Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Careful examination as well as biochemical and hormonal investigations should be performed in men suffering from vertebral crush fractures, in order to detect a destructive skeletal process (multiple myeloma, bone metastatic lesions, lympho and myeloproliferative disorders), a mineralization defect (osteomalacia) or a secondary osteoporosis: primary hyperparathyroidism, hypogonadism, hyperthyroidism, renal hypercalciuria, alcoholism and tobacco smoking. The diagnosis of idiopathic osteoporosis should be made only after these causes have been excluded; the pathogenesis of the disease is unclear but risk factors have been identified: family history of osteoporosis, low dietary calcium intake, delayed puberty, ethanol use, tobacco smoking, inactive lifestyle and lean body build. Correction of risk factors, calcium supplementation, regular program of weight bearing physical activity, in some instances correction of testosterone deficiency may be of benefit to reduce bone loss. Severe osteopenia or osteoporosis may require sodium fluoride therapy.
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PMID:[Male osteoporosis]. 793 30

Secondary osteoporosis may be associated with a number of endocrine dysfunctions and metabolic disorders. In this paper, osteoporosis in patients with Cushing's syndrome, hyperthyroidism, primary hyperparathyroidism, acromegaly, hypogonadism and some metabolic disorders such as diabetes mellitus, chronic renal failure and malabsorption syndrome are described. While the major manifestation of bone in these conditions is a reduction of bone mass and may be somewhat different from bone loss in primary osteoporosis histologically or radiologically, it is considered to be the same bone loss as primary osteoporosis in the present paper. In some conditions, for example, Cushing's syndrome, diabetes mellitus etc, factors responsible for bone loss are demonstrated.
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PMID:[Osteoporosis associated with endocrine dysfunctions or metabolic disorders]. 796 90

Bone is a living tissue; throughout life, new bone formation coexists with bone resorption. Although a large number of hormones and cytokines modulate osteoblast and osteoclast function, osteoporosis results from any disorder in which bone formation becomes uncoupled from bone resorption. Many disorders are associated with the uncoupling of bone formation and resorption. The most common is loss of gonadal steroid action on bone, as occurs in menopause or in male and female hypogonadism not associated with menopause. Other relatively common causes include primary hyperparathyroidism and endogenous or exogenous hypercortisolism and thyrotoxicosis. A large number of other, less frequent disorders also cause osteoporosis. Treatment of osteoporosis consists first of removing the cause if possible, for example, abolishing hypercortisolism, thyrotoxicosis, or hyperparathyroidism. In menopausal women or hypogonadal men or women, replacement of estrogens or androgens represents effective therapy. Estrogens and androgens given to hypogonadal subjects strikingly reduce bone resorption. For patients with established osteoporosis who either cannot take gonadal steroids or who are not hypogonadal, calcitonin decreases bone resorption and may stabilize bone mass. Estrogen replacement and calcitonin are approved by the Food and Drug Administration for treatment of osteoporosis. Experimental therapies presently include 1,25-dihydroxyvitamin D (calcitriol), bisphosphonates in intermittent treatment regimes, and fluoride in lower dosages than were used in previous studies. The use of fluoride is controversial, and to some extent it has fallen into disrepute. Effective use of any treatment is predicated on understanding the pathophysiology in any particular disease setting.
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PMID:Osteoporosis: pathophysiology, prevention, diagnosis, and treatment. 822 93

In children and the youth it is secondary osteoporosis (OP) rather than idiopathic one which occurs more often; its multidirectional pathogenesis is usually ascertainable. Secondary OP, mostly generalized, is diagnosed in the course of such hormonal disturbances as: primary hyperparathyroidism, hyperthyroidism, hyperadrenalocorticalism, hyperpituitarism (with excess of growth hormone) and in hypogonadism. Another group of diseases implicating OP are connective tissue pathologies: congenital (osteogenesis imperfecta, collagenopathies) and acquired (Juvenile chronic arthritis). A serious problem for a pediatrician is the iatrogenic OP resulting from a long-term use of some medicines (glucocorticosteroids, hydantoin derivatives, barbiturates), or long-lasting immobilization for surgical and orthopaedic reasons, or from chronic general diseases. Osteoporosis accompanying pathological states of the skeletal and nervous systems (with paralyses and pareses) is particularly intensive and difficult for treatment. Osteoporosis in developmental age may cause disturbances in natural development of the skeleton, which leads to deformities in the skeletal system and to the formation of faulty postures. Lower body height is a frequent complication resulting from OP in children and the youth.
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PMID:[Osteoporosis during development--selected problems]. 933 82

