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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have shown previously that chronic hyperchloremic metabolic acidosis (CMA) induces severe negative nitrogen balance and renal phosphate depletion and decreases serum insulin-like growth factor-1 (IGF-1) in association with growth hormone (GH) insensitivity in humans. The present study investigated whether acidosis-induced renal nitrogen wasting and renal phosphate depletion are mediated by GH insensitivity/low IGF-1 and thereby responsive to GH treatment. The effects of GH on acidosis-induced changes in divalent cation metabolism and acidosis-induced hypothyroidism were also investigated. CMA (delta[HCO3], -10.5 mmol/L) was induced in six healthy male subjects ingesting 4.2 mmol NH4Cl/kg body weight [BW]/d for 7 days. Recombinant human GH (0.1 U/kg BW/12 h subcutaneously) was administered for 7 days while acid feeding was continued. GH increased serum IGF-1 from 22.1 +/- 1.4 to 87 +/- 8.4 nmol/L (control level, 36.4 +/- 2.2). GH decreased urinary nitrogen excretion, resulting in a cumulative nitrogen retention of 2,404 mmol, thereby correcting the acidosis-induced cumulative increase in nitrogen excretion (2,506 mmol) despite continued acid feeding. GH attenuated the acidosis-induced hyperphosphaturia (cumulative phosphate retention, 91 mmol) and corrected the hypophosphatemia. GH did not affect acidosis-induced ionized hypercalcemia, but further exacerbated acidosis-induced hypercalciuria (cumulative loss, 27.3 mmol). GH significantly further increased serum 1,25-dihydroxyvitamin D (1,25(OH)2D) and further decreased intact PTH (from 10 +/- 1 to 6 +/- 1 pg/mL). Acidosis also induced hypomagnesemia and hypermagnesuria (cumulative loss, 9.4 mmol, ie, renal magnesium wasting), a novel finding, which was significantly attenuated by GH (cumulative retention, 5.0 mmol). In conclusion, GH corrected acidosis-induced renal nitrogen wasting, which may be caused, at least in part, by decreased IGF-1 levels. GH further increased serum 1,25(OH)2D and the systemic calcium load, which account for the suppression of parathyroid hormone (PTH) despite renal PO4 retention and correction of hypophosphatemia. GH attenuated acidosis-induced renal magnesium wasting.
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PMID:Growth hormone corrects acidosis-induced renal nitrogen wasting and renal phosphate depletion and attenuates renal magnesium wasting in humans. 1038 Nov 52

A 20-year-old Japanese man with a hypothalamic tumor (most likely germ-cell tumor) which caused secondary hypoadrenalism, hypogonadism and diabetes insipidus developed hypercalcemia and acute renal failure. The serum levels of intact PTH (iPTH), PTH-related protein (PTH-rP), 1,25-dihydroxy vitamin D (1,25- (OH)2 D), ACTH, cortisol, gonadotropins and testosterone were decreased, but his serum levels of triiodothyronine (T3) and thyroxine (T4) were within the normal range at admission, with depressed TSH and slightly increased thyroglobulin. The hypercalcemia was refractory to extensive hydration and calcitonin, but was ameliorated by pamidronate. After irradiation of the hypothalamic tumor, panhypopituitarism gradually developed. The patient has been normocalcemic for the last 2 years and is doing well under replacement therapy with glucocorticoid, L-thyroxine, methyltestosterone and 1-desamino D arginine vasopressin (dDAVP). As to the mechanism of euthyroidism at admission, transient destructive thyroiditis associated with hypopituitarism or delayed development of hypothyroidism following the hypoadrenalism was suggested. This is the first reported case of hypercalcemia in secondary hypoadrenalism due to hypothalamic tumor. Hypercalcemia was most likely induced by increased bone resorption, which was probably elicited by the combined effects of deficient glucocorticoid and sufficient thyroid hormones in addition to hypovolemia and reduced renal calcium excretion. Furthermore, severe dehydration due to diabetes insipidus and disturbance of thirst sensation caused by the hypothalamic tumor aggravated the hypercalcemia, leading to acute renal failure.
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PMID:Hypercalcemia in an euthyroid patient with secondary hypoadrenalism and diabetes insipidus due to hypothalamic tumor. 1039 33

