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 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin D deficiency is extremely prevalent in the elderly. Most often the first symptoms are caused by myopathy with muscle pain, fatigue, muscular weakness and gait disturbances. More severe deficiency causes osteomalacia with deep bone pain, reduced mineralization of bone matrix and low energy fractures. Recent data also suggest that hypovitaminosis D increases the risk of cancer of the prostate, colon and breast. Thus, hypovitaminosis D is associated with many diseases associated with aging. In order to diagnose hypovitaminosis D, the assessment of serum levels of 25-hydroxy vitamin D is mandatory. Screening based on other markers like alkaline phosphatase and parathyroid hormone (PTH) will be incomplete. The treatment of hypovitaminosis D is simple with administration of combined calcium (I g) and vitamin D supplements (calciferol, at least 800 IU). Severe cases may demand initial parenteral administration of vitamin D (repeated injections of 300,000 IU 2-3 times with monthly intervals). More potent analogues are rarely needed. One should aim at achieving S-25(OH)D values in the range 50-100 nmol/l.
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PMID:Vitamin D deficiency and aging: implications for general health and osteoporosis. 1201 47

An 80-year-old white woman who presented with fatigue, weakness, weight loss, constipation and polydipsia is reported. The patient was given a diagnosis of severe hypercalcemia and was subsequently found to have clinical, roentgenographic and pathological evidence of hepatocellular carcinoma. Further studies revealed a low parathyroid hormone level, excluding the possibility of primary hyperparathyroidism, and a negative bone survey, precluding metastatic bone disease. The patient's hypercalcemia was believed to emanate from the humoral secretion of a parathyroid hormone-related peptide, which was found to be elevated, and was abated with conservative management while her cancer was being treated with chemotherapy. The details of this rarely documented presentation, which can easily be mistaken for hepatic encephalopathy, are provided.
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PMID:Severe hypercalcemia as an initial presenting manifestation of hepatocellular carcinoma. 1236 13

Metabolic bone disease and some of the disorders of the skeleton are associated with alterations in calcium and phosphorus homeostasis. For example, calcium salts are not freely soluble in body fluids and increases in either calcium or phosphate or both can lead to deposition of calcium salts in the soft tissues. In addition, because the crystalline material in bone is very tiny, there is a rapid and very active exchange system with the extracellular space so that disorders of calcium or phosphorus are reflected by a change in bone structure and, in fact, contribute to the ease with which fractures occur. Also, in many disorders, bone formation and destruction are equal in activity but opposite in sign; in some conditions such as osteoporosis, destruction exceeds production and lead to weakness of bone structure. Finally, the transfer of calcium across lumens such as the gut, kidney, or bone requires a system, which consists of parathyroid hormone and 1,25-dihydroxyvitamin D and a low phosphate level.
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PMID:Metabolic bone disease: an update. 1269 Sep 1

In Japan, there are many dialysis patients because of the successful development and wide application of dialysis techniques. Almost all patients require long-term hemodialysis treatment because kidney transplantation is performed rarely. Renal hyperparathyroidism is one of the serious complications for hemodialysis patients. According to the overview of regular dialysis treatment reported by the Japanese Society for Dialysis Therapy, parathyroidectomy is required in 9.2%of patients who remain on hemodialysis more than 10 years and in 33.5%of those who so remain for more than 25 years. In this paper, we will describe the diagnosis, surgical indications, and operative strategy of renal hyperparathyroidism. The symptoms and biochemical variables were high serum parathyroid hormone (PTH) level, hyperphosphatemia, bone and joints pain, itching, irritability, muscle weakness, severe skeletal deformity, progression of ectopic calcification, and anemia. The clinical indications for performing parathyroidectomy to treat renal hyperparathyroidism in our institute are based on the indications reported by Tominaga et al. These are 1) high serum PTH level, 2) detection of enlarged parathyroid glands, 3) detection of osteitis fibrosa cystica on radiography or detection of high bone turnover by bone metabolic markers or bone scintigram, 4) resistance of symptoms to medical treatment. The routine operative procedure for renal hyperparathyroidism is total parathyroidectomy with forearm autograft. For autotransplantation, 30 pieces sliced 1x1x3 mm of diffuse hyperplasia are implanted into 30 pockets in the forearm without arteriorvenous (A-V) fistula for hemodialysis. In any surgical procedure for renal hyperparathyroidism, it is crucial to identify all parathyroid glands, including supernumerary glands and ectopic glands. At the initial operation for renal hyperparathyroidism, the surgeon must remove all parathyroid glands to avoid persistent and recurrent hyperparathyroidism and choose proper and adequate parathyroid tissue for autograft.
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PMID:[Endocrine surgery: the tenth report. Diagnosis, surgical indications and operative strategy of renal hyperparathyroidism]. 1292 32

Primary hyperparathyroidism is the most frequent cause of hypercalcemia in ambulatory patients. The condition is most common in postmenopausal women, although it can occur in persons of all ages, including pregnant women. If symptoms are present, they are attributable to hypercalcemia and may include weakness, easy fatigability, anorexia, or anxiety. However, most persons have no symptoms, and primary hyperparathyroidism usually is diagnosed after an elevated serum calcium level is found incidentally on multiphasic chemistry panel testing. Persistent hypercalcemia and an elevated serum parathyroid hormone level are the diagnostic criteria for primary hyperparathyroidism. Other causes of hypercalcemia are rare, and usually are associated with low (or sometimes normal) parathyroid hormone levels. Malignancy is the most frequent cause of hypercalcemia in hospitalized patients. Parathyroidectomy is the definitive treatment for primary hyperparathyroidism. When performed by experienced endocrine surgeons, the procedure has success rates of 90 to 95 percent and a low rate of complications. Asymptomatic patients who decline surgery and meet criteria for medical management must commit to conscientious long-term monitoring. Any unexplained elevation of the serum calcium level should be evaluated promptly to prevent complications from hypercalcemia.
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PMID:Hyperparathyroidism. 1566 24

