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Biomedical subjects

S Bridger

Publications and source records attributed to S Bridger.

27 records · Page 2Linked to original sources
PubMed1991

Acid secretory responses and parietal cell sensitivity following duodenal ulcer healing with omeprazole, sucralfate, and Maalox.

Acid secretory responses and parietal cell sensitivity (PCS) have been studied in 21 duodenal ulcer patients before and after successful treatment with omeprazole (n = 7), sucralfate (n = 7), or Maalox (n = 7). The second study was carried out 3 days after documented healing and withdrawal of treatment in the sucralfate- and Maalox-treated groups and 14 days after documented healing and withdrawal of treatment in the omeprazole-treated patients. Acid output (mmol/hour) was measured as basal secretion, and in response to 0.1 microgram/kg/hour pentagastrin (low-dose) and 6.0 micrograms/kg/hour pentagastrin (high-dose) stimulation. PCS was calculated as the ratio of low dose:high dose acid output (expressed as a percentage). Ulcer healing with sucralfate resulted in significant (p less than 0.05) decreases in low-dose acid output from 36.4% (13.2-51.0) (median [range]) to 8.4% (3.2-45.4) mmol/hour and PCS from 69.1% (44.9-91.4) to 22.0% (16.0-85.6), whereas no significant decreases in any of the measured parameters were noted following ulcer healing with Maalox. Ulcer healing with omeprazole resulted in significant (p less than 0.05) decreases in basal acid output from 6.3 (1.5-22.9) (median [range]) to 2.2 (0-6.9) mmol/hour, and low-dose acid output from 31.0 (6.0-58.0) to 23.0 (1.4-44.8) mmol/hour. These findings suggest that acid secretory responses following ulcer healing vary according to the therapeutic agent used.

Adult↗
PubMed1991

Basal and maximum acid output after continuous overnight gastric aspiration.

Basal and maximum acid outputs were measured on two occasions in a group of 15 duodenal ulcer (DU) patients in remission. The initial study was carried out after a nocturnal acid collection, whereas the second was carried out in the conventional manner without preceding nocturnal aspiration. No difference in the basal acid output, concentration, or volume of secretion was found between the two study days. Maximum acid output on the other hand, was significantly (p less than 0.02) reduced from 30.9 (14.2-41.2) mmol/h, median (+range), to 23.7 (8.1-33.7) mmol/h after overnight aspiration. The reduction in maximum acid output was attributable to a fall in the volume of gastric secretion from 280 (170-371) ml to 230 (142-280) ml. No fall in acid concentration was seen. We conclude that overnight gastric aspiration does not affect basal gastric secretion, but reduces the maximum acid output as a result of a reduced secretory volume.

Adult↗
PubMed1990

Duodenal ulcer healing and acid secretory responses to modified sham feeding and pentagastrin stimulation.

The effect of duodenal ulcer healing on the acid secretory responses to modified sham feeding and maximal pentagastrin stimulation has been studied in 17 patients treated successfully with ranitidine (n = 9) and sucralfate (n = 8). Parietal cell sensitivity was calculated as the ratio of the modified sham feeding response to the peak pentagastrin response, expressed as a percentage. Ulcer healing after sucralfate therapy resulted in significant falls in modified sham feeding stimulated acid output (P less than 0.02), from 9.4 (1.8-17.0) (median + range) to 3.7 (0.2-9.4) mmol/h; in peak acid output (P less than 0.05) from 42.8 (23.0-61.4) to 27.7 (7.2-51.0) mmol/h; and in the parietal cell sensitivity (P less than 0.05) from 19.2 (4.4-42.6) to 14.3 (2.8-19.7)%. No significant falls in any of these parameters were noted following ulcer healing with ranitidine. Duodenal ulcer healing with sucralfate results in decreased acid secretory responses to vagal and pentagastrin stimulation.

Adult↗
PubMed1989

Acid-secretory response and parietal cell sensitivity in patients with duodenal ulcer before and after treatment with sucralfate or ranitidine.

Patients with endoscopically proved duodenal ulcer were randomly assigned to treatment with either ranitidine 300 mg at bedtime or sucralfate 2 g twice daily for six weeks. Acid-secretory studies were performed before commencement and 60 to 84 hours after cessation of treatment and endoscopic healing was confirmed. Patients were randomly assigned to receive a constant infusion of secretory stimulant: either pentagastrin 0.1 and 6.0 micrograms/kg/hour or histamine acid phosphate 4.0 and 40 micrograms/kg/hour. Acid output in mmol/hour was measured for basal, low dose, and high dose output. Parietal cell sensitivity (PCS) was calculated as the ratio of low-dose acid output: high-dose acid output and expressed as a percentage. Values before and after treatment were compared and significance of differences was determined using the Student paired t test. There was an apparent decrease in basal acid output, low-dose acid output, high-dose acid output, and PCS with ulcer healing, regardless of treatment or stimulant used. Basal acid output, low-dose acid output, high-dose acid output, and PCS were significantly lower in the sucralfate-treated group, but only high-dose acid output decreased significantly in the ranitidine-treated group. These differences may be relevant to early duodenal ulcer relapse in ranitidine-treated patients.

Adolescent↗
PubMed1985

Congenital contractural deformities of the fingers and arthropathy.

Four patients are described who presented with congenital finger contractures and arthropathy. There was synovial cell hyperplasia and giant cells but no inflammatory process. Radiographs showed flattening of the metacarpal and metatarsal heads and the proximal femoral ossification centres. In the oldest patient the process had subsided leaving slight contractures but severe impairment of hip mobility. In another the arthropathy was still prominent in the early teens. In a third, finger contractures had failed to respond to conservative or surgical measures.

Contracture↗
PubMed1983

Causes and prevalence of blindness in the Northern Province of Sierra Leone.

The causes of blindness in Sierra Leone were studied in 7286 new patients attending the eye clinic in the year 1981. Blindness, defined as an inability to count fingers at 3 meters with the better eye (WHO, 1973), was present in 762 persons, due to cataract (39%), ocular onchocerciasis (30%), primary glaucoma (8%), measles keratitis (3%), trachoma (3%) and other causes. The prevalence of blindness was estimated from simple field surveys covering 41 villages with an estimated population of 10,559. The average prevalence of blindness was found to be 1.3% of the total population.

Adolescent↗