Cases reported "Hepatitis"

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1/25. A complex case of hepatitis in a patient with systemic lupus erythematosus.

    Liver involvement in patients with systemic lupus erythematosus (SLE) is considered rare. Previous treatment with potentially hepatotoxic drugs or viral hepatitis have usually been implicated as the main causes of liver disease in SLE patients. On the other hand, even after careful exclusion of these aetiologies, the problem remains whether to classify the patient as having a primary liver disease with associated autoimmune clinical and laboratory features resembling SLE, such as autoimmune hepatitis, or as having liver disease as a manifestation of SLE. We report the case of an elderly woman who presented with acute hepatitis, who had been diagnosed with SLE 14 years ago and who also had sjogren's syndrome and anti-phospholipid's syndrome for several years. The histology depicted chronic active hepatitis and, after drug-induced hepatitis and viral hepatitis were excluded, the serological and clinical features were shown to be typical of liver damage caused by SLE. The patient was treated with azathioprine 100 mg/d and prednisone 30 mg/d. The clinical symptoms resolved in 10 days and the laboratory values were normal at the end of the first month of therapy. prednisone was progressively reduced, during a period of 4 months, to 10 mg/d but azathioprine was kept to the same dose. One year after the diagnoses the patient is still in remission. Although uncommon, hepatic involvement is well recognised in SLE. The interest of this case lies in the differential diagnosis and recognition of this condition, which deserves an aggressive treatment.
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2/25. Hepatitis in disseminated bacillus Calmette-Guerin infection.

    Local immunotherapy with an attenuated live strain of mycobacterium bovis, bacillus Calmette-Guerin (BCG), is an effective and frequently used treatment for in situ transitional cell carcinoma (TCC) of the bladder. Success rates are high, and serious side effects are infrequent but can affect every organ system. A 79-year-old patient with recently diagnosed TCC who was treated with intravesical BCG for a recurrence after initial surgical treatment is reported. After unsuccessful attempts at bladder catheterization with the creation of a false passage for his third treatment, BCG was instilled via a suprapubic catheter the same day and again a week later. Two weeks after the third BCG instillation, the patient presented with profound lethargy and weakness to the point of not being able to get up out of a chair. He was febrile, anorexic, icteric and had hepatosplenomegaly. Disseminated BCG infection was suspected on the basis of history, clinical examination and a liver biopsy that showed noncaseating granulomatous hepatitis. Empirical treatment was started with antituberculous combination therapy. A short course of an oral corticosteroid was given. Clinical improvement was marked and sustained so that the patient could be discharged home for the full six-month course of his treatment. Disseminated BCG infection with granulomatous hepatitis can be severe and life-threatening in cases where a large intravascular inoculum of BCG may have been given inadvertently.
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3/25. scarlet fever associated with hepatitis--a report of two cases.

    Infection with group A beta-hemolytic streptococci (GABHS) is the most common bacterial cause of acute pharyngitis and tonsillitis beyond infancy. We report on two patients with scarlet fever associated with hepatitis. The patients (boys aged 6 and 7 years) both presented with a scarlatiniform rash, dark urine and light-colored stools. Laboratory studies revealed elevated liver transaminases and negative antibody tests against hepatitis viruses A, B and C, cytomegalovirus and Epstein-Barr virus. Both patients were treated with antibiotics and recovered completely within a few days. Although the association between scarlet fever and hepatitis has been known for many decades, the pathogenesis is still unknown. physicians treating patients with group A beta-hemolytic streptococcal infections should be aware of possible hepatic involvement.
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4/25. BCG immunotherapy: be cautious of granulomas. Disseminated BCG infection and mycotic aneurysm as late complications of intravesical BCG instillations.

    We describe a 65-year-old man with a granulomatous hepatitis and a progressive mycotic aneurysm of the abdominal aorta. One year before he received intravesical bacillus Calmette--Guerin (BCG) for carcinoma of the bladder without any complaints. Only post-mortem investigations could confirm that he suffered from a systemic BCG infection. literature is reviewed for this rare complication.
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5/25. Depletion of mitochondrial dna in the liver of an infant with neonatal giant cell hepatitis.

