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PubMed1983

Hypercalcemia in head and neck carcinoma. Incidence and prognosis.

A retrospective review of all head and neck cancers seen between January 1, 1975, and September 1, 1981, at Harper-Grace Hospitals, Detroit, Michigan, was performed. Of 1438 patients with head and neck cancers, 41 (2.9%) had hypercalcemia (calcium greater than 11.0 mg%) during the course of their disease. The incidence of hypercalcemia by site was 13 of 351 (3.7%) larynx, 7/280 (2.5%) pharynx, 19/733 (2.6%) oral cavity (floor of mouth 4/171, tongue 9/209, tonsil 5/176, palate 1/95, other 0/82, 2/26 (7.7%) nasal cavity, and 0/48 salivary gland carcinomas. Chest radiograph results were positive for mass lesions in 17/35 (49%). Bone scans and/or x-ray results were positive in 15/31 (48%), negative in 16/31 (52%), and were not evaluated in 10 patients. Of five patients tested, all had inappropriately elevated serum parathyroid hormone (PTH) for their serum calcium level. The hypercalcemia was medically treated in 29/41 (70%), with return-to-normal calcium levels in 17/29 (59%). Twelve patients (30%) received only terminal care. Survival from the diagnosis of hypercalcemia ranged from 1 to 514+ days (mean, 80+ days; median 33 days). It is concluded that hypercalcemia is unusual in head and neck carcinoma. Furthermore, hypercalcemia frequently is a late manifestation and terminal event. Finally, hypercalcemia in some patients may be mediated by PTH production.

Head and Neck Neoplasms↗
PubMed1993

Incidence of hypercalcemia in patients with malignancy referred to a comprehensive cancer center.

BACKGROUND: Hypercalcemia is a serious and not infrequent complication of malignant diseases; precise information about the incidence of hypercalcemia is not readily available. The study was designed to determine the incidence of hypercalcemia in patients with cancer. METHODS: Retrospective analysis was done of laboratory data from 7667 patients registered at M.D. Anderson Cancer Center for the first time during 1989 for whom serum calcium levels were determined during the first 2 months after registration. RESULTS: Severe hypercalcemia (serum calcium level of more than 12.0 mg/100 ml) was present in 40 patients (0.52%); it occurred most often in patients with renal cell cancer (1.42%) and non-small cell lung cancer (1.03%). Less frequent diagnoses were multiple myeloma (0.79%), leukemia (0.63%), non-Hodgkin lymphoma (0.26%), and cancer of the gastrointestinal tract (0.20%). Moderate hypercalcemia (calcium levels of 10.8-12.0 mg/100 ml) was present in 48 patients (0.63%); it occurred most often in patients with renal cell cancer (3.30%) and multiple myeloma (2.38%). Less frequent diagnoses were non-small cell lung cancer (0.89%), non-Hodgkin lymphoma (0.79%), leukemia (0.63%), and cancer of the gastrointestinal tract (0.51%). The presence of hypercalcemia was associated with increased frequency of distant metastases, bone metastases, and increased mortality consistent with other studies of the prognostic effect of this complication. CONCLUSIONS: Hypercalcemia may appear as a frequent complication in patients with cancer at some time during the course of their disease, but its incidence is relatively low.

Adolescent↗
PubMed2002

Hypercalcemia associated with parathyroid hormone-related protein at the terminal stage of uncomplicated squamous cell carcinoma in the head and neck region.

BACKGROUND: Parathyroid hormone-related protein (PTHrP) is mainly responsible for hypercalcemia in squamous cell carcinomas (SCCs). METHODS: We retrospectively checked the appearance of hypercalcemia among 33 patients who died with head and neck SCC. Serum concentrations of C-terminal region of PTHrP (C-PTHrP) were measured in 15 of them. The intracellular PTHrP expression was immunohistochemically stained in 42 SCC sections obtained from the 33 before the appearance of hypercalcemia. RESULTS: Hypercalcemia appeared in 24 of the 33, and increased serum C-PTHrP levels were confirmed in 11 of 12 hypercalcemic patients. PTHrP was identified in all SCC sections, and a stronger intensity than in normal squamous epithelia was observed in 50% of those obtained within 1 year before the onset of hypercalcemia. CONCLUSION: A high incidence of PTHrP-induced hypercalcemia was shown among patients dying with head and neck SCCs. The intracellular increase in PTHrP might be observed preceding hypercalcemia.

