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Biomedical subjects

R J Stenger

Publications and source records attributed to R J Stenger.

At least 37 records · Page 2Linked to original sources
PubMed1985

Hepatic cirrhosis in young adults: association with adolescent onset of alcohol and parenteral heroin abuse.

Hepatic cirrhosis is infrequently diagnosed in young adults. In a hospital for addictive diseases in New York City, we found cirrhosis in 53 patients under age 35 within just 40 months. The cirrhosis was biopsy-proven in 37 patients (group I) and diagnosed clinically in 16 patients with severe liver disease (group II). Alcohol abuse was found in 51 patients (96%), and parenteral heroin abuse was seen in 52 (98%). The duration of alcohol abuse was seven or fewer years in 24 patients (45%) and 10 or fewer in 39 (74%). In 44 (83%), the substance abuse began in adolescence. Comparison of group I cirrhotic patients with 65 non-cirrhotic biopsied patients showed that cirrhosis was significantly associated with abuse of both alcohol and parenteral heroin (p less than 0.001). The distribution of 66 HLA antigens from A, B, C, and DR loci showed no differences when 42 patients were compared with 42 ethnically-matched control substance abusers. The early development of cirrhosis in these young patients may be related to multiple hepatic injuries induced by alcohol and parenteral heroin abuse and to the onset of addictive diseases during adolescence or early adult life.

Adult↗
PubMed1984

Effects of bile acid oxazolines on gallstone formation in prairie dogs.

The effects of 2 bile acid analogs, chenodeoxy-oxazoline [2-(3 alpha, 7 alpha-dihydroxy-24-nor-5 beta-cholanyl)-4,4-dimethyl-2-oxazoline] and ursodeoxy-oxazoline [2-(3 alpha, 7 beta-dihydroxy-24-nor-5 beta-cholanyl)-4,4-dimethyl-2-oxazoline] were examined in the prairie dog model of cholesterol cholelithiasis. Gallstones and biliary cholesterol crystals were induced in 5 out of 6 male prairie dogs fed a semisynthetic diet containing 0.4% cholesterol for 8 weeks. Six animals maintained on a low cholesterol control diet (0.08% cholesterol) exhibited neither gallstones nor biliary cholesterol crystals. The addition of 0.06% chenodeoxy-oxazoline to the lithogenic diet did not prevent induced cholelithiasis or the appearance of cholesterol crystals in bile. In contrast, 0.06% dietary ursodeoxy-oxazoline prevented gallstones in 5 out of 6 prairie dogs (but cholesterol crystals were present in the bile of 4 of these animals). Histologically, most of the livers from the prairie dogs fed the cholesterol-supplemented semisynthetic diet showed bile duct proliferation, inflammatory infiltration and fibrosis along the portal tracts. These pathologic changes were generally not ameliorated by adding chenodeoxy-oxazoline or chenodeoxy-oxazoline plus chenodeoxycholic acid to the diet. Portal tract pathology was markedly reduced in most animals by adding ursodeoxy-oxazoline to the cholesterol-supplemented diet. The pathologic changes overall could best be correlated with the presence of gallstones, but not with the incidence of biliary cholesterol crystals.

Animals↗
PubMed1984

Prevention of cholesterol-induced gallstones by hyodeoxycholic acid in the prairie dog.

