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

In order to investigate the relationships between serum calcium, urate and kidney function, serum calcium, urate, creatinine and urea were measured at 100 occasions in hypercalcemic cancer patients together with 113 preoperative measurements in HPT subjects and 106 measurements in normocalcemic control persons. When compared to normocalcemic control subjects (serum urate 336 +/- 110 mumol/l) both HPT subjects (356 +/- 98 mmol/1, p less than 0.006) and the cancer patients (407 +/- 179 mmol/l, p less than 0.001) showed raised levels of serum urate. While serum urate was correlated to serum creatinine in all groups (r = 0.40-0.59, p less than 0.0001) a significant correlation to serum calcium was only seen in the HPT group (r = 0.28, p less than 0.004). This relation persisted also after correction for age, sex and serum creatinine in the multiple regression analysis. Serum creatinine was similar in all groups but significantly correlated to serum calcium only in the HPT subjects (r = 0.29, p less than 0.003). Serum urea was not significantly correlated to serum calcium in any of the groups but was elevated in the cancer group (8.3 +/- 4.4 vs 6.2 +/- 2.9 mumol/l in the control group, p less than 0.0001). This elevation in serum urea seen in the cancer patients might rather be explained by dehydration or catabolism than an impaired kidney function. In conclusion, while serum urate is related to the kidney function both in normo- and hypercalcemia, it also seems to be related to the hypercalcemia in HPT subjects but not in cancer patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum urate and renal function in different forms of hypercalcemia. 163 24

Patients suffering from malignant disease will probably develop some metabolic abnormality of electrolytes. Hypernatremia is defined as an elevation of serum natrium over 150 mEq/l and caused by decrease of water intake, low level of ADH secretion and impaired response of kidney to ADH. Hyponatremia below 135 mEq/l of serum natrium is caused by SI-DAH, sick cell syndrome and increased loss of natrium from the kidney. On the other hand, hyperkalemia is defined as an elevation of serum kalium over 5.0 mEq/l and caused by acute tumor cell lysis syndrome, adrenal and renal insufficiency. Hypokalemia is caused by kalium loss from kidney and hypersecretion of mineral corticoid. Hypercalcemia is found in the high frequency among patients with malignant disease. Hypercalcemia is defined as an elevation of serum calcium over 11.0 mg/dl, although the most important aspect is the level of ionized calcium. The excess calcium causes defective urinary concentration with polydipsia, nausea and vomiting leading to volume depletion. At serum calcium levels about 13.8 mg/dl, there may be rapid deterioration or renal function, dehydration, coma and cardiac arrhythmias. Hypercalcemia is rarely the first manifestation of cancer. There are three principle pathogenic causes of malignant hypercalcemia, 1) hypercalcemia is a feature of several hematological cancers, including Burkitt's lymphoma, T cell leukemia, but most commonly with myeloma. The hypercalcemia in these myeloma patients is due to the secretion of an osteoclast activator, a lymphokine by the myeloma cells. 2) all patients with bony metastases have biochemical evidence of increased bone resorption. However, not all patients with bony metastases develop hypercalcemia. Probably the hypercalcemia is due partially to increased renal tubular reabsorption of calcium, mediated by a humoral factor, with activity similar to that of parathormone. 3) hypercalcemia in the patients without bony metastases is due to increased bone resorption caused by the ectopic secretion by the tumor. Mildly symptomatic patients will benefit from modest salt loading. They are dehydrated and replacement of the extracellular fluid is the first line of treatment. This may require 4-10 l normal saline/24 h. In addition, frusemide will increase calcium excretion. Calcitonin may be given subcutaneously or intravenously to refuse the mobilisation of calcium from bone. Glucocorticoids are unhelpful, but will prolong the effect of calcitonin. A diphosphonate is also useful.
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PMID:[Palliative therapy in cancer. 4. Palliation of the symptoms from a malignant tumor. (2)]. 169 56