Hip fractures in men account for one third of all hip fractures and have a higher mortality than in women. The public health burden will increase as the increase in the numbers of elderly men in the community increases. In addition, the age-specific incidence of hip fractures may be increasing in some, but not all, countries. Vertebral fractures may be a public health problem as recent studies suggest that the prevalence in the community is 20-30%, similar to that reported in women. Forearm fractures should probably not be regarded as a public health problem. Peak bone mass is higher in men than women because men have bigger bones. Peak bone mineral density is the same. The amount of trabecular bone lost at the spine and iliac crest during ageing is similar in men and women. Cortical bone loss is less in men because endocortical resorption is less and periosteal formation is greater. Bone loss accelerates in elderly men because endocortical resorption and increasing cortical porosity increase the surface available for resorption. Bone fragility is less in men than women because: (a) the cross-sectional surface of the bone is larger; (b) trabecular bone loss is less as a percentage of the higher peak bone mass; (c) trabecular bone loss occurs by thinning rather than perforation; and (d) periosteal appositional growth compensates for endocortical resorption by maintaining the bending strength of bone. Reduced BMD in men with fractures may be due to reduced peak bone size and mass, and bone loss. Bone loss occurs by reduced bone formation. Whether men with fractures have increased bone fragility due to reduced periosteal appositional growth during ageing is unknown. The age-related decline in testosterone, adrenal androgens, growth hormone, and insulin-like growth factor 1 may contribute to reduced bone formation and bone loss. Men with vertebral fractures often have hypogonadism or illnesses with few clinical features that should be considered with a high index of suspicion (alcoholism, myeloma, malabsorption, primary hyperparathyroidism, haemochromatosis, Cushing's disease). Secondary hyperparathyroidism may contribute to bone loss by activating bone turnover and so increasing the number of bone remodelling units with impaired bone formation in each. There is no proven treatment for osteoporosis in men because there have been no trials using anti-fracture efficacy as an end point. Testosterone replacement should be considered in men with proven hypogonadism and vitamin D deficiency should be corrected if present. Calcium supplements and bisphosphonates are reasonable options given the lack of information.
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PMID:Osteoporosis in men. 936 40

Endocrine diseases may present with musculoskeletal complaints, and their outcome, even after endocrine control, can be impaired by bone and joint disorders. All musculoskeletal structures, including bone, cartilage, synovium, tendons and ligaments, can be involved by some processes triggered by the endocrine disorder and its related disturbances of homeostasis, including that of growth factors. Endocrine disorders may account for 20-30% of all cases of osteopenia or osteoporosis in adults, the main causes being central and peripheral hypogonadism, endogenous and exogenous hypercorticism or hyperthyroidism, and primary hyperparathyroidism. The physician should be aware of these identifiable and treatable causes of bone loss when interpreting bone mineral density measurements. It is also valuable to evaluate bone status in patients diagnosed with these endocrine disorders. Specific bone therapeutic measures could be discussed. Other frequent musculoskeletal features include myopathy and joint and soft tissue involvement. Endocrine myopathy is frequent in most of the endocrine disorders and is non-specific since proximal painless muscle weakness associated with normal serum enzyme levels and an uncommonly encountered electromyogram myopathic pattern are present in these diseases. Soft tissue involvement is also a frequent consequence of acromegaly, hypothyroidism and diabetes mellitus. There is also a risk of nerve entrapment syndromes in these conditions. Specific arthropathies are the hallmark of acromegaly at the spinal and peripheral joints. Neuroarthropathies are a severe complication of diabetes mellitus as a result of infection, neuropathy and vasculopathy. In all these settings, the physician should be aware that endocrine disorders are part of the differential diagnosis and, conversely, that these articular and peri-articular lesions should be managed independently of the control of the underlying endocrine condition, a specific outcome being borne in mind.
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PMID:Osteoarticular disorders of endocrine origin. 1092 44

