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Biomedical subjects

J A Clifton

Publications and source records attributed to J A Clifton.

At least 19 recordsLinked to original sources
PubMed1983

Gastric lipoma presenting as peptic ulcer: case report and review of the literature.

A 61-year-old housewife was diagnosed as having peptic ulcer disease for a period of 2 years. During this time she had episodes of abdominal cramping, dyspepsia, and one episode of severe upper gastrointestinal bleeding. She was subsequently found to have a large gastric lipoma. Gastric lipoma, a rare tumor, frequently mimics peptic ulcer disease in its clinical presentation and its complications. This point has not been previously emphasized.

Diagnosis, Differential↗
PubMed1977

Closing the circle.

Explore the source record for details and available documents.

Education, Medical↗
PubMed1974

Back diffusion of hydrogen ions across gastric mucosa of patients with gastric ulcer and rheumatoid arthritis.

Ionic permeability of the gastric mucosa was measured in six patients with an acute exacerbation of severe generalized rheumatoid arthritis receiving either aspirin and prednisone or aspirin and indomethacin as therapy. The results were compared with those in four patients with benign gastric ulcer and nine normal subjects. Compared with controls H(+) concentration was decreased and Na(+) concentration increased while corrected H(+) flux out of the lumen and Na(+) flux into the lumen were significantly increased in the patient groups, indicating increased mucosal permeability. Abnormality of the gastric mucosal barrier persisted in two patients despite healing of their ulcers. Mucosal permeability of patients with rheumatoid arthritis and gastric ulcer did not differ significantly from one another. One rheumatoid patient with a gastric ulcer showed no difference in mucosal permeability to that of the other rheumatoid patients. These studies suggest that increased H(+) ion loss contributes to the apparent hyposecretion of acid in patients gastric ulcer; persistence of an abnormal gastric mucosal barrier to H(+) ions may explain the high recurrence rate of gastric ulcers; and an abnormal gastric mucosal barrier may be a precursor to gastric ulceration in rheumatoid arthritis.

Adult↗
PubMed1971

Effect of intragastric bile salts on ionic movement across normal human gastric mucosa after intravenous atropine.

The effect of intravenous atropine (2.0 mg/70 kg) and intragastric bile salts (5.0-5.5 mM) on ionic fluxes across the gastric mucosa was studied. Serial instillations of bile salts, in 200 ml 160 m-equiv/l HCl with (51)Cr as a non-absorbable indicator, were performed in eight normal subjects. Five subjects received a bile salt mixture of 84% taurocholic acid, 14% taurodeoxycholic acid, and 2% taurochenodeoxycholic acid. With HCl alone (controls) the mean net flux into the lumen was 1.4 m-equiv H(+), 2.9 m-equiv Cl(-), 1.5 m-equiv Na(+), and 0.26 m-equiv K(+) per 15 minutes after the first instillation. Where atropine plus bile salt was given the loss from the lumen was 5.4 m-equiv H(+) (p < 0.01) and 1.9 m-equiv Cl(-) (p < 0.05) and movement into the lumen was 3.2 m-equiv Na(+) (p < 0.01) and 0.20 m-equiv K(+) in the corresponding period. Similar but smaller ion flux changes occurred in three subjects who received atropine and pure taurodeoxycholic acid. The net loss of H(+) from the gastric lumen was greater after atropine-bile salts than that shown in previous studies with bile salts alone. It is postulated that atropine reduced the volume of endogenous HCl secretion unmasking the loss of H(+).

Adult↗