We described a patient with the milk-alkali syndrome induced by the ingestion of small amount of milk (200 ml/day) and ice cream (145 g/day) and the administration of small dose of absorbable alkali (magnesium oxide 2.0 g/day) for the treatment of chronic constipation. The present case shows not only triads, i.e., hypercalcemia (s-Ca 14.3 mg/dl), metabolic alkalosis (s-HCO3- 37.4 mEq/L), and renal insufficiency (s-Cre 2.3 mg/dl) but also hypernatremia (s-Na 161 mEq/L) and hypertonic dehydration after the frequent episodes of elevated body temperature. The milk-alkali syndrome has been defined as the hypercalcemia with a metabolic alkalosis from a high amount of calcium intake and long term administration of absorbable alkali in any form, usually as calcium carbonate for the treatment of peptic ulcer. As the present case could be distinguished from any other cases previously reported with regard to the amount of calcium (0.4 g/day) and alkali (36 mEq/day) intake and the clinical situations that induced the syndrome, we compared the present case with the previous reports, calculating the amount of calcium and alkali intake from milk and absorbable alkali. After the introduction of the H2 blockers for peptic ulceration, the most cases with milk-alkali syndrome had provoked by the smaller amount of calcium than previously reported, which were associated with the treatment of relatively large amount of alkali (50-150 mEq/day), suggesting the role of sustained metabolic alkalosis for the development. In the present case the metabolic alkalosis induced by hypertonic dehydration and enhanced by absorbable alkali intake also could cause an increase of renal tubular reabsorption of calcium and a decrease of ionized calcium which might produce increased secretion of parathyroid hormone followed by vitamin D3 activation and increased Ca absorption from the gut. The metabolic alkalosis might be essential to the development of the milk-alkali syndrome without a high calcium and absorbable alkali intake.
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PMID:[A case of the milk-alkali syndrome with a small amount of milk and magnesium oxide ingestion--the contribution of sustained metabolic alkalosis induced by hypertonic dehydration]. 192 Sep 38

A variety of tumors and nontumorous lesions were used to illustrate some of the biologic, clinical, and pathologic aspects of inappropriate or ectopic endocrine and metabolic syndromes that have musculoskeletal repercussions. It is clear, both from the discussion and case material, that many mechanisms of ectopic endocrine syndromes have yet to be clarified. Elaborate techniques are available for hormonal estimations, but their routine use is prohibitively expensive and relatively unrewarding. Cells of a given lesion may be functionally heterogeneous or may fail to elaborate active products in substantial amounts. Different cells may produce similar peptides, while the same cells can produce more than one. Despite these difficulties, recognition of ectopic endocrine syndromes remains crucial to diagnosis and patient management, and thus corroboration or correlation must often rest on a cruder basis. In fact, the clinical significance of basic laboratory data, e.g., PTH elevation, may vary, as PTH may be immunoreactive but biologically inactive. As another example, hypercalcemia associated with myeloma may be variously related to coexistent hyperparathyroidism, renal disease, dehydration, or humoral osteolysis. Therefore, roentgenographic evidence of bone destruction or skeletal stigmata of hyperparathyroidism imbues laboratory data with greater significance. Paraneoplastic syndromes are of particular concern to the radiologist, as multiple systemic manifestations, occurring either synchronously or metachronously, may suggest the presence of an underlying or unifying lesion or even of a specific type of neoplasm. They may precede detection of neoplasms by months to years and can develop at any time during their course. Paraneoplastic syndromes may, furthermore, parallel the course of a lesion and be used as indicators of remission or recurrence. Conversely, those unassociated with overt symptoms possess endocrine markers that can reinforce sometimes silent skeletal stigmata. Familiarity with representative secretory products influencing the musculoskeletal system per se may often clarify seemingly innocuous and sometimes asymptomatic skeletal findings. Alert imagers may, therefore, detect, infer, or suspect particular syndromes when they present in a specific sequence or mosaic. Conversely, when apprised of their existence, imagers should know where their related effects may be sought or anticipated. Such relationships, sometimes serendipitously discovered, may be valuable assets in clinical diagnosis and patient management in both suspected and unsuspected cases.
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PMID:Skeletal manifestations of ectopic or inappropriate endocrine and metabolic syndromes. 198 23

