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Biomedical subjects

F B Thomas

Publications and source records attributed to F B Thomas.

At least 37 records · Page 2Linked to original sources
PubMed1977

Aortic aneurysm eroding the esophagus. Case report and review.

A 71-year-old woman developed dysphagia and hematemesis with an endoscopic diagnosis of esophageal submucosal hematoma. Post mortem examination demonstrated an aorto-esophageal fistula as the etiology of her hematemesis. The differential diagnosis of upper gastrointestinal bleeding in the elderly patient without cirrhosis is discussed. A review of the literature on aorto-esophageal fistula is included.

Aged↗
PubMed1977

Esophageal intramural pseudodiverticulosis.

Three cases of esophageal intramural pseudodiverticulosis (EIP) are described and the literature reviewed. We conclude that EIP is an inflammatory disease of unknown etiology characterized by dilatation of the esophageal submucosal glandular elements. The classic radiographic picture which is that of collar-button-shaped outpouchings projecting in a perpendicular fashion from the luminal surface is mainly related to dilatation in the glandular ductal system. It is usually diagnosed in the sixth and seventh decades, but all ages may be affected. Dysphagia is a very common but not universal symptom of the disease process. Approximately one third of these patients have diabetes mellitus. Strictures of the esophagus are frequently seen, and varying degrees of esophagitis may be manifest endoscopically. Esophageal motility disturbances are common and may be severe. Candida infestation with and without tissue invasion has been seen in a number of patients and should be searched for in all cases of EIP.

Candida albicans↗
PubMed1977

Acute pancreatitis secondary to furosemide with associated hyperlipidemia.

A patient is described with acute pancreatitis which was probably caused by furosemide. Administration of furosemide on two separate occasions was associated with increases in serum amylase concentrations and recurrence of abdominal pain. This case is of further interest because of the presence of hyperlipemia in the absence of an underlying lipid abnormality. Following recovery from pancreatitis, the lipoprotein pattern evolved from type V to type III, type IIA, and finally to normal.

Acute Disease↗
PubMed1977

Localization of gastric inhibitory polypeptide release by intestinal glucose perfusion in man.

To determine the site of endogenous release of gastric inhibitory polypeptide (GIP), glucose perfusions (556 mmoles per liter) of duodenum, proximal jejunum, midjejunum, and ileum were performed in human volunteers using an occluding balloon perfusion technique. Preperfusion GIP concentrations were below assay sensitivity (125 pg per ml) in all subjects. After glucose perfusion, maximal serum GIP concentrations for the four groups were: duodenum, 1383 +/- 152 pg per ml; proximal jejunum, 904 +/- 87 pg per ml; midjejunum, 545 +/- 91 pg per ml, and ileum 305 +/- 38 pg per ml. Integrated GIP secretion was significantly greater with duodenal perfusion (111 +/- 21 ng-min ml-1) d proximal jejunal perfusion (69 +/- 5 ng-min ml-1), as compared to either midjejunal (47 +/- 7 ng-min ml-1) or ileal (25 +/- 6 ng-min ml-1) perfusions. Peak serum insulin concentrations and integrated insulin secretion were also significantly greater with perfusion of the duodenum or proximal jejunum. Serum glucose concentrations, integrated serum glucose, and glucose absorption were similar for the four areas perfused. The results of this study indicate that the proximal small intestine is the primary site of endogenous GIP release in man, but that smaller quantities are also released by the distal small bowel.

Adult↗
PubMed1977

Stimulation of pancreatic secretion of water and electrolytes by furosemide.

The effect of furosemide on secretin-stimulated pancreatic secretion was examined in 12 normal subjects using a perfusion method to quantitate pancreatic output. During continuous secretin infusion (0.9 U per kg per hr), secretory volume rose to a steady state level of 32.5 +/- 10.2 ml per min. When a bolus injection of furosemide (20 mg) was given during continuous secretin infusion, mean secretory volume increased further to a maximum value of 110 +/- 14.7 ml per min. Similarly, the outputs of bicarbonate, sodium, and chloride increased significantly after furosemide, compared to values obtained with secretin infusion alone. Total bilirubin output fell after furosemide, suggesting that the effect of furosemide on secretory volume and electrolyte output was not due to a stimulatory effect on bile flow. Furosemide also had no effect on duodenal water transport. These observations demonstrate that furosemide stimulates pancreatic secretion of water and electrolytes, possibly via inhibition of pancreatic ductal absorption of sodium.

Adult↗
PubMed1976

Inhibition of intestinal iron absorption by laundry starch.

