Autoimmune hepatitis acute

Several types of immunosuppression have also been tried. Azathioprine alone was found to have no effect on PBC [82], but additional benificial effects were found in combination with ursodeoxychohc add and corticosteroids [78]. Cyclosporin showed some success, espe-dally in corticosteroid-resistant autoimmune hepatitis [83], but its use is generally considerably hmited by severe side-effects. Corticosteroids were effective in the management of several types of autoimmune chronic active hepatitis [84,85] and in the management of acute al-cohohc hepatitis [86]. Their use, however, has to be brief hi order to minimize side-effects. In the treatment of PBC, corticosteroids alone were found to be toxic and had only limited efficacy [77]. 

Hepatotoxicity Severe hepatic reactions, including acute liver failure, jaundice, hepatitis, and cholestasis, have been reported rarely in postmarketing data in patients receiving infliximab. Autoimmune hepatitis has been diagnosed in some of... 

A patient developed atorvastatin-induced severe autoimmune hepatitis and a lupus-like syndrome. Although the drug was immediately withdrawn, the disease persisted and deteriorated to a fulminant form with acute hepatic failure. There was no response to conventional immunosuppression with glucocorticoids and azathioprine. Only the introduction of intense immunosuppressive therapy, as used in solid organ transplantation, led to a complete and sustained recovery. The patient had the HLA haplotypcs DR3 and DR4, which are well-known genetic factors associated with autoimmune diseases. 

A 50-year-old woman with previous autoimmune thyroid disease taking atorvastatin developed acute hepatitis when she also was given ezetimibe (4). Further investigations, including liver biopsy, showed a probable drug-induced autoimmune hepatitis. 

Heyningen CV. Drug-induced acute autoimmune hepatitis during combination therapy with atorvastatin and ezetimibe. Ann Clin Biochem 2005 42 402-4. 

A 61-year-old woman developed symptoms of acute hepatitis 6 weeks after she began to take fluvastatin sodium 20 mg/day for hypercholesterolemia (3). Ultrasonography and liver biopsy confirmed the diagnosis of non-obstructive intrahepatic jaundice. Studies of viral markers and autoimmune factors excluded viral hepatitis and autoimmune hepatitis. There was a high serum concentration of a metabolite of fluvastatin, suggesting a possible anomaly of drug metabolism. All liver function tests normalized 8 weeks after the withdrawal of fluvastatin. 

Autoimmune hepatitis typically occurs in females, at puberty and between the ages of 40 and 70. It can also occur in males at any age. It may present in a number of ways as a mild hepatitis, as a severe acute hepatitis or as established cirrhosis. The functioning capacity of the liver will vary depending on the stage of disease. The diagnosis of AIH is based on serum biochemistry, liver histology, and the presence of certain autoantibodies in the serum. Exclusion of other potential causes of hepatitis, e.g. hepatitis B or C, alcohol consumption, is needed before a definitive diagnosis can be made. There are no featnres that are specifically indicative of AIH, but it usually responds to treatment with corticosteroids. Once remission is indnced azathioprine or... 

Patients with acute hepatitis (hepatitis A, B, C or autoimmune hepatitis) are usually jaundiced with extremely elevated transaminases. COCs should not be used during the acute phase, as oestrogen derivatives could exacerbate hepatitis when combined with active inflammation of the liver [2]. One author stated that COCs should not be prescribed in a hepatitis A patient until three months after the LFTs have returned to normal [23]. 

Nakadate, I., Nakamura, A., Endo, R., Iwai, M., Kaneta, H., Shimo-tono, H., Sasaki, S., Takikawa, Y., Yamazakl, K., Madarame, T., Kashi-wabara, T., Suzuki, K., Sato, S. Autoimmune hepatitis presenting with acute hepatic failure. Acta Hepatol. Xapon. 1993 34 665-671... 

In acute and chronic HCV infections, various antibodies such as ANA, SMA, LKM-1, anti-GOR, etc. (s. pp 118-121, 679) (up to 65% of cases) as well as a positive rheiunatoid factor (approx. 20% of cases) were detected. The differentiation between genuine autoimmune hepatitis and HCV infection with autoimmune phenomena is of paramount chnical significance. 

The cause of autoimmune hepatitis (AIH) is unknown. Autoimmune reactions lead to a chronic (rarely acute) inflammatory process (periportal piecemeal necrosis, infiltration of portal zones). AIH is frequently associated with autoimmune diseases of other organs. It occurs predominantly among women, particularly in younger years. Hypergammaglobulinaemia is invariably in evidence. Various autoantibodies to components of the liver parenchyma are found. The presence and specificity of these antibodies, together with the respective clinical symptoms, facilitate differentiation between the various subtypes of AIH. Diagnosis is substantiated by the response to immunosuppressive therapy. If left untreated, AIH progresses rapidly with transition to cirrhosis and/or liver failure. If treated adequately, the course taken by the disease is favourable. 

A female patient between 35 and 40 years of age with confirmed (in line with the methods of the time, including laparoscopy and biopsy) autoimmune hepatitis (ANA ++, SMA+, LMA +, LE factor+, IgG++, y-globulin++, GPT, GOT80-100 Utl, GDH ca. 12 UH, no cholestasis) had been undergoing treatment with prednisolone I azathioprine and had been in constant remission for over 3 years (maintenance dose of 4—6 mg prednisolone and 50 mg azathioprine for over 2 years). Physically and mentally stable, engaged in her profession, she had placed great confidence in us. Approximately 3 days after a sudden, severe emotional trauma with mental breakdown, the AlH deteriorated on a massive scale, and about 3 weeks later, the patient died in a coma hepaticum from acute liver failure. 

