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)

Guillain-Barre syndrome is known as one of the autoimmune disease, but the etiology, pathophysiology relating immune reaction, as well as the treatment are not established. It still causes physical handicap although its rate is low. The causes, clinical symptoms and outcome of 132 cases of Guillain-Barre syndrome have been analyzed. The patients' ages ranged from 4 months to 15 years. The antecedent events for 56.1% of the patients were known. These were upper respiratory tract infection, unexplained fever, vomiting, diarrhea, vaccination, measles, german measles, shigellosis, mumps, hepatitis, pertussis and surgery in order of frequency. The CSF protein level reached a maximum at 12.3 +/- 9.5 days. Steroids did not influence the outcome of this disease. More studies are necessary to conquer the disease.
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PMID:Guillain-Barre syndrome in Korean children. 274 76

Giant-cell hepatitis in adults is a rare event resembling either chronic non-A, non-B or autoimmune chronic active hepatitis. The etiology is unknown. Paramyxoviruses may be implicated. The clinical picture varies remarkably from mild chronic liver disease to subacute hepatic failure. Liver biopsy is diagnostic, showing giant cells as the common pathological finding. Due to the unknown cause of the disease, treatment is symptomatic. Steroids are applied, as in the case of autoimmune disease, with remarkable results in some patients. In fulminant cases, however, liver transplantation is the only option for cure.
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PMID:[Clinical aspects of giant cell hepatitis]. 797 78

From autoimmune hepatitis (AIH) classification which recognizes three types of AIH, we discuss the main relations between hepatitis C virus (HCV) infection and AIH. Type I AIH is associated with antinuclear and antismooth muscle antibodies, and with other autoimmune diseases. There is no relation between type I AIH and HCV. Type I anti-liver kidney microsome and anti-liver cytosol I antibodies represent the hallmark of type II AIH. Among type II AIH, two subgroups emerged: type IIa AIH (10-40%) are true AIH (sensitive to steroids but worsens with interferon alpha), whereas type IIb AIH (60-90%) appear as a particular form of HCV hepatitis. Type IIb AIH have a moderate activity, a low titer of autoantibodies, anti-GOR antibodies but never anti-liver cytosol I, no sensitivity to steroids but are sensitive to interferon alpha. The hallmark of type III AIH are anti-cytosol antibodies, but these AIH have the same characteristics as type I AIH. The classification between true AIH (I, IIa, III) or "pseudo-AIH" due to HCV infection has major therapeutic implications. Steroids or immunosuppressive treatments are effective in type I, IIa and III AIH but have no efficacy in type IIb AIH. Alpha interferon has an efficacy in type IIb AIH, but it has no efficacy and may even worsen hepatitis in type I, IIa and III AIH.
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PMID:[Autoimmune hepatitis and hepatitis C]. 878 84

Steroids are recommended in severe alcohol-induced hepatitis, but some data suggest that artificial nutrition could also be effective. We conducted a randomized trial comparing the short- and long-term effects of total enteral nutrition or steroids in these patients. A total of 71 patients (80% cirrhotic) were randomized to receive 40 mg/d prednisolone (n = 36) or enteral tube feeding (2,000 kcal/d) for 28 days (n = 35), and were followed for 1 year or until death. Side effects of treatment occurred in 5 patients on steroids and 10 on enteral nutrition (not significant). Eight enterally fed patients were prematurely withdrawn from the trial. Mortality during treatment was similar in both groups (9 of 36 vs. 11 of 35, intention-to-treat) but occurred earlier with enteral feeding (median 7 vs. 23 days; P =.025). Mortality during follow-up was higher with steroids (10 of 27 vs. 2 of 24 intention-to-treat; P =. 04). Seven steroid patients died within the first 1.5 months of follow-up. In contrast to total enteral nutrition (TEN), infections accounted for 9 of 10 follow-up deaths in the steroid group. In conclusion, enteral feeding does not seem to be worse than steroids in the short-term treatment of severe alcohol-induced hepatitis, although death occurs earlier with enteral nutrition. However, steroid therapy is associated with a higher mortality rate in the immediate weeks after treatment, mainly because of infections. A possible synergistic effect of both treatments should be investigated.
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PMID:Short- and long-term outcome of severe alcohol-induced hepatitis treated with steroids or enteral nutrition: a multicenter randomized trial. 1086 86