Primary hypoadrenocorticism was diagnosed in ten young to middle-aged cats of mixed breeding. Five of the cats were male, and five were female. Historic signs included lethargy (n = 10), anorexia (n = 10), weight loss (n = 9), vomiting (n = 4), and polyuria (n = 3). Dehydration (n = 9), hypothermia (n = 8), prolonged capillary refill time (n = 5), weak pulse (n = 5), collapse (n = 3), and sinus bradycardia (n = 2) were found on physical examination. Results of initial laboratory tests revealed anemia (n = 3), absolute lymphocytosis (n = 2), absolute eosinophilia (n = 1), and azotemia and hyperphosphatemia (n = 10). Serum electrolyte changes included hyponatremia (n = 10), hyperkalemia (n = 9), hypochloremia (n = 9), and hypercalcemia (n = 1). The diagnosis of primary adrenocortical insufficiency was established on the basis of results of adrenocorticotropic hormone (ACTH) stimulation tests (n = 10) and endogenous plasma ACTH determinations (n = 7). Initial therapy for hypoadrenocorticism included intravenous administration of 0.9% saline and dexamethasone and intramuscular administration of desoxycorticosterone acetate in oil. Three cats were euthanatized shortly after diagnosis because of poor clinical response. Results of necropsy examination were unremarkable except for complete destruction of both adrenal cortices. Seven cats were treated chronically with oral prednisone or intramuscular methylprednisolone acetate for glucocorticoid supplementation and with oral fludrocortisone acetate or intramuscular injections of repository desoxycorticosterone pivalate for mineralocorticoid replacement. One cat died after 47 days of therapy from unknown causes; the other six cats are still alive and well after 3 to 70 months of treatment.
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PMID:Primary hypoadrenocorticism in ten cats. 246 93

A 35-year-old man presenting with severe watery diarrhea was diagnosed as having the watery diarrhea, hypokalemia and achlorhydria (WDHA) syndrome with the elevation of plasma vasoactive intestinal peptide (VIP) level. Imaging diagnostic techniques revealed a hypervascular tumor at the tail of the pancreas as well as a solitary liver metastasis. During the patient's stay in hospital, he developed acute renal failure probably due to persistent dehydration and severe hypokalemia. Although these complications improved with artificial dialyses, severe watery diarrhea continued, which made it difficult to achieve surgical resection of the tumor. A new long-acting and potent somatostatin analogue, SMS 201-995 (Sandoz Ltd, Basel, Switzerland), was tested and was shown to be effective; after a few hours of subcutaneous injection of this agent, the watery diarrhea disappeared, which in turn improved the patient's hypokalemia, hypercalcemia and metabolic acidosis. Three weeks later, distal pancreatectomy with splenectomy and hepatic lobectomy were successfully performed, and the patient resumed his normal life. The somatostatin analogue has been reported to be useful in the long-term treatment of patients with inoperable WDHA syndrome. The present case demonstrated that short-term administration of this agent is also useful for improving the condition of WDHA patients at the preoperative stage.
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PMID:A case of the watery diarrhea-hypokalemia-achlorhydria syndrome: successful preoperative treatment of watery diarrhea with a somatostatin analogue. 255 28

Myeloma is a malignancy of plasma cells which are terminally differentiated B-lymphocytes. The diagnosis may be made incidentally at routine blood testing, when an abnormality is found in the plasma proteins on electrophoresis. More usually the patients are symptomatic, with bone pain, anaemia, evidence of renal failure, or the metabolic abnormalities associated with increased plasma calcium and urate levels. Effective treatment will extend survival from 7 to approximately 30 months and at the same time improve the quality of life. Treatment is multidisciplinary, prominently involves the professional nurse and may arbitrarily be divided into two stages. Firstly, reversible lesions, such as dehydration and plasma hyperviscosity must be corrected, hypercalcaemia and hyperuricaemia improved and, if necessary, renal dialysis undertaken. Secondly, but of equal importance, is the need for specific therapy to be directed against the tumour itself, and both cytotoxic agents and irradiation have an important role to play. More recently, newer approaches have included high dose chemotherapy and bone marrow transplantation.
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PMID:Myeloma--the integral role played by the professional nurse. 263 5

