Biomedical subjects
Publications and source records attributed to G A Weaver.
Five patients thought to have bleeding angiodysplasia in the distal duodenum and proximal jejunum were treated surgically after conservative measures failed to control hemorrhage. Aspiration through a long oral tube preoperatively and intraoperative endoscopy were most helpful in locating the site of bleeding.
Methanogens were in the isolated sigmoid colon but not in the colostomy bag of a woman with a left hemicolectomy with end colostomy and mucous fistula. The predominant methanogen was Methanobrevibacter smithii. An anaerobic bacterial community supported by nondietary substrates was present in the isolated sigmoid colon.
Erythrocytosis, increased whole blood oxygen affinity, and iron overload were found in a 37-yr-old man. Electrophoretic techniques to demonstrate a hemoglobin variant showed no abnormality. Structural studies of the hemoglobin from this patient revealed an abnormal hemoglobin previously described as Hemoglobin Olympia, a high-affinity variant. Study of three generations in this family showed increased hepatic iron or iron absorption in some members of all three generations studied. The findings in this family are consistent with an increase in iron absorption due to the consequences of Hemoglobin Olympia and the heterozygous state for hemochromatosis (allele for hemochromatosis associated with HLA-A3, B7) or the presence in the family pedigree of three different alleles for hemochromatosis (alleles for hemochromatosis associated with HLA-A3. B7, HLA-A3, B15, and HLA-A9, B44) with the heterozygous state being manifest with increased iron absorption.
A patient is presented who developed hepatic osteodystrophy after orthotopic liver transplantation in association with persistently low serum 25-hydroxyvitamin D levels. After successful liver transplantation there was a delay in the return to normal of the serum 25-hydroxyvitamin D levels until oral supplementation with vitamin D was instituted. This case emphasizes the need for effective treatment of hepatic osteodystrophy with vitamin D especially in patients considered for transplantation.
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Acute pancreatitis has been associated with multiple drugs. Some animal and autopsy studies have shown chronic focal changes. Most clinical reports have shown acute pancreatitis at autopsy or an acute clinical course. Herein we present a patient with chronic pancreatitis with cyst formation that was detected several months after steroid administration had been stopped. The histological findings in the resected pancreas showed ectatic ducts, acute and chronic inflammation, and laminated protein concretions in dilated pancreatic ducts. The findings in this patient suggest that drug therapy might be etiological in causing selected cases of chronic pancreatitis.
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Moniliformin (1-hydroxy-cyclobut-1-ene-3,4-dione), either purified (0, 8, and 16 mg/kg of diet) or from culture of Fusarium moniliforme strain NRRL 6322 on corn grits (8, 16, and 64 mg/kg of diet) was fed to growing broiler chicks from 1 to 21 days of age. Up to 16 mg moniliformin/kg of diet from either source was without effect on chick weight gain, feed consumption, and mortality. Chicks fed 64 mg moniliformin/kg of diet from culture had reduced weight gain and feed consumption. Total daily moniliformin consumption by these chicks was nearly twice the reported single oral 50% lethal dose. Three of 10 chicks fed 64 mg/kg of moniliformin in the diet died. No lesions were found upon necropsy. The LD50 of purified moniliformin upon intravenous injection of 7-week-old female broiler chickens was 1.38 +/- .035 mg/kg body weight. Average time to death was 65 minutes. Progressive symptoms noted included lack of muscular coordination, tachypnea from moderate to severe followed by slow labored respiration, coma, terminal agonal struggle, and death.
Purified diacetoxyscirpenol (DAS) mycotoxin fed to growing pigs at 0, 2, 4, 8, and 9 ppm for as long as nine weeks caused several lesions at all levels. The pigs developed multifocal, proliferative, gingival, buccal and lingual lesions. The small intestine had both glandular and mucosal cell hyperplasia. No other lesions were seen at necropsy or in any of the 19 tissues examined microscopically using haematoxylin and eosin stain. A one-way analysis of variance revealed statistically significant (P less than 0.05) decreased ration consumption and weight gain at all levels of DAS. Total ration refusal occurred at 10 ppm of DAS. There was no effect on the packed cell volume, haemoglobin concentration, total red blood cell count, total white blood cell count, 300 cell differential, terminal bone marrow smears or on the serum levels of aspartate transaminase, serum glutamic pyruvic transaminase and lactic dehydrogenase at any level of DAS. Based on the gross and microscopic lesions, decreased ration consumption and decreased weight gain the no-effect level was less than 2 ppm of DAS in the ration.
