Hepatitis A in most developing countries is a sporadic childhood disease, but lately focal outbreaks have been observed among children in India. During 2004, we investigated a large-scale outbreak of hepatitis among children living in a residential colony in Daund Taluka of District Pune in the western region of India. In total, 123 overt and 56 sub-clinical cases were detected. All the patients were reactive for IgM antibodies against hepatitis A virus (IgM anti-HAV) and were negative for IgM anti-hepatitis E virus, confirming HAV to be the etiological agent of the outbreak. Serum samples, feces and sewage samples were tested for HAV RNA and molecular characterization of the positives showed the presence of genotype IIIA. Further, IgM anti-HAV-positive sera from eight focal outbreaks were analyzed. The causative HAV in all these small-scale outbreaks also belonged to genotype IIIA, indicating the predominance of genotype IIIA in this region. This report of a large-scale, explosive outbreak of hepatitis A in Indian children once again emphasizes the need to evolve proper public health strategies, especially for vaccination, in countries in the transitional phase from hyperendemicity to intermediate endemicity.
Renal allograft recipients are prone to opportunistic infections, rarely multiple coexisting infections, due to the immunocompromised state. To the best of our knowledge, no case of a co-existing polyoma virus nephropathy and pulmonary histoplasmosis in a renal allograft recipient has been reported so far in the available literature. A 55-year-old male renal allograft recipient underwent graft biopsy for asymptomatic graft dysfunction. The graft biopsy showed features of polyoma virus nephropathy. Soon after, he developed fever with pulmonary nodules. Fine-needle aspiration from lung nodules showed intracellular yeast forms of histoplasma. The patient responded well to amphotericin B with subsidence of fever. The co-existence of renal allograft-limited infection like polyoma virus and systemic fungal infection such as histoplasmosis should be kept in mind in a transplant recipient with graft dysfunction and non-specific systemic symptoms. Prompt recognition of these infections permits the clinician to institute appropriate therapeutic modification and improved survival.
We evaluated important nontraditional cardiovascular risk factors, endothelial function and oxidative stress (OS) among stable peritoneal dialysis (PD) patients. Their association with carotid intimal medial thickness (CIMT) was also assessed. Thirty-eight adult patients (13 diabetics, 20 males) on PD for >6 months and 15 age and sex-matched controls were studied. Duration of dialysis (DOD), residual urine output (UO), weekly Kt/V urea, detailed biochemical and lipid profile were noted. OS was measured by serum concentration of antioxidants; vitamin C and ferric reducing ability of plasma (FRAP) and pro-oxidant; thiobarbituric acid-reactive substances (TBARS). High-resolution ultrasonography was used to determine CIMT and flow-mediated dilatation of brachial artery [endothelium-dependent dilatation (EDD)] and dilatation subsequent to nitrate spray [endothelium-independent dilatation (EID)]. Mean age, DOD, UO and Kt/V of study population were 49.3 ± 11.6 years, 19.4 ± 11.8 months, 508.2 ± 422.9 ml/day and 1.73 ± 0.24, respectively. As compared to controls PD patients had higher CIMT (0.46 ± 0.05 vs 0.50 ± 0.07 mm, P = 0.003) and TBARS (1.5 ± 0.4 vs 5.1 ± 2.3 nM/ml, P < 0.001) but lower Vitamin C (1.7 ± 0.3 vs 0.6 ± 0.2 mg%, P < 0.001), FRAP (990.8 ± 78.1 vs 328.7 ± 183.5 μM/L, P < 0.001) and EDD (26.2 ± 5.4 vs 9.8 ± 4.6 %, P < 0.001). TBARS correlated positively with DOD and negatively with hemoglobin. Vitamin C and FRAP correlated positively with serum albumin. EDD correlated positively with UO, Kt/V and hemoglobin. CIMT correlated negatively with Kt/V and hemoglobin. Among themselves CIMT correlated negatively with EDD and vitamin C. EDD correlated positively with vitamin C, while FRAP correlated positively with vitamin C and negatively with TBARS. PD patients have higher OS, poorer endothelial function and higher structural atherosclerosis. These parameters are closely linked to each other, hemoglobin, DOD, residual UO, serum albumin and small solute clearances.
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