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Biomedical subjects

B S Tomar

Publications and source records attributed to B S Tomar.

15 recordsLinked to original sources
PubMed2001

Intestinal infections.

Gastrointestinal infections are the significant cause of childhood morbidity and mortality worldwide. Gastrointestinal infections reflects the balance between the intrinsic virulence factors of the enteropathogens and host mechanisms which defend against enteric infections. Host defense factors include gastric acidity, intestinal motility, the normal indigenous intestinal microflora, mucous secretion, and specific mucosal and systemic immune mechanisms. Majority of GI infections are self limited so on one hand antibiotics are not needed and on the other hand the irrational use of antibiotics produces resistant strains. Acute diarrheal diseases which are one of the important intestinal infections, in majority of the cases are viral and have short course. Antibiotics are recommended only in specific cases and in immunocompromised individuals. Gastrointestinal disease is one of the most common manifestations of HIV infection. The gastrointestinal tract contains abundant quantities of lymphoid tissue and is likely to function as a reservoir of HIV infection, a site of profound immune dysregulation, and a target for opportunistic infections. In this situation specific antibiotics are indicated.

Anti-Bacterial Agents↗
PubMed2000

Hepatobiliary abnormalities and parenteral nutrition.

Hepatobiliary dysfunctions (TPN-HBD) occur during parenteral nutrition. In older children these are usually reversible whereas in newborns and infants these hepatobiliary abnormalities play a significant role in the morbidity. Cholestasis is a commonly occurring TPN-HBD. It correlates directly with the decreasing gestational age, low birth weight and increasing duration of TPN therapy. The pathogenesis of cholestasis of TPN is multifactorial and predisposed by necrotising enterocolitis, sepsis, cardiac failure, shock, and hypotension. Diagnosis is made with exclusion of other causes of direct hyperbilirubinemia. Most TPN-HBD appear within 4 weeks of starting of TPN but severe complications manifest usually after the 16th week. Histologically there is intralobular cholestasis. In few cases there may be severe portal fibrosis followed by development of micronodular biliary cirrhosis. Enteral starvation, defective bile acid carriers, hypercaloric TPN are the major factors responsible for TPN-HBD, including cholestasis. Biliary complications of TPN-HBD are acalculous, cholecystitis, and cholelithiasis. Bile stasis is a major pathological factor for these. If the calories are provided only by glucose or glucose-containing electrolyte solutions it may lead to cholestasis and other TPN-HBD. Even small oral alimentation (continuous or bolus) during TPN, prevent TPN-HBD. Choleretic agents have been useful in the prevention and management of cholestasis and other parenteral nutrition induced hepatobiliary abnormalities.

Biliary Tract Diseases↗
PubMedDate not supplied

Infantile cholestasis--advances in its understanding: new concepts.

Cholestasis is decrease or absence of bile flow into the duodenum. It can be either or in combination pathology of hepatocytes, intrahepatic bile ducts or extrahepatic bile ducts. Hepatocyte with their bile secretory apparatus and tight junction between hepatocytes are of specific importance in this. Bile is formed by several different energy-dependent transport processes. Secretion of bile is a complex metabolic process, which depends upon multiple structural and functional components in the hepatocytes and bile duct cells. The regulation of bile flow is regulated by many hormones. Bile is secreted in bile ducts having pressure of 15-25 cm of water. Rise in pressure in these bile ducts of more than 35 cm of water result suppression of bile flow and jaundice. A rise of conjugated serum bilirubin above the value of 400-500 mumol/L finds an alternate excretory pathway like urine. Various conditions are responsible for infantile cholestasis and can have different outcome of chronic cholestasis. These can be extrahepatic or intrahepatic and acute or chronic. Pathological consequences of infantile cholestasis are mainly because of malabsorption of fat and fat-soluble vitamins and hepatocellular dysfunctions. A battery of tests are required to diagnose the early infantile cholestasis. In the management of cholestasis diet rich in MCT is needed. Further, a high caloric intake up to 200 kcal/day to get adequate weight gain is desirable. Phototherapy, phenobarbitone and rifampicin is helpful in the pruritus of cholestasis by enhancing the excretion of bile. Ursodeoxycholic acid is specifically helpful in the cholestasis. A number of anti-inflammatory and immunosuppressive agents and a new compound, FK 506 has specific role in the management.

Bile↗
PubMedDate not supplied

Hepatitis E in India.

Institute of Pediatric Gastroenterology is superspecialised referral institute for all Pediatric Gastroenterological diseases from all over the country and for adjoining countries. We have our data and experience on 10,500 cases of proven Hepatitis E (HEV) in Pediatric population. HEV is non-enveloped 27-30 nm diameter RNA virus, prototype for alpha-like supergroup of positive stranded RNA virus. Indian HEV strain has 97% nucleotide and 98% amino acid sequence identity with Chinese strains but much diversity with Mexican strain. More than 70% acute hepatitis occurring in Pediatric population in this subcontinent are caused by HEV and 80% of these are sporadic. 90% cases were enterically transmitted, spread primarily by fecally contaminated drinking water (70%) and by food (20%), in 9.5% case spread probably was because of person to person and household contact. We could demonstrate HEV in urine, respiratory secretions. Interestingly we found HEV in insects like Flies, Cockroaches, and also in engorged Bedbugs and in Mosquitoes, apart from briefly boiled Mussels, and partially cooked cockles. Maternal-neonatal transmission could be seen if mother had HEV infection in third trimester of pregnancy. In 5 cases we could demonstrate HEV in breast milk. By studying on 10 volunteers, 40% have anicteric form only accompanied by anorexia, epigastric pain. HEV appeared in serum before the icteric phase. Shedding of virus in stool starts before the icteric phase and continued during the high levels of abnormal ALT. Hepatitis IgG anti-HEV persist up to 4 years. In 5 cases we could establish Transfusion associated Hepatitis (TAH). No chronicity could be documented. 5% cases had fulminant viral Hepatitis (FVH)/Sub fulminant viral Hepatitis (SVH), alpha-interferon (IFN) has been proved beneficial in these cases, further use of intravenous PGEl could also be beneficial. Inadequate chlorination of drinking water was an important additional factor for causing epidemics. A free residual chlorine concentration of at least 0.5 mg/l for minimum of 30 minutes is considered adequate as quality of drinking water.

Animals↗