Prairie dogs of both sexes were fed a semisynthetic diet containing 0.35% cholesterol for a period of 8 weeks. This lithogenic diet induced cholesterol gallstones in ten "lithogenic control animals", five males and five females. Three animals maintained with a high glucose, fat-free diet did not develop gallstones although the cholesterol saturation of their bile approached unity. The formation of gallstones was prevented in four out of five males and all five females fed the lithogenic diet plus 0.1% hyodeoxycholic acid (30 mg per kg body weight per day). The biles of the prairie dogs receiving hyodeoxycholic acid were abnormally colored, cloudy, and highly saturated with cholesterol but contained neither cholesterol crystals nor gallstones (with the exception of one male). Feeding the relatively hydrophilic bile acid, hyodeoxycholic acid, was associated with an increase in hepatic microsomal HMG-CoA reductase activity. Cholesterol 7 alpha-hydroxylase, on the other hand, was inhibited by the administered bile acid. The dietary hyodeoxycholic acid was transformed, in part, to 3 alpha, 6 beta-dihydroxy-5-beta-cholanoic acid and hyocholic acid. It is concluded that hyodeoxycholic acid and its metabolites did not prevent the induced cholelithiasis by causing a decrease in the concentration of biliary cholesterol. Instead, this hydrophilic bile acid apparently increases the amount of cholesterol in the bile, probably in the form of a liquid crystalline mesophase. Hyodeoxycholic acid apparently prevents gallstones by preventing the nucleation and aggregation of cholesterol crystals. The lithogenic diet induced moderate to marked bile duct proliferation together with portal fibrosis and inflammatory infiltration. The addition of hyodeoxycholic acid to the lithogenic diet reduced all of the portal tract changes.

Animals↗
PubMed1982

Tumors of the ampulla of Vater: early diagnosis by intraampullary biopsy during endoscopic cannulation. Two case presentations and a review of the literature.

In 2 cases of ampullary tumor, the diagnosis was made by intraampullary biopsy after an abnormality was discovered via the fluoroscope during endoscopic retrograde cholangiopancreatography. One case was a villotubular adenoma with dysplasia and carcinoma in situ, and the other, a polypoid adenocarcinoma of the ampulla of Vater. These tumors were not visualized on upper gastrointestinal barium studies and conventional duodenoscopy nor by direct vision during endoscopic retrograde cholangiopancreatography. In the past the diagnosis of ampullary neoplasm has been most often made of surgery and on autopsy. Only in 11 of 538 patients reviewed was the diagnosis made by biopsy of a tumor visible at endoscopy. As demonstrated by the two cases we report, intraampullary biopsy of lesions visualized on fluoroscopy during endoscopic retrograde cholangiopancreatography may facilitate early diagnosis.

Adenocarcinoma↗
PubMed1981

Methadone disposition in patients with chronic liver disease.

Chronic liver disease is common in methadone-maintained patients. We studied the disposition of this drug in 14 patients with biopsy-proved chronic liver disease and five otherwise healthy subjects receiving methadone maintenance treatment. The patients were divided into three groups based on the severity of liver disease, with group I having the most severe disease. The apparent terminal half-life of methadone was longer in group I than in group II and III (moderate and mild chronic liver disease, P less than 0.01) and the contrast group (P less than 0.05). All other kinetic indices determined for group I and all kinetic indices in groups II and III were essentially the same as those in the contrast subjects or in the other patient groups. Seven patients, including al five in group I, had flattened plasma methadone concentration-time curves. The data suggest that the maintenance dosage of methadone need not be changed in stable chronic liver disease.

Administration, Oral↗
PubMed1981

Hepatitis B serologic studies in narcotic users with chronic liver disease.

Hepatitis B surface antigen (HBsAG) and antibody (anti-HBs), and antibody to the hepatitis B core antigen ( anti-HBc) were measured by radioimmunoassay in 46 current or former narcotic users who underwent liver biopsy for evaluation of chronic liver disease. Significant alcohol abuse was found in 38 narcotic users (82.6%). On liver biopsy, 24 had cirrhosis (52.2%), nine had chronic active hepatitis (19.6%), five had lipid accumulation (10.9%) and eight had other diagnoses (17.4%). At least one marker for hepatitis B was found in 45 of 46 narcotic users (97.8%). Five had HBsAg and anti HBc (10.9%), one had anti-HBs alone (2.2%), 30 had anti-HBs and anti-HBc (65.2%) and nine had anti-HBc alone. Although almost all narcotic users with chronic liver disease have active or resolved hepatitis B infection, alcohol abuse appears to be the major factor in the development of cirrhosis in the subset of narcotic users studied.

Adult↗
PubMed1977

Liver disease.

Explore the source record for details and available documents.