Adult↗
PubMed1989

Hypercalcemia related to the poor prognosis of patients with squamous cell carcinoma of the esophagus.

A review of 208 cases of surgically treated squamous cell carcinoma of the esophagus revealed 16 (7.7%) with hypercalcemia. There was no evidence of bone metastases in 13 (6.3%) of the patients with hypercalcemia. Pathogenesis of this hypercalcemia without bone metastases was suggested to be multifactorial. Anastomotic leakage and malnutrition because of fasting were the most possible causes of mild hypercalcemia, and moderate to severe hypercalcemia was thought to be due to subclinical and clinical recurrence of the tumor, probably with PTH-like hormonal activity. Overall survival rates in the groups with and without hypercalcemia were 18.2 and 61.7% at the 12th postoperative month and 9.1 and 37.8% at the 24th month, respectively. Thus hypercalcemia is a significant prognostic factor linked to an unfavorable clinical course even in patients with no evidence of bone metastases.

Bone Neoplasms↗
PubMed2005

Acute lymphocytic leukemia in adolescence with multiple osteolytic lesions and hypercalcemia mediated by lymphoblast-producing parathyroid hormone-related peptide: a case report and review of the literature.

BACKGROUND: Osteopathy is one of the common initial symptoms of acute lymphocytic leukemia (ALL) in children and adolescents, but multiple osteolysis accompanied by hypercalcemia is rarely observed. PROCEDURE: We treated a 14-year-old female who had multiple osteolytic lesions and hypercalcemia at initial onset of ALL. In this case we examined some humoral factors, which are known to associate with hypercalcemia in malignancies. RESULTS: Parathyroid hormone-related peptide (PTHrP) was elevated in serum, and reverse transcriptase-polymerase chain reaction and immunohistochemistry revealed that the lymphoblasts produced PTHrP directly. Other humoral factors related to hypercalcemia were not detected. ALL relapsed in the bone marrow 3 months after achieving complete remission, and hypercalcemia and elevation of serum PTHrP were also observed. A second remission could not be achieved and hypercalcemia continued. The patient received allogeneic bone marrow transplantation. The serum calcium level became normal after the conditioning therapy. Before engraftment, however, the patient died of infection. CONCLUSIONS: The present case suggests that blast-producing PTHrP might be associated with multiple osteolytic lesions and hypercalcemia. PTHrP expressed in the lymphoblasts may, in itself, confer a survival advantage to lymphoblasts and contribute to the refractory nature of the disease.

Adolescent↗
PubMed1986

Bile secretion in acute and chronic hypercalcemia in the cat.

The reported coincidence of primary hyperparathyroidism and cholelithiasis led us to investigate the effects of acute and chronic hypercalcemia on bile secretion in cats. Acute hypercalcemia (6-7 mmol/liter) was induced by an intravenous calcium infusion. Chronic hypercalcemia (3-4 mmol/liter) was induced and maintained for 8-10 weeks by treatment with subcutaneous vitamin D3, oral dihydrotachysterol, and feeding a calcium-rich diet. Bile secretion was then studied in acute experiments. We found that calcium concentrations in serum and hepatic bile were similar during all experimental normo- or hypercalcemic conditions (y = 1.12x - 0.85; r = 0.76). Biliary volume outputs were significantly decreased during both acute (P less than 0.002) and chronic (P less than 0.05) hypercalcemia compared with normocalcemic controls. Acute hypercalcemia also decreased total bile acid outputs (P less than 0.05), but had no effect on biliary bile acid concentrations. The inhibitory effect of acute hypercalcemia on biliary fluid and bile acid secretion was dose dependent and not antagonized by atropine. These findings suggest that calcium is secreted in hepatic bile at similar concentrations as present in the serum and that elevations of serum calcium concentration inhibit biliary volume and bile acid secretion in cats. Similar effects of hypercalcemia on bile composition in humans might promote calcium salt precipitation in bile.

Acute Disease↗
PubMedDate not supplied

Management of hyperparathyroid patients with grave hypercalcemia.

