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Biomedical subjects

T E Bynum

Publications and source records attributed to T E Bynum.

At least 37 records · Page 2Linked to original sources
PubMed1980

Glucocorticoid and partial mineralocorticoid deficiency associated with achalasia.

A number of patients with ACTH unresponsiveness resulting in glucocorticoid deficiency with normal mineralocorticoid activity have been described. This could be due to an inherited defect within the adrenal gland causing primary unresponsiveness to ACTH or to an inherited progressive degenerative process. The association of achalasia, lack of lacrimation, and glucocorticoid deficiency in two pairs of siblings with normal mineralocorticoid activity has been recently reported. Our case describes an 8.8-yr-old female with glucocorticoid insufficiency, partial mineralocorticoid deficiency, achalasia, and evidence of decreased lacrimation. Sodium depletion produced hyponatremia, and she was unable to increase her plasma aldosterone levels sufficiently, although PRA was markedly elevated. Our case may be part of a progressive degenerative process, possibly affecting both the autonomic nerve structures and the adrenal gland, leading not only to glucocorticoid deficiency but also to abnormal mineralocorticoid secretion.

17-Hydroxycorticosteroids↗
PubMed1980

Failure of penicillin G benzathine in the treatment of neurosyphilis.

Although penicillin remains highly effective in syphilis, important questions exist regarding the optimal regimen for syphilitic involvement of the nervous system. Progression of neurosyphilis despite 7.2 million units of penicillin G benzathine occurred in the case reported here, with subsequent resolution following high-dose intravenous aqueous penicillin therapy. This and other recent reports support the conclusion that neurosyphilis should be treated with higher amounts of penicillin than is provided by the benzathine regimens.

Adult↗
PubMed1979

Gastric aspiration in localization of gastrointestinal hemorrhage.

We compared the findings from gastric aspiration for blood with the site of gastrointestinal (GI) hemorrhage ultimately identified by endoscopy or angiography in 1,190 patients whose cases were analyzed retrospectively and prospectively during a six-year period. Gastric aspirates were positive for blood in 837 patients. An upper GI site proximal to Treitz' ligament was identified in 93%, and none had a lower GI site. A negative aspirate was found in 353 patients; a lower GI site was identified in 60%, and 1% (three patients) had an upper GI site. In these three patients, hemorrhage occurred in clinical settings suggesting ulcer disease, and bleeding duodenal ulcers were found in all three. All of the other 180 patients with a bleeding duodenal ulcer had a positive gastric aspirate.

Aged↗
PubMed1979

Ischemic hepatitis.

Seven patients with cardiovascular disease had clinical episodes and marked transaminase elevations that suggested viral hepatitis, but all had morphologic evidence (from liver biopsy or autopsy specimens) that documented centrilobular necrosis (ischemic hepatitis) with no evidence of viral or drug injury. Several also had moderate or marked passive congestion of the liver so the liver biopsies of 15 additional patients were retrospectively reviewed. In this latter group congestion alone was associated with normal or minimal elevation in transaminases while all patients with notable (greater than 5 times normal) transaminase elevations had centrilobular necrosis. Congestion alone, no matter how severe or prolonged, seems to do little if any damage to the liver. Centrilobular necrosis, or ischemic hepatitis, correlates with significant hypertransaminasemia, appears to result from failure of hepatic perfusion (with or without preceding hypotension), and presents with clinical and laboratory manifestations that suggest viral hepatitis.

Adolescent↗
PubMed1979

Mesenteric vascular effects of prostaglandins F2 alpha and B2. Possible advantages over vasopressin in control of gastrointestinal bleeding.

Mesenteric vascular effects of prostaglandins B2 and F2 alpha were studied and compared to those of vasopressin in the dog, cat and baboon. Vasopressin reduced superior mesenteric blood flow (SMBF) 80-100%, and significantly increased hepatic arterial blood flow and systemic arterial pressure. Prostaglandin B2 produced vasodilatation at low doses and biphasic vasodilatation/vasoconstriction at high doses. Prostaglandin F2 alpha elicited only vasoconstriction, reducing SMBF, left gastric, and inferior mesenteric blood flow 80-100%. Systemic arterial pressure was not significantly changed. Thus, vasopressin and prostaglandin F2 alpha are equally effective mesenteric vasoconstrictors. Because of reduced systemic effects, prostaglandin F2 alpha has excellent potential as a mesenteric vasoconstrictor to control gastrointestinal hemorrhage.

Animals↗
PubMed1977

Hepatic and gastrointestinal disorders in pregnancy.

