAS. The venous blood sample was collected in the morning after PSG. Hematological and biochemical assays were also performed. Plasma levels of hypoxanthine/xanthine were measured by fluorometric analysis (normal laboratory reference <2.00 mmol/L). Data collected was analyzed statistically by SPSS version 14.0, student unpaired t test, chi-square test, Mann-Whitney U test, and Pearson correlation coefficient.RESULTSThe mean plasma level of hypoxanthine/xanthine in patients of OSAS was found to be 5.4 (5.1) mmol/L, and in controls it was 1.2 (0.4) mmol/L. A statistically significant (P=.000) difference was found between both groups. Among patients, a positive correlation between hypoxanthine/xanthine levels with age, AHI, and serum triglyceride levels was observed. The joint explanatory power of these significant factors was found to be 59.6% (P<.001).CONCLUSIONPlasma levels of xanthine/hypoxanthine were significantly elevated in patients of OSAS, and these were positively correlated with age, serum triglyceride levels, AHI, and severity of the disease.

Background:Sometimes etiological diagnosis of pleural effusion is difficult despite cytological, biochemical and microbiological tests and labeled as undiagnosed exudative pleural effusions.Aim of present study was to make an etiological diagnosis of pleural effusion.Materials and Methods:Study group included patients of exudative pleural effusion where etiological diagnosis could not be yielded by conventional cytological, biochemical and microbiological investigations. Pleural tissue was obtained by Cope’s pleural biopsy needle and or thoracoscopy. Pleural biopsy was subjected to histopathology, ZN staining and culture to find the mycobacterium tuberculosis.Results:Out of 25 patients, 17 (68%) and 8 (32%) were male and female, respectively. Age ranged from 15 to 65 years (mean 31.72). Mean value of serum and pleural fluid LDH was 170.56 U/L and 1080.28 U/L, respectively. Histopathology of 9 (36%) showed epitheloid granuloma with caseation necrosis. In other 9 (36%) patients, epitheloid granulomas (with or without giant cells) was reported. In 5 (20%) patients, histopathology report was of nonspecific chronic inflammation. Histopathology was reported as normal in one case; it turned out to be a case of malignancy. In two (8%) patients, pleural tissue obtained was inadequate for opinions; however, other tests revealed malignancy in one and tuberculosis in other. Ziehl-Neelsen (ZN) stain was positive for AFB in two patients and culture of pleural tissue showed presence of Mycobacterium tuberculosis in three patients.Conclusions:The role of percutaneous closed needle biopsy of pleura among patients of undiagnosed exudative pleural effusion is still accepted as a diagnostic tool, as this may lead to a specific diagnosis among 76% of cases. This is of particular importance in a developing country like India where the facilities of thoracoscopy and imaging guided cutting needle biopsies are not easily available.

BACKGROUND AND OBJECTIVESTissue hypoxia due to repeated sleep apneas leads to increased serum levels of uric acid (UA) and lactate in patients with obstructive sleep apnea syndrome (OSAS). Studies on assessment of serum level of UA in patients of OSAS are available. However, research on simultaneous evaluation of levels of serum lactate and UA is lacking.DESIGN AND SETTINGProspective, case-control study.PATIENTS AND METHODSForty patients suffering from OSAS, diagnosed by night polysomnography (PSG), were included in this study. Forty age- and sex-matched subjects in whom the presence of OSAS was ruled out by night PSG were included as healthy controls. Participants underwent a procedure for the measurement of serum UA and lactate before and after sleep.RESULTSBoth before and after sleep UA levels of patients with OSAS were found to be significantly higher (P=.001 and .002, respectively) as compared to UA levels of controls. A statistically significant (P=.02) overnight (after sleep) rise was observed in the serum lactate level of OSAS patients. The correlation between serum UA values and %TSTs (percentage of total sleep time spent) below 95% SaO2 (arterial oxygen saturation) (P=.02) was statistically significant. The correlation was positive with %TSTs below 90% SaO2, whereas it was found negative with normal basal oxygen. No significant correlation was observed between serum UA and the AHI (apnea-hypopnea index). Polysomnographic variables failed to show significant correlation with serum UA on respective multiple regression models controlling for age, body mass index, and waist-hip ratio. However, plasma lactate levels after sleep correlated with %TSTs below 95% of SaO2 and AHI with P values of .02 and .01, respectively.CONCLUSIONSBoth serum UA and lactate were positively correlated with the degree of hypoxia in OSAS. The measurement of serum lactate level was a better marker of oxidative stress among patients with OSAS.