Gene/Protein Disease Symptom Drug Enzyme Compound
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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 timely diagnosis and treatment of intra-abdominal conditions during pregnancy can challenge the surgical consultant. Familiarity with the anatomic and physiologic changes present in normal pregnancy is essential, as is the knowledge of relative risk by trimester. The general surgeon will be called upon to diagnose and treat appendicitis, biliary tract disease (including pancreatitis), and liver disease. Knowledge of how these conditions become manifest is essential. The surgical consultant should be aware that virtually all complications that occur in the management of these conditions are caused by delay in the detection of the disease process.
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PMID:The surgical management of intra-abdominal inflammatory conditions during pregnancy. 785 15

It is well known that the responses of serum gamma glutamyl transferase (GGT) to chronic alcohol drinking are different depending on the individual. In order to clarify the genetic backgrounds in the development of alcoholic liver and pancreatic diseases, the relationships between serum GGT response and alcoholic liver and pancreatic diseases in heavy drinkers were studied. The responses of GGT to alcohol drinking were classified into three groups: non-response, mild-response and hyperresponse. In alcoholic liver disease, non-responders were scarcely found and the response of GGT tended to increase in parallel with the progression of liver disease, when the hepatitis C virus (HCV) marker-positive patients were excluded. The differences in GGT levels between just after and at 4 weeks after abstinence in the HCV marker-negative patients were significantly higher than those in the HCV marker-positive patients. The rate of decrease in GGT activities during 4 weeks following abstinence was significantly higher in the HCV marker-negative patients than in the HCV marker-positive patients, indicating higher GGT induction in the HCV marker-positive patients. All patients with alcoholic pancreatitis, but without liver disease, were non-responders. All patients, except one, with severe pancreatitis were also non-responders. In alcoholic pancreatic disease, GGT induction correlated negatively with the development of pancreatitis. These results suggested that genetic polymorphism of GGT may link with the induction of GGT by alcohol drinking, and consequently link with the development of alcoholic liver and pancreatic diseases.
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PMID:The relationship between the development of alcoholic liver and pancreatic diseases and the induction of gamma glutamyl transferase. 791 69

Because of the almost universal recurrence of hepatitis B surface antigenemia (HBsAg) after liver transplantation, some centers have questioned whether these patients are appropriate allograft candidates. Since January 1984, 51 patients with hepatitis B (HBV) underwent OLT at our center. No therapy was given to prevent reinfection. Three patients underwent retransplantation. The indications for transplant included fulminant HBV (13 patients), chronic HBV (33 patients), and hepatocellular carcinoma (HCCA) in addition to HBV (5 patients). Incidental HCCA was found in 2 of the 33 patients thought to have only chronic HBV. Actuarial survival for the entire group was 57% at 1 year and 54% at 3 years. Of the 23 patients who died, only 4 deaths were attributable to recurrent HBV liver disease. Four patients survived less than 4 days due to primary graft nonfunction. Ten patients died in the first 3 months from sepsis. Although all patients who died beyond 30 days had recurrent HBsAg, only 4 deaths were attributable to recurrent HBV. The remaining 5 deaths were caused by portal vein thrombosis, bile leak, lymphoma, pancreatitis, and sepsis occurring at 15 months. Excluding the 4 patients who died from primary graft nonfunction, actuarial survival was 63% at 1 year and 60% at 3 years. Of the 28 survivors, 24 are HBsAg positive; however, only 5 have recurrent HBV liver disease. Multiple factors were evaluated to determine their influence on survival; i.e., HBV serology, United Network for Organ Sharing status, fulminant versus chronic HBV, incidence of rejection, immunosuppression, transfusion requirements, and presence of HCCA. Of these, only the presence of HCCA adversely affected outcome. Of the 7 patients with HCCA and HBV, 6 patients died within the first 6 months and 1 patient has recurrent HBV liver disease at 25 months. Actuarial survival excluding those patients with HCCA was 64% at 1 year and 61% at 3 years. Based on our results, patients with HBV and associated HCCA have a poorer prognosis and should probably be excluded from transplantation. Although the survival for patients with HBV undergoing liver transplantation is inferior to that expected in patients with some other diagnoses, long-term survival can be achieved in a majority of these patients despite recurrence of HBsAg. We believe that appropriately selected patients with a diagnosis of HBV alone should continue to be candidates for liver allografts.
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PMID:Should liver transplantation be performed for patients with hepatitis B? 800 92

