Prolonged survival after portal decompression of patients with non-cirrhotic intrahepatic portal hypertension

Zeegen, R.; Stansfeld, A. G.; Dawson, A. M.; Hunt, Alan H.

doi:10.1136/gut.11.7.610

Cited by 40 publications

(18 citation statements)

References 28 publications

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“…These findings agreed with our previous description and also with other papers including Zeegan et al [14], As for as IPO patients of idiopathic origin who had high portal vein pressure, the fibrosis apparently played a major role in the resis tance to the portal vein blood flow into the liver. The cause of the fibrosis is not known yet and is considered idiopathic.…”

Section: Resultssupporting

confidence: 82%

The Clinical Entity of Idiopathic Portal Hypertension: A Review of 17 Cases

Takeshige¹,

Yamamoto²

1983

Dig Dis

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Section: Resultssupporting

confidence: 82%

The Clinical Entity of Idiopathic Portal Hypertension: A Review of 17 Cases

Takeshige¹,

Yamamoto²

1983

Dig Dis

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“…Similarly the centrilobular venous distention of acute circulatory failure or the early phase of Budd-Chiari congestion was lacking. The prominence of the portal venous radicles is reminiscent of human idiopathic noncirrhotic portal hypertension [26], but the inflammatory and centrilobular changes clearly distinguished the condition.…”

Section: Discussionmentioning

confidence: 99%

Lobular Dissecting Hepatitis in the Dog

et al. 1983

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Abstract. Ascites and acquired portosystemic shunts were consistent findings in six dogs with a chronic hepatitis of unusual morphology and unknown etiology. The hepatitis was characterized by a mixed inflammatory infiltrate and dissection of the lobular parenchyma by reticulin and fine collagen fibers. While limiting plates were disrupted by this process, portal inflammation was inconstant and seldom marked. Biopsy samples generally had very small, sublobular regenerative nodules, but larger nodules sometimes were present postmortem. Dilated vascular channels, representing sinusoids and portal venous radicles were a prominent feature of most affected livers.The lesions differ from previously documented chronic hepatitis in the dog, and from the chronic hepatitides in man.Portosystemic shunts in the dog may be congenital [8] or acquired. Acquired shunts develop as the result of portal hypertension. They consist of multiple, frequently tortuous, anastomotic vessels which represent the opening up of preexistent portosystemic collaterals [23, 24]. The obstruction to blood flow responsible for the portal hypertension may be extrahepatic or intrahepatic. Acquired shunts resulting from intrahepatic portal hypertension have been described in dogs with chronic hepatitis/ hepatic fibrosis [5,6,10] and overt cirrhosis [5,10,21, 24]. Affected dogs ranged in age from nine months to 15 years.Chronic hepatitis is an etiologically diverse and morphologically variable condition which has been documented extensively in man. By contrast there are few descriptions of chronic hepatitis in the dog, and aggressive forms have been recognized only recently [3,6,13,17]. Portosystemic shunts have not been a common feature of the reports.Over the last five years we have recognized an unusual and histologically distinctive chronic hepatitis in six dogs with acquired portosystemic shunts. Case ReportsAs indicated in table I, three unrelated standard poodles were included. Males and females were represented in equal numbers, although all standard poodles were male. Ages at initial presentation ranged from seven months to five years. The common presenting sign was ascites of three to eight weeks duration. In addition, the dogs were inappetant (refusing, particularly, 179

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“…Three patients had less evidence of hepatocellular damage. Two of these were jaundiced, the diagnosis being cryptogenic macronodular cirrhosis with cholestatic features, and the third patient had non-cirrhotic intrahepatic portal hypertension (Zeegen, Stansfeld, Dawson, and Hunt, 1970). The tolerance tests were performed in the conventional manner, with blood samples being taken fasting and subsequently at regular intervals following the ingestion of fructose or glucose.…”

Section: Methodsmentioning

confidence: 99%

The effect of portacaval anastomosis on oral carbohydrate tolerance and on plasma insulin levels

Holdsworth¹,

Nye²,

King³

1972

Gut

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SUMMARY In patients with portal hypertension, plasma insulin levels were raised both fasting and after oral glucose or intravenous tolbutamide. This supports previous suggestions that resistance to endogenous insulin plays a major role in producing the impaired glucose tolerance found in chronic hepatic dysfunction.The operation of portacaval anastomosis was followed by impaired oral fructose tolerance, but did not significantly change oral glucose tolerance. Plasma insulin levels were unchanged by the operation, either fasting orfollowing the stimulus of an oral glucose load or intravenous tolbutamide.The insulin response after operation was only higher after intensive pancreatic P cell stimulation by a combination of glucose, tolbutamide, and glucagon. These results indicate that, in patients with hepatic dysfunction, little insulin is being removed by the liver from the portal blood except when the insulin secretory rate is unusually high.

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Prolonged survival after portal decompression of patients with non-cirrhotic intrahepatic portal hypertension

Cited by 40 publications

References 28 publications

The Clinical Entity of Idiopathic Portal Hypertension: A Review of 17 Cases

The Clinical Entity of Idiopathic Portal Hypertension: A Review of 17 Cases

Lobular Dissecting Hepatitis in the Dog

The effect of portacaval anastomosis on oral carbohydrate tolerance and on plasma insulin levels

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