    A boy presented with lactic acidosis, hepatomegaly, hypoglycemia, generalised icterus, and muscle hypotonia in the first weeks of life. At the age of 2 months, neonatal giant cell hepatitis was diagnosed by light microscopy. Electron microscopy of the liver revealed an accumulation of abnormal mitochondria and steatosis. Skeletal muscle was normal on both light and electron microscopy. At the age of 5 months, the patient died of liver failure. Biochemical studies of the respiratory chain enzymes in muscle showed that cytochrome-c oxidase (complex IV) and succinate-cytochrome-c oxidoreductase (complex II III) activities were (just) below the control range. When related to citrate synthase activity, however, complex IV and complex II III activities were normal. Complex I activity was within the control range. The content of mitochondrial dna (mtDNA) was severely reduced in the liver (17% to 18% of control values). Ultracytochemistry and immunocytochemistry of cytochrome-c oxidase demonstrated a mosaic pattern of normal and defective liver cells. In defective cells, a reduced amount of the mtDNA-encoded subunits II-III and the nuclear dna-encoded subunits Vab was found. cells of the biliary system were spared. immunohistochemistry of mtDNA replication factors revealed normal expression of dna polymerase gamma. The mitochondrial single-stranded binding protein (mtSSB) was absent in some abnormal hepatocytes, whereas the mitochondrial transcription factor A (mtTFA) was deficient in all abnormal hepatocytes. In conclusion, depletion of mtDNA may present as giant cell hepatitis. mtTFA and to a lesser degree mtSSB are reduced in mtDNA depletion of the liver and may, therefore, be of pathogenetic importance. The primary defect, however, is still unknown.
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6/25. Spectrum of bacille Calmette-Guerin (BCG) infection after intravesical BCG immunotherapy.

    Intravesical instillation of bacille Calmette-Guerin (BCG) effectively treats transitional cell carcinoma of the bladder. Occasionally, BCG infection complicates such treatment. In some patients, infection appears early (within 3 months after instillation) and is characterized by generalized symptoms, with pneumonitis and hepatitis. Late-presentation disease occurs >1 year after the first BCG treatment and usually involves focal infection of the genitourinary tract (the site at which bacteria were introduced) and/or other sites that are typical for reactivation of mycobacterial disease, such as the vertebral spine or the retroperitoneal tissues. Noncaseating granulomas are found in the majority of cases, whether early or late. Most patients respond to treatment with antituberculous drugs; in early-presentation disease, when features of hypersensitivity predominate, glucocorticosteroids are sometimes added. Late localized infection often requires surgical resection.
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7/25. Successful treatment with cyclosporin in adult-onset Still disease manifesting as acute hepatitis with marked hyperferritinemia.

    A 48-year-old woman was admitted because of spiking high fever, sore throat, and jaundice. A diagnosis was made of adult-onset Still disease (AOSD) presenting with acute hepatitis and very high serum ferritin levels (32,240 ng/mL), and she was treated with 2 courses of pulse therapy of methylprednisolone (2 g/day for 3 days) followed by 40 mg/day prednisolone. Subsequently, the serum level of ferritin decreased, but serum total bilirubin increased to 17.3 mg/dL. Therefore, cyclosporin was administered orally. Within the next 3 months, results of liver function tests, as well as serum levels of ferritin, soluble interleukin-2 receptor, interferon-gamma, interleukin-6, and tumor necrosis factor-alpha gradually returned to within normal limits, and cyclosporin administration was subsequently reduced gradually. The clinical presentation suggests that AOSD should be considered when liver dysfunction is accompanied with high fever and extreme hyperferritinemia, and that treatment with cyclosporin or other immunosuppressive drugs that selectively suppress cytokine production by helper T cells is a valuable option in the treatment of AOSD with very high serum ferritin levels.
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8/25. Reappearance of vanished bile ducts.

