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Elevated Serum (elevated + serum)
Terms modified by Elevated Serum Selected AbstractsElevated serum and cerebrospinal fluid levels of soluble human herpesvirus type 6 cellular receptor, membrane cofactor protein, in patients with multiple sclerosisANNALS OF NEUROLOGY, Issue 4 2001Samantha S. Soldan MS Membrane cofactor protein (CD46) is a member of a family of glycoproteins that are regulators of complement and prevent activation of complement on autologous cells. Recently, CD46 has been identified as the cellular receptor for human herpesvirus Type 6 (HHV-6). Elevated levels of soluble CD46 have been described in several autoimmune disorders and may be implicated in the pathogenesis of these diseases. As several reports have supported an association of HHV-6 and multiple sclerosis, it was of interest to compare levels of soluble CD46 in the sera of MS patients to that of healthy controls, other neurological disease controls, and other inflammatory disease controls. Using an immunoaffinity column comprised of immobilized monoclonal antibodies to CD46, serum levels of soluble CD46 were found to be significantly elevated in multiple sclerosis patients compared with healthy and other neurological disease controls. Moreover, multiple sclerosis patients who tested positive for HHV-6 DNA in serum had significantly elevated levels of soluble CD46 in their serum compared with those who were negative for HHV-6 DNA. A significant increase in soluble CD46 was also found in the serum of other inflammatory disease controls tested compared with healthy controls. Additionally, a significant correlation was demonstrated between levels of soluble CD46 in the serum and cerebrospinal fluid of multiple sclerosis patients. Collectively, these data suggest that elevated levels of soluble CD46 may contribute to the pathogenesis of inflammatory diseases, including MS. [source] Elevated serum heparanase-1 levels in patients with pancreatic carcinoma are associated with poor survivalCANCER, Issue 3 2006Roderick M. Quiros M.D. Abstract BACKGROUND It has previously been shown that heparanase-1 (HPR1), an endoglycosidase, is up-regulated in pancreatic carcinoma. The purpose of this study was to test whether serum HPR1 levels in pancreatic carcinoma patients are elevated, and whether higher serum HPR1 levels are associated with a shortened survival. METHODS Serum HPR1 levels in 40 healthy donors, 31 pancreatic carcinoma patients, and 11 patients treated with gemcitabine were measured by a novel enzyme-linked immunoadsorbent assay. HPR1 expression in tumors was analyzed by immunohistochemical staining. Patient overall survival time was determined according to the Kaplan,Meier method, and their difference was evaluated by the log-rank test. A P value < 0.05 was considered statistically significant. RESULTS The mean serum HPR1 activity in pancreatic carcinoma patients was 439 ± 14 units/mL, compared with 190 ± 4 units/mL in the control serum samples from healthy donors. Serum HPR1 levels were significantly higher in patients with HPR1-positive tumors (660 ± 62 units/mL) compared with those with HPR1-negative tumors (241 ± 14 units/mL). The mean survival of 19 pancreatic carcinoma patients with serum HPR1 activity > 300 units/mL was 7.9 ± 0.2 months, whereas the mean survival of 12 patients with serum HPR1 activity < 300 units/mL was 13.3 ± 0.6 months. A Kaplan,Meier plot of the patient survival curve followed by log-rank test revealed that patients in the high serum HPR1 group had a significantly shorter survival compared with those in the low serum HPR1 group. Mean serum HPR1 activity decreased by 64% in 11 pancreatic carcinoma patients after 2 weeks of treatment with gemcitabine. CONCLUSIONS Serum HPR1 activity in pancreatic carcinoma patients was found to be significantly elevated, in particular in those with HPR1-positive tumors. Increased serum HPR1 activity was associated with a shorter survival in patients with pancreatic carcinoma patients. Cancer 2006. © 2005 American Cancer Society. [source] Central nervous system dissemination in immunocompetent patients with aggressive lymphomas: incidence, risk factors and therapeutic optionsHEMATOLOGICAL ONCOLOGY, Issue 2 2009Andrés J. M. Ferreri Abstract Central nervous system (CNS) dissemination is a rare (4,5%) but usually fatal complication of aggressive lymphomas. Prophylaxis modalities to prevent CNS dissemination in aggressive lymphomas cannot be widely applied to every lymphoma patient since it is associated with increased risk of neurotoxicity. Therefore, identification of