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Biomedical subjects

Birger Pålsson

Publications and source records attributed to Birger Pålsson.

7 recordsLinked to original sources
PubMed2005

Partial splenic embolization as pretreatment for antiviral therapy in hepatitis C virus infection.

Chronic hepatitis C virus infection is frequently complicated by cirrhosis and hypersplenism, which together with several other factors, such as reduced thrombopoietin synthesis in the liver, cause cytopenia. The antiviral combination therapy with pegylated interferon and ribavirin itself is impaired by haematological toxicity. Partial splenic embolization (PSE) by the injection of microspheres via a catheter comprising approximately 30-70% of the splenic parenchyma is now a safe method, which significantly reduces the cytopenia induced by hypersplenism, especially thrombocytopenia. The effect is long lasting up to 20 years and has been documented in a variety of disorders. PSE is now carefully described in a combination modality as a pretreatment to reduce cytopenia in hepatitis C virus-induced cirrhosis patients with hypersplenism, making antiviral therapy possible per se at higher dosages with a sustained duration.

Antiviral Agents↗
PubMed2003

Partial splenic embolization: long-term outcome.

BACKGROUND: Partial splenic embolization (PSE) was introduced in the 1980s. We studied the long-term follow-up results of a PSE-treated patient cohort. PATIENTS AND METHODS: Twenty-six severely ill patients (median age 63.5 years) were treated with a graded PSE a total of 52 times, mainly due to bleeding esophageal varices and thrombocytopenia. The aggregated follow-up time was 1715 months. RESULTS: The mean values of hemoglobin, leukocytes and thrombocytes increased significantly after PSE. The frequency of bleeding episodes from esophageal varices was significantly reduced. No effect was observed concerning blood liver parameters in cirrhotic patients. The integrated PSE effect was judged as improvement in 19 patients, status quo in 5, and deterioration in 2. Median survival time was 50.5 months (range 0.5-272 months). Two patients underwent liver transplantation. Complications consisted mainly of fever, atelectasis, and abdominal pain. Two patients died of PSE-related complications. CONCLUSIONS: A standardized and graded PSE is reasonably safe even in patients with advanced disease in whom it is hazardous to splenectomize. It gives a long-term effect on the hematological parameters, bleedings from esophageal varices and good palliation, and improved clinical status contributing to symptomatic control.

Adult↗
PubMed2003

Follow-up after colorectal cancer surgery.

Although most institutions offer some kind of follow-up to patients operated on for colorectal cancer, its value with respect to prolonged survival has been challenged. However, improved results of liver surgery and chemotherapy make it reasonable to assume that a follow-up programme leading to detection of more asymptomatic recurrences would result in improved survival. Liver metastases and extramural local recurrences are the most common secondary lesions and 5-year survival rates of about 30% are reported after radical resection. From these observations a survival benefit could be expected when follow-up is directed to these forms of recurrence. From six randomized studies, six comparative cohort studies and four meta-analyses it can be concluded that an intensive follow-up programme results in more recurrences being resected for cure and about a 10% higher 5-year survival rate compared with less intensive or no follow-up. However, the differences in the follow-up protocols make it difficult to conclude how a follow-up programme should be designed. Liver imaging and carcinoembryonic antigen assay should probably be included, while the yield of frequent colonoscopies is small. A follow-up regimen based on these principles is suggested. Future studies should focus on which tests are the most cost-effective for follow-up after colorectal cancer resection.

Colorectal Neoplasms↗
PubMed2002

Cytogenetic abnormalities in a hemangiopericytoma of the spleen.

To date, only 16 cytogenetically abnormal hemangiopericytomas (HP) have been reported. Despite this low number, some characteristic karyotypic features have already emerged: most HP are near-diploid and breakpoints in 12q13, 12q24, and 19q13 seem to be common, with t(12;19)(q13;q13) being a recurrent translocation. Here, we report the first case of a probably benign splenic HP with chromosomal abnormalities. The abnormal karyotype was 47,XX,t(5;22;11)(q31;q11;q13),+10. None of these abnormalities have previously been reported in HP, suggesting that the karyotypic pattern of splenic HP may differ from soft tissue HP.

Chromosome Aberrations↗
PubMed2002

Cytogenetic aberrations and heterogeneity of mutations in repeat-containing genes in a colon carcinoma from a patient with hereditary nonpolyposis colorectal cancer.

The majority of tumors from patients affected by hereditary nonpolyposis colorectal cancer (HNPCC) exhibit a mutator phenotype characterized by widespread microsatellite instability (MSI) and somatic mutations in repeated sequences in several cancer-associated genes. An inverse relationship between MSI and chromosomal instability (CIN) has been demonstrated and HNPCC-associated tumors are generally characterized by diploid or near-diploid cells with few or no chromosomal rearrangements. We have studied MSI, somatic mutations in repeat-containing genes, DNA-ploidy, and cytogenetic aberrations in a colon carcinoma from a patient with a germline MLH1 mutation. Mutations in coding repeats were assessed in 10 macroscopically separate areas of the primary tumor and in two lymph nodes. Some of the genes studied (E2F4, MSH3, MSH6, TCF4, and TGFBRII) showed a consistent lack of mutations, whereas others (BAX, Caspase-5 and IGFIIR) displayed alterations in some tumor regions but not in others. The tumor had DNA-index 1.1-1.2 and a stable, aberrant karyotype with extra copies of chromosomes 7 and 12 and the structural aberrations i(1q), der(20)t(8;20), and der(22)t(1;22). The finding of CIN, MSI, and somatic mutations in coding repeats in this tumor suggests that these phenomena may act together in HNPCC tumorigenesis. Furthermore, the observed intratumoral heterogeneity of mutations in coding repeats implies these changes occur late in tumorigenesis and, thus, probably play a role in tumor progression rather than initiation.

Adaptor Proteins, Signal Transducing↗