The appearance of desialo-transferrin (De-TF) in serum has been reported to be a biochemical marker of chronic alcoholism. However, conclusive evidence of whether De-TF is a marker for chronic alcohol drinking or for alcoholic liver disease (ALD) has not yet been obtained. Glycoproteins can be divided into two groups, a transferrin (TF) group and an alpha 1-acid glycoprotein (A1-AG) group, based on the characteristics of microheterogeneity (M-HTG) of each protein. In the present study, the appearance of M-HTG in serum TF and A1-AG in alcohol drinkers was compared. In 96 patients with ALD, M-HTG of TF was found in 66 patients (68.8%), and M-HTG of A1-AG was found in 61 patients (63.5%). In 20 patients with alcoholic pancreatitis, the detection rate of M-HTG of A1-AG was significantly higher than that of TF. In six patients with pancreatitis but not liver disease, M-HTG of TF was not detected. In 14 alcoholics without liver or pancreas disease, M-HTG of TF was not detected, whereas M-HTG of A1-AG was detected in 6 cases--a significant difference. The amount of alcohol consumed was not different in patients with and without liver disease. In non-ALD, M-HTG of both proteins was detected only in patients with decompensated liver cirrhosis. The detection rate of M-HTG in TF was significantly higher than in A1-AG. These results suggest that M-HTG of serum TF is a marker of ALD and that of serum A1-AG is a marker of chronic alcohol drinking.
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PMID:Microheterogeneity of serum glycoproteins in alcoholics: is desialo-transferrin the marker of chronic alcohol drinking or alcoholic liver injury? 804 44

We have developed a convenient method combining fast protein liquid chromatography (FPLC) with sensitive radioimmunoassay (RIA) for thyrotropin-releasing hormone (TRH) to separate and identify TRH and its metabolite histidyl-proline diketopiperazine (CHP) and applied this to study inactivation of TRH by blood extracts from patients with liver cirrhosis (LC) and acute edematous pancreatitis (AP). Blood samples spiked with TRH and CHP were extracted by cold methanol and injected on a reverse-phase FPLC column. A linear gradient was applied for separation. Subsequent analyses of fractions by RIA for TRH revealed that only fractions 9-10 contained TRH. Separation by retention time (9.9 +/- 0.8 min for TRH, 10.5 +/- 0.6 min for CHP, mean +/- SEM) was highly reproducible. For degradation studies, pooled sera from patients with LC and AP were incubated with TRH and CHP for 60 min. Inactivation of TRH was less rapid in the presence of blood extract from LC patients than that from normal subjects or AP patients. CHP was more stable than TRH. These data suggest that activity of TRH-degrading enzymes is reduced in liver disease, whereas it does not appear to be altered in AP. Degradation of CHP does not closely reflect metabolic processing of its major precursor. This rapid and sensitive method may be applicable for further investigations on the metabolism of TRH in organic fluids.
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PMID:A fast protein liquid chromatography (FPLC) method for study of thyrotropin-releasing hormone (TRH) and its metabolite histidyl-proline diketopiperazine (CHP) in human blood: degradation in liver and pancreatic diseases. 812 15

Traumatic injury frequently follows alcohol abuse. Between October 1, 1988 and January 31, 1992, 2,219 patients were admitted to the Trauma Service at the University Medical Center of Eastern Carolina-Pitt County. Of the 1,602 who were tested for serum ethanol, 685 (43%) were found to have measurable levels. Thirty-seven patients had alcohol withdrawal and were treated with intravenous ethanol; 34 were male (21 black, 13 white) and 3 female (1 black, 2 white), with an average age of 46 years. Those who had withdrawal had an average serum ethanol level, on presentation, of 239 mg/dL (N = 34). Fourteen patients were involved in motor vehicle crashes, seven were pedestrians struck by cars, and the remaining 16 had various traumatic mechanisms of injury. The most common injuries were long-bone fractures and blunt abdominal trauma. The length of ethanol therapy averaged 4 days. A majority of patients had a favorable response to treatment. Relative contraindications to i.v. ethanol therapy were CNS trauma, liver disease, and pancreatitis. i.v. ethanol is a safe and effective method of alcohol detoxification in the trauma patient.
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PMID:Intravenous ethanol for alcohol detoxification in trauma patients. 828 18

