Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Triggered by a case of ischaemic hepatitis (shock liver) in a patient with severe respiratory insufficiency, we tried to gather information about clinical characteristics and incidence. To our surprise, this information could be found neither in major critical care, medical or gastroenterology textbooks nor in textbook indices or works on differential diagnosis. From Sept. 1989 to May 1990 we studied all possible cases of ischaemic hepatitis in a 390 bed general hospital, to establish incidence. Using computerised data from the clinical chemistry laboratory, all patients with grossly abnormal liver function tests were identified. In this nine-month period 27 adult patients had a peak ALAT level of > 500 U/l: 8 of these suffered from ischaemic hepatitis, using the criteria described by Gibson et al. In another 5 this diagnosis was suspected but could not be ascertained before death (30% and 18% of all cases). In all these cases ASAT, ALAT, LDH levels were 8-100 times normal, but bilirubin, alkaline phosphatase, gamma-glutamyl transferase and prothrombin time were only slightly abnormal. With correction of the underlying disorder enzyme levels returned to normal very rapidly, in 5-10 days. Ischaemic hepatitis could easily be distinguished from other causes such as alcoholic, viral or drug-induced hepatitis. Ischaemic hepatitis was the most frequent cause of severely elevated ASAT, ALAT and LDH in hospitalised patients. The diagnosis can easily be made on clinical characteristics and the typical biochemical pattern. An elaborate work-up or invasive procedure is redundant. Prognosis per se is excellent but depends on the underlying disorder.
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PMID:[Ischemic hepatitis]. 140 10

Ischemic hepatitis is not an uncommon complication of reversible severe hypotension or cardiac failure. The prognosis usually is determined by the cause of the initial hypotension or cardiac failure, rather than the subsequent hepatic dysfunction. We report a retrospective analysis of nine patients with ischemic hepatitis in which previously unreported clinical and biochemical abnormalities are noted. The clinical and biochemical course of the patients were reviewed until recovery or death from ischemic hepatitis. All the patients had a rapid striking elevation of aspartate aminotransferase, and lactic dehydrogenase, with an equally rapid resolution of these parameters. Abnormal serum glucose levels occurred in six patients (none of whom had a prior carbohydrate intolerance). Insulin therapy was given to three patients for a limited period. Renal impairment was manifest in all nine patients, and it resolved spontaneously within 10 days. Altered mental status was detected in six patients; the changes reverted to normal within 7 days of their onset. A preexisting anemia (hemoglobin less than 11.0 g/dl) was noted on admission in four patients, and it did not appear to potentiate the manifestations of the hepatic ischemia. We conclude that ischemic hepatitis should be anticipated in all patients with a recent history of systemic hypotension. It should be considered in the differential diagnosis of patients with unexplained hepatitis; the early massive rise in lactic dehydrogenase, the rapid fall in transaminases, and the early mild/moderate renal failure strongly suggest ischemic hepatitis. Patients with ischemic hepatitis can manifest reversible renal failure, mental confusion, and hyperglycemia which may require insulin for its control.
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PMID:Ischemic hepatitis: widening horizons. 848 Jul 56

In patients with pathological findings in tests of liver function, ischemic hepatitis is an important differential diagnosis. This condition is most often seen in patients with coronary heart disease. Acute circulatory failure may induce reduced liver perfusion with extreme elevation in transaminase levels within three to five days. The values return to normal within five to ten days and in uncomplicated cases there is minimal cholestasis. Ischemic hepatitis may progress to fulminant hepatic failure. The diagnosis can be made by clinical examination and biochemical tests alone. Biopsy gives a characteristic picture of centrilobular liver cell necrosis which confirms the diagnosis, but is seldom necessary.
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PMID:[Ischemic hepatitis. Important differential diagnosis of increased levels of transaminases in the liver]. 163 42

Twenty-nine patients of 18,000 inpatient admissions over a six-month period developed ischaemic hepatitis accompanied by peak aspartate aminotransferase (AST-EC 2.6.1.1) activity greater than 1,000 U/L. Seventeen of these 29 patients died either during or shortly after the episode of ischaemic hepatitis, with an overall mortality of 58.6%. Mortality was not due in any of the cases to the hepatitis but rather the underlying cause. Ischaemic hepatitis was the commonest cause of an AST activity greater than 1,000 U/L in this hospital population (29 of 52 patients i.e. 56%). This condition is more common than generally appreciated and is associated with a poor prognosis.
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PMID:Mortality associated with ischaemic hepatitis. 187 62

