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PubMed1992

Critical care hypercalcemia--a hyperparathyroid state.

Hypocalcemia is a well known finding in critically ill patients. Subsequent occurrence of mild hypercalcemia has also been reported. In order to investigate the incidence and nature of critical care hypercalcemia serum calcium was measured in 83 critically ill ICU patients (TISS score > or = 40) and related to the occurrence of acute renal failure (ARF) and severity of illness, evaluated by the APACHE-II and the multiple organ failure scoring systems. Thirty-two percent of the patients developed hypercalcemia (serum calcium > or = 2.60 mmol/l) during their ICU stay. These hypercalcemic episodes (mean maximal value 2.71 +/- 0.12 mmol/l) were more common and occurred earlier in patients with co-existing ARF. However, multiple regression analysis showed the number of failing organ systems in the first days to be the best predictors for later occurrence of hypercalcemia (p < 0.0001). When serum parathyroid hormone (PTH) was measured in 6 of the patients without ARF during their hypercalcemic episodes, PTH was not suppressed but slightly elevated, to a similar extent as in patients with mild primary hyperparathyroidism. In conclusion, a high incidence of hypercalcemia was found in critically ill ICU patients. The hypercalcemia was mild and was more frequently found in patients with co-existing renal failure. The most powerful predictor to later occurrence of hypercalcemia was however the severity of the illness in itself. The raised levels of PTH found during the hypercalcemic episodes suggest ICU hypercalcemia to be caused by parathyroid overactivity.

Acute Kidney Injury↗
PubMed1994

Case report: cholangiocarcinoma and hypercalcemia.

Hypercalcemia is a relatively common problem seen in the presence of malignancy, and is the most common life-threatening metabolic disorder in patients with cancer. In the hospitalized patient, malignancy is the most common cause of hypercalcemia. It is estimated that hypercalcemia occurs in 10% to 20% of patients with cancer. Usually, it is a sign of advanced disease. Approximately 85% of patients with cancer and hypercalcemia will have disease metastatic to bone. The remaining 15%, however, will have some other etiology for their hypercalcemia, typically squamous carcinomas of the head and neck, esophagus, and lung. This type of hypercalcemia has been termed humoral hypercalcemia of malignancy and has been associated with the secretion of various cytokines, including parathyroid hormone-related protein. In this case report, the authors document the production of parathyroid hormone-related protein by an adenocarcinoma-cholangiocarcinoma. This is documented both by measurement of the protein in the patient's serum and staining of the protein within the tumor by a monoclonal antibody. A general discussion of hypercalcemia and malignancy also is provided.

Bile Duct Neoplasms↗
PubMed1995

Case report: vitamin D-mediated hypercalcemia in fungal infections.

Hypercalcemia has been well described in a variety of neoplastic and granulomatous diseases. One mechanism for this hypercalcemia is via the excess production of 1,25-dihydroxyvitamin D from extra-renal sources. The authors describe an AIDS patient infected with Cryptococcus neoformans who had suggestive evidence of vitamin D-mediated hypercalcemia. He had an elevated serum 1,25-dihydroxyvitamin D value, a normal 25-hydroxyvitamin D value, and low values for parathyroid hormone and parathyroid hormone-related peptide. Most previously reported cases of hypercalcemia associated with fungal infections did not include sufficient evidence to implicate a role for excess 1,25-dihydroxyvitamin D production, except for two case reports involving patients with hypercalcemia with infections due to Pneumocystis carinii and Candida albicans. The authors' patient's hypercalcemia resolved during treatment of his underlying infection. Patients with hypercalcemia or in whom hypercalcemia develops during a disseminated fungal infection should have vitamin D metabolites measured as part of their work-up.

AIDS-Related Opportunistic Infections↗
PubMed1992

Hypercalcemia and parathyroid disorders.

Primary hyperparathyroidism and malignancy are responsible for the majority of reported cases of hypercalcemia. Suspected hypercalcemia should be documented on more than one occasion, preferably with the measurement of ionized calcium. Determination of intact parathyroid hormone with a modern two-site immunoassay is the single most important laboratory analysis in the differential diagnosis of hypercalcemia. Intact parathyroid hormone is increased or inappropriately high in primary hyperparathyroidism and suppressed or low normal in hypercalcemia of malignancy. Midregion and carboxylterminal radioimmunoassays are less effective in separating parathyroid and nonparathyroid hypercalcemia. In malignancy, hypercalcemia may result from local osteolysis or humoral factors. Although ectopic parathyroid hormone is produced rarely and certain lymphomas secrete 1,25-dihydroxyvitamin D, parathyroid hormone-related protein is elevated in the majority of patients with humoral hypercalcemia of malignancy. Recent developments in the measurement of parathyroid hormone-related protein should help to define the physiologic function of parathyroid hormone-related protein and its role in the differential diagnosis and therapy of hypercalcemia.

