PubMed Health⌕ Search

Biomedical subjects

Ashish Bavdekar

Publications and source records attributed to Ashish Bavdekar.

10 recordsLinked to original sources
PubMed2006

Triglyceride associated polymorphisms of the APOA5 gene have very different allele frequencies in Pune, India compared to Europeans.

BACKGROUND: The APOA5 gene variants, -1131T>C and S19W, are associated with altered triglyceride concentrations in studies of subjects of Caucasian and East Asian descent. There are few studies of these variants in South Asians. We investigated whether the two APOA5 variants also show similar association with various lipid parameters in Indian population as in the UK white subjects. METHODS: We genotyped 557 Indian adults from Pune, India, and 237 UK white adults for -1131T>C and S19W variants in the APOA5 gene, compared their allelic and genotype frequency and determined their association with fasting serum triglycerides, total cholesterol, HDL and LDL cholesterol levels using univariate general linear analysis. APOC3 SstI polymorphism was also analyzed in 175 Pune Indian subjects for analysis of linkage disequilibrium with the APOA5 variants. RESULTS: The APOA5 -1131C allele was more prevalent in Indians from Pune (Pune Indians) compared to UK white subjects (allele frequency 20% vs. 4%, p = 0.00001), whereas the 19W allele was less prevalent (3% vs. 6% p = 0.0015). Patterns of linkage disequilibrium between the two variants were similar between the two populations and confirmed that they occur on two different haplotypes. In Pune Indians, the presence of -1131C allele and the 19W allele was associated with a 19% and 15% increase respectively in triglyceride concentrations although only -1131C was significant (p = 0.0003). This effect size was similar to that seen in the UK white subjects. Analysis of the APOC3 SstI polymorphism in 175 Pune Indian subjects showed that this variant is not in appreciable linkage disequilibrium with the APOA5 -1131T>C variant (r2 = 0.07). CONCLUSION: This is the first study to look at the role of APOA5 in Asian Indian subjects that reside in India. The -1131C allele is more prevalent and the 19W allele is less prevalent in Pune Indians compared to UK Caucasians. We confirm that the APOA5 variants are associated with triglyceride levels independent of ethnicity and that this association is similar in magnitude in Asian Indians and Caucasians. The -1131C allele is present in 36% of the Pune Indian population making it a powerful marker for looking at the role of elevated triglycerides in important conditions such as pancreatitis, diabetes and coronary heart disease.

Adult↗
PubMed2006

Evaluation of immunogenicity and tolerability of a live attenuated hepatitis a vaccine in Indian children.

An open non comparative study of a live attenuated H2 strain Hepatitis A vaccine of Chinese origin was carried out in 143 healthy Indian children aged 1 to 12 years (mean age 4.87 2.76 years; 88 boys, 55 girls). At baseline, all were negative for IgG HAV antibodies and had normal hematological and biochemical indices. Two months after a single dose of the vaccine (given subcutaneously), 137 children (i.e. 95.8 %) developed protective antibodies of IgG > 20 mIU / mL. The hematological and biochemical parameters remained within normal limits. There were no adverse events in any except mild fever in one child. In conclusion, live attenuated H2 strain Hepatitis A vaccine in a single dose was found to be immunogenic and safe in Indian children.

Child↗
PubMed2005

Transcutaneous absorption of topically massaged oil in neonates.

OBJECTIVE: To study the transcutaneous absorption of traditionally massaged oil in newborns and to specifically compare the effects of (i) essential fatty acid (EFA) rich - safflower oil and (ii) saturated fat rich coconut oil, on fatty acid profiles of massaged babies. DESIGN: A short term randomised controlled study. SETTING: Tertiary care NICU of a large teaching hospital and a research laboratory of a University complex. METHODS: 120 study babies were randomly assigned to three oil groups (i) safflower oil (n = 40) (ii) coconut oil (n = 40) and (iii) no oil controls (n = 40). In each group, babies were selected in three subsets as per their gestational ages viz (a) less than 34 weeks, (b) 34-37 weeks, (c) greater than 37 weeks. 5 mL of the designated oil was massaged four times a day for five days under controlled conditions of temperature and feeding. Pre and post oil massage samples of blood were analysed for triglycerides and fatty acid profiles using gas chromatography. RESULTS: Post oil triglyceride values were significantly raised in both the oil groups and also in controls. However, the quantum of rise was significantly higher in oil groups as compared to controls. Fatty acid profiles (gas chromatography) showed significant rise in EFAs (linolenic acid and arachidonic acid) in safflower oil group and saturated fats in coconut oil group. Changes were more evident in term babies. There were no side effects associated with the massage. CONCLUSIONS: This study shows that topically applied oil can be absorbed in neonates and is probably available for nutritional purposes. The fatty acid constituents of the oil can influence the changes in the fatty acid profiles of the massaged babies.