high-risk patients as the best candidates to receive CNS prophylaxis constitutes a major endpoint in the management of these malignancies. Various risk factors and models for CNS recurrence have been described. Parameters reflecting the extent and proliferation of the disease, like elevated serum lactate dehydrogenase levels, involvement of multiple extranodal sites, advanced stage and high age-adjusted International Prognostic Index (IPI) score, as well as the involvement of specific anatomic sites, like testes, orbit, paranasal sinuses, have been identified and confirmed as important to predict CNS dissemination. Management of this complication in aggressive lymphomas with conventional-dose chemotherapy is associated with disappointing results, while some preliminary but encouraging experiences suggest a potential role of high-dose chemotherapy and stem cell transplantation. The analysis of recent clinical studies could lead to advancement in the prognosis of aggressive lymphomas, but several questions regarding the optimum chemotherapy combination, the best conditioning regimen and the role of radiation therapy and intrathecal chemotherapy remain still unanswered. The purposes of the present review are to critically analyse current data on the risk of CNS dissemination in aggressive lymphomas, the clinical presentation of secondary CNS lymphomas and the efficacy of CNS prophylaxis as well as to discuss the available therapeutic options for this devastating event. Copyright © 2009 John Wiley & Sons, Ltd. [source] Dissociation between liver inflammation and hepatocellular damage induced by carbon tetrachloride in myeloid cell,specific signal transducer and activator of transcription 3 gene knockout mice,HEPATOLOGY, Issue 5 2010Norio Horiguchi Liver injury is associated with inflammation, which is generally believed to accelerate the progression of liver diseases; however, clinical data show that inflammation does not always correlate with hepatocelluar damage in some patients. Investigating the cellular mechanisms underlying these events using an experimental animal model, we show that inflammation may attenuate liver necrosis induced by carbon tetrachloride (CCl4) in myeloid-specific signal transducer and activator of transcription 3 (STAT3) knockout mice. As an important anti-inflammatory signal, conditional deletion of STAT3 in myeloid cells results in markedly enhanced liver inflammation after CCl4 injection. However, these effects are also accompanied by reduced liver necrosis, correlating with elevated serum interleukin-6 (IL-6) and hepatic STAT3 activation. An additional deletion of STAT3 in hepatocytes in myeloid-specific STAT3 knockout mice restored hepatic necrosis but decreased liver inflammation. Conclusion: Inflammation-mediated STAT3 activation attenuates hepatocellular injury induced by CCl4 in myeloid-specific STAT3 knockout mice, suggesting that inflammation associated with a predominance of hepatoprotective cytokines that activate hepatic STAT3 may reduce rather than accelerate hepatocellular damage in patients with chronic liver diseases. Hepatology 2010 [source] Complete remission with intraperitoneal cisplatin followed by prolonged oral etoposide in a stage IIIc primary leiomyosarcoma of the fallopian tube patientJOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 4 2010Yoichi Kobayashi Abstract Leiomyosarcoma (LMS) of the fallopian tube is exceedingly uncommon. So far as we investigated, only eighteen cases of LMS of the fallopian tube have been reported. Here we report a nineteenth case which was International Federation of Gynecology and Obstetrics stage IIIc LMS of the fallopian tube successfully treated with intraperitoneal cisplatin followed by prolonged oral etoposide. A 70-year-old female was introduced to our institute due to intrapelvic tumor and ascites. Because of elevated serum lactate dehydrogenase and CA125 as well as the findings of pelvic magnetic resonance imaging and computerized tomography, the patient was suspected to have ovarian cancer. In laparotomy, the large pelvic tumor was seemed to originate from the right fallopian tube. Pathologically, the patient was diagnosed as stage IIIc fallopian tube LMS. At the end of the operation, cisplatin was given intraperitoneally followed by prolonged oral etoposide. Although a lot of dissemination was noted throughout the peritoneal cavity, the patient is alive without any evidence of recurrence for more than 6 years since the initial operation. In this uncommon entity, a cisplatin- and etoposide-based regimen could be considered. [source] Postrenal Transplant Hemophagocytic