Biomedical subjects

Solko W Schalm

Publications and source records attributed to Solko W Schalm.

39 records · Page 3Linked to original sources

PubMedDate not supplied

Pegylated interferon alfa-2b alone or in combination with lamivudine for HBeAg-positive chronic hepatitis B: a randomised trial.

BACKGROUND: Treatment of HBeAg-positive patients with chronic hepatitis B is not effective in most. A combination of immunomodulatory pegylated interferon alfa-2b and antiviral lamivudine might improve the rate of sustained response. METHODS: 307 HBeAg-positive patients with chronic hepatitis B were assigned combination therapy (100 microg/week pegylated interferon alfa-2b and 100 mg/day lamivudine) or monotherapy (100 microg/week pegylated interferon alfa-2b and placebo) for 52 weeks. During weeks 32-52 the pegylated interferon dose was 50 microg/week in both treatment groups. The analyses were based on the modified intention-to-treat population after exclusion of 24 patients from one centre withdrawn for misconduct, ten who lost HBeAg before the study start, and seven who received no study medication. All included patients were followed up for 26 weeks after treatment. FINDINGS: 49 (36%) of 136 patients assigned monotherapy and 46 (35%) of 130 assigned combination therapy had lost HBeAg at the end of follow-up (p=0.91). More of the combination-therapy than of the monotherapy group had cleared HBeAg at the end of treatment (57 [44%] vs 40 [29%]; p=0.01) but relapsed during follow-up. Patterns were similar when response was assessed by suppression of serum hepatitis B virus (HBV) DNA or change in concentrations of alanine aminotransferase. Response rates (HBeAg loss) varied by HBV genotype (p=0.01): A, 42 (47%) patients; B, ten (44%); C, 11 (28%); and D, 26 (25%). INTERPRETATION: Treatment with pegylated interferon alfa-2b is effective for HBeAg-positive chronic hepatitis B. Combination with lamivudine in the regimen used is not superior to monotherapy. HBV genotype is an important predictor of response to treatment.

Adult↗

PubMedDate not supplied

Benign versus malignant hepatic nodules: MR imaging findings with pathologic correlation.

According to the currently used nomenclature, there are only two types of hepatocellular nodular lesions: regenerative lesions and dysplastic or neoplastic lesions. Regenerative nodules include monoacinar regenerative nodules, multiacinar regenerative nodules, cirrhotic nodules, segmental or lobar hyperplasia, and focal nodular hyperplasia. Dysplastic or neoplastic nodules include hepatocellular adenoma, dysplastic foci, dysplastic nodules, and hepatocellular carcinoma (HCC). Many of these types of hepatic nodules play a role in the de novo and stepwise carcinogenesis of HCC, which comprises the following steps: regenerative nodule, low-grade dysplastic nodule, high-grade dysplastic nodule, small HCC, and large HCC. State-of-the-art magnetic resonance (MR) imaging facilitates detection and characterization in most cases of hepatic nodules. State-of-the-art MR imaging includes single-shot fast spin-echo imaging, in-phase and opposed-phase T1-weighted gradient-echo imaging, T2-weighted fast spin-echo imaging with fat saturation, and two-dimensional or three-dimensional dynamic multiphase contrast material-enhanced imaging.

Carcinoma, Hepatocellular↗

PubMedDate not supplied

Pseudo-Budd-Chiari Syndrome: decompensated alcoholic liver disease mimicking hepatic venous outflow obstruction.

Three patients with rapid onset decompensated liver disease who were referred to our hospital with presumed Budd-Chiari syndrome are described. This diagnosis was based on marked hepatomegaly, caudate lobe hypertrophy and failure to visualize hepatic veins by Doppler-ultrasound examination. Detailed history, biochemistry, and histology were, however, highly suggestive of alcoholic liver cirrhosis with steatohepatitis-induced hepatomegaly. On angiographic examination narrowed but patent hepatic veins were demonstrated in 2 patients. A third patient died before further work-up could be performed; autopsy showed patent hepatic veins. These cases show that the radiological diagnosis of Budd-Chiari syndrome due to hepatic vein obstruction can be false positive and that suspected hepatic vein occlusion on Doppler-ultrasound should be confirmed by angiographic studies and on liver histology.

Budd-Chiari Syndrome↗