Humans↗
PubMed2000

Hypercalcemia, arrhythmia, and mood stabilizers.

Recent findings in a bipolar patient receiving maintenance lithium therapy who developed hypercalcemia and severe bradyarrhythmia prompted the authors to conduct a retrospective study of bipolar patients with lithium-associated hypercalcemia. A printout of all cases of hypercalcemia that presented during a 1-year period was generated. After eliminating spurious hypercalcemias or those associated with intravenous fluids, the authors identified 18 non-lithium-treated patients with hypercalcemias related to malignancies and other medical conditions (group A) and 12 patients with lithium-associated hypercalcemia (group B). Patients in group B were not comparable to those in group A, as the latter were medically compromised and were receiving multiple pharmacotherapies. Thus, two control groups were generated: group C1, which included age- and sex-comparable lithium-treated bipolar normocalcemic patients, and group C2, which included bipolar normocalcemic patients treated with anticonvulsant mood stabilizers. The electrocardiographic (ECG) findings for patients in group B were compared with those of patients in groups C1 and C2. It was found that these groups did not differ in their overall frequency of ECG abnormalities; however, there were significant differences in the frequency of conduction defects. Patients with hypercalcemia resulting from medical diseases and bipolar patients with lithium-associated hypercalcemia had significantly higher frequencies of conduction defects. Patients in group A had significant mortality at 2-year follow-up (28%), in contrast to zero mortality in the other three groups. The clinical implications of these findings are discussed.

Adult↗
PubMed1977

Hypercalcemia and parathyroid function after renal transplantation.

Hypercalcemia after renal transplantation (post-T hypercalcemia) has been detected in 29 (16.7%) of 174 long-term survivors. The mean time of onset of hypercalcemia was 69 days after renal transplantation (range 3-210). In 18 patients the hypercalcemia was mild and resolved spontaneously (transient) from 2-65 months (mean 19) after onset. In 4 patients serum calcium normalized concurrently with rejection episodes. In 7 patients the hypercalcemia was more pronounced (permanent), being terminated by subtotal parathyroidectomy in 5 and persisting in 2 recipients. The hypercalcemia was asymptomatic except in one patient, who developed calculi in the graft and a fall in graft function, all of which disappeared after parathyroidectomy. At operation the parathyroid glands showed hyperplasia, except in one case with an adenoma in one of the hyperplastic glands. Serum phosphorus was markedly decreased, to the same extent in transiently and permanently hypercalcemic recipients. Serum parathyroid hormone (S-PTH) was increased in all of 5 patients with permanent and in 3 of 8 with transient post-T hypercalcemia. In normocalcemic and in transiently hypercalcemic recipients the mean S-PTH was identical, but significantly lower than in the permanently hypercalcemic recipients. S-PTH was suppressed to the same extent during an i.v. calcium infusion in patients with post-T hypercalcemia and with primary hyperparathyroidism.

Adolescent↗
PubMed1996

Acute management of cancer-related hypercalcemia.

OBJECTIVE: To review the pathogenesis and pharmacologic treatment of acute hypercalcemia associated with malignancy. DATA SOURCES: A MEDLINE search (1966 to 1995) of the English-language literature pertaining to acute hypercalcemia was performed. Additional literature was obtained from reference lists of articles identified through the search. STUDY SELECTION AND DATA EXTRACTION: All articles discussing the etiology and medical management of cancer-related acute hypercalcemia were considered in this review. Clinical trials reporting efficacy and safety of antihypercalcemic agents were also included. Information selected in the review was based on the discretion of the authors. DATA SYNTHESIS: Hypercalcemia is a life-threatening disorder associated with malignancy. It occurs in approximately 10-20% of patients with cancer. A variety of medications have been used in the management of hypercalcemia including bisphosphonates, calcitonin, furosemide, gallium nitrate, glucocorticoids, NaCl 0.9%, and plicamycin. Each of these agents has been reviewed with consideration of pharmacologic mechanism of action, evaluation of clinical trials, recommended dosages, efficacy, safety, cost, and role in treating cancer-related acute hypercalcemia. CONCLUSIONS: Immediate management of cancer-related acute hypercalcemia to prevent death and provide symptomatic relief is warranted. Severity determined by symptoms, calcium concentrations, and the overall status of the patient are important considerations in selecting appropriate therapy. Although the specific role of individual agents may vary, hydration remains the cornerstone of therapy. NaCl 0.9%, calcitonin, and pamidronate disodium have established roles as dominant first-line agents for the management of acute hypercalcemia associated with malignancy.

