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Armin E Heufelder and Lorenz C Hofbauer

Human immunodeficiency virus (HIV) infection and the resulting acquired immunodeficiency syndrome (AIDS) may involve, directly or indirectly, virtually every endocrine organ system, including the thyroid gland (1–3). A variety of potential pathogenetic mechanisms may account for thyroid dysfunction in HIV disease. These include alterations of thyroid tissue by hemorrhagic, infectious or neoplastic processes, changes in thyroid hormone secretion or action due to HIV infection, interference with hormone secretion and binding and effects of antibodies, cytokines or other biologically active molecules (Table 1). A further cause of thyroid dysfunction in patients with HIV disease is therapy with drugs that can disturb various endocrine systems and affect thyroid gland integrity or function, as well as hepatic metabolism of thyroid hormones (4). Interpretation of thyroid function tests and thyroid status in patients with HIV infection is complicated further by the well-recognized effects that any acute or chronic illness may have on thyroid function

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Lorenz C Hofbauer and Armin E Heufelder

Medical terminology provides many terms for diseases of yet unknown etiology, including idiopathic, essential, or cryptogenic. Fortunately, some of them at some point in time need to be renamed, when their true identity becomes better known. Idiopathic acquired hypoparathyroidism might be such an example. This disorder, characterized by decreased levels of intact parathyroid hormone, usually affects children in their first decade of life, with a female preponderance, and eventually leads to hypocalcemia and hyperphosphatemia. Clinically, individuals with acquired hypoparathyroidism may display neuromuscular signs and symptoms of persistent hypocalcemia, including episodes of tetany, calcification of the basal ganglia, increased prevalence of seizures, mental retardation, and papilledema, as well as cataract formation and dental abnormalities (1).

In search of an autoimmune etiology of acquired hypoparathyroidism (AH), investigators have rounded up several suspects during recent years. First, autoantibodies directed against parathyroid tissues have been detected in some individuals with AH (1, 2). Second,

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Lorenz C Hofbauer, Michael Rafferzeder, Onno E Janssen and Roland Gärtner

Hofbauer LC, Rafferzeder M, Janssen OE, Gartner R. Insulin-like growth factor I messenger ribonucleic acid expression in porcine thyroid follicles is regulated by thyrotropin and iodine. Eur J Endocrinol 1995;132:605–10. ISSN 0809–4643

Insulin-like growth factor I (IGF-I) has been shown to be released from thyrocytes in vitro. We investigated IGF-I mRNA expression during treatment with thyrotropin (TSH), forskolin and potassium iodide (KI) in intact porcine thyroid follicles ex vivo. Porcine thyroid follicles were prepared by collagenase digestion and cultured in the presence of TSH, forskolin or KI. After different incubation times, mRNA was isolated and examined by Northern hybridization with a porcine IGF-I cDNA probe of 405 bp in length. In untreated follicles no IGF-I mRNA was found, whereas in follicles stimulated with TSH an IGF-I mRNA of 7.0 kb was detected after 24 h, which persisted for another 24 h. Forskolin treatment mimicked the TSH effect, indicating that IGF-I mRNA expression may be stimulated by the adenylate cyclase pathway. Preincubation of the porcine follicles with KI decreased dose dependently the TSH-induced IGF-I mRNA expression, with complete inhibition at 10 μmol/l KI. These results suggest that TSH acts via the cAMP pathway to enhance IGF-I mRNA expression, which then may lead to an autocrine IGF-I stimulation. The IGF-I mRNA expression is under negative control of iodide.

Roland Gärtner, Medizinische Klinik, Ludwig Maximilians University, Ziemssenstrasse 1, 80336 München, Germany

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Lorenz C Hofbauer, Christine Hamann and Peter R Ebeling

Abstract

Secondary osteoporosis is characterized by low bone mass with microarchitectural alterations in bone leading to fragility fractures in the presence of an underlying disease or medication. Scenarios that are highly suspicious for secondary osteoporosis include fragility fractures in younger men or premenopausal women, very low bone mineral density (BMD) values, and fractures despite anti-osteoporotic therapy. An open-minded approach with a detailed history and physical examination combined with first-line laboratory tests are aimed at identifying clinical risk factors for fractures, osteoporosis-inducing drugs, and underlying endocrine, gastrointestinal, hematologic, or rheumatic diseases, which then need to be confirmed by specific and/or more invasive tests. BMD should be assessed with bone densitometry at the hip and spine. Lateral X-rays of the thoracic and lumbar spine should be performed to identify or exclude prevalent vertebral fractures which may be clinically silent. Management of secondary osteoporosis includes treatment of the underlying disease, modification of medications known to affect the skeleton, and specific anti-osteoporotic therapy. Calcium and vitamin D supplementation should be initiated with doses that result in normocalcemia and serum 25-hydroxyvitamin D concentrations of at least 30 ng/ml. Oral and i.v. bisphosphonates are effective and safe drugs for most forms of secondary osteoporosis. Severe osteoporosis may require the use of teriparatide.

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Elena Tsourdi, Tilman D Rachner, Martina Rauner, Christine Hamann and Lorenz C Hofbauer

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Elena Tsourdi, Tilman D Rachner, Martina Rauner, Christine Hamann and Lorenz C Hofbauer

Signalling of receptor activator of nuclear factor-κB (RANK) ligand (RANKL) through RANK is a critical pathway to regulate the differentiation and activity of osteoclasts and, hence, a master regulator of bone resorption. Increased RANKL activity has been demonstrated in diseases characterised by excessive bone loss such as osteoporosis, rheumatoid arthritis and osteolytic bone metastases. The development and approval of denosumab, a fully MAB against RANKL, has heralded a new era in the treatment of bone diseases by providing a potent, targeted and reversible inhibitor of bone resorption. This article summarises the molecular and cellular biology of the RANKL/RANK system and critically reviews preclinical and clinical studies that have established denosumab as a promising novel therapy for metabolic and malignant bone diseases. We will discuss the potential indications for denosumab along with a critical review of safety and analyse its potential within the concert of established therapies.