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Biomedical subjects

I R Wanless

Publications and source records attributed to I R Wanless.

At least 55 records · Page 3Linked to original sources
PubMed1990

Hepatic vascular disease and portal hypertension in polycythemia vera and agnogenic myeloid metaplasia: a clinicopathological study of 145 patients examined at autopsy.

The pathogenesis of portal hypertension arising in patients with myeloproliferative disorders has been difficult to understand because liver biopsy findings often show minimal changes. It has been suggested that increased splenic blood flow, hepatic infiltration with hematopoietic cells or sinusoidal fibrosis may be important. We have reviewed the autopsy findings and clinical histories of 97 patients with polycythemia vera and 48 patients with agnogenic myeloid metaplasia collected from three institutions and from the Polycythemia Vera Study Group. Cirrhosis was present in seven patients, one of whom had bleeding varices. Esophageal varices were present clinically in 10 patients without cirrhosis (seven polycythemia and three agnogenic myeloid metaplasia). All of these patients had lesions in small or medium-sized portal veins and four had stenosis of the extrahepatic portal vein with histology compatible with organized thrombi. Nodular regenerative hyperplasia occurred in 14.6% and correlated closely with the presence of portal vein lesions. Thirty patients had greater than 500 ml of ascites, seven of these patients also had varices and six of them had hepatic vein thrombosis. Ascites also correlated with hepatic vein disease confined to small intrahepatic branches. No correlation was seen between hepatic hematopoietic infiltration and signs of portal hypertension. We conclude that esophageal varices are common and are almost always associated with portal vein lesions visible by light microscopy. These portal vein lesions, and the secondary effects of nodular regenerative hyperplasia and portal hypertension, are most likely a result of portal vein thrombosis in patients with myeloproliferative disorders.

Adult↗
PubMed1990

Histopathology of cocaine hepatotoxicity. Report of four patients.

Although cocaine is believed to be hepatotoxic for humans, the hepatic histopathology has been reported in only 1 patient. That patient had zone-1 necrosis. We have encountered 4 patients with liver injury secondary to cocaine use, 1 of whom died. The biopsies from two patients showed well-demarcated zone-3 necrosis identical to that seen with acetaminophen toxicity. The patient who died had necrosis of almost all hepatocytes as found at biopsy and autopsy. Biopsy was performed on another patient after resolution of the illness, and showed hyperplastic endoplastic reticulum but no necrosis. All patients had mild large- and small-droplet steatosis in surviving hepatocytes. Inflammation was mild. Drug screenings performed on all patients showed the presence of a cocaine metabolite and the absence of acetaminophen, alcohol, and other potential toxins. Patients typically had early marked increase and rapid decrease of serum aminotransferases, mild-to-moderate increase in prothrombin time, myoglobinuria, and moderate azotemia. The predominant pattern of zone-3 necrosis is similar to that reported of mice given cocaine.

Adult↗
PubMed1989

Subcapsular steatonecrosis in response to peritoneal insulin delivery: a clue to the pathogenesis of steatonecrosis in obesity.

Hepatic steatosis and steatonecrosis occur in nonalcoholic individuals, usually in a setting of obesity, type II diabetes mellitus, and after jejunoileal bypass. We propose an hypothesis for the pathogenesis of these hepatic lesions based on an observation in peritoneal dialysis patients. Hepatic histology was examined at autopsy in 11 patients with type I diabetes mellitus and renal failure who had received i.p. insulin in conjunction with continuous ambulatory peritoneal dialysis (CAPD). Steatosis in a unique subcapsular distribution occurred in 10 of 11 patients treated with i.p. insulin and in 0 of 9 controls receiving CAPD without insulin. Three of the 11 had steatonecrosis, 2 of whom had Mallory bodies. We suggest that insulin has an important role in the pathogenesis of steatosis and steatonecrosis. In CAPD patients the lesions occurred only under the capsule where concentrations of insulin are high secondary to its i.p. administration. In obese patients the lesions occur throughout the liver where insulin concentrations are high because of elevated levels in the portal vein. Free fatty acids (FFA) are oxidized in the liver by a pathway that is blocked by insulin. In the presence of insulin, FFA are preferentially esterified into triglycerides which accumulate in large quantities leading to steatosis; small amounts of FFA escaping local control may lead to membrane injury and steatonecrosis. Steatosis and/or steatonecrosis will occur when there is insulin secretion sufficient to block FFA oxidation but not sufficient to block FFA mobilization from adipose tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Multiple focal nodular hyperplasia of the liver associated with vascular malformations of various organs and neoplasia of the brain: a new syndrome.