The presentation, nonradiologic diagnostic evaluation, and course (including complications and outcome) of gastrointestinal disorders in pregnancy are not substantially different than for the nonpregnant patient. The possible exception is the higher mortality for pancreatitis when it occurs during pregnancy. With the exception of nausea/vomiting and hyperemesis gravidarum, there does not appear to be a gastrointestinal tract disorder that is peculiar to the pregnant state. Hepatic disorders are somewhat different in that the excretory defect-pruritus gravidarum-cholestatic jaundice spectrum and perhaps part of what presents as acute hepatic failure are intimately associated with pregnancy and have an onset and course that are tied to the gestational period. Otherwise, hepatic diseases that occur during pregnancy share the characteristic of gastrointestinal diseases, that their manifestations are not clearly different from the nonpregnant state. As is true for the diagnostic approach to all medical diseases that occur during pregnancy, radiographic procedures are prohibited. Furthermore, therapy must be reconsidered with concern for its effect on the fetus. This leads to elimination of many or all measures used for purely symptomatic or nonspecific benefit. If no harm or potential harm will accrue for the fetus, therapy for hepatic and gastrointestinal disorders preceeds in pregnancy very much as it does in the nongravid individual.

Acute Disease↗
PubMed1977

Pancreatic ascites: diagnosis of leakage site by endoscopic pancreatography.

A case with pancreatic ascites is presented in which the site of leak from a pancreatic pseudocyst was identified by oral endoscopic pancreatography. It is suggested that this procedure be done early in the clinical course of most patients with pancreatic ascites, since the information obtained will facilitate medical and surgical management.

Adult↗
PubMed1976

Hypocalcemia as a complication of jejunoileal bypass for morbid obesity.

Hypocalcemia following jejunoileal bypass for morbid obesity is not an uncommon occurrence. Three cases of severe hypocalcemia after bypass operation are presented with emphasis on the altered physiology of calcium homeostasis. Recognition and treatment of bypass hypocalcemia can avert a potentially serious complication.

Adult↗
PubMed1975

Stimulation of human pepsin output by tropical hydrochloric acid.

Pepsin secretion is stimulated by the back-diffusion of acid across the mucosa of the vagally denervated canine pouch. If back-diffusion is enhanced by damage, pepsin secretion increases. The current study investigates whether this mechanism exists in man. The stomach of normal human volunteers were irrigated for 1 hour with either buffer of 0.01 N HCl, 1 hour with 0.2 N HCl, and a final hour with buffer or 0.01 N HCl. During the middle hour both the concentration and output of pepsin increased three- or fourfold. From these studies it appears that the human gastric mucosa contains a mechanism similar to the dog's which results in the stimulation of pepsin secretion when exposed to acid. This mechanism could be of etiologic significance in gastric ulcer disease, which has been shown to be associated with increased gastric-mucosal permeability.

Adolescent↗
PubMed1975

Digoxin induced intestinal vasoconstriction. The effects of proximal arterial stenosis and glucagon administration.

Previous studies have been shown that intravenous cardiac glycosides produce mesenteric vasoconstriction (MVC). The possibility that this might critically compromise blood flow in patients with mesenteric vascular disease was suggested. To evaluate whether MVC occurs with intravenous cardiac glycosides in the presence of proximal mesenteric artery stenosis, blood flow in the superior mesenteric artery (SMA) of thirteen dogs was measured with a Doppler flowmeter. The SMA was constricted and pressures were measured in the aorta, SMA, and superior mesenteric vein. Superior mesenteric vascular resistance (SMVR) was calculated by dividing the pressure difference between the SMA and superior mesenteric vein by the total blood flow to the superior mesenteric vasculature and was reported as mm Hg/cc-min. Blood flow was measured simultaneously by a drop rate meter in the vein of a surgically isolated intestinal segment supplied by a single arterial arcade. Venous outflow pressure from this segment was also monitored, which allowed calculation of isolated gut segment resistance (IGSR) in mm Hg/cc-min per 100 g gut. Stenosis of the SMA produced pressure gradients of 10 to 75 mm Hg and decreased resting blood flow by as much as 82%. Digoxin produced an increase in both SMVR and IGSR throughout the 30 to 120 minute period of the study in thirteen dogs despite the presence of severe grades of SMA stenosis. There was no relationship between the degree of proximal SMA stenosis and the magnitude of resistance change due to digoxin. To determine if this MVC was reversible, glucagon was administered to eleven dogs 30 to 60 minutes after digoxin and completely overcame the constriction. Thus, digoxin produced MVC in the presence of proximal SMA stenosis. This MVC was pharmacologically reversible. These data suggest that intravenous digoxin might contribute to intestinal ischemia in patients with preexisting vascular disease.

Animals↗