Hepatic hypoperfusion can result in ischemic hepatitis, a clinical syndrome characterized by a sudden rise in serum transaminases followed by resolution to near normal levels within 7 to 10 days. Although described in adults, this syndrome has not been well defined in pediatric patients. We report 22 children who developed ischemic hepatitis during an acute illness. Fifteen of 22 patients had a documented hypotensive episode or no cardiac output before the onset of the ischemic hepatitis episode. Four of the seven patients without documented hypotension required pressor therapy to maintain their BP. SGOT showed a marked rise (mean 2294 IU/L, range 438 to 6652) from admission to 96 h (mean 34) with a rapid decline to near normal levels within 9 days (mean 5.1). Serum bilirubin levels also rose transiently, but generally not to the extent of transaminase levels. A clinically significant coagulopathy occurred in six patients. Although nine patients expired, none died as a direct result of the hepatic damage. Ischemic hepatitis can occur during illnesses associated with diminished hepatic blood flow and follows a characteristic course that usually can be differentiated from viral or drug-induced hepatitis on clinical and biochemical criteria.
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PMID:Ischemic hepatitis in children: diagnosis and clinical course. 319 36

Ischemic hepatitis represents a condition in which an acute circulatory failure determines a striking elevation of both serum transaminases and total bilirubin and a prolongation of prothrombin time. Such impairment of liver function tests is due to a haemodynamic hepatocyte injury, showing focal centrilobular necrosis as the specific pathologic correlate. In this paper the authors describe four different cases of ischemic hepatitis, in which an acute derangement of liver function tests occurred as a consequence either of myocardial failure or of systemic venous congestion. Finally, the authors review all current international literature concerning the various clinical, pathologic and therapeutic features of ischemic hepatitis.
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PMID:[Ischemic hepatitis: case reports and a review of the literature]. 750 Dec 28

We report two cases of ischemic hepatitis in patients with alcoholic cirrhosis. In both, hepatic ischemia was induced by hemorrhagic shock and severe sepsis. Despite control of the bleeding and restoration of normal hemodynamics, liver failure deteriorated to hepatic coma and death in both cases. Ischemic hepatitis occurred in 1.5% of 130 consecutive cases of cirrhosis admitted for hemorrhage on our medical intensive care unit. Although cirrhotic patients run an increased risk of ischemic hepatitis, our experience and our review of the literature indicate that this condition is rare in these patients.
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PMID:Ischemic hepatitis in cirrhosis. Rare but lethal. 840 9

Ischaemic hepatitis, a condition to be distinguished from cardiac liver or stasis cirrhosis, can occur as an acute episode in patients with advanced stage congestive heart failure. The mechanism is massive necrosis in the central lobules resulting from acute hypoxia when low cardiac output reduces oxygen supply further aggravating the underlying condition of congestion due to poor venous outflow. We report 4 cases which illustrate the difficulties in diagnosis and treatment. All four patients (age range 79-86 years) were seen in an emergency situation caused by an acute drop in cardiac output aggravating their underlying heart failure. Clinical signs included jaundice, oligouria, abdominal pain and cardiovascular shock. The first element suggesting the diagnosis of ischaemic hepatitis was a sudden and massive peak in transaminase levels (> 20 times normal) which rapidly returned to normal. Prothrombin and fibrinogen levels fell rapidly and functional renal failure was present in all cases. Viral serology was negative and no hepatotoxic drugs could be incriminated. Despite symptomatic intensive care one patient died on day 15 due to cardiovascular shock. Enzyme movements, together with the lack of evidence for another cause, is the key to diagnosis of acute ischaemic hepatitis which thus is often established after the emergency situation has been controlled. Initially, viral hepatitis or drug-induced hepatotoxicity may be suspected, especially if the episode of low cardiac output goes unrecognized. Cases with signs of encephalopathy may also be difficult to distinguish from fulminating hepatitis and would be the only indication for needle biopsy in this acute situation. Outcome is generally unfavourable with mortality at 6 months estimated at 50%.
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PMID:[Acute ischemic liver]. 854 28

Ischemic hepatitis is rare in patients with liver cirrhosis and is usually precipitated by hypotension due to gastrointestinal bleeding. We describe a cirrhotic patient who developed ischemic hepatitis as a consequence of toxic epidermal necrolysis (TEN) caused by cefuroxime.
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PMID:Ischemic hepatitis associated with toxic epidermal necrolysis in a cirrhotic patient treated with cefuroxime. 911 Sep 27

Ischemic hepatitis can occur as an acute episode in advanced congestive heart failure (CHF). The mechanism is massive necrosis of the central lobules resulting from acute hypoxia when low cardiac output further reduces oxygen supply, aggravating underlying congestion due to poor venous outflow. We describe a 70-year-old woman with congestive heart failure for 7 years who was admitted with jaundice, vomiting, abdominal pain and oliguria after an episode of hypotension. The diagnosis of ischemic hepatitis was established by a documented episode of severe hypotension, followed by elevation of serum transaminases, a rise in serum bilirubin and LDH levels, prolonged prothrombin time and acute renal failure. Other causes of acute hepatitis, such as a virus or drugs were excluded, and improved liver and renal function followed hemodynamic stabilization. We conclude that ischemic hepatitis should be considered whenever acute hepatitis follows a recent episode of systemic hypotension, especially in the context of concomitant CHF.
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PMID:[Ischemic hepatitis in congestive heart failure after an episode of hypotension]. 915 12


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