Biomedical subjects
J C O'Laughlin
Publications and source records attributed to J C O'Laughlin.
Resistance to medical therapy of gastric ulcers in rheumatic disease patients taking aspirin. A double-blind study with cimetidine and follow-up.
Little is known about healing or recurrence of aspirin-induced gastric ulcers if aspirin intake is continued. A double-blind controlled study compared cimetidine plus antacids as needed (prn) with placebo plus prn antacids in healing aspirin-associated gastric ulcers during continued salicylate ingestion in 18 rheumatic disease patients over a 2-month period. Healing occurred in 44% of the placebo and 56% of the cimetidine-treated patients (P greater than 0.05). Subjects in both groups ingested potentially therapeutic doses of antacid. Ulcer size had an effect on healing rate, irrespective of treatment. Ninety percent of gastric ulcers less than 0.5 cm in diameter healed in 2 months but only 25% of ulcers greater than 0.5 cm. Six of seven patients with unhealed ulcers at 2 months eventually healed medically at intervals of 6--26 months. Of 11 patients managed medically and followed endoscopically for a mean of 15 months after healing, only one had a recurrent ulcer. In conclusion, placebo and antacid therapy were as effective as cimetidine and antacids in healing ulcers over a 2-month period. In spite of continued aspirin intake, most benign gastric ulcers less than 0.5 cm in diameter heal medically in two months. Aspirin-induced ulcers greater than or equal to 1 cm in diameter are relatively resistant to therapy but can be healed with prolonged cimetidine and antacid treatment; once healed, recurrence rate is low with prophylactic therapy even with continued aspirin intake.
Effects of 24 hours of aspirin, Bufferin, paracetamol and placebo on normal human gastroduodenal mucosa.
Aspirin causes gastroduodenal erosions and/or ulcers in man when taken for prolonged periods. The effects of shorter periods of aspirin, Bufferin, or paracetamol (acetaminophen) intake as used for self-medication are unknown. In a four way, crossover, blinded endoscopic study, we compared the effects of aspirin, Bufferin, paracetamol, and placebo, two tablets four times a day for 24 hours, on the gastroduodenal mucosa of 10 normal volunteers. Both regular aspirin and bufferin produced multiple gastric (p less than 0.005) and duodenal erosions (p less than 0.05, compared with baseline and placebo studies). Paracetamol did not cause significant gastric or duodenal mucosal damage. Two subjects developed duodenal ulcer-like lesions in the course of the study. We conclude that the use of unbuffered aspirin and Bufferin, but not paracetamol, in recommended doses for one day causes significant gastroduodenal mucosal damage.
Does aspirin prolong bleeding from gastric biopsies in man?
Aspirin prolongs skin bleeding time in man by inducing abnormal platelet function. Prolongation of gastric bleeding time has been postulated as a mechanism for gastric hemorrhage after aspirin in man. To determine whether endoscopic gastric biopsy is safe in patients taking aspirin, we studied the effects of acute and chronic aspirin use on gastric bleeding time in four groups of subjects. Gastric bleeding time was assessed directly following endoscopic biopsy. Skin bleeding time was done by the Mielke method. Control subjects (group I) were studied twice at one-week intervals to determine reproducibility of the gastric bleeding time technique. The effect of aspirin on gastric and skin bleeding time when given to normal volunteers for 24 hours (group II) and for two weeks (group III) and to rheumatic disease patients on a chronic basis (group IV) was also studied. In normal volunteers given aspirin for 24 hours or two weeks, gastric bleeding time was not affected in spite of skin bleeding time being significantly prolonged over baseline. Gastric bleeding time was less then skin bleeding time in all groups including patients with rheumatoid arthritis (p less than 0.05). We conclude that aspirin ingestion does not prolong gastric bleeding time in man and that gastric biopsy is not contraindicated on th basis of recent aspirin ingestion.