Primary hyperparathyroidism (pHPT), caused by solitary parathyroid adenomas in 85% of cases and diffuse hyperplasia in most of the remaining cases, overproduces parathyroid hormone (PTH), which mobilizes calcium to the blood stream. Renal stones, osteoporosis and diffuse symptoms of hypercalcaemia, such as constipation, fatigue and weakness are well-known complications. However, in Western Europe and North America, patients with pHPT are nowadays usually discovered during an early, asymptomatic phase of the disease. It has been reported that patients suffering from symptomatic pHPT have increased mortality, mainly due to an overrepresentation of cardiovascular death. pHPT is reported to be associated with hypertension, disturbances in the renin-angiotensin-aldosterone system, and structural and functional alterations in the vascular wall. Recently, studies have indicated an association between pHPT and heart disease, and studies in vitro have produced a number of theoretical approaches. An increased prevalence of cardiac structural abnormalities such as left ventricular hypertrophy (LVH) and valvular and myocardial calcification has been observed. Associations have been found between PTH and LVH, and between LVH and serum calcium. LV systolic function does not seem to be affected in patients with pHPT, whereas any influence on LV diastolic performance needs further evaluation. The aim of this review is to clarify the connection between pHPT and cardiac disease.
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PMID:Primary hyperparathyroidism and heart disease--a review. 1547 92

The most important step in calcium homeostasis is the regulation of parathyroid hormone (PTH) secretion. The discovery and characterization of the calcium sensing receptor (CaR) of the parathyroid cell has led to a better understanding not only of the physiology of the parathyroid glands, but also of the development of hyperparathyroidism. Drugs acting on CaR can now be designed to treat hyperparathyroidism and osteoporosis. The workshop on primary hyperparathyroidism held at the National Institutes of Health in 2002 has recommended new guidelines for the treatment of asymptomatic hyperparathyroidism. Controversy still exists regarding the treatment of patients with non-classical symptoms, such as weakness, fatigue and depression. Primary hyperparathyroidism as a risk factor for cardiovascular disease and mortality is also debated. Improved techniques for the preoperative localization of pathological parathyroid glands have led to a shift in surgical strategy: surgeons abandon the traditional bilateral neck exploration in favor of a more limited approach. This change of strategy has not been based on the results of prospective randomized studies and the long term results are not known.
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PMID:Primary hyperparathyroidism. Update on pathophysiology, clinical presentation and surgical treatment. 1565 69

Vitamin D deficiency among hospitalized patients may be more widespread than realized. Vague musculoskeletal complaints in these chronically ill patients may be attributed to multiple underlying disease processes rather than a deficiency in vitamin D. However, the failure to diagnose an underlying deficiency places the patient at risk for continued pain, weakness, secondary hyperparathyroidism, osteomalacia, and fractures. The causes of hypocalcemia and hypophosphatemia in the chronically ill patient are many, and the patient may respond to simple replacement therapy. Elderly hospitalized patients with ionized hypocalcemia and hypophosphatemia, with or without an elevated parathyroid hormone level, are most likely deficient in vitamin D. Initiating treatment during hospitalization is reasonable once the diagnosis has been confirmed by finding a low 25-hydroxyvitamin D level. Treatment with high doses of vitamin D is safe. Unfortunately, some hospital formularies continue to provide multivitamin supplements that contain less vitamin D than currently is recommended.
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PMID:Undiagnosed vitamin D deficiency in the hospitalized patient. 1568 95

A 37-year-old patient with severe hypokalemia (approximately 1.7 mEq/L) and muscular weakness had a very high serum renin level. No renin-producing tumor was found and she was diagnosed with Bartter Syndrome The parathyroid hormone level was high due to concomitant renal calcium loss. Tc-99m-DTPA captopril scintigraphy was performed to confirm the diagnosis.
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PMID:Abnormal captopril scintigraphy in Bartter syndrome. 1576 90

Although acute nonoliguric renal failure is a well-known nephrotoxic effect of aminoglycoside antibiotics, less recognized is acquired Bartter-like syndrome. Herein, we describe four female patients who presented with marked paresthesia, muscle weakness, and tetany following gentamicin therapy with total dose ranging from 1.2 g to 2.6 g. All were normotensive. Biochemical abnormalities included hypokalemia (K+ 1.8-2.3 mmol/L), metabolic alkalosis (HCO(3-) 31.9-34.2 mmol/L), hypomagnesemia (Mg2+ 0.9-1.2 mg/dL), hypermagnesiuria (fractional excretion of Mg 3-6%), hypocalcemia (free Ca2+ 2.0-4.1 mg/dL), and hypercalciuria (molar ratio of Ca2+/creatinine 0.23-0.53), all consistent with Bartter-like syndrome. Serum immunoreactive parathyroid hormone concentration was low despite the hypocalcemia. The Bartter-like syndrome lasted for 2 to 6 weeks after cessation of gentamicin, coupled with supplementation of K+, Ca2+, and Mg2+. These biochemical abnormalities resembled those seen in patients with gain-of-function mutations in the calcium-sensing receptor. We hypothesize that gentamicin, a polyvalent cationic molecule, induces the action of calcium-sensing receptor on the thick ascending loop of Henle and distal convoluted tubule to cause renal wasting of Na+, K+, Cl-, Ca2+, and Mg2+.
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PMID:Acquired bartter-like syndrome associated with gentamicin administration. 1576 21


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