Search PubMed⌕ Search

Biomedical subjects

E A Shaffer

Publications and source records attributed to E A Shaffer.

121 records · Page 7Linked to original sources
PubMed1978

Diagnosis of hepatobiliary disease by 99mTc-HIDA cholescintigraphy.

99mTc-HIDA is concentrated by the hepatocytes and excreted into the biliary system; the gallbladder, common bile duct, and early accumulation in the duodenum are visualized within 30 minutes of intravenous administration. The authors studied the utility of 99mTc-HIDA imaging in both acute and chronic cholecystitis and hepatobiliary disease in the presence of jaundice: (a) all normal gallbladders exhibited filling, (b) absence of visualization indicated gallbladder disease and/or cystic duct obstruction, (c) visualization of the gallbladder after cholecystokinin-induced emptying excluded an obstructed cystic duct and acute cholecystitis, and (d) a definitive diagnosis of hepatocellular disease, partial and complete obstruction, is possible in jaundiced patients with hyperbilirubinemias up to 5 mg%. Beyond that level, 99mT-HIDA imaging was of qualified value. The technique is useful in assessing biliary drainage in jaundiced patients with surgically altered biliary tract anatomy.

Acute Disease↗
PubMed1977

Endoscopic removal of a foreign body perforating the duodenum.

Perforation of the intestine by an ingested foreign body usually results in peritonitis or abscess formation and the treatment is surgical. In one case the duodenum was perforated by a toothpick, and hemorrhage from the upper gastrointestinal tract occurred 3 months later. Diagnosis and management were accomplished by operative endoscopy.

Aged↗
PubMed1977

Biliary lipid secretion in cholesterol gallstone disease. The effect of cholecystectomy and obesity.

Cholesterol gallstone disease is initiated in a liver which produces abnormal bile with excess cholesterol relative to bile salts and phospholipid. To define the responsible secretory mechanism(s), the rate of biliary lipid secretion was measured by a duodenal marker perfusion technique, while the bile salt pool was simultaneously estimated by isotope dilution. Two groups of control patients expected to have normal biliary lipid composition--14 subjects without hepatobiliary disease and 6 patients with pigment gallstones, were compared to two experimental groups expected to have abnormal bile--10 nonobese patients with cholesterol gallstones and 7 obese subjects without gallstones. Both control groups had nearly identical biliary lipid secretion rates, and a corresponding low relative molar concentration of cholesterol. Two different secretory mechanisms were found to be responsible for the abnormal bile in the experimental groups. In the nonobese patients with cholesterol gallstones, bile salt and phospholipid secretion rates were both significantly reduced. Conversely, the grossly obese subjects had an increased cholesterol secretion. To determine how cholecystectomy improves biliary lipid composition, three groups of gallstone patients --6 with pigment stones, 4 grossly obese with cholesterol stones, and 13 nonobese with cholesterol stones --were all examined after full recovery from surgery. In the nonobese patients with cholesterol gallstones, both bile salt and phospholipid secretion significantly increased, causing a definite improvement in bile composition. Cholecystectomy produced a similar but less marked trend in the obese patients with cholesterol stones, and in the patients with pigment stones. Cholesterol secretion, however, was unaffected by surgery. The bile salt pool was definitely small in the nonobese patients with cholesterol gallstones and became slightly smaller after cholecystectomy. The pool was significantly reduced by cholecystectomyin the patients with cholesterol gallstones. Removal of the gallbladder in all three groups caused a greater fraction of the pool to cycle around the enterohepatic circulation each hour. This more rapid cycling produced the increase in bile salt and phospolipid secretion, and was responsible for the improved composition found after cholecystectomy.

Adult↗
PubMed1976

Bilirubin secretion and conjujation in the Crigler-Najjar syndrome type II.

Features characteristic of the Crigler-Najjar syndrome (type II) are described in an adolescent boy with severe congenital unconjugated hyperbilirubinemia. Bilirubin encephalopathy developed only in early puberty after surgery and fasting, coincident with a dramatic rise in serum bilirubin, which responded to intensive therapy. Fasting was later shown to increase markedly the serum bilirubin levels and probably was a major factor in precipitating the initial acute event. One year later, while the patient was in a metabolic steady state, the secretion rate of bilirubin was measured by aduodenal marker-perfusion technique, and the nature of the secreted bilirubin conjugates was characterized. Total bilirubin secretion rates were low, 4.39 mg per hr and 4.44 mg per hr on two separate studies. The major pigment detected in bile was bilirubin monoglucuronide. Bilirubin diglucuronide comprised only a minor fraction of the pigments, and other conjugates were not detected. The present study documents a reduced biliary bilirubin secretion and suggests that the addition of the second glucuronic acid moiety to the bilirubin molecule may be defective in Crigler-Najjar syndrome (type II).

Adolescent↗
PubMedDate not supplied

Reticuloendothelial system Fc receptor-mediated clearance of IgG-tagged erythrocytes from the circulation of patients with idiopathic ulcerative colitis and chronic liver disease.

