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      Endocrine and metabolic disorders in HTLV-1 infected patients

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          Abstract

          Human T-cell leukemia virus type 1 (HTLV-1) infection is endemic in Japan and several countries in South America, Caribbean and Africa. Endocrine and metabolic disorders have been variably reported to be associated with human T-cell leukemia virus type 1 (HTLV-1) infection. Therefore, the aim of this article was to critically evaluate the current knowledge of the endocrine and metabolic disorders associated with HTLV-1 infection. The literature search used PubMed, Web of Science, and LILACS databases in the past 10 years, utilizing, in various combinations, the following keywords: HTLV-1, adult T-cell leukemia, diabetes mellitus, GLUT-1, osteoporosis, hypercalcemia, autoimmune thyroid disorders, diabetes insipidus, inappropriate antidiuretic hormone secretion; pseudohypoparathyroidism; pseudopseudohypoparathyroidism. The proven endocrine manifestations of the HTLV-1 infection are calcium disorders which occur in some patients with acute HTLV-1/Adult T-cell leukemia/lymphoma. The few reports about thyroid, parathyroid, antidiuretic hormone and diabetes mellitus are insufficient to prove a causal association with HTLV-1 infection. The evidence for an association between endocrine disorders and HTLV-1 infection in general, and in asymptomatic patients is lacking. Given all these uncertainties, the endocrine expression of the HTLV-1 infection composes a promising research line for understanding the pathophysiology of this infection

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          Most cited references125

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          Osteoprotegerin: a novel secreted protein involved in the regulation of bone density.

          A novel secreted glycoprotein that regulates bone resorption has been identified. The protein, termed Osteoprotegerin (OPG), is a novel member of the TNF receptor superfamily. In vivo, hepatic expression of OPG in transgenic mice results in a profound yet nonlethal osteopetrosis, coincident with a decrease in later stages of osteoclast differentiation. These same effects are observed upon administration of recombinant OPG into normal mice. In vitro, osteoclast differentiation from precursor cells is blocked in a dose-dependent manner by recombinant OPG. Furthermore, OPG blocks ovariectomy-associated bone loss in rats. These data show that OPG can act as a soluble factor in the regulation of bone mass and imply a utility for OPG in the treatment of osteoporosis associated with increased osteoclast activity.
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            osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification.

            Osteoprotegerin (OPG) is a secreted protein that inhibits osteoclast formation. In this study the physiological role of OPG is investigated by generating OPG-deficient mice. Adolescent and adult OPG-/- mice exhibit a decrease in total bone density characterized by severe trabecular and cortical bone porosity, marked thinning of the parietal bones of the skull, and a high incidence of fractures. These findings demonstrate that OPG is a critical regulator of postnatal bone mass. Unexpectedly, OPG-deficient mice also exhibit medial calcification of the aorta and renal arteries, suggesting that regulation of OPG, its signaling pathway, or its ligand(s) may play a role in the long observed association between osteoporosis and vascular calcification.
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              Impaired endochondral ossification and angiogenesis in mice deficient in membrane-type matrix metalloproteinase I.

              Membrane-type matrix metalloproteinase I (MT1-MMP)-deficient mice were found to have severe defects in skeletal development and angiogenesis. The craniofacial, axial, and appendicular skeletons were severely affected, leading to a short and domed skull, marked deceleration of postnatal growth, and death by 3 wk of age. Shortening of bones is a consequence of decreased chondrocyte proliferation in the proliferative zone of the growth plates. Defective vascular invasion of cartilage leads to enlargement of hypertrophic zones of growth plates and delayed formation of secondary ossification centers in long bones. In an in vivo corneal angiogenesis assay, null mice did not have angiogenic response to implanted FGF-2, suggesting that the defect in angiogenesis is not restricted to cartilage alone. In tissues from null mice, activation of latent matrix metalloproteinase 2 was deficient, suggesting that MT1-MMP is essential for its activation in vivo.
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                Author and article information

                Journal
                bjid
                Brazilian Journal of Infectious Diseases
                Braz J Infect Dis
                Brazilian Society of Infectious Diseases (Salvador, BA, Brazil )
                1413-8670
                1678-4391
                December 2010
                : 14
                : 6
                : 613-620
                Affiliations
                [01] orgnameUniversidade Federal da Bahia orgdiv1Faculty of Medicine orgdiv2Hospital Universitário Prof. Edgard Santos
                [02] orgnameUniversidade Federal da Bahia orgdiv1Faculty of Medicine orgdiv2Hospital Universitário Professor Edgard Santos
                Article
                S1413-86702010000600011 S1413-8670(10)01400611
                10.1590/S1413-86702010000600011
                56709818-8c25-4111-8355-5e9ac1118bd1

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

                History
                : 10 March 2010
                : 28 April 2010
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 75, Pages: 8
                Product

                SciELO Brazil

                Self URI: Full text available only in PDF format (EN)
                Categories
                Review Article

                HTLV-1,adult T-cell leukemia,metabolic disorders,endocrine disorders

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