Steroids have been 1 of the primary modes of immunosuppression since the inception of transplantation and have been credited with both the prevention and treatment of rejection. Steroids also have been held responsible for increased infections, posttransplantation diabetes, and recurrent hepatitis after orthotopic liver transplantation (OLT). The purpose of this ongoing prospective randomized trial is to eliminate steroid use in OLT through induction with rabbit antithymocyte globulin (RATG). This is the first report of a prospective randomized trial in OLT achieving complete absence of steroids. Seventy-one adult patients were prospectively randomized to administration of RATG or steroids. Thirty-six patients were randomized to the administration of RATG induction at a dose of 1.5 mg/kg intravenously (IV) beginning during the anhepatic phase. No steroids were administered. Patients were administered a second 1.5-mg/kg dose of RATG post-OLT day 1. Thirty-five patients were randomized to the administration of methylprednisolone, which had been our standard immunosuppressive protocol. These patients were administered methylprednisolone, 1,000 mg IV, initiated during the anhepatic phase and followed by steroid taper. Maintenance immunosuppression consisted of tacrolimus and mycophenolate, with or without prednisone. Three patients died in each group, for an overall survival rate of 91% in each group. One patient in each group required re-OLT, for a graft survival rate of 89% in each group. Seven patients administered RATG had biopsy-proven rejection (20.5%), all of whom were successfully treated by increasing tacrolimus doses. Eleven patients administered steroid had biopsy-proven rejection (32%), 7 (64%) of whom required additional steroids for treatment, whereas 4 patients (36%) were successfully treated by increasing tacrolimus doses. The incidence of rejection was not statistically significant; however, there was a significant difference in the incidence of steroid-requiring rejection (P =.01). The incidence of recurrent hepatitis C was 50% in RATG patients and 71% in steroid patients (P = not significant). The incidence and severity of infectious complications were slightly lower in RATG patients, accounted for by a greater incidence of cytomegalovirus (CMV) infection in the steroid patients. RATG induction enables complete avoidance of steroid use in OLT with a trend toward a lower rejection rate, decreased incidence of post-OLT diabetes and recurrent hepatitis C, and decreased CMV infection. This prospective randomized trial gives encouraging support that steroids can be safely eliminated in OLT.
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PMID:Steroid-free liver transplantation using rabbit antithymocyte globulin induction: results of a prospective randomized trial. 1151 14

A 43-year-old woman with Hashimoto's thyroiditis (HT), euthyroid on levothyroxine since 1999, developed thyroid-associated ophthalmopathy (TAO) in February 2002. She had involvement of the eye muscles, as shown by computed tomography (CT) scan. She was started on methylprednisolone pulse therapy 7.5 mg/kg of body weight, (one cycle every 2 weeks, each cycle comprising two infusions on alternate days), with rapid improvement of soft tissue inflammation and of eye motility, as confirmed by the reduction of clinical activity score (CAS) and eye muscles size on CT scan. At the end of treatment the patient showed a marked and rapid increase of serum aminotransferases (up to 1200 U/L). She had negative hepatitis A, B, and C viruses serology, but circulating antinuclear antibodies. A liver biopsy, performed at 4 weeks after the discontinuation of intravenous steroids, led to the diagnosis of autoimmune hepatitis (AIH). The patient was treated with oral steroids with a rapid reduction of serum aminotransferases concentrations. To our knowledge, there have been only two reports of liver dysfunction after intravenous steroids for TAO, but the etiology of such hepatitis had not been established. AIH may develop in patients with multiple autoimmunity and may not become overt until immune rebound occurs (i.e. after cessation of or between immunosuppressive treatment cycles). Steroids are the first line of treatment for AIH, hence their use would not be contraindicated when patients with TAO have chronic hepatitis, provided that the modalities of treatment are appropriate.
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PMID:Onset of autoimmune hepatitis during intravenous steroid therapy for thyroid-associated ophthalmopathy in a patient with Hashimoto's thyroiditis: case report. 1532 Sep 78