Immune complexes may be important in the pathogenesis of the liver disease associated with idiopathic ulcerative colitis. In the present study, we documented Fc receptor-mediated clearance by the reticuloendothelial system of immune complex-like material from the systemic circulation of 25 healthy control subjects, 19 patients with ulcerative colitis alone, 9 patients with ulcerative colitis and elevated liver enzyme tests and 8 patients with various other forms of chronic liver disease. Following an intravenous infusion of IgG-tagged 51Cr-labeled autologous erythrocytes, serial blood samples were drawn over a 2-hr period of time, and computer-generated clearance curves were obtained. The time required for clearance of 50% of infused erythrocytes (T1/2) was then calculated. Serum immunoglobulin (IgA, IgG and IgM), complement (C3 and C4) and immune complex-like activity (IgG and IgM types) were also determined. Sixteen of 19 (84%) ulcerative colitis patients and 7 of 8 (88%) chronic liver disease patients had normal clearance T1/2's (when compared to 25 healthy controls). Conversely, only 1 of 9 (11%) ulcerative colitis + chronic liver disease patients demonstrated normal clearance function. Aside from serum IgM levels, the results of serum immunoglobulin, complement and immune complex-like determinations were similar in ulcerative colitis and ulcerative colitis + chronic liver disease patients. Serum IgM levels, however, were significantly decreased in ulcerative colitis patients and increased in ulcerative colitis + chronic liver disease patients (p less than 0.001). The results indicate that the reticuloendothelial system of patients with ulcerative colitis and chronic liver disease is impaired in its ability to dear immune complex-like material from the systemic circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

A comparative study of the effects of insulin/glucagon infusions, parenteral amino acids and high dose corticosteroids on survival in a rabbit model of acute fulminant hepatitis.

Acute fulminant hepatitis was induced in 55 healthy adult male rabbits with the potent hepatotoxin galactosamine hydrochloride (3.75 mmoles per kg i.v.). Control rabbits (n = 27) were divided into three groups: Group I (n = 10) underwent sham surgery for placement of an indwelling central venous catheter; Group II (n = 9) received 5% dextrose and water via an indwelling central venous catheter, and Group III (n = 8) received daily intramuscular injections of 0.9% sodium chloride. Treated rabbits (n = 28) also consisted of three groups: Group IV (n = 9) received 12-hr intravenous infusions of insulin (0.029 units per kg per hr) and glucagon (2.86 micrograms per kg per hr) daily; Group V (n = 10) received a continuous infusion of parenteral amino acids (Travasol), and Group VI (n = 9) received daily intramuscular methylprednisolone (0.69 mg per kg). In each case, treatment was initiated 16 hr following galactosamine injection. Serum aminotransferase activity was determined on Days 0, 1, 4 and 10 of the 10-day study. Liver histology was obtained immediately after death and graded under code on a scale of 1 to 4 for severity of hepatitis. Rabbits surviving 10 days were sacrificed on Day 10 for histologic examination. The extent of galactosamine-induced hepatic injury was similar in all six groups as manifest by peak mean SGPT (range: 2,662 to 3,568 IU per liter), SGOT (range: 4,435 to 5,625 IU per liter) levels and hepatic histologic findings. The overall survival rate in controls was 6/27 (22%); in insulin/glucagon-treated animals 2/9 (22%), and in the amino acid-treated group 2/10 (20%).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMedDate not supplied

Ascending infection of the biliary tract after surgical sphincterotomy and biliary stenting.

It has been widely accepted that there is an ascending route of bacterial infection of the biliary tract but there is a lack of direct evidence. This hypothesis was tested in an animal experiment using the cat as an animal model. The implantation of biliary stents and surgical sphincterotomy were performed in these animals, with sham controls. Stents bypassing the sphincter of Oddi with the tip in the duodenal micro-organisms and the biliary tract was heavily contaminated. Blockage of these stents resulted in biliary obstruction. Stents implanted within the common bile duct, proximal to the sphincter were largely unaffected by biofilm formation. After surgical sphincterotomy the biliary tract was also contaminated but, in the absence of obstruction, the animals did not develop any symptoms. It was concluded that ascending infection by duodenal biliary reflux, via the sphincter of Oddi, is an important route of infection in the biliary system.

Animals↗
PubMedDate not supplied

Bacterial biofilm, brown pigment stone and blockage of biliary stents.

Bacterial pathogens gain access into the biliary system by descending via the portal venous circulation or ascending through the sphincter of Oddi in duodenal-biliary reflux. Bacteria thrive as glycocalyx-enclosed microcolonies, coalescing to form an adherent biofilm. The establishment of biofilm is a key event in the formation of biliary sludge and pigment gallstones, and the blockage of biliary stents. The biofilm mode of growth is very effective because it provides bacteria with a measure of protection from antibacterial agents and phagocytic leucocytes. Calcification of the matrix confers further protection for the micro-organisms living inside the biofilm. To date, attempts to prevent blockage of biliary stent have employed physical methods by using large self-expandable stents and stents without side hole. Incorporation of antibiotics within stents has not been successful presumably because bacteria once living in their biofilm are quite resistant to antimicrobial agents. Even the most toxic bile salts have no effect on the biofilm bacteria. Yet, hydrophobic bile salts reduce bacterial adhesion on biomaterial, suggesting that incorporation of such bile salts might prevent the formation of bacterial biofilm.

Animals↗