If cholestasis is not present, the additional application of ursodeoxycholic acid (UDCA) is worth considering because of its pharmacological properties and lack of side effects or interactions. Initial results on the treatment of chronic hepatitis with UDCA were reported by F. IcHiDA (1961), T. Nakahara et al. (1975) and K. Miyaji (1976). (s. p. 705) In 1988 our study group also noted obvious and permanent effects of UDCA on the course of disease in terms of clinical and laboratory indices in severe acute viral hepatitis B. (s. p. 437) Such observations were confirmed by A. Jorge in 1993. Owing to the multiple mechanisms of action of UDCA, in particular its immunomodulatory effect, adjuvant therapeutic efficacy can be anticipated in autoimmune hepatitis, as reported by P. Janowitz et al. in 1996. In autoimmune-associated chronic hepatitis C, UDCA proved to be a successful therapeutic agent (K. Nakamura et al., 1999). 

Singh, R., Nair, S., Farr, G., Mason, A., PerriBo, R.P. Acute autoimmune hepatitis presenting with centrizonal liver disease case report and review of the Uterature. Amer. J. Gastroenterol. 2002 97 2670-2673... 

Lobular inflammation Whereas lobular, diffusely distributed inflammation is more evident, in acute hepatitis portal and periportal inflammation predominates in chronic hepatitis and lobular hepatitis is less pronounced. Generally, it consists of separate small clusters of mononuclear cells. Scattered necrotic hepatocytes (= acidophilic / Councilman bodies) are found the hepatocellular nuclei are in disarray (= anisonucleosis) there is swelling of the hepatocytes, and mitoses are present. Marked lobular hepatitis in conjunction with considerable portal and periportal inflammation is typical of flares of chronic viral hepatitis or autoimmune hepatitis. In addition to single-cell necroses, there are confluent necroses, which affect entire lobules. Bridging necroses link portal tracts with other portal tracts or with terminal venules, (l)... 

A 7-year-old boy with Duchenne muscular dystrophy and attention deficit hyperactivity disorder (ADHD) developed acute hepatic failure, with features of autoimmune hepatitis (2). The only medications he had taken were pemoline (56 mg/day) and cjrproheptadine (2 mg/day). Pemoline was withdrawn after 8 months as the presumed cause of his raised transaminases. Two weeks later he developed an altered mental state, jaundice, and encephalopathy. The histological features of the liver and his autoimmune antibody panel were consistent with autoimmune hepatitis. He was treated with corticosteroids and azathioprine and recovered. 

Crapper R, Bhathal P, Mackay I, Frazer I. Acute autoimmune hepatitis. Digestion 1986 34 216-25. 

It has been well documented that the anaemia of chronic disease, ACD, results in a lowering of various haematological parameters. Several mediators are involved, among them histamine, serotonin, bradykinin, prostaglandins and, as found more recently, cytokines and nitric oxide. ACD is a parameter of systemic autoimmune disorders. The severe inflammatory stimuli lead to several systemic changes, mediated by inflammation-associated cytokines, e.g. IL-6, IL-1 TNFa, TGF beta that regulate hepatic synthesis of the acute phase proteins. 

Mercaptopurine [6-MP] (Purinethol) [Antineoplastic/ Antimeta lite] Uses Acute leukemias, 2nd-line Rx of CML NHL, maint ALL in children, immunosuppressant w/ autoimmune Dzs (Crohn Dz) Action Antimetabolite, mimics hypoxanthine Dose Adults. 80-100 mg/mVd or 2.5-5 mg/kg/d maint 1.5-2.5 mg/kg/d Peds. Per protocol X w/ renal/hepatic insuff on empty stomach Caution [D, ] Contra Severe hepatic Dz, BM suppression, PRG Disp Tabs SE Mild hematotox, mucositis, stomatitis, D rash, fever, eosinophilia, jaundice. Hep Interactions T Effects W/ allopurinol T risk of BM suppression W/ trimethoprim-sulfamethoxazole X effects OF warfarin EMS May falsely T glucose OD May cause NA and liver necrosis symptomatic and supportive Meropenem (Merrem) [Antibiotic/Carbapenem] Uses lntra-abd Infxns, bacterial meningitis Action Carbapenem X cell wall synth, a [3-lactam Dose Adults. 1 to 2 g IV q8h Peds. >3 mo, <50 kg 10-40 mg/kg IV q 8h in renal insuff Caution [B, ] Contra [3-Lactam sensitivity Disp Inj 500 mg, 1 g SE Less Sz potential than imipenem D, thrombocytopenia Interactions T Effects W/ probenecid EMS Monitor for signs of electrolyte disturbances and... 

A 60-year-old woman with normal liver function tests developed acute hepatitis 6 weeks after starting to take gliclazide. No viruses, autoimmune factors, or metabolic factors that could have caused hepatitis could be found. A lymphocyte transformation test was not performed. A liver biopsy was compatible with drug-related acute hepatitis. When gliclazide was withdrawn she improved. She took glibenclamide and recovered fully within 6 weeks. 

A 50-year-old obese woman taking glipizide 5 mg/day who had been drinking a bottle of rum daily for 2 months developed an acute hepatitis and died (115). The viral hepatitis profile was negative. At autopsy the liver weighed 1800 g and there was focal necrosis without evidence of autoimmune or alcoholic hepatitis. There was no brain edema. 

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