Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Common thyroid and parathyroid disorders present with reversible neurologic signs and symptoms affecting the central and peripheral nervous system, musculature, and mental function. Patients with thyrotoxicosis may have myopathy, spasticity, seizures, and multiple psychiatric symptoms. A deficiency of thyroid hormone also causes muscle weakness and may be accompanied by reversible muscle hypertrophy or movement disorders. The chronic hypercalcemia that develops secondary to hyperparathyroidism produces many psychiatric and cognitive symptoms, as well as a reversible myopathy. Calcium deficiency leads to neuromuscular irritability, paresthesias, and tetany. Psychiatric disorders are also common in this disorder.
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PMID:Neurologic complications of thyroid and parathyroid disease. 841 21

This article discusses several unusual forms of primary thyroid neoplasms. The TCV of PTC and insular thyroid carcinoma appears to have a more aggressive clinical behavior than DTC in most patient groups and may respond to thyroid hormone suppression and radioiodine. Anaplastic thyroid carcinoma, which may develop from differentiated thyroid tumors, has a poor prognosis which may be altered by surgery and radiation therapy but not typically by radioiodine and thyroid hormone suppression. Primary squamous cell carcinoma of the thyroid is an unusual entity that may be associated with a clinical syndrome that includes leukocytosis, fever, and hypercalcemia. Primary thyroid lymphoma is frequently associated with Hashimoto's thyroiditis and should be considered especially in older patients with rapidly enlarging thyroid masses. Although there are no studies assessing this issue, it seems reasonable that patients who have undergone thyroidectomy for neoplasms of thyroid cells that are poorly differentiated and do not concentrate radioiodine (e.g., squamous cell, anaplastic) should receive sufficient thyroid hormone suppression, if tolerated, to reduce TSH (third-generation assay) to approximately 0.1 to 0.3 mu U/mL, because TSH may be a growth factor. If, however, the tumor concentrates or responds to radioiodine, suggesting more differentiated cells (e.g., TCV, insular carcinoma), the target TSH level (third-generation assay) should range from 0.01 to 0.1 mu U/mL, as tolerated. Patients with primary thyroid neoplasms arising from cells other than thyrocytes (e.g., lymphoma) can be maintained at a TSH level of 0.5 to 1.5 mu U/mL. Our conclusions and analyses are often based upon small, retrospective, poorly controlled reports, and further studies are required to allow a better understanding of the evaluation and treatment of these neoplasms.
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PMID:Unusual types of thyroid neoplasms. 890 80

Calcium pyrophosphate dihydrate crystal arthropathy (CPPA) is a well known but heterogeneous disease with a variable presentation and course. We present a cross-sectional study undertaken in a Portuguese rheumatology unit with the aim of analysing clinical and radiological patterns of CPPA in our population. The study population included 50 patients, 34 (68%) women and 16 (32%) men. The mean age was 69.8 +/- 8.8 years. The onset features were acute arthritis in 19 (38%) patients and chronic joint complaints in 26 (52%); five (10%) patients were asymptomatic at the time of diagnosis, which was based only on radiological findings. The diagnosis was established in 37 (74%) cases by clinical and radiographic features, in eight (16%) by clinical, X-ray and synovial fluid analysis, and in five (10%) by clinical features and fluid analysis. The disease course was characterised by acute episodic arthritis in 16 (32%) patients and by persistent symptoms (with or without synovitis) in 34 (68%). The pattern of CPPA in 20 (40%) patients was pseudo-osteoarthritis with synovitis, pseudo-osteoarthritis without synovitis in nine (18%), pseudogout in nine (18%), monoarthropathy in eight (16%) and pseudorheumatoid arthritis in four (8%). The phosphocalcium balance was altered in nine (18%) cases: six patients had hypercalciuria two hyperphosphaturia, two hypocalciuria, one hypophosphaturia and one hypercalcemia. Five patients had abnormal thyroid hormone levels, but only one presented with clinical hypothyroidism. Four patients showed increased parathormone levels, but only one presented with clinical hyperparathyroidism. Radiographic findings showed that 43 (86%) patients had meniscus calcifications, 20 (40%) radiocarpal and 16 (32%) calcification of the symphysis pubis. The study confirms the clinical variability of the disease in a population of Portuguese patients. The knee meniscus calcifications were the most sensitive single finding for establishing the diagnosis of CPPA. Almost all our patients had sporadic idiopathic CPPA without associated pathological conditions.
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PMID:Cross-sectional study of 50 patients with calcium pyrophosphate dihydrate crystal arthropathy. 1134 23