The clinical features and laboratory findings of 91 Thai patients (33 males and 58 females) with CPPD crystal deposition disease were studied. Their average age was 71.54 years. Acute monoarthritis and oligoarthritis were the two most common forms of presentation and were seen in 89 per cent of cases. The knee, wrist and ankle were the three most common joints involved. Associated diseases were common and included hypertension (30 cases), renal insufficiency (23 cases), chronic obstructive pulmonary disease (17 cases), coronary heart disease (13 cases) and diabetes mellitus (12 cases). Eleven patients had malignancies. Five patients had concomitant gout and CPPD crystal deposition disease. The knee and the wrist were the two most common sites of chondrocalcinosis. Of 67 patients who had thyroid function tested, 2 had hyperthyroidism and 5 had hypothyroidism. Hypomagnesemia was seen in 19 per cent. None had hypercalcemia, hypophosphatasia, hemochromatosis or hyperparathyroidism. In contrast to the western series, acute arthritis in our series responded well to oral colchicine alone.
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PMID:Calcium pyrophosphate dihydrate crystal deposition: a clinical and laboratory analysis of 91 Thai patients. 1044 78

Renal and metabolic adverse effects of lithium therapy are illustrated by the case report of a manic depressive woman aged 78 years, so treated for about 25 years. Long term lithium therapy with plasma lithium level in the therapeutic range impairs renal concentrating ability in 25-50% of the patients (when the total ingested amount reaches 100-200 mol, 700-1400 g). About 10-15% of the patients have overt nephrogenic diabetes insipidus (NDI) with elevated antidiuretic hormone plasma level and unresponsiveness to desmopressin. In rats, lithium treatment down regulates expression of the main water channel, aquaporin 2, in the renal collecting duct. NDI may be complicated by hypernatremic dehydration if the access to water is restricted, whatever the cause. Treatment of NID is best started with nonsteroidal antiinflammatory drugs, being then substituted for amiloride. Prolonged lithium therapy may induce chronic interstitial nephritis. In some patients this may result in mild or moderate non progressive chronic renal insufficiency. Acute lithium intoxication (with supratherapeutic doses) may be complicated by acute renal failure (ARF); even in the absence of ARF hemodialysis is indicated when plasma lithium level reaches 4 mmol/l or more. Other metabolic adverse effects of lithium therapy include: hypercalcemia due to hyperparathyroidism (in 5-10% of the patients); hypothyroidism (often latent); hyperthyroidism. In conclusion, these renal and metabolic adverse effects are generally mild or moderate, allowing the continuation of lithium therapy in most affected patients.
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PMID:[Renal and metabolic complications of lithium]. 1079 6

Thyroid hormones are believed to influence calcium metabolism. In the present prospective study we investigated the influence of various thryroid diseases on serum calcium levels. In addition to screening for thyroid diseases we measured serum calcium concentrations (S-Ca) in individuals who came to our outpatient service for thyroid diseases from 1992 to 1998. 13,387 persons, among them 9017 patients with thyroid diseases and 4370 persons without thyroid dysfunction, were studied. S-Ca was found to be higher in patients with hyperthyroidism (2.36 +/- 0.11 mmol/L n = 1201, p < 0.05) than in those with subclinical hyperthyroidism (2.33 +/- 0.11 mmol/L, n = 494), with euthyroid goiter (2.32 +/- 0.10 mmol/l, n = 5599), with hypothyroidism (2.31 +/- 0.11 mmol/L, 344), with subclinical hypothyroidism (2.32 +/- 0.10 mmol/L, n = 1290) and in healthy persons (2.31 +/- 0.11 mmol/L, n = 4370). 173/13,387 persons had serum calcium levels < 2.1 mmol/L, among them 31 patients with hypoparathyroidism after strumectomy (31/592) and 2 patients with primary hypoparathyroidism. 106/13,387 persons showed a S-Ca of > 2.6 mmol/L, which in 30 cases was due to primary hyperparathyroidism. Of 55 persons with S-Ca of > 2.6 mmol/L and without any other reason for hypercalcaemia, 31 were found to be in a hyperthyroid state. In conclusion, a clinically not relevant influence on S-Ca was demonstrated in patients with hyperthyroidism as compared with other thyroid diseases and individuals with no thyroid diseases. Measurement of S-Ca in every patient being referred to a thyroid outpatient department is recommended because of the frequent occurrence of postoperative hypoparathyroidism and primary hyperparathyroidism in this setting.
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PMID:Serum calcium in thyroid disease. 1123 72