Effect of aspirin on the human stomach in normals: endoscopic comparison of damage produced one hour, 24 hours, and 2 weeks after administration.
We studied the effects of regular aspirin on the human stomach by endoscopy in 15 volunteers divided equally into three groups. Each had a normal baseline endoscopy. In Group I, two aspirin or placebo tablets were administered suspended in 100 cc of water and endoscopic assessment made over on hour, at four hours, and 24 hours. In Group II, in a two way cross-over, blinded study we compared the effects of 24 hours' ingestion of 3.25 g of aspirin and placebo. Group III subjects received aspirin, two tablets four times daily for two weeks. In Group I, multiple petechiae (p less than 0.05) developed in the fundus and antrum by one hour and were still visible at 24 hours in 80%. In Group II, aspirin produced multiple antral erosions (p less than 0.05 vs. placebo) in all subjects and duodenal erosions in half. Antral and duodenal petechiae were common. In Group III, all subjects developed antral erosions (p less than 0.05 vs. control) and 50% duodenal erosions but only on subject developed petechiae. Acute aspirin administration appears to cause predominantly petechial hemorrhage in the fundus and antrum while longer term administration causes antral and duodenal erosions. Regular aspirin in recommended doses for one hour, 24 hours and two weeks produces endoscopically visible gastroduodenal damage in the majority of normal subjects.
Healing of aspirin-associated peptic ulcer disease despite continued salicylate ingestion.
Patients who have rheumatic disease and who are undergoing long-term aspirin therapy have a high incidence of peptic ulcer disease. Whether it is possible to heal long-term aspirin-related peptic ulcer disease if aspirin intake is continued is unknown. Nine patients with rheumatic disease who were receiving long-term aspirin therapy and who had 15 endoscopically verified gastric and/or duodenal ulcers were studied. Patients were treated daily with 1,200 mg of cimetidine plus at least 120 mL of antacid (Mylanta II), while continuing aspirin therapy at the same dose and type. By eight weeks, 14 ulcers had healed. This study shows that some aspirin-associated peptic ulcers can be healed, despite continued aspirin intake, by intensive medical therapy aimed at lowering intragastric acidity.
Treatment of systemic mastocytosis.
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Hypertonic upper esophageal sphincter in the oculopharyngeal syndrome.
The oculopharyngeal syndrome (OPS) is a rare variant of muscular dystrophy characterized by progressive ptosis and dysphagia. Previous esophageal motility studies in OPS have yielded conflicting results because of low-fidelity esophageal recording systems. Although cricopharyngeal myotomy improves symptoms, accurate postoperative manometric findings have not been reported. Using a low-compliance, high-fidelity system and a radially oriented esophageal motility catheter in an OPS patient we found a hypertonic upper esophageal sphincter (UES), a hypotonic proximal esophagus, and elevated pressures in the distal two-thirds with prolonged duration of contraction. Clinical improvement followed myotomy. We also found a similar manometric pattern but a normotensive UES in an asymptomatic sibling.
Portal hypertension secondary to a congenital splenic arteriovenous fistula.
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Esophageal intramural pseudodiverticulosis. Case report.
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Malabsorption and gastric hyperacidity in systemic mastocytosis. Results of cimetidine therapy.
Visceral infiltration by mast cells (systemic mastocytosis) is an unusual manifestation of cutaneous mastocytosis. Symptomatic gastrointestinal disease occurs in approximately one-fourth of patients having systemic mastocytosis. An unusual gastrointestinal complication is malabsorption, described in sporadic case reports. A patient with gastric acid hypersecretion and malabsorption is described. Treatment using the histamine H2 antagonist, cimetidine, ameliorated the patient's gastrointestinal symptoms; however, the malabsorption was not resolved.
Osteopaths, podiatrists and the "sixth pathway".
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Saccular dilatations in the LeVeen shunt.
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Psoriatic enteropathy: report of case and review of literature.
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Endoscopy in family practice.
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