In this study, we found that the rate at which radiographically diagnosed simultaneous pleural and peritoneal effusions (double effusion [DE]) developed was highest in dogs and cats with infectious causes of pleuritis and/or peritonitis and in those with pancreatitis. However, DE were observed more frequently in dogs and cats with neoplastic and cardiovascular diseases. Nonneoplastic liver disease was also documented as a cause of DE in the population of this study. Frequency of DE was increased in males and in animals > 6 years old. The finding of simultaneous pleural and peritoneal effusions can be considered an indicator of disease severity, and warrants a poor to grave prognosis.
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PMID:Radiographic, epidemiologic, and clinical aspects of simultaneous pleural and peritoneal effusions in dogs and cats: 48 cases (1982-1991). 842 43

The aim of this work was to perform ultrasonographic measurements of normal pancreas in the Chilean population. Among 5000 subjects referred for an ultrasound abdominal examination, those without history of alcoholism, pancreatitis or liver disease were selected for the study. 261 individuals (157 female) aged 20 to 79 years were studied. The size of the head of the pancreas ranged from 6 to 28 mm (17.7 +/- 4.2 mm), the body size ranged from 4 to 23 mm (10.1 +/- 3.8 mm) and the tail size from 5 to 28 mm (16.4 +/- 4.2 mm). These figures are lower than those reported in Europe and North America. No size differences were observed according to sex or body frame. Progressive declines in size with age, were observed in all pancreatic segments. No hypoecogenic pancreas were observed. A new technique to improve pancreatic ultrasonographic vision is proposed.
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PMID:[Size and echogenicity of the pancreas in Chilean adults: echotomography study in 261 patients]. 852 25

Some recent proposals in management of alcoholic liver disease are discussed focusing on early diagnosis and treatment of alcohol abuse itself, alcoholic hepatitis early mortality, clinical meaning of nutritional therapy, serological approach and treatment of hepatic fibrosis, and problems in liver transplantation for end stage alcoholic liver cirrhosis. CAGE or similar systematized brief questionnaires, and desialylated transferrin/total transferrin ratio as serological marker, seems to be interesting contributions to "hidden" alcohol abuse diagnosis and abstinence control while psycho-social support and voluntary incorporation to self-aid groups are the best weapons to reach persistent abstinence. Corticosteroids seems to improve survival in a selected group of patients with severe alcoholic hepatitis, specially in those presenting encephalopathy but free of GI bleeding, decompensated diabetes, active infections, pancreatitis, and other contraindications or adverse effects of these drugs. Relationship between direct toxicity and nutritional deficiencies in pathogenesis of alcoholic liver injury are not clear enough, but malnutrition is generally present in patients requiring hospitalization, and related to clinical severity; oral, enteral or parenteral nutritional supplementation in this order of preference according to patients condition, associated or not with steroid anabolics, are useful in cases with moderate to severe alcoholic hepatitis or decompensated cirrhosis to eliminate the catabolic state, reaching a better nitrogen balance and liver function tests, without special adverse effects. A special role on liver regeneration is discussed. Antioxidants and supernutrients are special "modern" aspects of nutritional therapy in alcoholic liver disease generally related to the MEOS activation in chronic alcoholism, the excessive production of free radicals, and the depletion of glutathione, membrane phospholipids (specially phosphatidycholine), and vitamin A, E, and C. Natural supplements as soybean polyunsaturated lecithin, with high concentration of phosphatidycholine, or oral supplementation with natural metabolic products depleted from the liver of chronic heavy drinkers, such SAMe, have an interesting rationale based on experimental and clinical findings besides availability and costs. Carotenoids and tocopherols supplementation seems to be an useful tool, but are limited in the case of vitamin A because its special toxicity in chronic alcoholism. Serological markers of metabolism of liver connective tissue are clearly involved in fibrogenesis process and other inflammatory connected events; standardization of laboratory methods surely will result in new possibilities of non-invasive valuation of liver injury, evolution and therapeutic response; special histological damage such as sinusoidal "cappilarization" (type i.v. collagen and laminin), endothelial sinusoidal cell function (seric hyaluronate), or collagenase activity (TIMP-1 or tissue inhibitor of metalloproteinases-1) seems to be valuable by these new technologies.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[New suggestions for the management of alcoholic liver diseases]. 852 63


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