Although hypercalcaemia in young children or adolescents immobilized by fractures or spinal cord injury is well recognized, hypercalcaemia in adult immobilized patients is rare without a pre-existing bone disease. To our knowledge, hypercalcaemia in a head-injured, immobilized patient has not been previously reported. We report here a case where a previously normocalcaemic, immobilized, head-injured adult patient developed cognitive decline secondary to hypercalcaemia five months after injury, when transient interruption of enteral feedings led to mild dehydration. Indices of bone turnover were elevated and parathyroid hormone was appropriately suppressed. Possible predisposing factors in our patient included a severe degree of immobilization and a very high level of athletic activity prior to injury. Careful fluid management and specific monitoring of calcium levels, even several months post-injury, should be performed to avoid the added complications of hypercalcaemia in head-injured patients.
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PMID:Hypercalcaemia causing declining cognitive function in a head injured patient. 275 93

Based on the author's experience with more than 20 cases of immobilization hypercalcemia following spinal cord injury, current concepts of this condition are presented. Symptoms may be mild or severe: laboratory findings are essential for differential diagnosis in older individuals, in whom preinjury Paget's disease and mild primary hyperparathyroidism must be ruled out. Most cases of immobilization hypercalcemia are seen in adolescent boys following recent spinal cord injury. Besides sex (male), risk factors include age (less than 21 years), complete neurologic injuries, high cervical levels of spinal cord injury, dehydration, and a prolonged period of immobilization. A preinjury history of large ingestion of milk and/or extreme exposure to sunshine may also be contributory factors. Therapy includes vigorous hydration, saline infusions and diuretics, calcitonin, and steroids. The clinical course, without treatment, may be prolonged to 14 months, but the condition is always self-limiting.
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PMID:Immobilization hypercalcemia following spinal cord injury. 293 20

Renal failure (RF) occurring in the course of multiple myeloma is often judged irreversible and generally considered an ominous complication. The aim of the present study was to re-evaluate the outcome, triggering conditions and prognostic factors of severe RF in a series of 34 patients, 33 to 90 years old. RF was totally reversible in 7 patients and partially reversible in 9 although 6 of them had to be temporarily dialyzed. However, the improvement in renal function was often very slow as indicated by an average recovery time of 115 days. The high rate of RF reversibility was associated with markedly lengthened survival. Review of triggering events confirmed the leading role of dehydration and hypercalcemia, but further suggested that intake of nonsteroidal anti-inflammatory drugs and renal infection might play a part in the development of RF. Systematic statistical analysis of potential prognostic factors showed that the outcome was significantly more severe in females, but age, myeloma characteristics including tumor mass, calcemia, and triggering events had no predictive value. The most reliable prognostic indicators were provided by analysis of kidney biopsy performed in 30 patients. Complete recovery from RF was observed only in the absence of global tubular atrophy and interstitial damage. In contrast, cast-induced tubular obstruction detected by the presence of Tamm-Horsfall protein in urinary space of glomeruli did not seem to influence the outcome of RF. Finally, we analyzed the prognostic value of immunochemical properties of light chains (LC). Lambda LC were unexpectedly detected in 2 of 3 patients, as compared to a ratio of 1 to 3 in the population of normal and monoclonal Ig, but LC type did not correlate with the course of RF. Isoelectric points of LC measured in 32 patients were dispersed from 5.2 to 8.9 and bore only weak prognostic significance. These results underline the value of kidney biopsy and justify aggressive treatment including dialysis and chemotherapy.
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PMID:Multiple myeloma and severe renal failure: a clinicopathologic study of outcome and prognosis in 34 patients. 310 93


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