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)

Severe alcoholic liver injury has been relatively rare, but is gradually increasing in Japan. The clinical features and prognostic factors in severe alcoholic liver injury were retrospectively investigated in 105 patients, consisting of 3 with severe alcoholic hepatitis (SAH), 43 with cirrhosis with superimposed alcoholic hepatitis [liver cirrhosis (LC)+alcoholic hepatitis (AH)], 38 with AH, and 21 with alcoholic cirrhosis. Seven of the 105 patients (6.7%, 2 with SAH and 5 with LC+AH) died of hepatic failure. Patients with SAH showed severe hyperbilirubinemia, reduced hepatic biosynthetic capacity, and marked acute inflammatory reactions, and developed multiple organ failure, such as disseminated intravascular coagulation (DIC), renal failure, acute pancreatitis, or pneumonia. Two SAH patients died within 1 month, whereas five with LC+AH died within 77 days during the second episode of AH. In these nonsurvivors, the serum total bilirubin (T.Bil) level was not normalized, and the hepaplastin test (HPT), serum albumin, cholesterol, and platelet count were not markedly improved after the first episode of AH. In the survivors, elevation of AST lasted longer, and the improvement of T.Bil, hepatic biosynthetic capacity, and the platelet count were much less in patients with LC+AH than in those with AH. Multivariate analysis using the Cox proportional hazards model showed serum C-reactive protein (CRP) and DIC as significant independent prognostic factors among SAH, LC+AH, and AH groups. When factors related to multiple organ failure, such as DIC and renal failure, were excluded, T.Bil and CRP were selected as independent prognostic factors. In patients with LC+AH and AH, CRP, and HPT were shown to be significant independent prognostic factors. These results suggest that SAH with multiple organ failure, and another episode of AH in advanced LC with hyperbilirubinemia and reduced hepatic biosynthetic capacity, are indicative of an extremely poor prognosis in chronic alcoholics.
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PMID:Prognostic factors in severe alcoholic liver injury. Nara Liver Study Group. 1023 76

Association of hepatitis viruses with acute pancreatitis in the setting of nonfulminant viral hepatitis is rare. We report six cases of nonfulminant viral hepatitis complicated by acute pancreatitis, including the first documented case of hepatitis E virus (HEV) associated acute pancreatitis. The other five patients had acute viral hepatitis caused by hepatitis A infection. Besides features of viral hepatitis, the presence of typical abdominal pain, high serum amylase, and ultrasound or CT scan features suggested the diagnosis of acute pancreatitis. This complication generally developed in the initial phase of the hepatitic illness. All of the patients had mild to moderate pancreatitis that recovered uneventfully with conservative treatment.
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PMID:Acute pancreatitis associated with viral hepatitis: a report of six cases with review of literature. 1044 66

A 63-year-old man with seronegative rheumatoid arthritis developed acute pancreatitis, severe hepatitis, and sensorimotor polyneuropathy after receiving 150 mg of intramuscular aurothioglucose (gold). Positive lymphocyte transformation test to gold indicated a cell mediated hypersensitivity to the drug, while multiple investigations ruled out other underlying causes for his illness. After cessation of gold therapy a complete recovery occurred.
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PMID:Reversible pancreatitis, hepatitis, and peripheral polyneuropathy associated with parenteral gold therapy. 1049 91

