Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two studies investigating the association of liver disease with acute and chronic pancreatitis in alcoholics are presented. In a retrospective study of 50 patients, no clinical liver disease was found in 9 patients with acute pancreatitis, while 23 (56%) of 41 patients with chronic pancreatitis had liver disease by clinical criteria. Of this latter group, 8 were confirmed histologically; thus 19% of patients with chronic pancreatitis had biopsy-proven cirrhosis. Fifty alcoholic patients with pancreatitis were prospectively evaluated. All who had clinical evidence of liver disease were biopsied. No cases of liver disease were encountered in the 4 patients with acute pancreatitis. Although 28 (60%) cases of clinically diagnosed liver disease were present in 46 patients with chronic pancreatitis, only 20 of these seemed significant (cirrhosis, alcoholic hepatitis, severe fatty liver), for an incidence of 43%. Thus, clinically significant alcoholic liver disease occurs quite frequently in association with alcoholic pancreatitis. This association is meaningful in more effective management of these patients in general and in preoperative assessment of the risk of surgery in particular.
 ...
PMID:Associated liver disease in alcoholic pancreatitis. 68 26

Twenty patients with longstanding alcoholism and biopsy-proven alcoholic liver disease presented with marked elevation of serum alkaline phosphatase (in excess of four times the upper limit of normal). None had a past or present history to suggest pancreatitis or biliary tract disease, nor had any of these patients recently taken medication which could be implicated in cholestatic jaundice. Thirteen (65%) of this group either had radiologic or post mortem confirmation of nonobstructed biliary systems. The histologic findings in this group of patients were compared with those of a group of patients with alcoholic liver disease and normal or only mild elevation of serum alkaline phosphatase. Significantly more hepatocellular necrosis (P less than 0.05), alcoholic hyaline (P less than 0.02), and cholestasis (P less than 0.002) were noted in the severely hyperphosphatasemic group. Minimal degrees of steatosis were found in both groups. These data indicate that intrahepatic cholestasis occurs in patients with alcoholic liver disease, and this may often be secondary to alcoholic hepatitis. Overemphasis has previously been given to alcoholic fatty liver as a cause of this syndrome.
 ...
PMID:Alcoholic liver disease presenting with marked elevation of serum alkaline phosphatase. A combined clinical and pathological study. 73 13

Thirty-four patients with severe delirium tremens were allocated randomly to treatment with paraldehyde (10 ml rectally very 30 minutes) or diazepam (10 mg then 5 mg intravenously every 5 minutes) until they were calm but awake. Diazepam-treated patients became calm in one half the time needed to calm patients with paraldehyde. Half of the patients had delirium tremens in association with pneumonia, pancreatitis, or alcoholic hepatitis; these patients required twice as much paraldehyde or diazepam for initial calming as patients with delirium tremens alone. Maintenance of a calm state was accomplished easily with either diazepam, intramuscularly, or paraldehyde, rectally. Adverse reactions occurred in nine patients, all of whom had been treated with paraldehyde; these patients had greater degrees of fever, tachypnea, and tachycardia and required three times longer for initial calming than patients without adverse reactions. Diazepam given under this regimen is a safe and effective sedative for management of combative patients with severe delirium tremens.
 ...
PMID:Diazepam and paraldehyde for treatment of severe delirium tremens. A controlled trial. 109 Feb 22

Alcoholic liver disease includes steatosis, alcoholic hepatitis and cirrhosis. Other liver diseases of genetic origin, but with a curious association with alcohol intake, are hemochromatosis and porphyria cutanea tarda. The attribution of chronic hepatitis to alcohol intake remains speculative, and the association may reflect hepatitis C infection. Hepatic injury attributed to alcohol includes the changes reported in the fetal alcohol syndrome. Steatosis, the characteristic consequence of excess alcohol intake, is usually macrovesicular and rarely microvesicular. Acute intrahepatic cholestasis, which in rare instances accompanies steatosis, must be distinguished from other causes of intrahepatic cholestasis (e.g., drug-induced) and from mechanical obstruction of the intrahepatic bile ducts (e.g., pancreatitis, choledocholithiasis) before being accepted. Alcoholic hepatitis (steatonecrosis) is characterized by a constellation of lesions: steatosis, Mallory bodies (with or without a neutrophilic inflammatory response), megamitochondria, occlusive lesions of terminal hepatic venules, and a lattice-like pattern of pericellular fibrosis. All these lesions mainly affect zone 3 of the hepatic acinus. Other changes, observed at the ultrastructural level, are of importance in progression of the disease. They include widespread cytoplasmic shedding, and capillarization and defenestration of sinusoids. Progressive fibrosis complicating alcoholic hepatitis eventually leads to cirrhosis that is typically micronodular but can evolve to a mixed or macronodular pattern. Hepatocellular carcinoma occurs in 5 to 15% of patients with alcoholic liver disease. The clinical syndrome of alcoholic liver disease is the result of three factors--parenchymal insufficiency, portal hypertension and the clinical consequences of extrahepatic damage produced by alcohol. At the several phases of the life history of alcoholic liver disease, the individual factors play a different role. The clinical manifestations of alcoholic steatosis are mainly extrahepatic in origin. Those of alcoholic hepatitis reflect mainly parenchymal insufficiency and those of cirrhosis are mainly those of portal hypertension. Alcoholic liver injury appears to be generated by the effects of ethanol metabolism and the toxic effects of acetaldehyde, perhaps the immune responses to alcohol- or acetaldehyde-altered proteins, and questionably enhanced by viral hepatitis. Alcoholic hepatitis may be mimicked histologically, and to a varying degree clinically, by a number of conditions (obesity, diabetes, several drug-induced injuries, jejunoileal bypass, and related "shortcircuiting" of the bowel). Perhaps the most important facet of the hepatotoxicity of alcohol is its enhancement of the effects of a number of other hepatotoxic agents, among which acetaminophen is the prime example.
 ...
PMID:Alcoholic liver disease: pathologic, pathogenetic and clinical aspects. 205 45