The endocrine adaptations to critical illness are varied. In the diabetic patient, counterregulatory hormones predispose to insulin resistance and hyperglycemia, a derangement accentuated by the use of glucocorticoids and enteral or parenteral nutrition. Thyroid abnormalities include the euthyroid sick syndrome, which may manifest as a low T3, low T4, low TSH, or all three. Illness in patients with pre-existing hypothyroidism or hyperthyroidism may precipitate myxedema coma or thyroid storm, respectively. The most important issue related to calcium is that of acute hypercalcemia, which, in the intensive care unit, usually is caused by malignancy and dehydration. Hyponatremia, a frequently encountered electrolyte disturbance, is evaluated best and treated according to volume status.
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PMID:Endocrine problems in the chronically critically ill patient. 1131 56

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

Idiopathic slow-transit constipation is a clinical syndrome predominantly affecting women, characterized by intractable constipation and delayed colonic transit. This syndrome is attributed to disordered colonic motor function. The disorder spans a spectrum of variable severity, ranging from patients who have relatively mild delays in transit but are otherwise indistinguishable from irritable bowel syndrome to patients with colonic inertia or chronic megacolon. The diagnosis is made after excluding colonic obstruction, metabolic disorders (hypothyroidism, hypercalcemia), drug-induced constipation, and pelvic floor dysfunction (as discussed by Wald ). Most patients are treated with one or more pharmacologic agents, including dietary fiber supplementation, saline laxatives (milk of magnesia), osmotic agents (lactulose, sorbitol, and polyethylene glycol 3350), and stimulant laxatives (bisacodyl and glycerol). A subtotal colectomy is effective and occasionally is indicated for patients with medically refractory, severe slow-transit constipation, provided pelvic floor dysfunction has been excluded or treated.
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PMID:Slow-transit Constipation. 1146 89

We report here a 47-year-old woman with isolated adrenocorticotropin (ACTH) deficiency (IAD). She presented impaired renin-angiotensin-aldosterone (R-A-A) system and suppressed parathyroid hormone (PTH)-vitamin D system. She showed severe hyponatremia due to secondary adrenocortical insufficiency, which was deteriorated by hypoaldosteronism. She also showed hyperphosphatemia and relative hypercalcemia with suppressed PTH-vitamin D axis. Moreover, she showed hypothyroidism, which was thought to be important to maintain normal Ca levels under secondary hypoadrenalism via decrease in bone resorption by T3. Replacement with glucocorticoid completely normalized PTH-vitamin D axis and R-A-A system. Thus, the present case implicates that severe adrenocortical deficiency due to IAD might affect both R-A-A system and PTH-vitamin D axis. These findings suggest that the ACTH-cortisol axis has an important role in mineral metabolism in vivo.
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PMID:Isolated adrenocorticotropin deficiency presenting with impaired renin-angiotensin-aldosterone system and suppressed parathyroid hormone-vitamin D axis. 1213 25

A 48-year-old woman was referred to our hospital because of secondary hypothyroidism. Upon admission a left adrenal tumor was also detected using computed tomography. Laboratory data and adrenal scintigraphy were compatible with Cushing syndrome due to the left adrenocortical adenoma, although she showed no response to the TRH stimulation test. Hypercortisolism resulting in secondary hypothyroidism was diagnosed. After a left adrenalectomy, hydrocortisone administration was begun and the dose was reduced gradually. After discharge on the 23rd postoperative day, she began to suffer from anorexia. ACTH level remained low, and serum cortisol, free thyroxine and TSH levels were within the normal range. Since her condition became worse, she was re-admitted on the 107th postoperative day at which time serum calcium level was high (15.6 mg/dl). Both ACTH response to the CRH stimulation test and TSH response to the TRH stimulation test were restored to almost normal levels, but there was no response of cortisol to CRH stimulation test. We diagnosed that the hypercalcemia was due to adrenal insufficiency. Although the serum calcium level decreased to normal after hydrocortisone was increased (35 mg/day), secondary hypothyroidism recurred. It was suggested that sufficient glucocorticoids suppressed TSH secretion mainly at the pituitary level, which resulted in secondary (corticogenic) hypothyroidism. However, both postoperative glucocorticoid deficiency and adequate amounts of thyroxine due to the elimination of inhibition of TSH secretion by glucocorticoids might cause hypercalcemia possibly through increased bone reabsorption of calcium.
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PMID:A case of cushing syndrome with both secondary hypothyroidism and hypercalcemia due to postoperative adrenal insufficiency. 1500 16


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