Calcitonin↗
PubMed1997

The role of interleukin-6 in the induction of hypercalcemia in renal cell carcinoma transplanted into nude mice.

Hypercalcemia is a well known complication of renal cell carcinoma (RCC). As RCCs can produce IL-6, and IL-6 may stimulate bone resorption and cause mild hypercalcemia, we examined whether IL-6 is involved in renal cancer-associated hypercalcemia in vivo. Three human renal cell carcinoma tumor lines (RC-8, RC-9, and NC-65) growing in nude mice were studied. Tumors were implanted s.c., and parameters of bone metabolism and serum human IL-6 levels were determined in relation to tumor volume (TV). All three tumor lines secreted human IL-6, although in different quantities. The maximum level of IL-6 in RC-8 was 434 pg/ml (TV, 200 mm3), that in RC-9 was 81 pg/ml (TV, 1800 mm3), and that in NC-65 was 2368 pg/ml (TV, 1800 mm3). Hypercalcemia developed in RC-8 and RC-9 tumor-bearing animals, but not in NC-65-bearing animals. The hypercalcemia in both RC-8 and RC-9 tumor lines was associated with elevated levels of PTH-related peptide (PTHrP) and loss of trabecular bone volume. Serum calcium and phosphate concentrations showed an almost linear relationship with plasma PTHrP independently of the tumor line and serum IL-6 levels. No hypercalcemia occurred in the NC-65 animals, which had the highest levels of IL-6, but no detectable plasma PTHrP and PTHrP messenger RNA expression in the tumor. Administration of neutralizing antibodies to IL-6 to RC-8 animals normalized serum calcium concentrations and PTHrP values and induced a significant inhibition of tumor growth. No such effect on tumor growth of anti-IL-6 was seen in the other two tumor lines. The normalization of serum calcium in RC-8 mice is most likely attributed to the growth-inhibiting effect of anti-IL-6 on RC-8 tumor. We conclude that IL-6 secreted by RCC does not contribute directly to hypercalcemia, but may enhance hypercalcemia by stimulating the tumor growth of a subpopulation of PTHrP-secreting carcinomas.

Animals↗
PubMed1981

Maximal urine-concentrating ability: familial hypocalciuric hypercalcemia versus typical primary hyperparathyroidism.

Impairment of urine-concentrating ability is common in persons with chronic hypercalcemia. We assessed urine-concentrating ability in 40 patients with typical primary hyperparathyroidism and 10 patients with familial hypocalciuric hypercalcemia, a disorder resembling typical primary hyperparathyroidism but lacking some of its clinical complications. Urine-concentrating ability was determined during a dehydration test of 18-22 h. The two patient groups were comparable with respect to serum calcium concentration and creatinine clearance. In the group with familial hypocalciuric hypercalcemia, the duration of hypercalcemia was probably greater, because it commences during infancy; the urinary excretion rate for calcium was lower [6.6 +/- 5.4 (mean +/- 1 SD) vs. 14.8 +/- 7.5 meq/day; P less than 0.005]. Patients with familial hypocalciuric hypercalcemia showed higher maximal urinary osmolality (800 +/- 150 vs. 664 +/- 130 mosmol/kg; P less than 0.0005). Among the patients with typical primary hyperparathyroidism, there was a negative association between maximal urinary osmolality and urinary cAMP (r = -0.40; P less than 0.05), but there was no significant relation between maximal urinary osmolality and the urinary excretion rate for calcium. Among 18 patients retested within 1 month after surgical correction of typical primary hyperparathyroidism, urine-concentrating ability did not improve. In patients with typical primary hyperparathyroidism, impairment in urine-concentrating ability reflects features of the chronic disease state, as it is not rapidly reversible by correction of that state. However, in patients with familial hypocalciuric hypercalcemia, longstanding hypercalcemia is not associated with obvious impairment of urine-concentrating ability. Complete or partial freedom from impairment of urine-concentrating ability and from calcareous renal disease are expressions of the generally mild course in familial hypocalciuric hypercalcemia.