Coxsackieviral infections have been linked etiologically to multiple diseases. The serotype CB4 is associated with acute pancreatitis and autoimmune type 1 diabetes. To delineate the mechanisms of host survival after an acute infection with CB4 (strain E2), we have investigated the role of nitric oxide (NO), generated by the inducible form of nitric oxide synthase (NOS2), in viral clearance and pancreatic beta-cell maintenance. Mice deficient in NOS2 (NOS2-/- mice) and their wild-type (wt) counterparts were injected with CB4, after which both groups developed severe pancreatitis, hepatitis, and hypoglycemia within 3 days. Within 4 to 7 days postinfection (p.i.), most of the NOS2-/- mice died and at a strikingly higher mortality rate than wt mice. Histological examination of pancreata from both infected NOS2-/- and infected wt mice revealed early and complete destruction of the pancreatic acinar tissue, but intact, insulin-stained islets. When examined up to 8 weeks p.i., neither surviving NOS2-/-mice nor surviving wt mice developed hyperglycemia. However, the clearance of infectious CB4 was different between the mice. The spleens of NOS2-/- survivors were cleared of infectious virus with kinetics similar to that of wt mice, but the livers, pancreata, kidneys, and hearts of the NOS2-/- groups cleared virus more slowly than those of the wt group. This delayed clearance was particularly prominent in the livers of infected NOS2-/- mice, which also showed prolonged histopathological features of viral hepatitis. Taken together, this outcome suggests that NOS2 (and NO) is not required for the prevention of pancreatic beta-cell depletion after CB4 infection. Instead the critical actions of NOS2 apparently occur early in the host immune response, allowing mice to survive and clear virus. Moreover, the data support the existence of an organ-specific dependency on NO for a rapid clearance of CB4.
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PMID:A critical role for inducible nitric oxide synthase in host survival following coxsackievirus B4 infection. 1127 93

A 33-year old female was diagnosed as Graves' disease and started on carbimazole. One month later when she was already euthyroid only on carbimazole therapy, she developed acute pancreatitis associated with mild cholestatic hepatitis and erythema nodosum. Carbimazole therapy was interrupted, pancreatic and liver function gradually improved and became normalized two weeks later. Other potential etiological causes of acute pancreatitis, hepatitis and erythema nodosum were excluded. Rechallenge with a single dose of carbimazole led to a new episode of acute pancreatitis and cholestatic hepatitis one day later. The appearance of different hypersensitivity reactions including pancreatitis, hepatitis and erythema nodosum, together with the observation that the interval between drug intake and onset of symptoms became shorter with repeated exposure to carbimazole, point to an immune-mediated mechanism. Carbimazole has to be added to the list of drugs capable of inducing acute pancreatitis, and should be emphasized the need to discontinue this medication as soon as there is evidence of pancreatic dysfunction.
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PMID:Acute pancreatitis, hepatic cholestasis, and erythema nodosum induced by carbimazole treatment for Graves' disease. 1220 Dec 14

Renal transplantation is often associated with severe complications. Except for acute rejection, infections and toxicity of immunosuppressive treatment are the most frequent problems observed after transplantation. Infections with hepatic viruses (HBV, HDV, HCV, HGV) and cytomegalic virus (CMV) are the main infectious complications after renal transplantation. Cyclosporine toxicity is not unusual for a patient with renal transplantation and is even more frequent for patients with hepatic impairment due to viral infections. The subjects of this report are two renal transplant recipients with acute pancreatitis, severe hepatitis and acute renal failure on graft, receiving immunosuppressive therapy for maintaining renal graft function
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PMID:Acute pancreatitis, acute hepatitis and acute renal failure favourably resolved in two renal transplant recipients. 1267 79

Although rare, encephalitis and hepatitis are major complications of measles that are more common in adults than in infants. On the other hand, although several other complications of measles, such as pneumonia and myocarditis, are found in all ages, acute pancreatitis in measles is very rare in both children and adults. We describe a 16-year-old female patient with measles encephalitis who developed acute pancreatitis. The response to steroid therapy was favorable.
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PMID:Measles encephalitis and acute pancreatitis in a young adult. 1516 56

Interleukin 18 has been known since 1989 and since its properties have been recognized, an interest in it is constantly growing. IL-18 induces synthesis and release of proinflammatory cytokines, chemokines and nitric oxide. Thus, it modulates the function of many immunocompetent cells: macrophages, monocytes, lymphocytes and granulocytes. In the paper, properties of IL-18 are reviewed and its implications for pathogenesis of some gastrointestinal diseases, particularly inflammatory bowel diseases, i.e. Crohn Disease and colitis ulcerosa, inflammatory liver diseases such as persistent active hepatitis and primary biliary cirrhosis and acute pancreatitis are discussed.
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PMID:[Interleukin 18 as a new immunomodulator of some digestive tract diseases]. 1519 Jun 10

