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Biomedical subjects

R H Kalro

Publications and source records attributed to R H Kalro.

At least 37 records · Page 2Linked to original sources
PubMed1994

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↗
PubMed1993

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↗
PubMed1993

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↗
PubMed1993

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↗
PubMed1993

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↗
PubMed1993

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↗
PubMed1993

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↗
PubMed1993

Ultrastructural changes in esophageal mucosa of chronic tobacco chewers.

Seventeen chronic tobacco chewers and three control subjects underwent clinical evaluation, upper gastrointestinal endoscopy and esophageal mucosal biopsies. The esophageal biopsies were processed and examined under the electron microscope. A large number of ultrastructural abnormalities such as discontinuous, fragmented basement membrane, with reduction in hemidesmosomes, widened intercellular spaces were found in the esophageal mucosa of chronic tobacco chewers which resembled the ultrastructural features of experimental carcinogenesis and leukoplakia. It is concluded that chronic chewing of tobacco produces ultrastructural abnormalities in the esophageal mucosa which could be important precursors for esophageal malignancy.

Basement Membrane↗
PubMed1992

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↗
PubMed1992

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↗
PubMed1992

Frequency of hepatitis B, C and D and human immunodeficiency virus infections in multi-transfused thalassemics.

Of forty multi-transfused thalassemia patients (26 males, 14 females; mean age 8.1 +/- 5.3 years, range 1-35) with no clinical or biochemical evidence of liver disease, HBsAg, anti-hepatitis C virus and anti-human immunodeficiency virus antibodies were present in 18 (45%), 7 (17.5%) and 1 (2.5%) cases respectively. Three of the 18 (16.7%) HBsAg positive patients were anti-delta antibody positive. Our results indicate that more than 50% of multi-transfused thalassemia patients show serological evidence of one or more of hepatitis B, C and D and human immunodeficiency virus infection.

Adolescent↗
PubMed1992

Prevalence of spontaneous bacterial peritonitis.

To assess the prevalence of spontaneous bacterial peritonitis (SBP), ascitic fluid cell count, and ascitic fluid culture by conventional method and by bedside inoculation in blood culture bottles were performed in 31 consecutive patients of liver cirrhosis. Seven (22.58%) patients had ascitic fluid polymorphonuclear count (PMN) more than 500/mm. Ascitic fluid culture by conventional method was negative in all the patients, while in 4 patients culture was positive by bedside inoculation method. Six of 7 patients with SBP or its variant were in Child class C. Clinical features in these patients were abdominal pain (5 patients), fever (4) and encephalopathy (2); serum bilirubin level was 6.8 +/- 5.5 mg/dl, serum albumin 1.98 +/- 0.2 g/dl, prothrombin index 59.8 +/- 12.2%, ascitic fluid protein 0.78 +/- 0.24 g/dl. Three of 7 patients with SBP or its variant expired during hospital stay; the other 4 patients recovered after appropriate antibiotic therapy. We conclude that SBP is a serious complication in patients of liver cirrhosis with ascites. Ascitic fluid PMN count and bedside inoculation of blood culture bottles with ascitic fluid are sensitive indicators of SBP. Hence they should be performed routinely for early detection of SBP.

Adult↗
PubMed1992

Prevalence of delta virus infection in high risk population and hepatitis B virus related liver diseases.

Two hundred and fifty four high risk persons or patients with hepatitis B virus related liver disease (209 men, 45 women; age range 1-78 years) were tested for anti-delta antibody and IgM anti-HBc to determine the prevalence of delta agent coinfection and superinfection. The prevalence of delta infection was as follows: acute viral hepatitis 23/148 (16%) and chronic liver disease 17/92 (19%), and asymptomatic HBsAg carriers 1/6 (17%). In the high risk population, the delta antibody prevalence was as follows: multiple transfusion recipients 3/8 (38%), patients with chronic renal failure 1/5 (20%) and medical professionals 2/7 (29%). Of 44 patients (34 men, 10 women; age 3-63 years) with delta infection, 26 (59%) had coinfection and 18 (41%) had superinfection. Six patients with anti-delta antibody had received blood transfusion(s) and six others gave history of parenteral exposure.

Adolescent↗
PubMed1991

Effect of acute ingestion of tobacco on gastric mucosa. An endoscopic study.