Calcium↗
PubMed2007

The causes of hypercalcemia in Okinawan patients: an international comparison.

OBJECTIVE: Our objective was to determine the causes and relative prevalence of hypercalcemia in patients at a major community hospital in Okinawa, Japan. Additionally, we compared these causes of hypercalcemia with the previously published international data. MATERIALS AND METHODS: We analyzed all patients with hypercalcemia in a community teaching hospital in Okinawa, Japan, from 1999 to 2002 and determined the cause of hypercalcemia in each patient. We also performed a literature review of the original articles describing causes of hypercalcemia in patients from Eastern as well as Western countries. RESULTS: We identified 145 patients with hypercalcemia (median age, 69; range, 22 to 97). Major causes included malignant disorders (n=100; 69%), primary hyperparathyroidism (n=31; 21%), vitamin D-induced (n=4; 3%), and miscellaneous or unknown cause in 11 (8%). Among malignant disorders, adult T cell leukemia was the most frequent (n=35), being followed by lung cancer (n=25). Breast carcinoma was less prevalent (n=4). CONCLUSION: The major causes of hypercalcemia are malignancy and primary hyperparathyroidism in Okinawan Japanese patients. Adult T cell leukemia and lung carcinoma are among the top leading malignancies, while breast carcinoma is less frequent in this patient population. The etiologic prevalence of hypercalcemia in the Eastern population including Okinawans is significantly different from that in the Western population.

Adult↗
PubMedDate not supplied

Causes of hypercalcemia in a population of military veterans in the United States.

OBJECTIVE: To determine the various causes of hypercalcemia in a population of US veterans at the San Diego Veterans Affairs Medical Center. METHODS: A retrospective analysis of medical records was performed on 212 US veterans encountered between 1998 and 2002 with serum calcium measurements between 10.5 and 10.9 mg/dL on multiple readings or 11.0 mg/dL (or greater) on any single determination. Data were collected from the clinical records for each patient and used to determine the cause of each patient's hypercalcemia. Patients undergoing hemodialysis were excluded from this study. RESULTS: The study population consisted of 201 men (95%) and 11 women (5%), with a median age of 63 years (range, 25 to 95). Of the 212 patients, 59 (28%) had a diagnosis of malignant disease, 38 (18%) had primary hyperparathyroidism, and 114 (54%) had hypercalcemia due to a range of other causes. The mean total serum calcium concentration for all patients in this study was 11.69 mg/dL. Lung carcinoma was the most prevalent malignant condition (in 17 patients or 29% of those with cancer). A single parathyroid adenoma (in 20 of 22 patients who underwent surgical intervention) accounted for the majority of cases of primary hyperparathyroidism. Among the other identified causes of hypercalcemia, acute renal failure was the most common (in 37 patients or 17% of all patients). In 37 patients, no specific cause for the hypercalcemia was identified. CONCLUSION: To our knowledge, this is the first study to focus on hypercalcemia within the US veterans population. Although the 2 most common causes of hypercalcemia, hyperparathyroidism and malignant disease, were represented in this study, the majority of cases of hypercalcemia in this population of US veterans related to other etiologic factors.

Acute Kidney Injury↗
PubMedDate not supplied

Immobilization-related hypercalcemia after renal failure in burn injury.

OBJECTIVE: To describe a patient with hypercalcemia presumably due to immobilization in the setting of burn injury and acute renal failure. METHODS: We present a case report of a man who sustained a severe burn injury and then had renal failure and hypercalcemia. An additional series of patients with burns and immobilization was assessed for the presence of hypercalcemia. RESULTS: In a 43-year-old man with burns on 65% of his body surface area, acute renal failure developed. Renal function failed to return, and he continued to require hemodialysis. Because of the severity and extensiveness of his burns, he remained immobilized. Serum calcium levels were low during the early part of the hospitalization. On the 57th day, generalized tonic-clonic seizures developed, and he was found to have a high ionized calcium level (1.41 mmol/L). Low values were recorded for intact parathyroid hormone (2 pg/mL), 25-hydroxyvitamin D (5 ng/mL), and 1,25-dihydroxyvitamin D (4 pg/mL). Persistent and recurrent hypercalcemia eventually responded to pamidronate and calcitonin. Other than immobilization, we could identify no predisposing factors such as confounding illnesses or medications that could have caused the hypercalcemia. A review of serum ionized calcium levels in 50 consecutive patients admitted to a burn unit and immobilized for at least 20 days failed to reveal any episodes of persistent hypercalcemia. CONCLUSION: In our patient with burns and renal failure, symptomatic hypercalcemia was most likely attributable to prolonged immobilization. As patients with catastrophic illnesses survive for longer periods, additional problems such as hypercalcemia from immobilization may occur.