80 patients (P) (68 men and twelve women) with the diagnosis of delirium tremens were retrospectively analyzed and reexamined over a period of ten years (1974 to 1984). Included were only patients who--after failure of oral medication--required intravenous therapy with Chlomethiazol and thereby intensive care treatment. Mean age was 46.2 (26 to 75) years. During the observation period delirium tremens increased in frequency by 11% each year. Nine patients had two, six patients three and two patients four episodes of delirium tremens. In 86.7% delirium tremens occurred with fatty liver and alcoholic hepatitis, epileptic seizures, cirrhosis and hepatic coma, gastrointestinal hemorrhage and pancreatitis. Eight patients (10%) died in hospital at a mean age of 53.2 years. None of the deceased had less than three (on average four) complicating or associated diseases. These were mostly pneumonia, cirrhosis, hepatic coma, and gastrointestinal hemorrhage. The mean duration of intravenous Chlomethiazol therapy was 4.7 (0.25 to 20) days, the applied dose 26.2 (0.8 to 78.6) grams, there being no significant difference between survivors and non-survivors. Of the 72 survivors 62 were invited for follow-up examination after an average of five years. During this period another twelve patients (15%) died of pneumonia, gastrointestinal bleeding, cardiocirculatory failure and accidents. Life expectancy was only 9.3 years. Of 29 patients who came for follow-up, 55% showed clinical evidence of alcohol dependency, 65% had elevated gamma-glutamyl-transferase.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Severe course of delirium tremens. Results of treatment and late prognosis]. 262 19

A 33-yr-old white woman treated for alcoholic hepatitis developed acute pancreatitis during her hospital stay. At autopsy, two major pathological processes were found: alcoholic cirrhosis and chronic pancreatitis. In both, there was evidence of an acute episode, i.e., acute alcoholic hepatitis and acute hemorrhagic pancreatitis superimposed on the chronic alcoholic lesions. The sequence of events would indicate that the acute pancreatic pathology was precipitated by supranormal ecbolic stimulation of the acinar segment of the "pancreon" units, triggered as a result of a high protein and fat diet.
 ...
PMID:Acute pancreatitis in a patient treated for alcoholic hepatitis. The hypothesis of supranormal ecbolic stimulation of the pancreon. 276 May 14

Spontaneous bacterial peritonitis (SBP), a fascinating disease that had been reported perhaps 50 times in varying guises over the preceding century, suddenly burst forth in the 1960s and was recognized in clusters of cases almost simultaneously in Paris, London, and West Haven, Connecticut. The spectrum of the disease has broadened. Initially, it was associated almost exclusively with alcoholic cirrhosis, but it has now been found in association with posthepatitic cirrhosis, cryptogenic cirrhosis, chronic active liver disease, and, occasionally, in biliary cirrhosis and cardiac cirrhosis. Recently, it has been reported in alcoholic hepatitis and acute viral hepatitis. It occurs occasionally in malignant ascites and in pancreatitis in the absence of cirrhosis. It is surprisingly common in disseminated lupus, in which it occurs relatively more commonly than in alcoholic cirrhosis. A similar syndrome, primary peritonitis, occurs frequently in children with nephrotic ascites. The clinical pattern of SBP has broadened. Initially it consisted of abdominal pain, fever, rebound tenderness, hypoactive bowel sounds, hypotension, encephalopathy, and cloudy ascites with large numbers of polymorphonuclear leukocytes in ascitic fluid. Each and every symptom, sign, and laboratory abnormality may be absent; indeed, the syndrome can be completely silent. Initially, the causative bacteria appeared to be almost exclusively enteric, but now the list of bacteria isolated in cases of SBP looks like a bacteriology textbook. Anaerobes are rare. Multiple organisms usually suggest nonspontaneous origin such as perforation or vasopressin induction. The differentiation between spontaneous and nonspontaneous bacterial peritonitis is crucial in the differential diagnosis. The great majority of cases of SBP develop in the hospital, 80% more than one week after admission. It is therefore a nosocomial disease that may be precipitated by procedure-induced bacteremia, gastrointestinal bleeding, or diarrhea, and it tends to occur in patients with low ascitic fluid protein (complement) concentrations and severe portal-systemic shunting.
 ...
PMID:Spontaneous bacterial peritonitis: variant syndromes. 368 33