Adenoma↗
PubMed1977

The spectrum and causes of liver diseases in narcotic addicts.

Fifty charts of patients discharged with a diagnosis of liver disease from the acute care service of a hospital for the treatment of addiction were analyzed. Among 42 active heroin users or former heroin addicts maintained on methadone, 79% were heavy alcohol abusers. Seventeen cases of cirrhosis were encountered. All occurred in those abusing alcohol. Reversible liver disease was seen in both alcohol abusers and nonalcoholics. This study suggests that alcohol is a major factor in the development of irreversible liver disease in active heroin addicts and ex-addicts on methadone maintenance.

Acute Disease↗
PubMed1976

Influence of acute and chronic administration of methadone hydrochloride on NADPH-cytochrome c reductase and cytochrome P-450 of mouse liver microsomes.

Administration of a single acute dose (20 mg/kg body weight) of methadone hydrochloride to both male and female mice increased the specific activity of NADPH-cytochrome c reductase and did not change much the content of cytochrome P-450 of their liver microsomes. Administration of multiple acute doses of methadone in male mice increased the specific activity of cytochrome c reductase and the content of cytochrome P-450 of their liver microsomes. Chronic administration of progressively increasing doses of methadone (up to 40 mg/kg body weight) to male mice increased the specific activity of c reductase. Similar chronic administration of methadone up to 28 mg/kg body weight also increased the microsomal content of P-450, but with higher doses of methadone, the content of P-450 declined and finally dropped slightly below control levels. The levels of c reductase activity and P-450 content returned to normal about two weeks after discontinuation of methadone administration.

Animals↗
PubMed1976

Effects of morphine sulfate on NADPH-cytochrome c reductase and cytochrome P-450 of mouse liver microsomes.

Three hr after i.p. administration of a single dose of 30 mg/kg of morphine to male mice, an increase in specific activity of NADPH-cytochrome c reductase by about 10% and the content of cytochrome P-450 by about 14% of their liver microsomes was observed.Administration of 30 mg/kg of morphine, once daily,during 5 days, caused about 16% and 9% increases in specific activity of c reductase and the content of P-450 respectively. Administration of a single dose of morphine to male and female mice caused no sex-dependent differences in the specific activity of c reductase and the content of P-450. Repeated administration of morphine up to 100 mg/kg to male mice increased the specific activity of microsomal c reductase by about 70%. Repeated administration of morphine up to 55 mg/kg also increased the microsomal content of P-450 by about 22%, but with higher doses of morphine, the content of P-450 declined and finally dropped below control levels. The levels of c-reductase activity and P-450 content returned to normal levels about 2 weeks after termination of morphine administration.

Animals↗
PubMed1975

CEA levels in patients with colorectal polyps.

Preoperative plasma CEA levels were measured in 93 selected patients with histologically defined colorectal adenomata removed at fibroptic colonoscopy in order to determine whether CEA levels are elevated in patients with colonic polyps, or vary with different histologic patterns. None of the patients had inflammatory bowel disease, previous history of carcinoma, or evidence of liver disease. Fifteen percent of the patients had elevated CEA levels (greater than or equal to 2.5 ng/ml; Hansen method), and two-thirds of these were between 2.5 and 4.0 ng/ml. Increased association of elevated CEA levels was noted with old age, villous adenomas (2- to 4-fold), and increased tumor size (greater than 2.3-cm diameter; 2-fold), but not with foci of dysplasia or carcinoma in situ as such. One-half (7/14) of the patients with elevated CEA levels showed the following: two patients had villous tumors with carcinoma in situ, one had a villous adenoma, two had mixed villous and tubular adenomas (with a high proportion of villous pattern), and two were subsequently shown to have carcinoma elsewhere in the colon. It is uncertain that the polyps were the source of the elevated circulating CEA levels; other factors including smoking and patient selection need to be considered. This preliminary study suggests that patients with colorectal adenomata and elevated circulating CEA may be at higher risk for the development of carcinoma. Further follow-up studies of the malignant potential of the polyp-bearing colon are essential.

Adenoma↗