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Curr Gastroenterol Rep. 2001 Feb;3(1):49-53.
Should patients with chronic hepatitis C who have normal ALT levels be treated?

Russo MW, Brown RS Jr.

Center for Liver Disease and Transplantation, Columbia University College of Physicians and Surgeons, Weill-Cornell School of Medicine, New York-Presbyterian Hospital, 622 West 168th Street, PH14, New York, NY 10032, USA.

Up to 25% of patients with chronic hepatitis C have persistently normal serum alanine aminotransferase (ALT) levels. Reports from some studies indicate that patients with normal ALT levels are more likely to be female and nondrinkers. Patients with persistently normal aminotransferase levels often have mild disease on liver biopsy with little or no fibrosis, but a small number of patients may have substantial fibrosis or cirrhosis. Treatment with interferon monotherapy has been disappointing. Combination therapy with interferon and ribavirin is controversial, but early clinical results have shown good response rates. Currently, therapy for chronic HCV patients with normal ALT levels should be based upon results from liver biopsy and preferably be done in the context of a clinical trial.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11177694&dopt=Abstract [PubMed - in process]

Curr Gastroenterol Rep. 2001 Feb;3(1):79-83.
Kidney disease in patients with chronic hepatitis C.

Philipneri M, Bastani B.

Division of Nephrology, Saint Louis University School of Medicine, 3635 Vista Avenue, St. Louis, MO 63110, USA. philipmlu.edu

There is an increasing recognition of the association between chronic hepatitis C virus infection and glomerular diseases. Renal complications may be the presenting manifestation of hepatitis C virus infection. Patients may present with signs and symptoms of cryoglobulinemic systemic vasculitis, proteinuria, microscopic hematuria, acute renal failure, or nephrotic syndrome. The pathogenesis of hepatitis C virus associated with renal disease remains incompletely understood; however, deposition of circulating immune complexes in the subendothelial space and mesangium in the glomeruli seems to play a major role. The most common renal pathology associated with hepatitis C virus infection is type I membranoproliferative glomerulonephritis with or without cryoglobulinemia. In patents who do not have significant renal impairment, combination therapy with interferon alfa (IFN-alpha) and ribavirin seems to be the treatment of choice, although the experience with this combination is quite limited in patients with renal involvement. A prolonged course of high-dose IFN-alpha has been most commonly used for these patients with significant success, but relapse of hepatitis C viremia and renal disease after discontinuation of therapy have frequently occurred.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11177699&dopt=Abstract [PubMed - in process]

Am J Respir Crit Care Med. 2001 Feb;163(2):484-9.
Antiapoptotic effects of IL-15 on pulmonary Tc1 cells of patients with human immunodeficiency virus infection.

Agostini C, Siviero M, Facco M, Carollo D, Binotto G, Tosoni A, Cattelan AM, Zambello R, Trentin L, Semenzato G.

Department of Clinical and Experimental Medicine, Padua University School of Medicine, Clinical Immunology Branch, Padua, Italy.

In the early phases of human immunodeficiency virus (HIV) disease a T-cell alveolitis sustained by cytotoxic T lymphocytes (CTL) with anti-HIV activity occurs in the lung. With the progression of HIV disease, pulmonary CTL become infected and their cytotoxic activity declines. To investigate the potential causes leading to this phenomenon, we evaluated T cells obtained from the bronchoalveolar lavage (BAL) of 18 HIV-infected patients with T-cell alveolitis. BAL T cells were CD45R0+/CD8+ defined as Tc1 cells because they expressed cytoplasmic interferon gamma (IFN-gamma) and were CXCR3+/IL-12Rbeta2+. Furthermore, they bore the interleukin (IL)- 15 receptor, Fas antigen, and tumor necrosis factor receptor (TNFR) type II. When cultured for 24 h highly purified BAL T cells showed an excessive spontaneous apoptosis; after activation with anti-CD3 or ionomycin, the proportion of T cells undergoing cell death increased. Interestingly, we found a direct relationship between the predisposition to undergo spontaneous apoptosis and the levels of Fas expression by BAL T cells. Alveolar macrophages (AMs) expressed high levels of IL-15 which paralleled the intensity of T-cell infiltration in most patients. The predisposition of CD8 T cells to undergo cell death was downregulated by the incubation with IL-15; the protective effect of the cytokine was dose-dependent. Nonetheless, AMs also expressed proapoptotic molecules, including membrane TNF-alpha (mTNF-alpha). Based on these observations it may be suggested that an excessive, spontaneous, and activation-induced apoptosis of pulmonary lymphocytes may be observed in HIV lung and that AMs are major regulators of T-cell homeostasis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11179127&dopt=Abstract

Am J Respir Crit Care Med. 2001 Feb;163(2):532-9.
Induction and regulation of nitric oxide synthase in airway epithelial cells by respiratory syncytial virus.