Heart failure may lead to subclinical circulatory disturbances and remain an unrecognized cause of ischemic liver injury. We present the case of a previously healthy 40-year-old bodybuilder, referred to our Intensive-Care Unit of Hepatology for treatment of severe acute liver failure, with the suspicion of toxic hepatitis associated with anabolic steroid abuse. Despite the absence of symptoms and signs of congestive heart failure at admission, an anabolic steroid-induced dilated cardiomyopathy with a large thrombus in both ventricles was found to be the underlying cause of the liver injury. Treatment for the initially unrecognized heart failure rapidly restored liver function to normal. To our knowledge, this is the first reported case of severe acute liver failure due to an unrecognized anabolic steroid-induced cardiomyopathy. Awareness of this unique presentation will allow for prompt treatment of this potentially fatal cause of liver failure.
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PMID:Anabolic steroid-induced cardiomyopathy underlying acute liver failure in a young bodybuilder. 1953 18

Autoimmune Hepatitis (AIH) is a periportal hepatitis with increased immunoglobulins and auto antibodies, which primarily responds to immunosuppression. It affects women 3.6 times more commonly than men. It is postulated that an environmental agent, either a drug or a virus or another agent seems to trigger a T-cell mediated cascade directed against liver antigens in genetically predisposed individuals to cause AIH. Diagnosis requires exclusion of other causes of liver disease. The diagnostic criteria have been defined in a simplified scoring system introduced by the International Autoimmune Hepatitis Group (IAIHG) in 2008. Current treatment of AIH is based on guidelines published by the American Association for the Study of Liver Diseases (AASLD) in 2002 and comprises of corticosteroids with azathioprine. Steroids tend to carry a high complication risk profile; hence several newer immunomodulators and biologics are in different stages of trials to assess their efficacy and safety.
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PMID:Autoimmune hepatitis: a review. 2052 13

Autoimmune hepatitis (AIH) is a chronic autoimmune inflammation of the liver usually requiring life-long immunosuppression. Steroids and azathioprin are the standard therapy, but the therapy is accompanied by strong side effects. Due to the fact that AIH is often recognized during late course of disease, it is difficult to obtain knowledge about the immunological mechanisms responsible for initiation of the disease. Current AIH models were helpful for understanding and modulating liver immune responses, but are not suited to study mechanisms in chronic AIH or to develop new therapies. While transgenic AIH models deal with short-term hepatitis, models with natural antigens are either self-limited or have unknown target antigens. Therefore, new animal models with defined onset of AIH and a standard course of the disease are essential for a more defined understanding of the disease and its pathophysiology. To obtain a preclinical platform for new therapeutic approaches or to be able to prevent onset of AIH, a positive impact of conventional standard therapeutic interventions in the model would be helpful. For decades, AIH research has lacked such a reliable preclinical model with chronic immune response against the liver. Initial results in breaking tolerance against hepatocytes have only led to mild and transient hepatitis. Transgenic models were helpful in understanding different aspects for hepatic immune regulation. Nowadays, the fate of T cells, especially CD8+ T cells, is the focus of research. Especially ignorance, anergy, deletion or TCR downregulation of T cells are mechanisms of tolerance against hepatic antigens. Furthermore, the importance of professional antigen-presenting cells and particularly liver sinusoidal cells in liver tolerance has been demonstrated in many studies. Other models have shown the mechanism of interaction of adaptive and innate immune cells in the liver. Recently, approaches have been made to establish AIH models reflecting the situation in AIH patients. This will allow new studies in the field and will provide an opportunity to study the onset and pathophysiology of AIH. Furthermore, these models will try new options for therapeutic approaches and might show options of how to prevent onset of disease.
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PMID:Requirements and challenges of a preclinical autoimmune hepatitis mouse model. 2189 11

Autoimmune hepatitis (AIH) is a chronic autoimmune inflammation of the liver usually requiring lifelong immunosuppression. Steroids and azathioprine are the standard therapy, but the therapy is accompanied by strong side effects. Due to the fact that AIH is often recognized during the late course of disease, it is difficult to obtain knowledge about the immunological mechanisms responsible for initiation of the disease. Current AIH models have been helpful for understanding and modulating liver immune responses, but are not suited to study mechanisms in chronic AIH or to develop new therapies. While most common hepatitis models are more models of injury, transgenic AIH models deal with short-term hepatitis leading to tolerance, and models with natural antigens are either self-limited or have unknown target antigens. Therefore, new models with defined onset of AIH and a standardized course of disease are essential for a better understanding of the disease and to develop new therapies.
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PMID:Animal models for autoimmune liver disease--what is relevant for immune-mediated liver disease. 2307 63


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