Concurrent Graves' disease and primary hyperparathyroidism in the same patient is rare, probably accounts for hypercalcemia in no more than 1 percent of thyrotoxic patients. Hypercalcemia may be noted during the course of hyperthyroidism in as many as 22 percent of cases. The cause of hypercalcemia in a thyrotoxic patient might be due to the activation of osteoclastic bone resorption by the excess thyroid hormone, as the severity of hyperthyroidism correlates positively with osteoclastic activity in trabecular and cortical bone. In 1936, Noble JF et al reported the first case in the world. To our knowledge, only 49 such cases have been described in the literature until the year of 1989. No case has been reported again afterward. The occurrence of hypercalcemia in a patient with hyperthyroidism may present a challenging diagnostic problem. In this communication, we described the first case in mainland of China with hypercalcemia caused by concurrent hyperthyroidism and primary hyperparathyroidism, and the clinical and laboratory characteristics were studied before and after therapy with anti-thyroid medication.
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PMID:Concomitant Graves' disease and primary hyperparathyroidism: the first case report in mainland of China and literature review. 1213 11

1alpha, 25-dihydroxyvitamin D3 [1,25 (OH)(2)D(3)], the active metabolite of vitamin D3, is known for the maintenance of normal skeleton architecture and mineral homeostasis. Apart form these traditional calcemic actions, 1,25 (OH)(3)D(1) and its synthetic analogs are increasingly recognized for their potent anti-proliferative, prodifferentiative and immunomodulatory activities. The calcemic and non-calcemic actions of 1,25 (OH)(2)D(3) and its synthetic analogs are mediated through vitamin D receptor (VDR), which belongs to the superfamily of steroid/thyroid hormone nuclear receptors. Physiological and pharmacological actions of 1,25 (OH)(2)D(3) in various systems, along with the detection of VDR in target cells, have indicated potential applications of VDR ligands in inflammation, dermatological indications, osteoporosis, cancers and autoimmune diseases. VDR ligands have shown therapeutic potential in limited clinical trials as well as in animal models of these diseases. As a result, a VDR ligand, calcipotriol is in clinic for psoriasis and another, OCT, [2-oxa-1,25 (OH)(2)D(3)] is being developed as a topical agent for the same indication. Further, 1alpha,-hydroxyvitamin D3 (alphacalcidol), a prodrug of 1,25 (OH)(2)D(3) is in clinic and a synthetic VDR ligand, ED-71, is under consideration for approval in Japan for the treatment of osteoporosis. Interestingly, VDR ligands have shown not only preventive but also potent therapeutic anabolic activities in animal models of osteoporosis. However, the wide spread use of VDR ligands in above-mentioned indications is hampered by their major side effect, namely hypercalcemia. In view of this associated toxicity, synthetic VDR ligands with reduced calcemic potential have been synthesized with the ultimate aim of improving their therapeutic efficacy. This review presents recent advances in VDR biology, novel VDR ligands and therapeutic applications of VDR ligands.
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PMID:Vitamin D receptor as a drug discovery target. 1257 Aug 35

Primary hyperparathyroidism (PHPT) is one of the most common endocrine disease processes, however the clinical presentation in 2003 is typically characterized by minimal signs or symptoms of hypercalcaemia or para-thyroid hormone (PTH) excess. Recent developments in imaging and management of PHPT have been published, however the area of biochemical investigation has been relatively neglected. A group of experts convened in April 2002 to consider whether changes were needed to the 1990 consensus guidelines which defined criteria for the diagnosis and management of asymptomatic PHPT. It is appropriate to review the revised recommendations, which have been disseminated by the panel and were recently published. Each of the laboratory -analytes used to establish the diagnosis of PHPT and exclude alternative diagnoses or complications will be considered in succession in this review: (i) calcium, (ii) intact PTH, (iii) urinary calcium and (iv) 25 hydroxy-vitamin D. Furthermore, critical appraisal of the new diagnostic criteria and their applicability to Australian laboratories will be addressed. Finally, limitations and problems associated with the measurement of each analyte will be reviewed.
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PMID:Diagnosis of primary hyperparathyroidism: controversies, practical issues and the need for Australian guidelines. 1554 67