The pathogenesis of iron deficiency anemia associated with amylophagia is usually attributed to dietary iron lack. However, large quantities of starch may inhibit intestinal iron absorption. Accordingly, studies were carried out to determine the effect of laundry starch on the intestinal absorption of inorganic and hemoglobin iron. In vitro, laundry starch bound 19 to 80% of the available 59FeSO4 and 34 to 68% of the available 59Fe-hemoglobin. Binding of both forms of iron was pH-dependent, with maximal binding at pH 7.0. In vivo, laundry starch significantly inhibited mucosal uptake of 59FeSO4 from isolated duodenal loops. In nonanemic rats, administration of laundry starch (100 mg) 1 hr before a 100-mug dose of 59FeSO4 significantly decreased the absorption of 59FeSO4, as compared to saline or low iron chow controls (6.2 +/- 2.0 versus 14.9 +/- 2.1 and -1.8 +/- 1.7, respectively, P less than 0.001). In anemic rats the absorption of either a 100-mug dose of 59FeSO4 or a 500-mug dose of 59Fe-hemoglobin was also significantly decreased by prior administration of laundry starch. The data obtained indicated that laundry starch (1) binds appreciable quantities of inorganic and hemoglobin iron in vitro; (2) inhibits the mucosal uptake or inorganic iron by isolated intestinal loops; (3) inhibits the intestinal absorption of inorganic iron in normal nonanemic rats, and (4) blunts the compensatory increase in inorganic and organic iron absorption in anemic rats.

Anemia, Hypochromic↗
PubMed1976

Stimulation of secretion of gastric inhibitory polypeptide and insulin by intraduodenal amino acid perfusion.

The effect of intraduodenal or intravenous administration of a 30-gm mixed amino acid solution of serum gastric inhibitory polypeptide (GIP), alpha-amino nitrogen (AAN), glucose, and insulin concentrations was studied in 10 normal subjects. Initially, an intraduodenal amino acid perfusion (15 ml per min X 60 min) was performed in each subject and was followed in 1 to 2 weeks by an intravenous infusion. Peak AAN concentrations occurred at 60 min after both routes of administration, but were greater with intravenous infusion, 145 +/- 5.7 mug per ml vs. 89 +/- 4.4 mug per ml (P less than 0.001). Although serum AAN levels were significantly lower after intraduodenal administration, incremental insulin concentrations were greater after intraduodenal perfusion, 77.3 +/- 8.8 muM per ml vs. 43.1 +/- 5.6 muU per ml (P less than 0.005). Total integrated insulin secretion was also greater after intraduodenal amino acids, 5000 vs. 2400 muU-min ml-1 (P less than 0.005). With intravenous amino acid infusion, serum GIP concentrations remained below the assay detection limit. After intraduodenal perfusion, a mean maximum GIP increment of 468 pg per ml occurred at 15 min. In all subjects peak GIP concentrations occurred at 15 min and preceded the maximum insulin rise by 15 to 30 min. Total integrated GIP secretion was significantly greater after intraduodenal amino acid perfusion, 13,000 pg-min ml-1 vs. no measurable response with intravenous infusion. In separate studies performed in 12 subjects, no significant changes in serum GIP concentrations occurred after intraduodenal perfusion of 0.45% saline, 0.9% saline, or 10% mannitol. The results of this study demonstrate that intraduodenal amino acid administration stimulates the secretion of GIP and suggest that endogenously released GIP may be important in the enteric mediated release of insulin.

Adult↗
PubMed1975

Silent pancreatic pseudocyst. An unusual cause of extrahepatic biliary obstruction.

Extrahepatic biliary obstruction due to mechanical obstruction of the common bile duct is a relatively rare complication of pancreatic pseudocyst. When jaundice does occur, clinical or laboratory evidence of associated primary hepatobiliary disease or acute pancreatitis has invariably been present. The patient described had a 3-month history of painless juandice, 40-lb weight loss, pruritus, and hepatomegaly, but no clinical or biochemical evidence of acute or chronic pancreatitis. After initial evaluation, including an abdominal echogram and a transhepatic cholangiogram, carcinoma of the head of the pancreas was diagnosed preoperatively. At laparotomy, a small pancreatic pseudocyst obstructed the terminal portion of the common bile duct. This case illustrates that a pancreatic pseudocyst should be considered in the differential diagnosis of obstructive jaundice, even in the absence of clinical evidence of pancreatitis or pseudocyst formation.

Adult↗
PubMed1975

Lymphopenic infectious mononucleosis.

Lymphopenic IM is a real phenomenon. It is likely to appear as a more severe clinical illness and, in contrast to the benign course to typical IM, may have a poorer prognosis. The clinical spectrum of IM should be extended to included to include lymphopenic patients if their diagnosis is supported by appropriate heterophil and EBV antibody titers.

Acute Kidney Injury↗