Kao YJ, Piedra PA, Larsen GL, Colasurdo GN.

Department of Pediatrics, University of Texas-Houston Medical School, Houston 77030, USA.

In this study, we evaluated the effects of respiratory syncytial virus (RSV) infection on nitric oxide (NO) production in human airway epithelial cells. In addition, we evaluated whether T-helper type 1 (Th1)- and Th2-type cytokines modulate the release of NO in response to RSV infection. To do this, we infected monolayers of A549 cells with RSV and determined nitrite levels in the supernatant fluids. We also measured nitrite levels in human small-airway epithelial cells (SAEC) in primary culture and in the bronchoalveolar lavage fluid (BALF) obtained from Balb/c mice after RSV infection. To further support our observations in these analyses, we performed immunocytochemistry and Western blot analysis for inducible nitric oxide synthase (iNOS) in A549 cells. To evaluate the regulation of NO production in response to RSV, we performed experiments in the absence and presence of the Th1 and Th2 type cytokines: interferon (IFN)-gamma, interleukin (IL)-4, and IL-13. In addition, we assessed the inhibitory effect of dexamethasone on iNOS in RSV infected A549 cells. Results were expressed in terms of nmol/mg protein and shown as percents of control values (mean +/- SE). RSV increased the release of nitrites in A549 cells, SAEC, and BALF. The increase in nitrite levels was supported by immunocytochemistry and Western blot analysis for iNOS protein in A549 cells, indicating activation of iNOS in response to RSV infection. IFN-gamma and IL-13 did not affect the RSV-induced increase in NO production. By contrast, IL-4 and dexamethasone suppressed the release of NO in response to RSV infection. These observations show that RSV infection leads to activation of iNOS within the airway epithelium and that IL-4 and dexamethasone inhibit the production of NO in response to RSV infection.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11179135&dopt=Abstract

Infect Immun. 2001 Mar;69(3):1256-64.
Role of T cells and gamma interferon during induction of hypersensitivity to lipopolysaccharide by toxic shock syndrome toxin 1 in mice.

Dinges MM, Schlievert PM.

Department of Microbiology, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA.

The superantigenic function of toxic shock syndrome toxin 1 (TSST-1) is generally regarded as an important determinant of its lethal effects in humans or experimental animals. This study examined the role of superantigenicity in a BALB/c mouse model of lethal TSST-1-induced hypersensitivity to lipopolysaccharide (LPS). In this model, TSST-1 greatly potentiated both LPS-induced lethality, as well as LPS-induced serum tumor necrosis factor alpha (TNF-alpha) activity. Although BALB/c-SCID mice were resistant to these LPS enhancement effects of TSST-1, BALB/c-SCID mice reconstituted with T cells were completely susceptible to the enhancement effect of TSST-1 on LPS-induced serum TNF-alpha. Mice pretreated with cyclosporine (Cs) or neutralizing antibodies against gamma interferon (IFN-gamma) did not develop lethal LPS hypersensitivity when injected with TSST-1, and these agents reduced the enhancement effect of TSST-1 on LPS-induced serum TNF-alpha by 99 and 85%, respectively. Cs pretreatment also completely inhibited the known capacity of TSST-1 to amplify LPS-induced levels of IFN-gamma in serum. In contrast, mice given Cs after a priming injection of TSST-1, but before LPS, still exhibited lethal hypersensitivity to LPS. Cs given after TSST-1 also did not inhibit enhancement of LPS-induced serum TNF-alpha by TSST-1 but inhibited the enhancement effect of TSST-1 on LPS-induced serum IFN-gamma by 50%. These experiments support the theory that TSST-1-induced hypersensitivity to LPS is mediated primarily by IFN-gamma derived from superantigen-activated T cells.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11179286&dopt=Abstract

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