    A 36-year-old Surinam woman with a severe form of toxic epidermal necrolysis of unknown origin is presented. skin lesions healed gradually without scarring within 3 to 4 weeks, but eye lesions progressed to symblepharon and corneal opacification, resulting in almost complete blindness. In addition, toxic epidermal necrolysis was associated with severe intrahepatic cholestasis caused by vanished bile duct syndrome; viral hepatitis, primary biliary cirrhosis and primary sclerosing cholangitis were excluded. After about six months, intrahepatic chole-stasis improved spontaneously and a third liver biopsy taken after 51 weeks of illness revealed that the bile ducts had reappeared. At present, the patient is relatively well, with no jaundice, although parameters of cholestasis are still elevated: alkaline phosphatase three times, and gamma GT thirty times the normal values. This sequence of events has to our knowledge never been reported in the literature.
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9/25. Strategy for hepatic hyperplastic nodules in heavy drinkers.

    BACKGROUND: Increased detection of nodular lesions that have not yet been definitively diagnosed as hepatocellular carcinoma (HCC) has occurred with the use of advanced imaging techniques. In heavy drinkers, the differential diagnosis between a hyperplastic nodule and early HCC on the basis of results of fine-needle biopsy is often difficult. Negation of diagnosis of HCC after surgical resection has been reported, and nodular lesions have been found to decrease during follow-up observation. On the basis of findings, a suitable strategy for the management of such lesions is suggested. methods: We identified six patients who had hepatic nodular lesions on ultrasonography and were heavy drinkers. This group included five men and one woman with a mean age of 45.3 /- 3.8 years. Two patients had solitary lesions; four had multiple lesions, and of these, two were hepatitis c virus antibody positive (C ). In the five men, the nodular lesions were detected during hospitalization for ruptured or prophylactic treatment of gastroesophageal varices. RESULTS: Five of the six patients had hypervascular lesions characterized by increased hepatic artery blood flow. However, dynamic computed tomography and magnetic resonance imaging studies during late-phase imaging could not confirm any decrease in portal blood flow. HCC was diagnosed by detailed imaging studies and liver biopsy in one C patient with a solitary nodule. In two of the other four patients, imaging findings were compatible with hypervascular HCC. Findings on liver biopsy do not always permit an easy differential diagnosis between a regenerative lesion (hyperplastic nodule) and a dysplastic or neoplastic lesion. One patient with a hypovascular lesion was C , and liver biopsy showed a dysplastic nodule. CONCLUSION: Heavy drinkers with alcoholic liver disease often develop hypervascular, hyperplastic nodules. The accurate diagnosis of these nodules requires careful consideration of clinical factors, including a combination of images and histologic examination. However, some cases were still difficult to distinguish between HCC by applying advanced imaging techniques and biopsy results.
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10/25. bacillus Calmette-Guerin-induced granulomatous hepatitis in a patient with a superficial bladder carcinoma.

    A 71-year-old male patient with a superficial transitional cell carcinoma of the urinary bladder developed high fever and jaundice, accompanied by progressively increasing serum aminotransferase activities, 2 weeks after the fourth local instillation with an attenuated live strain of mycobacterium bovis [bacillus Calmette-Guerin (BCG)]. A liver biopsy showed non-caseating granulomatous hepatitis. Cultures for mycobacteria were negative. Mycobacterial dna was not detected in liver tissue using the polymerase chain reaction. Empirical treatment with rifampicin and isoniazid was started, resulting in partial recovery. After 6 months of therapy, however, serum aminotransferase activities were still twice the upper limit of normal. A second liver biopsy still demonstrated several granulomas. Only after addition of prednisolone, liver tests completely normalized. Also histologically the lesions improved dramatically. This suggests that the BCG hepatitis was at least partially caused by a hypersensitivity reaction. Our patient is the first reported case of BCG hepatitis with histological follow-up under therapy.
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