Focal nodular hyperplasia (FNH) is a lesion of the liver in which a large anomalous artery is located within a region of hyperplastic hepatic parenchyma. Patients with FNH commonly have other lesions, often vascular in nature, in the liver or other organs. We have noted that these associated lesions almost always occur in patients with multiple FNH. We therefore studied 27 autopsied patients with FNH. All 13 with multiple FNH had other lesions such as hemangioma of liver, meningioma, astrocytoma, telangiectasis of the brain, berry aneurysm, dysplastic systemic arteries, and portal vein atresia. One patient had several of these lesions including multiple FNH, meningioma, astrocytoma, vascular malformation of the brain stem, and hemangioma of the liver. In contrast, among the 14 patients with solitary FNH there were no associated lesions, except for hepatic hemangioma in one patient. The prevalence of this syndrome was estimated by examination of 2500 serial autopsies and autopsies with various components of the syndrome. On review of 73 consecutive autopsies with meningioma, three had multiple FNH, compared with seven of 2500 consecutive adult autopsies (P less than 0.001). Multiple FNH was found in two of 83 autopsies with astrocytoma (P less than 0.05) and in one of 139 autopsies with berry aneurysm (not significant). We describe a telangiectatic subtype of FNH which occurs in this syndrome as well as in a minority of patients with solitary FNH. The existence and character of this syndrome suggest that there may be an underlying systemic abnormality in some patients having components of the syndrome. Investigation of patients with multiple FNH lesions may reveal significant treatable lesions.

Adolescent↗
PubMed1987

Hepatic cysts of periductal gland origin presenting as obstructive jaundice.

Retention cysts may arise from periductal glands of the hepatic ducts. These cysts are usually asymptomatic. Presented here is the first case with jaundice secondary to obstruction of the hepatic ducts by periductal cysts. Two other cases involved asymptomatic cysts in the presence of cirrhosis, portal vein thrombosis, and hepatocellular carcinoma. This confirms the previously noted association of cysts and portal vein thrombosis. The possibility of obstruction caused by benign cysts should be considered when investigating patients with intrahepatic bile duct obstruction.

Aged↗
PubMed1987

The use of morphometry in the study of nodular and vascular lesions of the liver.

This paper summarizes the use of morphometry on human autopsy livers to investigate three conditions characterized by the presence of hepatocellular nodules: nodular regenerative hyperplasia (NRH), partial nodular transformation (PNT) and focal nodular hyperplasia (FNH). Vascular abnormalities were seen in all cases. The nodules can be explained in all three conditions as a response to a greater blood supply in the nodules as compared to the surrounding parenchyma. In NRH, there appears to be ischemia caused by arteritis and secondary oblitertion of small portal veins. In PNT, ischemia may be caused by portal vein thrombosis. In FNH, there appears to be hyperemia caused by a spiderlike arterial anomaly.

Arteritis↗
PubMed1987

The hepatitis B carrier state--a follow-up study of 100 consecutive cases.

The clinical, demographic, serologic, and histopathologic features of 100 consecutive patients with chronic hepatitis B were studied. The subjects were from diverse racial backgrounds; 59 had emigrated to Canada from geographical areas with high hepatitis B carrier rates. A reduced 5-year survival rate was seen only in those with cirrhosis; death was most commonly related to sepsis. The male to female ratio was 4.0 in the total study group but was higher in those with elevated transaminases (6.0 vs 2.0, p less than 0.05). Those patients with mild-to-heavy alcohol consumption were more likely to have elevated transaminase values than those who drank no alcohol (p less than 0.05). The mean annual sero-conversion rate from HBeAg to Anti-HBe was 8.0%. The HBeAg status did not correlate with the presence of histologic activity or fibrosis.

Adolescent↗
PubMed1986

Voluntary alcohol intake in the hypertension prone Dahl rat.

