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Biomedical subjects

H G Desai

Publications and source records attributed to H G Desai.

At least 19 recordsLinked to original sources
PubMed2005

Acute viral E hepatitis with chronic liver disease (autoimmune hepatitis).

A 36 years old male presented with anorexia, jaundice and ascites. He was suffering from acute viral E hepatitis. In view of ascites, he was investigated for associated asymptomatic chronic liver disease (CLD). The CLD was diagnosed as cirrhosis with autoimmune hepatitis and was treated with steroid with good response. He is maintaining good health with low dose steroid, on follow up for 1 year.

Acute Disease↗
PubMed2005

Is the presence or absence of Helicobacter pylori in gastric mucosa a greater risk?

Helicobacter pylori is a unique organism which is pathogenic for stomach-duodenum (chronic gastritis, duodenal ulcer, gastric ulcer, gastric malignancy, mucosa-associated lymphoid tissue (MALT) lymphoma) and protective for oesophagus (Barrett's oesophagus, oesophageal adenocarcinoma) at the same time in an individual. For prevention of diseases, the necessity of presence of some bacteria throughout the gastrointestinal lumen needs to be emphasized. The concept--only good Helicobacter pylori is a dead Helicobacter pylori, is dangerous and humans should learn to live in harmony with a few bacteria throughout the gastrointestinal tract.

Adenocarcinoma↗
PubMed2001

Apolipoprotein deficiency and chronic liver disease.

Deficiency of apolipoprotein can be of genetic origin or due to diseases like advanced chronic liver disease. Deficiency of apolipoprotein A causes Tangier disease without any major hepatic involvement being reported. Deficiency of apolipoprotein B causes abetalipoproteinemia or familial hypobetalipoproteinemia; with hepatic involvement in the form of raised transaminases, fatty liver and cirrhosis. Advanced chronic liver disease itself can cause reduction of apolipoprotein A and apolipoprotein B levels and acanthocytosis. In patients with chronic liver disease of undetermined etiology, lipid profile and apolipoprotein levels should be obtained routinely. If it suggests apolipoprotein B deficiency, then liver biopsy can be avoided, as the etiology of chronic liver disease is established. Isolated deficiency of either apolipoprotein A or apolipoprotein B suggests etiology of chronic liver disease, while deficiency of both apolipoprotein A and apolipoprotein B is a manifestation of advanced chronic liver disease.

Apolipoproteins A↗
PubMed2001

Fatty liver and elevated transaminases with heterozygous apolipoprotein B deficiency.

Asymptomatic fatty liver and elevated transaminases is a common occurrence with varied etiology. Apolipoprotein (apo) B deficiency is an uncommon cause of fatty liver and elevated transaminases. The typical lipid profile low cholesterol low LDL (low density lipoprotein) suggests diagnosis of apo B deficiency and an invasive procedure like liver biopsy can be avoided in such patients.

Adult↗
PubMed1998

Subacute hepatic failure: diagnosis of exclusion?

Subacute hepatic failure has been a controversial diagnosis ever since it was first identified more than 15 years ago. The Working Committee on Subacute Hepatic Failure has attempted to redefine this entity in which exclusion of preexisting cirrhosis on liver biopsy has been emphasized. Acute viral hepatitis in a patient with asymptomatic chronic liver disease (e.g., hepatitis B or C, Wilson's disease) can be misdiagnosed as subacute hepatic failure in the absence of a liver biopsy. This situation is common in developing countries where the prevalence of feco-orally transmitted (hepatitis A [<20 years] and hepatitis E [>20 years]) and parenterally transmitted (hepatitis B) viruses is high. To obtain and interpret liver biopsy specimens in such a situation is difficult and hazardous, and hence rarely performed. Acute viral hepatitis in a patient with asymptomatic chronic liver disease should be carefully looked for and excluded, especially in developing countries, before a diagnosis of subacute hepatic failure is confirmed.

Diagnosis, Differential↗
PubMed1997

Persistent transaminase elevation due to heterozygous (familial) apolipoprotein B deficiency.

Homozygous apolipoprotein B deficiency can present with fatty liver and raised levels of transaminases. Subjects with heterozygous deficiency are almost always asymptomatic. We report an asymptomatic 26-year-old man with persistently raised transaminases, in whom the diagnosis of heterozygous (familial) apolipoprotein B deficiency was made on the basis of characteristic lipid profile.

Adult↗
PubMed1995

Relationship of serum gastrin and Helicobacter pylori in the gastric antral and body mucosa.

OBJECTIVE: To evaluate the relationship between serum gastrin and Helicobacter pylori status in the antrum and body of gastric mucosa. METHODS: Fasting and post-meal serum gastrin levels were studied by radioimmunoassay in 41 patients with dyspepsia. These patients were divided into three groups depending on H pylori status ie H pylori present in both antrum and body; (A + B+; n = 13), present in antrum but not in the body; (A + B-; n = 7) and absent in both antrum and body; (A - B-; n = 21). RESULTS: There was no difference in fasting or post meal serum gastrin levels between the groups A + B+ and A - B-. Serum gastrin values 20 and 40 minutes post meal were significantly higher (p < 0.05) in the group A + B+ as compared to A + B-. CONCLUSION: Post meal serum gastrin levels are higher in patients with dyspepsia in whom Helicobacter pylori is present in the antral and body mucosa as compared to those in whom it is present in the antrum only.

Adolescent↗