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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dr. Wagner's description of an advanced macronodular cirrhosis is compatible with end-stage liver disease due to a variety of causes. An alcoholic etiology seems more probable than chronic viral hepatitis since such a diagnosis might also account for the chronic pancreatitis, unless it was related to the cholelithiasis. However, Dr. Wagner's description favors a diagnosis of biliary pigment sludge related to hemolysis. Furthermore, the controversy over the extent of Beethoven's alcohol consumption and the absence of mention of pancreatic calcification weakens the case for an alcoholic etiology. On the other hand, Dr. Wagner's emphasis of bluish-green pigmentation of the liver, blackish pigmentation of the spleen, and an arteropathy of the hepatic vessels suggests the probability of hemochromatosis, which diagnosis is also in keeping with Beethoven's medical history. In this regard the composer's history of recurrent obscure abdominal pain, commencing in his third decade, is especially in keeping with hemochromatosis. As many as a third of patients present with recurrent abdominal pain, and eventually up to 40% of cases develop significant abdominal pain in the course of their disease. While some of these cases of abdominal pain have been attributed to hepatoma, ascites, pancreatitis, perisplenitis, or diabetic neuropathy, the majority remain ill-defined (32). Even so, the diagnosis of hemochromatosis remains unproved in the absence of a histological examination and measurement of hepatic iron concentration. It is proposed that the combined additive, toxic effects of alcohol and iron were the most likely cause of Beethoven's cirrhosis.
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PMID:Was Beethoven's cirrhosis due to hemochromatosis? 777 Jun 48

The paper reports a case of splenic rupture during the course of chronic pancreatitis, an event rarely reported in the literature. The anatomical arrangement of organs and peripancreatic vessels is a predisposing factor for this complication. There are essentially three different but correlated pathogenetic hypotheses. The first refers to thrombosis of the splenic vein with portal hypertension documented by some researchers even in angiographical terms: during the course of chronic pancreatitis the spleen is sometimes palpable. Thrombosis and/or vascular compression make the spleen more fragile and its rupture more likely: this is particularly true during the course of calcific chronic pancreatitis and cases involving the tail. An enzymatic factor may also be responsible and this appears more clearly in pancreatitis with pseudocysts. In this case it is the direct action of pancreatic enzymes on the ileum or splenic parenchyma, which may also affect all organs surrounding the pancreas, which leads to hemorrhage or hematoma. Sometimes the cause of bleeding is a pseudoaneurysm of the splenic artery which is eroded by the contents of the pseudocysts themselves. There is also a mechanical hypothesis which some authors consider the sole possibility: in chronic pancreatitis the splenic compartment presents severe perisplenitis which fixes the spleen making it more vulnerable and even a mini-trauma will cause rupture. The patient is almost always an emaciated young alcoholic suffering from chronic pancreatic pathology.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Splenic rupture in chronic pancreatitis. A clinical case. Observations]. 820 60