Previous work in our laboratory has shown that alterations in the sodium content of the diet which alter salt appetite, can modify ethanol self-selection and intoxication. The present experiment investigates the relationship between the intakes of sodium and ethanol on the one hand and the development of hypertension, by measuring voluntary ethanol consumption and blood pressure in two rat lines, the salt sensitive (SS) and salt resistant (SR) Dahl rats, specially bred to show differential sensitivity to dietary sodium supplements. All rats were given 24 hr access to 6% (v/v) ethanol and water and first offered a control diet (0.5% Na) followed by a 4% and then an 8% sodium supplemented diet. While on the control diet there were significant between strain differences in ethanol consumption, suggesting that the SS animals came genetically prepared to consume more ethanol. Blood pressure measured at regular intervals indicated significant changes only in the SS rats even though both lines as well as a group of Wistar rats, added for purposes of comparison, all increased their ethanol intake to the salt supplemented diets. A second experiment suggested that the initial difference in consumption between the SS and SR lines may be related to central nervous system sensitivity since differences were found in salt appetite but not in taste sensitivity or in the absorption, distribution or metabolism of the drug. These findings demonstrate that the Dahl SS rat is predisposed to consume more ethanol than the SR rat even before exposure to the hypertension-inducing diet, and that this predisposition is probably central in origin.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohol Drinking↗
PubMed1986

Nodular transformation of the liver in hereditary hemorrhagic telangiectasia.

A case of hereditary hemorrhagic telangiectasia with prominent nodular transformation of the liver is described. The presence of enlarged arteries was documented morphometrically. Artery-to-portal vein shunts were also found. The association of abnormal vessels with hepatic nodules supports the hypothesis that abnormalities of blood flow cause nodular transformation. Nodular transformation may be the lesion that has heretofore been termed cirrhosis hepatis telangiectasia or atypical cirrhosis.

Female↗
PubMed1985

Mineral oil lipogranulomata in liver and spleen. A study of 465 autopsies.

Lipogranulomata (LG) are commonly seen in human tissues but the location and significance of these lesions are incompletely documented. In a study of 465 autopsies LG were found in 48% of livers and 46% of spleens. Hepatic LG were more common in portal tracts than adjacent to the terminal hepatic venules. There was a close correlation between hepatic LG in liver and in spleen. The incidence and severity of hepatic LG were higher in older adults, especially men. There was no evidence that LG caused hepatic dysfunction or portal hypertension. The absence of correlation with hepatic steatosis supports the suggestion that LG are secondary to mineral oil deposition rather than to steatosis.

Aging↗
PubMed1985

Partial nodular transformation of liver in an adult with persistent ductus venosus. Review with hypothesis on pathogenesis.

Partial nodular transformation of the liver (PNT) is a rare condition of unknown pathogenesis in which nodules composed of hepatocytes replace portions of the parenchyma. There is usually evidence of portal hypertension and portal vein thrombosis. We present a case of PNT in a man with persistent ductus venosus and hypoplasia of the major intrahepatic portal veins but without evidence of portal hypertension or portal vein thrombosis. Portal venules were largely absent between nodules, as documented by morphometry. We suggest the pathogenesis of PNT is similar to that previously proposed for nodular regenerative hyperplasia, that is, atrophy occurs in parenchyma with insufficient blood supply and nodules arise by hyperplasia in areas with adequate supply. Partial nodular transformation and nodular regenerative hyperplasia differ mainly in the cause and distribution of the portal vein obliteration.

Adult↗
PubMed1984

The effect of dietary cholesterol on platelet survival in the rabbit--a study using 14C-serotonin and 51chromium double-labelled platelets.

Hypercholesterolemic men and monkeys have shortened platelet survival but attempts to demonstrate this in rabbits have been unsuccessful. The present study examines platelet survival in cholesterol-fed rabbits. Platelets were double-labelled in vitro with 51Cr and 14C-serotonin or in vivo by intravenous injection of 14C-serotonin. In the double-label experiments 51Cr survival was always shorter than 14C survival but changes in survival of one label were accompanied by similar changes in the other label. Survival was shortened after 4 and 7 weeks of cholesterol feeding. This was demonstrated when the donor platelets were from normal rabbits for both cholesterol and control recipients but no shortening was demonstrated when cholesterol-rich platelets were injected into cholesterol-fed recipients and normal platelets were injected into the control rabbits. When 14C-serotonin was injected intravenously 14C survival was the same as when platelets were labelled ex vivo prior to injection and 14C survival was shortened in rabbits fed cholesterol for 1, 2, and 6 weeks. These results indicate that cholesterol-feeding shortens platelet survival. This effect may be masked if the test platelets are not identical in both test and control groups.