Fatty Acids↗
PubMed2003

The canine copper toxicosis gene MURR1 does not cause non-Wilsonian hepatic copper toxicosis.

BACKGROUND: Non-Wilsonian hepatic copper toxicosis includes Indian childhood cirrhosis (ICC), endemic Tyrolean infantile cirrhosis (ETIC) and the non-Indian disease known as idiopathic copper toxicosis (ICT). These entities resemble the hepatic copper overload observed in livers of Bedlington terriers with respect to their clinical presentation and biochemical and histological findings. We recently cloned the gene causing copper toxicosis in Bedlington terriers, MURR1, as well as the orthologous human gene on chromosome 2p13-p16. AIM: To study the human orthologue of the canine copper toxicosis gene as a candidate gene for ICC, ETIC, and ICT. METHODS: We sequenced the exons and the intron-exon boundaries of the human MURR1 gene in 12 patients with classical ICC, one patient with ETIC, and 10 patients with ICT to see whether these patients display any mutations in the human orthologue of the canine copper toxicosis gene. RESULTS: No mutations in the MURR1 gene, including the intron-exon boundaries, were identified in a total of 23 patients with non-Wilsonian hepatic copper toxicosis. CONCLUSIONS: Our results demonstrate that copper toxicosis in Bedlington terriers is not an animal model for the non-Wilsonian hepatic copper toxicosis described in this study.

Adaptor Proteins, Signal Transducing↗
PubMed2002

Nutrition management in chronic liver disease.

Liver has a central role in nutritional homeostasis and any liver disease leads to abnormalities in nutrient metabolism and subsequent malnutrition. All children with chronic liver disease (CLD) must undergo a periodic nutritional assessment--medical history, anthropometry esp. skinfold thickness and mid-arm circumference, and biochemical estimation of body nutrients. Nutritional rehabilitation is catered to the individual child but generally the caloric intake is increased to 130% of RDA by adding glucose polymers and/or MCT oil (coconut oil) with essential fatty acid supplementation (sunflower oil). The enteral route is preferred and occasionally nasogastric and/or nocturnal feeding are required to ensure an adequate intake. Proteins rich in branched chain amino acids are given in moderation (2-3 gm/kg/day) in compensated cirrhotics unless encephalopathy occurs when protein restriction may be necessary (1 gm/kg/day). Fat-soluble vitamins are supplemented in large quantities esp. in cholestasis along with other vitamins and minerals. Dietary therapy is the mainstay of management of some metabolic liver diseases and may be curative in disorders like galactosemia, fructosemia and glycogen storage disorders. Pre and postoperative nutritional support is an important factor in improving survival after liver transplantation.

Cholestasis↗
PubMed2002

Wilson's disease.

Wilson's disease (WD), an inborn error of copper (Cu) metabolism, is now one of the leading liver diseases in children in India. The clinical presentation can be extremely varied viz.,--all forms of acute and chronic liver disease, minimal to severe neurological disease, psychiatric problems, bony deformities, hemolytic anemia and endocrine manifestations. A high index of suspicion is necessary along with a judicious battery of investigations for diagnosis. Hepatic copper estimation is the most reliable test but is not easily available in India. Liver biopsy may not be possible because of bleeding problems and histological features are often not diagnostic of WD. In the absence of hepatic Cu, a low ceruloplasmin, high 24 hour urinary copper and presence of KF rings aid in making the diagnosis. The mainstay of initial therapy is Cu-chelators like D-Penicillamine, and Trientine for reduction in body copper to sub-toxic levels. Subsequent maintenance therapy is necessarily lifelong with D-Penicillamine, Trientine or Zinc. Children on therapy must be monitored regularly for response, side-effects, compliance and rehabilitation. Response to therapy may be unpredictable, but acute and early presentations like fulminant hepatic failures have a poor outcome. All siblings must be screened for WD as early diagnosis and treatment result in a good outcome. The identification of the WD gene on chromosome 13 has led to the possible use of molecular genetics (haplotype and mutational analyses) in the diagnosis of WD. Parent groups/associations must take active part in holistic management of WD.

