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Biomedical subjects

R H Kalro

Publications and source records attributed to R H Kalro.

At least 19 recordsLinked to original sources

Frequency analysis of proliferating and cytotoxic T cells in livers and peripheral blood of patients with chronic hepatitis B.

Frequencies of proliferating and cytotoxic lymphocytes from liver biopsy samples and peripheral blood of chronic hepatitis B (CHB) patients and control subjects were monitored by limiting dilution analysis. Precursor frequencies of proliferating T lymphocytes were not significantly different in the liver and peripheral blood compartments of patients and controls. Moreover, similar frequencies of natural killer cells and cytotoxic T lymphocytes were observed in the peripheral blood of patients and controls. A higher frequency of cytotoxic T cells (1 of 22) compared to NK cells (1 of 306) was observed in liver tissues of CHB patients. Dual colour flow cytometric analysis revealed the presence of both CD4+ HLA-DR+ and CD8+ HLA-DR+ T cells in the liver tissues. These results suggest that in livers of CHB patients not only activated CD8+ T cells but also activated CD4+ T cells may play a significant role in the pathogenesis of chronic hepatitis B.

Adolescent

Congestive gastropathy: factors influencing development, endoscopic features, Helicobacter pylori infection, and microvessel changes.

OBJECTIVES: To study 1) the factors influencing the development of congestive gastropathy (CG) in patients with portal hypertension (PHT), 2) the changes in gastric microvessels in patients with PHT with and without CG, and 3) to determine whether Helicobacter pylori plays any role in the pathogenesis of CG. METHODS: One hundred eighteen patients with PHT (102 cirrhosis, 16 noncirrhotic portal fibrosis) were evaluated by videogastroscopic examination. Antral biopsy tissue was examined for microvessel changes, histological gastritis, and H. pylori infection in 85 of 118 patients and 45 controls. Portal venous pressure (PVP) was determined by hepatic venous pressure gradient in 17 patients with CG. RESULTS: CG was present in 71 (60%) patients with PHT, of whom 41 (58%) had mild and 30 (42%) had severe CG. CG was observed with equal frequency in cirrhosis (63%) and noncirrhotic portal fibrosis (44%). The incidence of CG was higher in patients with severe liver disease, a past history of hemetemesis, in those with esophageal varices, and in those with gastric varices. Severe CG was commonly observed in patients with large size esophageal varices and in those with gastric varices. There was significant dilation of gastric mucosal vessels in patients with PHT, but in this regard there was no significant difference between patients with and without CG. The presence of H. pylori, histological gastritis, degree of PVP, or degree of capillary dilation did not influence the severity of CG. CONCLUSIONS: CG occurs commonly in patients with PHT, especially those with severe liver disease, past history of hemetemesis, and esophagogastric varices. Patients with PHT have significant gastric microvessel changes. The severity of CG appears to be independent of PVP, capillary dilation, H. pylori infection, or histological gastritis.

Adolescent

Role of routine estimation of creatinine clearance in patients with liver cirrhosis.

BACKGROUND: Frequent occurrence of renal dysfunction without azotemia in patients with decompensated cirrhosis, and its prognostic and therapeutic importance, are not well appreciated. METHODS: Creatinine clearance (CrCl), 24-hour urinary sodium excretion, fractional excretion of sodium, and urine flow were estimated in 68 non-azotemic uncomplicated cirrhosis patients; all these patients were followed up for a period of 6 months. Eighteen patients with ascites and edema were treated with large volume paracentesis without colloid replacement and renal function was evaluated before, and 48 hours and 7 days later. Eight patients with abnormal CrCl were treated with 10 mg of enalapril daily and CrCl estimated at the end of 7 days. RESULTS: Of 68 patients, 22 had CrCl > 80 mL/min (Group I), 21 had CrCl of 50-80 mL/min (Group II) and 25 had CrCl < 50 mL/min (Group III). Renal dysfunction correlated with Child's class. During a mean follow up period of 180 days, patients in Groups II and III had higher mortality rates than those in Group I (23.8% and 36.0% vs 9.1%; p < 0.001). Following large volume paracentesis, CrCl decreased at 48 h and continued to be low at the end of 7 days even though blood urea nitrogen and serum creatinine remained normal. CrCl improved with 10 mg enalapril at 7 days (46.5 +/- 15.4 to 73.2 +/- 19.7 mL/min; p < 0.05). CONCLUSION: More than two-thirds of patients with advanced cirrhosis have abnormal CrCl despite normal blood urea nitrogen and serum creatinine; they also have a higher mortality as compared with patients with normal CrCl. CrCl decreases after large volume paracentesis even though blood urea nitrogen and serum creatinine remain unchanged. Enalapril improves CrCl in patients with liver cirrhosis but its exact clinical utility needs further evaluation.