During recent years the total number of patients undergoing surgery for hyperparathyroidism has markedly increased, but the annual number of cases with substantial hypercalcemia has remained unchanged. Parathyroid carcinoma and water clear cell hyperplasia cause more severe hypercalcemia than other kinds of hyperparathyroidism. Grave hypercalcemia due to hyperparathyroidism is more common among the elderly, but can occur during pregnancy and also among children. Occasionally, a patient with hyperparathyroidism can also have another cause of the hypercalcemia and does not become normocalcemic until adequately treated for both. The suspicion of grave hypercalcemia should arise due to its clinical features. Determination of serum calcium and intact parathyroid hormone concentrations establishes the diagnosis. The basic treatment of grave hypercalcemia is to rehydrate the patient and to restore the sodium losses. To further lower the serum calcium value we have found bisphosphonates to be very effective. The definitive treatment of grave hypercalcemia due to hyperparathyroidism is surgery. As a last resort, frail patients with grave hyperparathyroidism can undergo surgery under local anesthesia. Repeat operations can improve the prognosis of patients with metastatic parathyroid carcinoma. Selective venous catheterization with blood sampling for determination of intact parathyroid hormone can be helpful in localizing recurrent disease.

Acute Disease↗
PubMed1996

Does tuberculosis really cause hypercalcemia?

Hypercalcemia has been known to be associated with tuberculosis. In some studies it has been reported to occur commonly. It seems that the studies in which tuberculosis was complicated by hypercalcemia were retrospective and therefore the other causes of hypercalcemia could not be excluded. We have a great deal of experience concerning tuberculosis and have not seen a patient with hypercalcemia due to tuberculosis itself. Therefore we aimed to investigate whether tuberculosis really cause hypercalcemia in a prospective study. We evaluated 104 patients with tuberculosis aged between 14-85 (mean +/- SD 38.5 +/- 15) years, 73 males and 31 females, and 50 age-matched healthy subjects aged between 19-70 (mean +/- SD 39 +/- 13) years, 33 males and 17 females. No significant differences between the patients and healthy subjects were detected in terms of 250HD3, calcium and phosphate levels. Albumin levels were significantly higher in the control group than in the tuberculous group (p < 0.02). No significant difference was found between the calcium levels measured before the therapy (2.4 +/- 0.1 nmol/L) and after the therapy (2.4 +/- 0.2). We think that patients with tuberculosis are not at risk for hypercalcemia either before or during treatment and the development of hypercalcemia as a result of tuberculosis is rather doubtful and needs to be clarified.

Adolescent↗
PubMed1976

Hypercalcemia in acute uremia and following citric acid administration: differential effect on parathyroid gland microtubule content.

Hypercalcemia, which occurs 4 hr after bilateral nephrectomy in normal rats, is not seen 4 hr after either bilateral ureterotomy or sham surgery. These results indicate that it is loss of renal mass per se, not the uremic syndrome, which is responsible for the hypercalcemia. Citric acid levels also increase 4 hr after nephrectomy, and a degree of hypercalcemia and hypercitricemia comparable to that which follows nephrectomy can be produced by administration of citric acid to normal rats. In an attempt to evaluate the role of the parathyroid gland in the development of hypercalcemia in these two situations, the microtubule content of parathyroid gland chief cells was determined by ultrastructural sterologic techniques 4 hr after either bilateral nephrectomy or citric acid administration. The results of these measurements indicate that parathyroid gland chief cell microtubule content increases after citric acid administration but not following bilateral nephrectomy. The significance of these results is not clear. However, since a previous study has suggested a correlation between increased microtubule content and increased secretory status in the chief cell, one may speculate that increased microtubule content resulting from citric acid administration may also be associated with increased parathyroid hormone secretion. By this formulation, citric acid-induced hypercalcemia would be secondary to increased parathyroid hormone secretion, but the transient hypercalcemia that occurs after nephrectomy would take place in the absence of an increase in parathyroid hormone secretion. In this latter instance, it is possible that loss of the kidney, a major site of parathyroid hormone removal from plasma, leads to an increase in circulating parathyroid hormone level, and hypercalcemia, in the absence of an increase in hormone secretion rate.

Animals↗
PubMed2005

Prognosis of hypercalcemia in aerodigestive tract cancers: study of 136 recent cases.