Adolescent↗
PubMed2002

Hepatitis B vaccination in premature and low birth weight (LBW) babies.

OBJECTIVE: To assess the immune response of preterm and low birth weight babies (LBW) to hepatitis B (HB) vaccine. SETTING: Neonatal Intensive Care Unit (NICU), postnatal ward and follow up clinics of KEM Hospital, Pune. DESIGN: Open trial. METHODS: 100 babies were enrolled in four study groups. Group I - preterm, gestational age (GA) < 34 weeks; Group II - GA 34 to 36 weeks; Group III full term <2.5 kg (LBW babies); and Group IV full term >2.5 kg (controls). A recombinant DNA HB vaccine was given at 0, 1, 2 and 12 month schedule. The first injection was administered as soon as the neonate was stabilized. Immune response in terms of anti HBs titres (AUSAB EIA Diagnostic kit) was measured one month after each of the first three injections and at the time of one year booster. Adverse events were monitored. RESULTS: 88 and 62 babies completed the study till the third dose and one year booster dose respectively. Immune response of HB vaccine was uniformly good in all the study groups with 100 % sero-conversion after the second dose itself. By one year (i.e. before the booster dose), very high titres were recorded in all 100%, with 85% demonstrating titres >1000 mIU/ml. Preterm and LBW babies had higher GMT as compared to full term babies till one month after third dose. By one year (before booster), full term babies had higher GMT than preterm and LBW babies. However, these differences were not statistically significant. The vaccine was well tolerated and safe and there were no adverse reactions. CONCLUSION: Immune response of preterm, LBW and full term babies to the new generation recombinant DNA HB vaccine was uniformly good. High and long term seroprotective levels were achieved after the second dose itself.

Female↗
PubMed2002

Diagnosis and outcome of acute bacterial meningitis in early childhood.

OBJECTIVE: To estimate frequency of acute bacterial meningitis (ABM) in early childhood in hospital admissions, to describe clinical and diagnostic features, and to analyze mortality, complications and long term sequelae. DESIGN: Prospective study. SETTING: Pediatric wards and Rehabilitation Center of KEM Hospital, Pune. METHOD: Study subjects between the ages of 1 months to 5 years with ABM were recruited. Clinical details were recorded. CSF was analysed by routine biochemical methods, antigen detection tests (Latex agglutination LAT) and microbiological studies on special media. Management was as per standard protocols. Survivors were followed up long term with neurodevelopmental studies and rehabilitation programmes. RESULTS: In a study period of 2 years, 54 children (1.5% of all admissions) satisfied the criteria of ABM in early childhood; 78% were below one year and 52% were under the age of six months. Chief presentation was high fever, refusal of feeds, altered sensorium and seizures. Meningeal signs were present in only 26%. CSF C-reactive protein was positive in 41%, gram stain was positive in 67% LAT in 78% and cultures grew causative organisms in 50% of the cases. The final etiological diagnosis (as per LAT and/or cultures) were Streptococcus pneumoniae 39% Hemophilus influenzae type b 26% and others in 35% The others included one case of Neisseria meningitidis and 10 who were LAT negative and culture sterile. 39% patients developed acute neurological complications during the hospital course. 31% children with ABM died in hospital or at home soon after discharge. Six were lost to follow up. Of the 31 children, available for long term follow up (1-3 years), 14 (45%) had no sequelae. The remaining had significant neurodevelopmental handicaps ranging from isolated hearing loss to severe mental retardation with multiple disabilities. CONCLUSION: ABM in early childhood has a considerable mortality, morbidity and serious long term sequelae. Neurodevelopmental follow up and therapy should begin early. Etiological diagnosis can be enhanced by LAT and good culture media. H. influenzae b and S. pneumoniae account for more than 60% of ABM in early childhood.

Acute Disease↗