Adult

Electron microscopic observations in gastric mucosa of habitual tobacco chewers.

Clinical evaluation, upper gastrointestinal endoscopy and electron microscopy of mucosal biopsies from antrum, body and fundus of stomach were performed in three control subjects and 17 habitual tobacco chewers. Electron microscopic abnormalities such as discontinuous, fragmented basement membrane with reduction in hemidesmosomes, and widened intercellular spaces filled with clusters of desmosomes were found in the gastric mucosa of habitual tobacco chewers; these were similar to those reported in experimental carcinogenesis and leukoplakia. It is concluded that habitual chewing of tobacco produces electron microscopic alterations in the human gastric mucosa which may be important precursors for gastric malignancy.

Adult

Gastric metaplasia and Helicobacter pylori infection in intestinal tuberculosis.

BACKGROUND: Gastric metaplasia occurs in intestinal epithelium of patients with Helicobacter pylori infection as well as intestinal tuberculosis, but the relationship between the three is not clear. SETTING: Teaching hospital. METHODS: Staining of intestinal sections from patients with ileocecal tuberculosis for H pylori and for metaplasia. RESULTS: Twenty seven of 92 (29.3%) patients demonstrated gastric metaplasia (superficial epithelial and pyloric gland metaplasia) in resected specimens of ileum. Gastric metaplasia was of antral type in all 27 patients. Helicobacter pylori was present in 3 of 27 (11%) patients with gastric metaplasia and was absent in all 65 patients without metaplasia. CONCLUSION: Gastric metaplasia (both superficial epithelial and pyloric gland) occurs in one-third of patients with ileocecal tuberculosis and such mucosa is poorly colonized by H pylori.

Adult

Is gastric metaplasia essential for duodenal ulcer?

Multiple biopsies were taken from the duodenum of 100 patients (46 active duodenal ulcer, 14 healed duodenal ulcer, 40 control subjects) to detect duodenitis, gastric metaplasia and Helicobacter pylori (Hp). Histamine-induced congo-red staining of the duodenal bulb was performed in additional 25 cases of active duodenal ulcer to determine the presence of functioning parietal cells in the duodenum. The incidence of duodenitis was 45% in control subjects and 76.7% in patients with duodenal ulcer (active or healed) (p < 0.01). Superficial gastric metaplasia was present in 2.5% of control subjects and 13.3% patients with duodenal ulcer (active or healed) (p > 0.05). Hp in the duodenum was detected in 10% of control subjects and 8.3% of patients with duodenal ulcer. Congo-red test was positive in two of 25 (8%) patients of active duodenal ulcer indicating "functioning" parietal cells in the duodenum. In Indian patients with duodenal ulcer, a low incidence of gastric metaplasia and Hp in the duodenum is observed in contrast to its high incidence in patients from Western countries.

Adult

Pancreatic ascites.