Recent data issuing the prognostic impact of hypercalcemia on outcome of aerodigestive tract cancers are spare. To assess the prognosis and the survival of head and neck cancer patients with hypercalcemia, we reviewed 136 recent successive cases, including also oesophageal and lung cancers. Data were collected from a retrospective database (July 2002-January 2004). Hypercalcemia was defined by calcemia level above 2.55 mmol/l. Univariate analysis for prognosis was performed with Mann-Whitney test (continuous variables) and Odd Ratio with 95% confidence interval (categorical variables). The primary locations were : oropharynx and oral cavity (79, 58%), hypopharynx (13, 9.5%), larynx (10, 7.3%), oesophagus (17, 12.5%) and lung (17, 12.5%). There were 23 females and 123 males, with a median age of 53 (18-86). The incidence of bone metastasis was low: 20/136, 14.5%. At cancer diagnosis, 32 hypercalcemia were observed. With a median follow-up of 88 days (2-553), we observed 98 deaths (overall mortality=72%). The median overall survival was 35 days (2-553+). The pejorative prognostic factors were: male gender (OR=2.64 CI 95% 1.07-6.82), age inferior to 50 (OR=2.67 CI 95% 1.23-5.8), presence of distant metastasis (OR=4.45 CI 95% 1.8-11.01), elevation of alkaline phosphatases (OR=7 CI 95% 2.73-17.9) and need of hospitalization for intravenous hydratation (OR=5.11 CI 95% 1.99-13.17). We observed 39 recurrences of hypercalcemia. The predictive factors for recurrence of hypercalcemia were: age superior to 50 (OR=4.61 CI 95% 2.02-10.52), male gender (OR=38.22 CI 95% 12.2-89), calcemia level superior to 2.7 mmol/l (OR=3.08 CI 95% 1.42-6.64) and absence of diphosphonates (bisphosphonates: OR=2.16 CI 95% 1.01-4.63). Despite use of diphosphonates (infusions of pamidronate), hypercalcemia is associated with very poor prognosis. Tumour location and level of calcemia had no prognostic value.

Adolescent↗
PubMed1983

Hypercalcemia associated with renal cell carcinoma: probable role of neoplastic stromal cells.

Sarcomatous proliferation of the fibroblast-like stromal cells in renal cell carcinoma was found in three patients who had apparently tumor-associated hypercalcemia but no evidence of bone metastases. The proliferation of stromal cells was not found in 20 patients who also had renal cell carcinoma without hypercalcemia. Immunoreactive parathormone-like substance was detected in two of the three patients with hypercalcemia, despite high levels of serum calcium. The parathormone assay was not conducted on the third hypercalcemic patient, however. Buffer extract from one of the tumors associated with hypercalcemia was able to elicit an increase of the serum calcium in rats, whereas buffer extract from a tumor not associated with hypercalcemia failed to induce hypercalcemia in rats. Findings suggest that the stromal cells of renal cell carcinoma may play a role in the tumor-associated hypercalcemia. The exact nature of the hypercalcemic agent is uncertain. However, in the case studied it appears that a parathormone-like substance was responsible.

Adenocarcinoma↗
PubMed1992

Reduced risk of hypercalcemia for hemodialysis patients by administering calcitriol at night.

Renal osteodystrophy therapy in dialysis patients with calcitriol and intestinal phosphate binders containing calcium entails the risk of hypercalcemia. A study was performed using 35 hemodialysis patients to see whether the time of day when calcitriol is administered influences the incidence of hypercalcemia. It was shown that simply by administering at night (11:00 PM), the occurrence of hypercalcemia was significantly reduced. While greater than 80% of patients developed hypercalcemia when calcitriol was administered in the morning, when administered at night, this figure was only 50% (P less than 0.013). At the same time, the extent of hypercalcemia when calcitriol was administered at night was significantly lower than when it was administered in the morning. The incidence of hypercalcemia occurred regardless of the type of phosphate binder containing calcium used, whether it was calcium acetate or calcium carbonate. In addition, hypercalcemic episodes were always associated with hyperphosphatemia. On the basis of the above information, it would be expedient to administer calcitriol at night to dialysis patients, in order to reduce the risk of hypercalcemia and to preserve the hypophosphatemic effect of the applied intestinal phosphate binders.