A 36-yr-old woman began to suffer from headache, anorexia and general fatigue at 35 weeks' gestation. About 2 or 3 months after the delivery, fever, tachycardia and generalized musculoskeletal disorder appeared. Thereafter, they worsened rapidly, accompanied by a disturbance of consciousness and hypercalcemia. Thyrotoxicosis, due to a post-partum thyroiditis, and glucocorticoid deficiency, due to a pituitary failure, probably associated with lymphocytic hypophysitis, were also observed. All the symptoms and hypercalcemia disappeared after the glucocorticoid replacement therapy and the normalization of thyroid hormone levels. Serum and urinary bone resorption markers, such as urine pyridinoline (U-Pyr), urine deoxypyridinoline (U-DPD), urine amino-terminal telopeptide of type I collagen (U-NTx) and serum carboxy-terminal telopeptide of type I collagen (ICTP), were extremely high at the hypercalcemic state. In this case, they were 10 to 20 times higher than the normal upper limits, and then markedly decreased in a normocalcemic state, thereby showing an extreme acceleration of bone resorption in a state of both thyrotoxicosis and glucocorticoid deficiency.
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PMID:Elevated bone resorption markers in a patient with hypercalcemia associated with post-partum thyrotoxicosis and hypoadrenocorticism due to pituitary failure. 1563 35

1alpha, 25-Dihydroxyvitamin D3 [1,25-(OH)2D3], the biologically active form of vitamin D, is an important hormone that is critically required for the maintenance of mineral homeostasis and structural integrity of bones. 1,25-(OH)2D3 accomplishes this by facilitating calcium absorption from the gut and by a direct action on osteoblasts, the bone forming cells. Apart form its classical actions on the gut and bone, 1,25-(OH)2D3 and its synthetic analogs also possess potent anti-proliferative, differentiative and immunomodulatory activities. 1,25-(OH)2D3 exerts these effects through vitamin D receptor (VDR), a ligand-dependent transcription factor that belongs to the superfamily of steroid/thyroid hormone/retinoid nuclear receptors. The presence of VDR in various tissues other than gut and bone, along with their ability to exert differentiation, growth inhibitory and anti-inflammatory action, has set the stage for therapeutic exploitation of VDR ligands for the treatment of various inflammatory indications and cancer. However, the use of VDR ligands in clinic is limited by their major dose-related side effect, namely hypercalcemia/hypercalciuria. Efforts are being undertaken to develop vitamin D receptor modulators (VDRMs) that are tissue-selective and/or gene-selective in their action and these ligands may exhibit increased therapeutic indices. This review explores the recent advances in VDR biology, non-secosteroidal VDR ligands and the current and potential clinical applications of VDR ligands in inflammation and cancer.
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PMID:Vitamin D receptor modulators for inflammation and cancer. 1610 12

1alpha,25-Dihydroxyvitamin D3 (1,25-(OH)2D3), the biologically active metabolite of vitamin D, mediates its actions via the vitamin D receptor (VDR), a member of the superfamily of steroid/thyroid hormone/retinoid receptors. 1,25-(OH)2D3 is required for calcium and phosphorus homeostasis, and for normal skeletal development as well as maintenance of skeletal architecture. Two VDR ligands, calcitriol (1,25-(OH)2D3) and its synthetic analog alfacalcidol (1alpha-hydroxyvitamin D3), have been approved for the treatment of osteoporosis. However, the use of calcitriol and alfacalcidol is limited by their major side effect, hypercalcemia, which is mediated mainly by VDR activity in the small intestine. In order to identify VDR ligands with less hypercalcemia liability, a number of pharmaceutical companies are pursuing efforts to develop synthetic vitamin D analogs. This review discusses the mechanism of action of vitamin D, and summarizes the currently approved anti-osteoporotic VDR agonists and compounds that are under development. The future directions of vitamin D research for the discovery of novel VDR agonists for osteoporosis are also discussed.
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PMID:Vitamin D receptor ligands for osteoporosis. 1708 35

Primary hyperparathyreosis and tumour diseases are the two most frequent causes of hypercalcaemia. Surgical removal of parathyroid adenoma is the permanent solution for hypercalcaemia. Hypercalcaemia may occur in 20-30% of patients with cancer in the course of the disease. It causes progressive deterioration of the overall condition of the patient which culminates in a coma-like state with renal failure and means a bad prognosis for the affected person. Evaluation of clinical condition and obtaining the immunoreactive parathormone level data are of extreme importance for correct diagnosis. Normal or even low parathormone levels almost surely exclude primary hyperparathyreosis as the source of hypercalcaemia. Additional, less frequent causes of hypercalcaemia should also be taken into consideration, such as diseases caused by the granulomatose tissue, familial benign hypocalciuric hypercalcaemia, drug provoked hypercalcaemia, high thyroid hormone doses and patient dehydration. Fast replenishment of liquids and administration of bisphosphonates are the cornerstones of hypercalcaemia therapy.
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PMID:[Differential diagnosing of hypercalcemias]. 1791 27


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