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Acute toxic effects of purified zearalenone were studied in growing female White Leghorn chickens. In the first experiment, zearalenone in gelatin capsules was administered to 10 chickens (zearalenone-treated chickens [ZC]) in a single oral dose of 15.0 g/kg. Another 10 control chickens (CC) received empty gelatin capsules. All chickens survived the 10-day experiment and did not show any noticeable gross or histopathological lesions. There were no differences between CC and ZC in weight gain, oviduct, comb and liver weights, hematological parameters, and serum cholesterol. ZC had significantly less (P less than 0.05) serum calcium but significantly greater (P less than 0.01) serum phosphorus than CC. In the second experiment, zearalenone was administered orally or intramuscularly (pectoral muscle) at levels of 0, 50, 200, 400, and 800 mg/kg for 7 consecutive days. The oviduct weight increased with increasing toxin levels in both orally (OZC) and intramuscularly (IZC) administered groups: there were more pronounced effects in the IZC. The liver weight increased and comb weight decreased in IZC. The relative estrogenic biopotency of zearalenone in IZC, using estradiol dipropionate as a standard, was 1.37%. The results of this experiment demonstrate that chickens are highly tolerant to zearalenone and that the estrogenic effects of the toxin are greater when it is administered in multiple doses than in a single dose and in IZC than in OZC.
A Holstein cow was intubated with 182 mg of 97% pure T-2 toxin (0.44 mg/kg of body weight) for 15 days. A dairy ration containing 50 mg/kg (50 ppm) of T-2 toxin was refused. A calf, born four days after onset of maternal treatment, was intubated with 26.2 mg of purified T-2 toxin (0.6 mg/kg of body weight) for seven consecutive days and then on alternate days for a total of 16 days. The calf was severely affected clinically by the T-2 toxin. The T-2 toxin failed to cause bovine hemorrhagic syndrome in either animal. Unspecific gastrointestinal lesions were noted in the cow but none were detected in the calf. In the calf, severe depression, hindquarter ataxia, knuckling of the rear feet, listlessness and anorexia were caused by the T-2 toxin.
A patient is presented with Barrett's esophagus (lower esophagus lined with columnar epithelium) who also has a band of columnar epithelium in the upper esophagus separated from that below by normal squamous epithelium in the midesophagus. The upper most squamocolumnar junction coincided with or formed a mucosal ring as seen at endoscopy. This ring, which was first seen on barium swallow, has the radiographic appearance of that associated with the Paterson-Kelly syndrome. This patient's unique findings may provide further insight into the etiology of upper esophageal webs or rings (Paterson-Kelly syndrome).
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Twelve patients with angiodysplasia of the gastrointestinal tract were seen at The Mary Imogene Bassett Hospital are presented. Six share the features of gastric or duodenal angiodysplasia, advanced age, and aortic valve disease. Of these 6 patients, 4 who bled repeatedly were treated with endoscopic coagulation of areas of gastric and duodenal angiodysplasia. Six patients with other types of gastrointestinal angiodysplasia are presented for comparison. Two had gastric angiodysplasia and no aortic valve disease, 2 had hereditary hemorrhagic telangiectasia, 1 had received irradiation, and 1 could not be classified. We suggest that angiodysplasia of the gastrointestinal tract can be regarded as a spectrum with a clearly inherited etiology on one extreme and an acquired etiology on the other. A subset of these patients may be associated with aortic valve disease. Angiodysplasia of the upper gastrointestinal tract may account for a significant fraction of previously unexplained bleeding. It is hoped that this paper will aid in their more frequent recognition.
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