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P S Anklesaria

Publications and source records attributed to P S Anklesaria.

7 recordsLinked to original sources
PubMed1995

Gastric bacterial overgrowth accompanies profound acid suppression.

BACKGROUND: Suppression of gastric acid may lead to gastric colonization by aerobic and anaerobic bacteria, and consequent clinical manifestations. The risk is likely to be higher with poor environmental hygiene. AIMS: To study the effect of short-term acid suppression with omeprazole on gastric bacterial flora. METHODS: Twenty-five ambulatory patients with acid-peptic diseases underwent clinical assessment and gastric juice collection (for pH and culture) prior to start of therapy with 20 mg omeprazole daily, on days 7 and 14 of therapy, and 7 days after omission of therapy (day 21). RESULTS: Eighteen patients completed the study. The median gastric pH was 1.8, 7.5, 7.5 and 3.4 on days 0, 7, 14 and 21 respectively. Positive gastric cultures were obtained in 13 of 25, 17 of 21, 18 of 18 and 14 of 18 patients on respective study days, with median colony counts of 1.5 x 10(4), 7.5 x 10(5), 8.7 x 10(7) and 7.3 x 10(4) cfu/mL respectively. Three patients developed self-limiting diarrhea during therapy and two more immediately after discontinuing therapy. CONCLUSIONS: Gastric colonization is common with short-term profound acid-suppression, and may cause diarrhea. Acid suppressive therapy should be used with caution especially in patients with poor environmental hygiene.

Adult↗
PubMed1993

Involvement of prostaglandins in chilli-induced early gastric vascular damage in adult Wistar rat.

OBJECTIVE: To explore the role of prostaglandins in protecting against chilli-induced early gastric vascular damage. METHODS: Early gastric vascular damage was induced in rats by oral administration of 8 mg/Kg chilli extract. The damage was assessed by estimating spectrophotometrically the amount of Evan's blue leaking into gastric tissue and luminal contents 10 min after exposure to chilli. Further groups of rats were pretreated with misoprostol (10, 25 or 50 micrograms/Kg) or dazmegrel (1, 5 or 25 mg) to evaluate their protective effects. RESULTS: Both misoprostol and dazmegrel were able to reduce gastric vascular damage induced by chilli in a dose-dependent fashion. CONCLUSION: Prostaglandins may play a role in protecting against chilli-induced early gastric vascular damage.

Animals↗
PubMed1991

Polymorphonuclear and monocyte functions in measles.

The depression of immune responses during measles infection has been recognized since the early 20th century. Acute bacterial infections are the most common cause of morbidity and mortality in measles. This study investigated the phagocytic and bactericidal or fungicidal capacities of polymorphonuclear cells (PMN) and monocytes during measles infections. When 14 children with measles were compared with 25 healthy controls, a significant depression in PMN and monocyte function was found. Of these 14 children, seven developed acute bacterial infections. These seven children were compared with 11 children who had acute bacterial infections without measles. It was found that PMN in patients with measles did not achieve an activated state, as expected with acute infections. Serum immunoglobulins were not altered in these patients. These results confirm previous reports of depressed phagocytic and bactericial capacities of PMN in measles, and further document that peripheral blood monocyte functions are also depressed in measles.

Acute Disease↗
PubMedDate not supplied

Portal venous pressure and the serum-ascites albumin concentration gradient.

CLINICAL ISSUE: Other investigators have found the serum-ascites albumin concentration gradient to be 1.1 g/dL or greater in the presence of portal hypertension and less than that in its absence. OBJECTIVE: To determine if any correlation exists between the serum-ascites albumin concentration gradient (which reflects the net serum oncotic pressure) and the portal venous pressure. METHODS: The study group comprised 15 patients who had alcoholic cirrhosis. The portal venous pressure was calculated as the difference between the measured hepatic venous wedge and inferior vena cava pressures and was expressed as the hepatic venous pressure gradient. SUMMARY: All patients had portal hypertension; the mean hepatic venous pressure gradient was 14.81 +/- 6.91 (SD) mm Hg. Fourteen of the 15 patients had a serum-ascites albumin concentration gradient of at least 1.1 g/dL; the mean value was 2.168 +/- .709 g/dL. No correlation was found between these variables (r = .0459, P > .05). CONCLUSIONS: Although the serum-ascites albumin concentration gradient is a sensitive indicator of portal hypertension in patients with alcoholic cirrhosis, it does not reflect the portal venous pressure.

Albumins↗