A 29-year-old man presented with symptoms suggestive of acute pancreatitis of 3 day's duration. No definite aetiology was identifiable at admission. The patient had been receiving corticosteroids for the preceding 1 month, after the evacuation of a traumatic subdural haematoma. During the hospital stay, he developed a macular skin rash, which evolved over a period of 48 hours to a papulovesicular rash typical of varicella infection. Liver function tests were suggestive of anicteric hepatitis. Acyclovir therapy was instituted. However, the patient succumbed to an episode ventricular arrhythmia of sudden onset, possibly due to varicella myocarditis. A high index of suspicion for varicella infection in immunocompromised patients presenting with acute pancreatitis is necessary for early diagnosis. The rash may at times be atypical and may rarely appear after the onset of pancreatitis. Whenever any rash develops in the setting of pancreatitis of unknown aetiology, rapid diagnostic tests should be undertaken to establish the diagnosis and start appropriate therapy.
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PMID:Acute pancreatitis: presenting manifestation of varicella infection. 1547 23

Acute pancreatitis develops immediately after the causative impulse, while chronic pancreatitis develops after the long-term action of the noxious agent. A typical representative of acute pancreatitis is biliary pancreatitis, chronic pancreatitis develops in alcoholism and has a long latency. As alcoholic pancreatitis is manifested at first as a rule by a potent attack, it is classified in this stage as acute pancreatitis. The most frequent etiological factors in our civilization are thus cholelithiasis and alcoholism (both account for 20-50% in different studies). The assumed pathogenetic principles in acute biliary pancreatitis are the common canal of both efferent ducts above the obturated papilla, duodenopancreatic reflux and intrapancreatic hypertension. A detailed interpretation is however lacking. The pathogenesis of alcoholic pancreatitis is more complicated. Among others some part is played by changes in the calcium concentration and fusion of cellular membranes. Idiopathic pancreatitis occurs in up to 10%, part of the are due to undiagnosed alcoholism and cholelithiasis. Other etiologies are exceptional. Similarly as in cholelithiasis pancreatitis develops also during other pathological processes in the area of the papilla of Vater such as dysfunction of the sphincter of Oddi, ampulloma and juxtapapillary diverticulum, it is however usually mild. The incidence of postoperative pancreatitis is declining. Its lethality is 30% and the diagnosis is difficult. In the pathogenesis changes of the ion concentration are involved, hypoxia and mechanical disorders of the integrity of the gland. Pancreatitis develops in association with other infections--frequently in mumps, rarely in hepatitis, tuberculosis, typhoid and mycoses. Viral pancreatitis is usually mild. In parasitoses pancreatitis develops due to a block of the papilla Vateri. In hyperparathyroidism chronic pancreatitis is more likely to develop, recent data are lacking. As to dyslipoproteinaemias, pancreatitis develops in the Ist, IVth and Vth type of Frederikson's classification, in rare recessive disorders and other conditions such as hypothyroidism, renal insufficiency, oestrogen substitution and others. In pancreas divisum chronic pancreatitis is more likely to develop. In exotic countries tropical pancreatitis is most frequent. It is however similarly as alcoholic pancreatitis primarily chronic. A very serious course is usual in traumatic pancreatitis. Risk factors of pancreatitis after ERCP are in particular undilated biliary pathways, dysfunction of the sphincter of Oddi and the use of a needle knife (bistoury). Medicamentous prevention is not substantiated. Drug induced pancreatic damage is much rarer than hepatotoxicity. Pancreatitis is caused most frequently by immunosuppressives, methyldopa, corticoids and oestrogens. The question remains to what extent the course of pancreatitis is influenced by its etiology. Biliary, alcoholic, traumatic and postoperative pancreatitis is usually severe, pancreatitis associated with viroses and induced by drugs is usually mild.
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PMID:[Etiological factors of acute pancreatitis]. 1673 20


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