The lifetime risk of any fracture of the hip, spine or distal forearm in men aged 50 years has been estimated to be 13%, compared with 40% in women. Although the overall incidence of osteoporosis is less in men than in women, the disease still represents an important public health problem. In particular, hip fractures are associated with substantial mortality and morbidity, even more so than in women. In male patients presenting with osteoporotic fractures, major causes of skeletal fragility, such as hypogonadism, glucocorticoid excess, primary hyperparathyroidism and alcohol abuse, can often be identified. In as many as 50% of osteoporotic men, however, no aetiology can be found: these men suffer from a syndrome commonly referred to as idiopathic osteoporosis, which is presumably related to some type of osteoblast dysfunction. Recent evidence indicates that the loss of skeletal integrity in ageing men may be partially related to endocrine deficiencies, including vitamin D, androgen and/or oestrogen deficiency. While the consequences of vitamin D or oestrogen deficiency in women have been well established, the skeletal impact of these (partial) age-related deficiencies in men remains to be clarified. Osteoporosis in elderly men is a multifactorial disease, as it is in women. The prevention of osteoporosis should therefore focus not only on increasing the bone strength, but also on decreasing the risk of falls. However, the prevention and therapy of osteoporotic disorders in men are virtually unexplored. To date, the use of specific osteoporotic drugs in osteoporotic men is still based on reasonable but untested assumptions.
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PMID:Osteoporosis and osteoporotic fractures in men: a clinical perspective. 1103 8

In order to assess properly the diagnosis of osteoporosis, a short clinical investigation is required to address potential causes for bone loss. Osteoporosis used to be suspected in a patient with vertebral demineralization, but nowadays it is often diagnosed in a patient with a low bone mass on a screening dual-energy X-ray absorptiometry (DEXA). In this setting, it is important for the clinician to look for secondary osteoporosis, especially in men in whom secondary osteoporosis is more frequent than in women, before discussing any specific therapy. The major causes are longterm glucocorticoid therapy, endocrine (hypogonadism, primary hyperparathyroidism, hyperthyroidism), or digestive diseases.
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PMID:[Secondary osteoporosis and glucocorticoid-induced osteoporosis]. 1110 30

The objective of this study was to define the types of disease seen at the only endocrine clinic in Jamaica. The diagnoses of all patients attending the endocrinology clinic of the University Hospital of the West Indies over a 7-year period were analysed. Of the 1503 patients attending 263 weekly endocrinology clinics, 1251 patients had thyroid-related diseases, of which 684 patients had thyrotoxicosis and 233 patients had hypothyroidism. There were 17 pituitary tumours, eight cases of Cushing's syndrome and four of acromegaly. Cases of Sheehan's syndrome (n=11), hypopituitarism (n=17), hypoadrenalism (n=13), hypogonadism (n=9), primary hyperparathyroidism (n=3) and phaeochromocytoma (n=3) were rare. Thyroid disease was the most common diagnosis. New emerging endocrine disorders that are public health problems, such as obesity (n 21) and hyperlipidaemia (n=1), were rare. More traditional diseases, such as Sheehan's syndrome have become rare with improvements in obstetric care.
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PMID:Endocrine disorders in a specialist hospital in Jamaica. 2130 97

Multiple endocrine neoplasia type I or Wermer syndrome is characterized by primary hyperparathyroidism, enteropancreatic endocrine tumor, and a pituitary pathology. A 35-year-old male presented with visual field defects, hyperprolactinemia, and hypogonadism. He also had multiple infraumbilical skin-colored nodules. A syndromal association of Wermer syndrome was derived using the dermal, pituitary, parathyroid, and gastrointestinal hormonal manifestations of the tumor. The radiological and histological findings of lesion which underwent biopsy are discussed. The presence of collagenomas, lipomas, and hypopigmented macules in a patient with neuroendocrine symptoms should raise the suspicion of an underlying multiple endocrine neoplasia.
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PMID:Neurocutaneous spectrum of multiple endocrine neoplasia-1. 2219 68


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