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Query: UMLS:C0039483 (giant cell arteritis)
 3,204 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 67 patients with giant cell arteritis (GCA) and 133 control patients, the value of eight clinical parameters and five laboratory findings for the diagnosis of GCA was analyzed. Out of the clinical parameters characteristic for GCA, headaches, visual disturbance, pains of the shoulder or hip regions and fever were of diagnostic value. Of the laboratory findings, only the BSR was of diagnostic value. Inappetence, exhaustion and fatigue, although characteristic of GCA, as well as blood count, alpha-globulins, CRP and alkaline serum phosphatase were of no value in differentiating between GCA and other diseases. Each of the valuable parameters increased the probability of diagnosing GCA from 33% (incidence of GCA in our patients) up to between 48% and 52%. The simultaneous evaluation of several parameters elevated the probability of diagnosing GCA to up to 88%. These results provide a basis for a rational decision in favor of or against biopsy of the temporal artery. In the case of a negative histology, they help to decide in favor of or against long term corticoid therapy.
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PMID:[The value of anamnesis, clinical findings and laboratory parameters in the diagnosis of giant cell arteritis]. 323 46

Varicella-zoster virus (VZV) is the causative agent of chicken pox (varicella) and shingles (zoster). Although considered benign diseases, both varicella and zoster can cause complications. Zoster is painful and can lead to post herpetic neuralgia. VZV has also been linked to stroke, related to giant cell arteritis in some cases. Vaccines are available but the attenuated vaccine is not recommended in immunocompromised individuals and the efficacy of the glycoprotein E (gE) based subunit vaccine has not been evaluated for the prevention of varicella. A hallmark of VZV pathology is the formation of multinucleated cells termed polykaryocytes in skin lesions. This cell-cell fusion (abbreviated as cell fusion) is mediated by the VZV glycoproteins gB, gH and gL, which constitute the fusion complex of VZV, also needed for virion entry. Expression of gB, gH and gL during VZV infection and trafficking to the cell surface enables cell fusion. Recent evidence supports the concept that cellular processes are required for regulating cell fusion induced by gB/gH-gL. Mutations within the carboxyl domains of either gB or gH have profound effects on fusion regulation and dramatically restrict the ability of VZV to replicate in human skin. This loss of regulation modifies the transcriptome of VZV infected cells. Furthermore, cellular proteins have significant effects on the regulation of gB/gH-gL-mediated cell fusion and the replication of VZV, exemplified by the cellular phosphatase, calcineurin. This review provides the current state-of-the-art knowledge about the molecular controls of cell fusion-dependent pathogenesis caused by VZV.
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PMID:Varicella-zoster virus: molecular controls of cell fusion-dependent pathogenesis. 3325 90