Animals↗
PubMed1984

Occurrence of alpha-1-antitrypsin deficiency in 155 patients with alcoholic liver disease.

Liver biopsies from 155 patients with alcoholic liver disease were examined for periodic-acid-Schiff-positive, diastase-resistant (PAS-DR) intracytoplasmic globules in hepatocytes. Seven patients had these PAS-DR globules: each was a heterozygote for a deficiency allele of alpha-1-antitrypsin (AAT), or alpha-1-protease inhibitor, with the PAS-DR globules distributed in a pattern characteristic of this deficiency. One further patient with normal AAT had a few intracytoplasmic PAS-DR globules in occasional hepatocytes. The prevalence of AAT heterozygotes in this series did not differ from that in the reference population. The seven heterozygotes included five of PI (protease inhibitor) type MZ, one of PI type SZ, and one heterozygous for a rare deficiency allele, PI type MMmalton. The M and Mmalton alleles may be difficult to distinguish because they have similar mobilities with isoelectric focusing technics. Therefore, if PAS-DR inclusions are found in the liver of a patient with an apparently normal phenotype, the presence of a defective M variant allele, such as Mmalton, should be considered.

Adult↗
PubMed1984

Nodular regenerative hyperplasia of the liver in a patient with rheumatoid vasculitis: a morphometric study suggesting a role for hepatic arteritis in the pathogenesis.

Nodular regenerative hyperplasia (NRH) of the liver commonly occurs as a complication of Felty's syndrome but the pathogenesis of the hepatic lesion is not certain. We present a patient with rheumatoid arthritis, leukopenia, glomerulonephritis, NRH and portal hypertension who had histologic evidence of widespread intrahepatic arteritis and paucity of arteries less than 40 micron diameter. We postulate that in this patient the arterial lesions caused secondary portal venous obliteration, portal hypertension, and nodular transformation.

Arteritis↗
PubMed1983

The cellular distribution of vitamin A in the liver.

Hepatic vitamin A (VA) is concentrated in lipocytes (fat-storing cells) but the actual concentration in various cell types has not been measured. In this study hepatocytes from normal and VA-pre-treated rats were isolated and the VA content was measured. Because most lipocytes were lysed in the procedure, VA content within lipocytes was estimated indirectly by subtracting total hepatic VA from hepatocellular VA. Hepatocytes contained 10.9% of the total hepatic VA (7.2% in VA-treated rats). The volume density of lipocytes in whole liver was 0.23% as determined morphometrically (1.45% in VA-treated rats). From these results it is estimated that the VA concentration in lipocytes is 39 mg/ml (3015 times that in hepatocytes) in normal rats and 69 mg/ml in VA-treated rats. Lipocyte lipid droplets are estimated to be 26% retinyl palmitate (by volume) in normal rats and 31% in VA-treated rats.

Animals↗
PubMed1983

Fibrous thickening of the splenic capsule. A response to chronic splenic congestion.

Fibrous thickening of the splenic capsule is often seen in patients with hepatic cirrhosis or portal hypertension from other causes. However, most cases of capsular thickening have been considered idiopathic, with no obvious abnormality of the portal circulation. The possibility that these "idiopathic" cases also have evidence of portal hypertension was examined in a retrospective study. The splenic capsule thickness was measured in 434 consecutive autopsy specimens. Various clinical and autopsy parameters relevant to vascular disease were recorded and correlated with splenic capsular thickness. Thickened capsules were significantly more frequent in patients with advanced age, clinical history of severe congestive heart failure, cirrhosis, and hepatic portal sclerosis. It is suggested that most cases of splenic capsular thickening are caused by splenic congestion with organization of capsular and subcapsular hemorrhages.

Adolescent↗