One hundred patients with non ulcer dyspepsia with history of chronic tobacco chewing were examined endoscopically to assess the effect of tobacco ingestion on the gastric mucosa. Gastric erosions were seen in 20 patients in the fasting state. The remaining 80 patients in whom gastroscopy did not reveal erosions were subjected to repeat gastroscopy after tobacco ingestion. In 40 patients, endoscopy was repeated 30 minutes after 200 mg of tobacco ingestion (Group I) and in another 40 patients endoscopy was repeated 1 hour after 400 mg of tobacco ingestion (Group II). Eleven patients (27.5%) in Group I and 19 (47.5%) in Group II developed gastric erosions. Erosions were observed mainly along the lesser curvature, and in the fundus and the body of stomach. Gastric pH, determined after tobacco ingestion, was 2.4 +/- 0.43 in patients with erosions and 3.0 +/- 0.67 in patients without erosions. It is concluded that tobacco ingestion produces dose-dependent damage to the gastric mucosa as seen on endoscopy. Hence, history of tobacco ingestion should always be asked for in patients with gastric erosions.

Gastric Acidity Determination↗
PubMed1991

Mono and dual therapy for Helicobacter pylori associated gastritis.

Sixty patients with Helicobacter Pylori positive non ulcer dyspepsia were randomly allocated to one of the following treatment groups: Group I--norfloxacin 400 mg bid for 10 days, Group II--amoxycillin 500 mg bid plus tinidazole 500 mg bid for 15 days, Group III--colloidal bismuth subcitrate (CBS) 240 mg bid for 4 weeks. H pylori elimination was achieved in 14%, 81%, and 62% in Groups I, II and III respectively. Eradication of H pylori was not observed in Groups I and II, but was achieved in 25% of patients in Group III. Antral gastritis improved in 69% in Group II and 50% in Group III. We conclude that norfloxacin is not effective in H pylori infection. A combination of amoxycillin and tinidazole is highly effective in H pylori elimination with improvement in associated gastritis, but H pylori eradication is not observed with this therapy. CBS is also effective in H pylori elimination though H pylori eradication is achieved in only 25%.

Adult↗
PubMed1991

Peritoneoscopy in diagnosis of ascites.

Diagnostic peritoneoscopies were performed in 226 patients with ascites. Satisfactory examination was possible in 220 patients. Clinical diagnosis was confirmed at peritoneoscopy in 82.7% of patients. Peritoneoscopic examination corrected the clinical diagnosis in 13.7%, was inconclusive in 2.6% and was incorrect in 0.8% of cases. It was 100% diagnostic in malignant peritonitis and 89.5% in patients with tuberculous peritonitis. Pseudomyxoma peritoneai and mesothelioma were suspected in one patient each at peritoneoscopy and was confirmed histologically. The utility of routine ascitic fluid examination was reviewed in all patients. The ascitic fluid was transudative in 81.9%, exudative in 8.6% and indeterminate in 9.5% of patients with cirrhosis of liver. Patients with tuberculous pertitonitis had exudative, transudative and indeterminate ascites in 71.8%, 3.2% and 25% respectively. The ascites in patients with malignant peritonitis was either exudative (80%) or indeterminate (20%). There was considerable overlap in the nature of ascites present in the three groups of patients. We therefore conclude that peritoneoscopy is the most valuable investigation in the diagnosis of ascites, particularly in exudative and indeterminate types.

Ascites↗
PubMed1991

Ascitic fluid protein and cellular changes during diuretic therapy in cirrhosis of liver.

Thirty four patients with peritoneoscopy and/or biopsy proven uncomplicated cirrhosis of liver with ascites were studied for the effect of diuretic therapy on ascitic fluid protein and cell count. Renal function tests, liver function tests, ascitic fluid protein concentration and cell count were estimated prior to diuretic therapy and once every week till the end of therapy. There was no change in mean total serum protein (5.71 +/- 0.58 g/dl to 5.72 +/- 0.63 g/dl). The rise in mean ascitic fluid protein from 1.55 +/- 0.77 g/dl to 1.76 +/- 0.79 g/dl was not significant (P greater than 0.05). Twenty one patients (Group I) showed a rise in ascitic fluid protein concentration while 13 patients (Group II) did not show a rise or showed a fall in protein concentration during diuretic therapy. The rise in ascitic fluid protein concentration in Group I from 1.62 +/- 0.69 g/dl to 2.05 +/- 0.67 g/dl was statistically significant (P less than 0.05). Group I patients had a mean weight loss of 6.21 +/- 3.66 kg as compared to 3.15 +/- 2.00 kg in Group II patients (p less than 0.05). There was no other difference between Group I and Group II patients. Only 5 patients showed a rise in ascitic fluid cell count (more than 50 cell/mm3). It is concluded that diuretic therapy alters ascitic fluid protein concentration in a majority of patients but has no significant effect on cell count.

Adolescent↗