Pancreatic ascites is rarely considered in the differential diagnosis of exudative ascites, and is in fact missed in a majority of patients. Eleven cases of pancreatic ascites are described. 63.6% were chronic alcoholics. The clinical diagnosis was cirrhosis of liver (5/11), tuberculous peritonitis (5/11) or malignant peritonitis (1/11). In all patients ascites was exudative and the ascitic fluid amylase was markedly elevated (mean +/- SD: 7815 +/- 6507 SU/dl). Endoscopic retrograde pancreatography (ERP) performed in 4 patients demonstrated the site of leak in 3. Laparoscopy performed in 8 patients helped in the diagnosis of pancreatic ascites in all, which was confirmed on histology. Laparoscopy ruled out other causes of exudative ascites in all. We conclude that pancreatic ascites should be suspected in any patient with exudative ascites, especially chronic alcoholics and that ascitic fluid amylase should be routinely performed in all such cases. High ascitic fluid content is virtually diagnostic of pancreatic ascites. ERP is essential in preoperative assessment or planning endoscopic treatment. Laparoscopy is an invaluable investigation to rule out other conditions such as tuberculous or malignant peritonitis and cirrhosis of liver.

Adolescent

Alternate-day therapy with omeprazole for duodenal ulcer.

BACKGROUND: Maximal acid suppression produced by a single dose of 20 mg omeprazole has been reported to persist for over 24 hours, with acid secretion returning to normal after 2 days. OBJECTIVES: (i) To study the effect of single oral dose of 20 mg omeprazole on maximal acid output (MAO) and peak acid output (PAO) in duodenal ulcer patients and healthy volunteers. (ii) To compare the efficacy of omeprazole 20 mg daily versus 20 mg on alternate days in the treatment of duodenal ulcer. STUDY DESIGN: Open randomized comparative trial. METHODS: MAO and PAO were estimated in five duodenal ulcer patients and five healthy volunteers before, and 24 hours and 48 hours after, a single 20 mg oral dose of omeprazole. Fifty eight consecutive uncomplicated duodenal ulcer patients were randomized to receive omeprazole 20 mg either daily (n = 30) or on alternate days (n = 28) for four weeks. The two groups were matched for age, sex, duration of ulcer symptoms, smoking, NSAID use, and ulcer size at entry. Symptom scores using a pre-defined scoring system and endoscopic ulcer healing rates were evaluated at 2 and 4 weeks. RESULTS: MAO and PAO showed significant reduction in both duodenal ulcer patients and healthy controls 24 hours after 20 mg omeprazole. Reduction at 48 hours was significant in duodenal ulcer patients but not in controls. Endoscopic healing rates of duodenal ulcer at 2 and 4 weeks were 80% and 93.3% respectively in the daily treatment group and 71.4% and 85.7% respectively in the alternate-day treatment group. These differences were not statistically significant. CONCLUSION: 20 mg omeprazole on alternate days is as effective as 20 mg daily (i) in suppressing MAO and PAO and (ii) in the treatment of duodenal ulcer.

Adult

Stomach in portal hypertension.

365 consecutive patient of portal hypertension [Cirrhosis 285, Non-cirrhotic portal fibrosis (NCPF) 50, Extrahepatic portal vein obstruction (EHPVO)-30] were evaluated prospectively over a period of 2 years. Of these, 33 patients underwent successful sclerotherapy with evaluation before and after the same. Portal hypertensive gastropathy (PHG) was found in 56.4% (mild 28.2%, Severe 28.2%) of total patients; while its incidence was 60.6% in cirrhosis, 54% in NCPF and 20% in EHPVO. Incidence of PHG was significantly higher in cirrhotics when compared with non-cirrhotics (60.7% vs 41.25%: p < 0.05). PHG is more common in patients with large esophageal varices as compared to those with small varices (64.1% vs 50.8%: p < 0.05). Overall incidence of gastric varices was 29.3% while its incidence in cirrhosis, NCPF and EHPVO was 22.1%, 44% and 73.3% respectively. Incidence of gastric varices was significantly higher in non-cirrhotics (NCPF + EHPVO) when compared with cirrhotic (p < 0.05) and in patients with large esophageal varices when compared with patients having small esophageal varices (p < 0.05). Peptic ulcer was found in 10.9% patients with portal hypertension. (More than 90% were cirrhotics, mainly alcoholics). 33 patients underwent successful sclerotherapy of which 11 had PHG (mild--6, severe--5) at the beginning of sclerotherapy. After successful sclerotherapy 26 patients had PHG (mild--14, severe--12) p < 0.001). There was no significant difference in incidence of gastric varices before and after sclerotherapy. Incidence of PHG was significantly higher in cirrhotics while gastric varices were seen more commonly in patients with non-cirrhotic portal hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent

Heterotopic gastric mucosa and Helicobacter pylori infection in Meckel's diverticulum in Indian subjects.

Two of twenty nine (6.8%) patients who had undergone resection of Meckel's diverticulum demonstrated heterotopic gastric mucosa. In both these patients gastric mucosa was of antral type. Remaining 27 of 29 (93.2%) patients with Meckel's diverticulum had intestinal mucosa. 9 of 29 (31%) patients with Meckel's resected were symptomatic (8 bleeding, 1 perforation) and all 9 were negative for heterotopic gastric mucosa. Helicobacter pylori (H. pylori) was absent in both patients with intestinal mucosa. Antral biopsy from 13 partial gastrectomy specimens (surgery done for carcinoma stomach) were used as methodological controls and 7 of 13 (54%) showed H. pylori colonization. We conclude that (i) incidence of gastric mucosa is 6.8% in Meckel's diverticulum in our population, (ii) presence of heterotopic gastric mucosa is unlikely to be associated with complications of Meckel's diverticulum and (iii) heterotopic mucosa in Meckel's diverticulum is not commonly colonized by H. pylori.

Adolescent

Gastric mucosa in acute viral hepatitis.

In acute viral hepatitis, gastric biopsy and augmented histamine test were performed in 63 patients. Gastric histology was abnormal in 12 of 63 (19%) patients; 3 with superficial and 9 with atrophic gastritis. Maximal acid output was less than 10 mEq/h in 35 of 63 (55.5%) patients. Acid load tests were performed in 23 patients measuring H+, K+, Na+ fluxes; the results showed increased loss of acid from lumen to mucosa in 16 of 23 (69.6%) patients, indicating damage to the gastric mucosal barrier.

Acute Disease

Hepatitis C virus infection in chronic liver disease in Bombay.

To find out the prevalence of antibody of hepatitis C virus (anti-HCV) in patients with chronic liver disease in Bombay, sera from 126 patients (93 men, 33 women; aged 9-70 years, mean 39.7) with chronic liver disease (cirrhosis 103, cirrhosis with hepatocellular carcinoma 3, chronic active hepatitis 20) were tested for HBsAg and anti-HCV antibody. HBsAg positive sera were tested for anti-delta antibody and IgM anti-HBc. All the tests were carried out by ELISA. Of 126 patients, 51 (40.5%) were HBsAg positive, 49 (38.8%) alcoholic and 21 (16.6%) anti-HCV positive. The prevalence of anti-HCV in HBsAg positive, alcoholic and cryptogenic (HBV negative and no alcohol) liver disease patients was 13.7%, 14.7% and 20.5% respectively. Of 21 anti-HCV antibody positive patients, 8 (38%) had received blood transfusions previously. HCV is present in 15-20% of patients with chronic liver disease in Bombay.

Adolescent

HIV infection in patients of liver cirrhosis.

A total of 130 patients of liver cirrhosis (97 males, 33 females; aged 9-70 yr) of various etiologies were subjected to anti HIV antibodies testing by ELISA and supplementary Western Blot (WB) tests. Eleven patients were positive by ELISA. Of these 11 patients, 5 were WB positive, 4 were WB negative and 2 were indeterminate. Of the 5 WB positive patients none had received blood transfusions and one was a homosexual. These results indicate that HIV infection was present in 3.8 per cent patients of liver cirrhosis. Further studies are required on a large number of patients to recommend HIV testing routinely in cirrhotic patients.

Adolescent