[Focal nodular hyperplasia of the liver in a young female]. / Ogniskowa hiperplazja watroby u mlodej kobiety.

Focal nodular hyperplasia (FNH) of the liver is a lesion characterized by a well circumscribed region of hyperplastic liver tissue with stellate fibrosis. The pathogenesis of FNH is unknown but various authors consider that this lesion may be a response to a preexisting vascular abnormality. A 27-year-old woman was referred because of large liver lesion detected by ultrasound abdominal examination. Doppler ultrasound, computed tomography and magnetic resonance suggested this was FNH. The patient was conducted to resection of the tumor because of size of the tumor and presence of clinical signs and symptoms. Pathological examination of the surgical resection confirmed diagnosis of FNH. Follow-up after 1 and 2 years showed that the patient remained well but she complained of general weakness and we found unexplained elevation of GGT. Liver biopsy was performed 1 year after resection of the tumor and histopathological examination showed only minimal reactive changes.

Autoimmune reactions in HBV and HCV.

BACKGROUND: Hepatotropic viruses HBV and HCV are capable of triggering autoimmune reactions (AIH). The aim of the study was the assessment of clinical course of AIH in patients with HBV and HCV, and the revision of treatment methods employed in these cases. MATERIAL AND METHODS: Among 120 patients with AIH and those qualified for antiviral therapy, 21 (17.5%) subjects were selected, including 16 with HCV (7 men and 9 women) and 5 with HBV (including 2 men and 3 women). AIH diagnosis was based on international criteria taking into account biochemical tests, autoantibodies and morphological picture of the liver. HBV infection was confirmed with the determination of HBV markers and HCV--with the presence of antiHCV and HCV RNA. RESULTS: The duration of infection at AIH diagnosis was difficult to assess in patients with HCV. AIH was diagnosed when patients were qualified for antiviral treatment. Three patients displayed high anti-LKM1, 8--ANA and SMA, two pts--ANA, two pts--SMA, one pt--ANA + pANCA and one--SMA + pANCA. Nine patients did not show hyperproteinaemia, and hypergammaglobulinaemia was not observed in 2 patients. Six patients suffered from other immunity disorders--thrombocytopenia, vasculitis, arthritis, visceral lupus erythematosus. The diagnosis of chronic hepatitis was confirmed by morphological examinations in 15 patients. Ten subjects received adrenocortical hormones, 3 patients were treated with adrenocortical hormones and azathioprine, 4 received interferon and 3 received no treatment. All patients with HBV proved HBeAg(-). In these patients, AIH symptoms developed 5-18 years after the diagnosis of HBV infection. Liver biopsy confirmed the diagnosis in 4 patients. SMA was observed in 2 subjects, ANA and SMA--in the remaining patients. All the subjects manifested typical biochemical changes as well as high IgG values. Extrahepatic exponents of immune process were observed in 3 patients. Three subjects were treated with Encorton (Prednisone), while 2 patients received Encorton and Azathioprine. CONCLUSIONS: Patients with HBV and HCV infections may manifest the features of AIH in the course of the disease, which requires careful attention while selecting treatment.

Correlation between liver damage and degree of gastric mucose colonization by Helicobacter pylori in subjects with parenchymatous liver damage.

BACKGROUND: Helicobacter pylori (H. pylori) is an important factor responsible for chronic inflammatory conditions of the gastric mucosa. It has been demonstrated in numerous animal studies that some Helicobacter species may cause parenchymatous liver damage. The aim of the study was to investigate whether there is any correlation between the incidence of parenchymatous liver damage, and the incidence and degree of colonization of the gastric mucosa by H. pylori. MATERIAL AND METHODS: The study was carried out in the group of 30 patients (14 females, 16 males) whose mean age was 37 years, hospitalized because of parenchymatous liver damage without clinical symptoms of cirrhosis. All the patients had gastroscopy and urease tests performed, and mucosal biopsies were taken for immunomorphological investigations. The patients were divided into groups, group I comprising those with positive, and group II with negative urease test results. RESULTS: Positive urease tests were obtained in 26/30 patients (group I), 18/26 of whom demonstrated macroscopic changes of the gastric mucosa visible in gastroscopy. Group II with negative urease test results comprised 4/30 patients, 2/4 of whom had detectable changes in the gastric mucosa. The presence of H. pylori antigens was demonstrated by gastric mucosa immunomorphology in all 30 patients. The degree of invasion of H. pylori was visualized by immunofluorescence, which allowed to differentiate deep mucosal invasion of H. pylori (bacterial antigens present in lymph follicles and at the base of muciferous glands) observed in group I in 14/26 and in group II in 1/4 cases and superficial invasion (epithelium and mucosal surface) observed in group I in 12/26, in group II in 3/4. CONCLUSIONS: The obtained results may suggest more frequent H. pylori infections in subjects with parenchymatous liver damage than in the population without liver damage. Immunofluorescence seems to be a highly sensitive method allowing for detection of even small degrees of gastric mucosa colonization by H. pylori.

[Antibiotic-associated diarrhea in light of personal observations]. / Zespoly biegunkowe po antybiotykoterapii w swietle wlasnych obserwacji.

Examination was performed in a group of 539 adult patients with diarrhea admitted to the Department of Infectious Diseases in Gdansk from 1991 to 1994. The group of 17 patients with antibiotic-associated colitis (AAC) was analysed. The antibiotics responsible for AAC were lincosamides, cephalosporins and penicillins. AAC was diagnosed by anamnesis, medical examination and detection of toxin A Clostridium difficile in stool samples. The contrast enema, colonoscopy and histopathological examination of colon mucosa were performed only in severe, protracted cases. The course of disease was mild in 2 cases, moderate in 13 and severe in 2 patients. Relapses of AAC were observed in 2 cases. Initial treatment of AAC included discontinuation of the antibiotic therapy that precipitated the disease and the replacement of fluid and electrolyte losses. Moreover, oral metronidazole and oral vancomycin were administered. All patients made a complete recovery.