Acute Kidney Injury↗
PubMed2002

A case of lung cancer with hypercalcemia which was incidentally complicated with primary hyperparathyroidism due to parathyroid adenoma.

In lung cancer patients, hypercalcemia is a fairly common metabolic problem associated with malignancy. However, the occurrence of hypercalcemia in lung cancer patients means an ominous prognostic sign. As hypercalcemia often causes early death, quick diagnosis and treatment for hypercalcemia are required. A 69-year-old woman was admitted to our hospital with anorexia caused by hypercalcemia. On admission, serum level of PTH was elevated and PTHrP was normal. From the results of CT findings and transbronchial lung biopsy, the cause of the hypercalcemia was determined as lung cancer incidentally complicated with primary hyperparathyroidism. First, serum calcium level was returned to normal through hydration with saline and bisphosphonates. Next, left hemithyroidectomy for primary hyperparathyroidism was performed. Histologically, the tumor was diagnosed as parathyroid adenoma. Fifteen days later, left lower lobectomy for primary lung cancer was performed under a video-assisted thoracoscopic approach. Histologically, the tumor was diagnosed as a moderately differentiated adenocarcinoma. Four years and three months after the operation, the patient is alive and well with no sign of recurrence. When a lung cancer patient is complicated with hypercalcemia, we need to consider that primary hyperparathyroidism is a possible cause of the hypercalcemia.

Adenocarcinoma↗
PubMed1989

Signs and symptoms associated with malignancy-induced hypercalcemia.

Hypercalcemia is a common life-threatening complication that often produces discomfort for the oncology patient. Prompt detection of this complication is imperative to prevent death and reverse uncomfortable symptoms. Laboratory analysis of a serum blood sample is presently the only means available to quantify hypercalcemia. A descriptive study was undertaken to determine what symptoms prompt oncology patients and their families to seek treatment of the hypercalcemia and to identify symptoms commonly associated with mild, moderate, and severe hypercalcemia. Seven hypercalcemic oncology patients were interviewed and observed on admission and during hospitalization for treatment of hypercalcemia. An identified significant other was also interviewed on admission and throughout the hospitalization to provide the researcher with information about subtle behavioral changes. A check-list of symptoms identified in the literature as being associated with hypercalcemia was completed. Symptoms that commonly led to admission included constipation, confusion, weakness, and anorexia. The most evident changes in a particular symptom within a given degree of hypercalcemia occurred in the mental status symptoms. The resulting data have implications for nurses in terms of patient assessment and of teaching patient and family about signs and symptoms of hypercalcemia that are observable at home.

Calcium↗
PubMed1983

Association of hypercalcemia with tumors producing colony-stimulating factor(s).

Two human malignant tumors, which we previously reported to produce colony-stimulating factors (CSFs), were found to be accompanied by remarkable hypercalcemia. A patient with a CSF-producing lower jaw cancer (squamous cell carcinoma) developed a marked granulocytosis (150,000/microliters) and hypercalcemia (more than 215 mg/dl). The tumor was successfully transplanted into nude mice, which developed marked granulocytosis (300,000/microliters) and hypercalcemia (20 mg/dl). White blood cell and serum calcium concentrations of these mice decreased promptly to normal levels when the tumor was excised. Treatment with prednisolone (1.5 mg/kg) or indomethacin (5 mg/kg) had no effect on the serum calcium level of these mice. Parathyroid hormone or prostaglandin E was not increased in the serum of the mice or in the tumor tissue. However, the mice bearing the tumor excreted extremely large amounts of calcium in their urine, and their bony tissues contained less calcium and phosphorus than controls. Moreover, histology of bony tissues of these nude mice clearly demonstrated the decrease in trabecular tissues and cortical thickness as well as remarkable activation of osteoclasts. Another patient with a CSF-producing bronchogenic squamous cell carcinoma showed mild granulocytosis and hypercalcemia. The biopsied tumor tissue was transplanted into nude mice, which developed marked granulocytosis (300,000/microliters) and also severe hypercalcemia (18 mg/dl). These results suggest the presence of a new syndrome of granulocytosis and hypercalcemia associated with CSF-producing tumors. The causal mechanism of the hypercalcemia was shown to be some humoral factor which activates osteoclasts other than parathyroid hormone. Neither prostaglandins nor osteoclast-activating factor seemed to be the cause of the hypercalcemia.