The significance of megamitochondria in the alcoholic liver injury of humans was investigated as part of a large Veterans Administration cooperative study of the natural history of alcoholic hepatitis. Two hundred twenty patients were clinically stratified into the following three groups according to disease severity using serum bilirubin and prothrombin time as indicators: Group 1 (mild disease), serum bilirubin levels less than 5 mg/dl and prothrombin time prolonged for less than 4 s; group 2 (moderate disease), serum bilirubin levels greater than 5 mg/dl but prothrombin time prolonged for less than 4 s; and group 3 (severe disease), serum bilirubin levels greater than 5 mg/dl and prothrombin time prolonged for greater than 4 s. Megamitochondria were observed in 20% of the patients (45 of 220). Of these, 43 patients were in groups 1 and 2 of severity and only 1 patient belonged in group 3. The association of megamitochondria with cirrhosis was infrequent (33%, 15 of 45 patients). The differences in severity correlated with the differences in mortality: in patients with megamitochondria, only 1 had died at 6 mo compared with 40 deaths in patients without megamitochondria. By 12 mo, there were two deaths in patients with megamitochondria versus 51 deaths in those patients without. No complications were present in 72% of patients with megamitochondria versus 39% for those without. Infection, gastrointestinal bleeding, pancreatitis, hyperglycemia, azotemia, delirium tremens, seizures, and hepatic encephalopathy were all more common in patients without megamitochondria. The patients with megamitochondria appear to represent a subcategory of alcoholic hepatitis with a milder degree of clinical severity, lower incidence of cirrhosis, fewer complications, and good long-term survival.
 ...
PMID:Significance of megamitochondria in alcoholic liver disease. 369 4

Pathogenetic associations between benign hepatic tumours and liver damage were studied in an autopsy series of 91 males with high incidence of alcoholism. Information on the consumption of alcohol was obtained by interviewing a family member or a close friend of the deceased. The reported use of alcohol correlated well with the increase of fatty and fibrotic changes and with the occurrence of liver cirrhosis, alcoholic hepatitis or pancreatitis. Benign bile duct tumours (bile duct adenomas and von Meyenburg's complexes) (n = 26) were associated with the occurrence of bridging (P less than 0.0005) and periportal (P less than 0.025) fibrosis of the liver and, independently from these, with chronic pancreatitis (P less than 0.05) and with non-parasitic liver cysts (n = 14) (P less than 0.01). The weight of the liver was greater (P less than 0.01) in males with focal nodular hyperplasia (n = 3). Cavernous hemangioma (n = 19) occurred independently of the parameters studied. None of the tumours showed significant correlation to liver cirrhosis, alcoholic hepatitis, fatty liver or diseases of the gallbladder. The results are in line with observations on the reactive nature and connections to fibropolycystic liver disease of benign bile duct tumours in laboratory animals and in man. Their presence in human liver specimens should be taken into account as a sign of liver damage, in this study related to heavy use of alcohol or to chronic inflammation of the pancreas.
 ...
PMID:Benign bile duct tumours, non-parasitic liver cysts and liver damage in males. 395 Mar 64

It has been our impression that clinical deterioration and worsening of liver tests of patients with alcoholic liver disease (ALD) is common immediately following hospitalization and cessation of ethanol intake. In order to determine the frequency of such deterioration and characterize features which may identify those patients who initially deteriorate, we analyzed the standard liver tests and clinical parameters of liver function following hospitalization of 273 cases of ALD, and correlated these with histologic patterns and hospital course. We found that moderate liver test worsening following hospitalization is frequent in patients with ALD, especially alcoholic hepatitis. The presence of alcoholic hyalin in patients with alcoholic hepatitis did not correlate with liver function or frequency of biochemical worsening, but did correlate with mortality. Biochemical deterioration did not correlate with clinical deterioration or mortality, unless complications such as bleeding, sepsis, or pancreatitis occurred. Spontaneous clinical deterioration of our patients in the absence of precipitating factors was rare. We conclude that worsening of liver tests following hospitalization frequently occurs in patients with ALD, does not necessarily imply presence of complications (e.g., biliary obstruction, sepsis, other liver injury), but should suggest the presence of alcoholic hepatitis.
 ...
PMID:Clinical and biochemical course of alcoholic liver disease following sudden discontinuation of alcoholic consumption. 635 82


1 2 Next >>