Lymphohistiocytosis and Thrombotic Microangiopathy Associated with Parvovirus B19 InfectionAMERICAN JOURNAL OF TRANSPLANTATION, Issue 6 2008M. R. Ardalan Persistent anemia is a known consequence of Parvovirus B19 (B19) infection following renal transplantation. However, to date, no description of B19-related hemophagocytic lymphohistiocytosis (HLH) exists in renal transplant recipients. We report a 24-year-old male kidney recipient, who presented with fever, severe anemia and allograft dysfunction two years following transplantation. Hyperferritinemia, hypertriglyceridemia, elevated serum lactate dehydrogenase, pancytopenia and fragmented red blood cells on the peripheral blood were also noted. Bone marrow examination revealed giant pronormoblasts and frequent histiocytes with intracellular hematopoietic elements, consistent with HLH. Renal allograft biopsy revealed closure of the lumen of glomerular capillaries and thickening of the capillary walls compatible with thrombotic microangiopathy. The presence of anti-B19 IgM antibody and viral DNA in the patient's serum (detected by real-time PCR) confirmed an acute B19 infection. Following high-dose intravenous immunoglobulin therapy, the anemia gradually resolved and renal function improved. As far as we know, this is the first report of B19-associated HLH and thrombotic microangiopathy in a renal transplant recipient. [source] Lung disease in ataxia-telangiectasiaACTA PAEDIATRICA, Issue 7 2007L Bott Abstract Ataxia-telangiectasia (AT) is a multi-systemic disease caused by mutational inactivation of the ATM gene. We report a retrospective study of lung disease in 15 patients. Patients and methods: A diagnosis of AT was made if the patient met the following criteria: neurological features and at least one the following: oculo-cutaneous telangiectasia, elevated serum ,-feto-protein level. Results: Recurrent sino-pulmonary infections were usually present in 11 of the cases and occurred during the first 2 years of life. Other lung injuries noted were bronchiectasis, obstruction and restriction of the airways, fibrosis, pneumothorax and haemoptysis. Eleven children had immunodeficiencies. Discussion: Recurrent sino-pulmonary manifestations precede neurological complications, but the severity of neuro-degeneration and pulmonary disease were not correlated. Pulmonary status was a prognosis factor. Immunodeficiency was the main, but not the only, aetiology for lung disease in AT. Conclusion: There is little dispute over the role of ATM in lung and respiratory epithelium. To reduce the morbidity associated with AT, there needs to be greater awareness of respiratory complications. Early management and monitoring lung function is necessary to minimize lung damage. [source] Clinical outcomes of persistent radioiodine uptake in the neck shown by diagnostic whole body scan in patients with differentiated thyroid carcinoma after initial surgery and remnant ablationCLINICAL ENDOCRINOLOGY, Issue 2 2010Eui Young Kim Summary Objectives, To evaluate the clinical outcomes of persistent radioiodine uptake (RAIU) in the neck by diagnostic whole body scan (DxWBS) after initial therapy and the efficacy of the second ablation in patients with differentiated thyroid carcinoma (DTC). Design, Patients with DTC who underwent bilateral surgery and high-dose remnant ablation between 2000 and 2004 were included. Patients with elevated serum stimulated thyroglobulin (sTg) or extensive lateral neck lymph node involvement at initial surgery underwent a second ablation, and patients with undetectable sTg or in very low-risk groups were observed. Results, Among 572 patients, 25 had persistent RAIU in the neck at first DxWBS. After a median 65·7 months of follow-up, five of these patients (20%) had persistent disease, whereas another 20 patients had no abnormal findings by ultrasonography (US) or other imaging modalities. Seven of 20 patients underwent second ablation and 13 were observed. RAIU disappeared spontaneously in about half of the patients in the observation group. There were no significant between-group differences in change of RAIU at follow-up DxWBS (P = 0·62). Serum sTg decreased and eventually disappeared over a few years in both groups. Ablation failure was not an independent risk factor for recurrence (P = 0·169). Conclusions, Neck US and serum sTg, but not DxWBS, were useful diagnostic tools during follow-up of patients with persistent uptake in the neck at DxWBS. A second ablation was not necessary when neck US showed no evidence of disease, especially in patients with very low sTg concentration. [source] | ||||||||||