Adult↗
PubMed1995

[The value of the parathyrin-related protein (PTH-RP) in the diagnosis of cancer-associated hypercalcemia].

BACKGROUND: The parathyrine related protein (PTH-RP) is very similar, both in structure and in function, to the PTH and is considered as a mediator in humoral hypercalcemia in cancer. The aim of this study was to know the clinical value of PTH-RP measurement. METHODS: Serum PTH-RP concentrations were studied in 22 healthy subjects, 13 patients with primary hyperparathyroidism, 9 patients with solid neoplasms and normocalcemia, 26 patients with solid neoplasms and hypercalcemia and 4 patients with hematologic neoplasms and hypercalcemia. The PTH-RP was quantified by a competitive radioimmunoassay technique using a specific antibody of the PTH-RP 1-40 fragment. Intact parathyrine (i-PTH) was quantified by an IRMA method using 2 polyclonal antibodies (INCSTAR). RESULTS: Fifteen (68%) of the healthy controls presented undetectable serum PTH-RP concentrations. The serum PTH-RP concentration was normal in all those patients with hyperparathyroidism. Elevated serum PTH-RP values were not found in patients with solid neoplasms and normocalcemia or in those with hematologic neoplasms and hypercalcemia. High values of PTH-RP were observed in 8 out of 9 (88%) of the patients with solid neoplasms and hypercalcemia with bone metastasis and in 7 out of 11 (63%) of the patients with bone involvement. CONCLUSIONS: Serum parathyrine-related protein was found to be high in a large proportion of patients with solid neoplasms and hypercalcemia. Serum PTH-RP determination is useful in the clinical investigation of patients with hypercalcemia. Even in patients with bone metastasis, hypercalcemia may have a humoral background.

Adult↗
PubMed1993

Update on the medical treatment of hypercalcemia of malignancy.

Recent information on the pathophysiology and treatment of hypercalcemia of malignancy is reviewed, and the roles of two new agents, gallium nitrate and pamidronate, are discussed. Current evidence suggests that parathyroid hormone-related protein is the most important mediator of humoral hypercalcemia of malignancy. In patients with local osteolytic hypercalcemia, cytokines have been implicated as mediators. Effective treatment of hypercalcemia of malignancy may improve patients' quality of life, although an episode of hypercalcemia is a poor prognostic indicator for survival. Gallium nitrate is more effective than salmon calcitonin and possibly more effective than etidronate in the treatment of hypercalcemia of malignancy. The primary adverse effect of gallium nitrate is nephrotoxicity, and its use must be avoided in patients who have renal dysfunction or who are receiving nephrotoxic drugs. Pamidronate is more effective than etidronate in the treatment of hypercalcemia of malignancy and can be administered as a single i.v. dose. The adverse effects of pamidronate include mild fever, hypocalcemia, and hypophosphatemia. Compared with gallium nitrate, pamidronate offers a more convenient dosing regimen, is less frequently associated with nephrotoxicity, and is less expensive. Single i.v. doses of either pamidronate or plicamycin effectively lower serum calcium levels and are reasonable choices for maintenance therapy. Gallium nitrate and pamidronate may be slightly more effective than previously available agents for initial treatment of hypercalcemia. Pamidronate currently offers the best combination of effectiveness, ease of administration, and a low rate of adverse effects.

Animals↗
PubMed1980

Incidence of hypercalcemia and malignant neoplasm.

Hypercalcemia often complicates the course of patients with malignant neoplasms. Since this metabolic derangement is potentially lethal, knowledge of the expected relative incidence of hypercalcemia in various malignant neoplasms is of importance. The incidence of hypercalcemia and malignant neoplasm at the Clinical Center, National Institutes of Health, Bethesda, Md, was reviewed. Of 17,706 admissions (multiple admissions counted once), the overall incidence of hypercalcemia for all disorders was 5.0%; of these, 38.0% (338 patients) had associated neoplasms (99.4% malignant). Primary hyperparathyroidism represented 19.6% of those admitted with hypercalcemia, and nonneoplastic disorders represented 10.7%. Of the 338 patients with hypercalcemia associated with neoplasia, 44.1% had hematologic and 41.4% had solid neoplasms. The relative incidences of hypercalcemia and neoplasia are reported for each of the solid and hematologic neoplasias evaluated.

Endocrine System Diseases↗