Acetates↗
PubMed2003

Treatment of malignancy-associated hypercalcemia and cachexia with humanized anti-parathyroid hormone-related protein antibody.

Parathyroid hormone-related protein (PTHrP) plays a central role in humoral hypercalcemia of malignancy (HHM), which is one of the most frequent paraneoplastic syndromes. PTHrP produced by the tumor acts through a common PTH/PTHrP receptor to promote bone resorption, inhibit calcium excretion from the kidney, and induce hypercalcemia. Patients with HHM often develop cachexia associated with typical symptoms such as anorexia, malaise, nausea, constipation, polyuria, polydipsia, and confusion. The etiology of the cachexia is not fully understood but is thought to be caused by hypercalcemia and various cytokines such as interleukin-6, tumor necrosis factor-alpha, leukemia inhibitory factor, and others. In this study, we investigated the role of PTHrP in hypercalcemia and cachexia in HHM by using humanized anti-PTHrP antibody. A mouse monoclonal antibody that binds to PTHrP amino acid sequence 1-34 and inhibits PTHrP function has been humanized to create a specific and potent agent for the treatment of patients with HHM. The mouse monoclonal antibody has been shown to have antihypercalcemic activity against nude mice bearing human tumors. Because a mouse antibody is highly immunogenic in human patients, the complementarity-determining regions from the mouse antibody were grafted into a human antibody. The resulting humanized antibody specifically recognizes PTHrP(1-34) and neutralizes PTHrP functions in vitro and in vivo. The humanized anti-PTHrP antibody was administered intravenously to HHM model animals bearing tumors such as LC-6 human lung carcinoma. These animals showed symptoms similar to those of patients with HHM (eg, hypercalcemia and cachexia). The humanized anti-PTHrP antibody-treated animals responded with normalization of blood ionized calcium level through an improvement of bone metabolism and calcium excretion. Moreover, the treated animals also showed an improvement in body weight, ultromotivity, metabolic alkalosis, food consumption, water intake, serum phosphorus, and renal function. Consequently, the humanized antibody-treated animals experienced complete resolution of hypercalcemia and cachexia. These results suggest that the humanized antibody would be an effective and beneficial agent for patients with HHM, and that PTHrP is a major pathogenetic factor of hypercalcemia and cachexia in patients with HHM.

Animals↗
PubMed1996

The humoral hypercalcemia of benignancy. A newly appreciated syndrome.

It has become recently appreciated that the hypercalcemia of malignancy is commonly caused by the increased production of parathyroid hormone-related protein (PTHrP) by the cancer. In fact, the demonstration of increased PTHrP production in a patient with hypercalcemia is regarded as pathognomonic of malignancy. The authors describe a patient with a benign ovarian lesion that produced PTHrP and caused hypercalcemia. They identify other reports of hypercalcemia associated with hypercalcemia and benign tumors, and refer to this syndrome as the humoral hypercalcemia of benignancy. Although apparently rare, a benign PTHrP-producing tumor should be considered in the differential diagnosis of hypercalcemia.

Adult↗
PubMed2002

Poorly differentiated colon carcinoma with neuroendocrine features presenting with hypercalcemia and cutaneous metastases: case report and review of the literature.

Humoral hypercalcemia is rarely associated with colon carcinoma; cutaneous metastases from colon carcinoma are also infrequent. To the authors' knowledge, no cases of colon carcinoma presenting with both hypercalcemia and cutaneous metastases have been reported to date. A case of advanced poorly differentiated colon carcinoma with neuroendocrine features with both humoral hypercalcemia of malignancy (HHM) and cutaneous metastases is presented. A poorly differentiated colon carcinoma with neuroendocrine features occurred in a 42-year-old patient with metastases to the liver, both femurs, left orbit, and scalp. The hypercalcemia was caused by the expression of a parathyroid hormone related peptide by both the primary and cutaneous metastatic tumors. Bisphosphonate treatment helped normalize serum calcium in a few days, but hypercalcemia recurred approximately 3 weeks later. Chemotherapy only mildly reduced the size of the cutaneous metastases. The patient died 8 months after initial diagnosis. To the authors' knowledge, the case presented in the current study is the first to be reported with both HHM and cutaneous metastases. Hypercalcemia and cutaneous metastases are separately associated with a poor prognosis and indicate advanced and widely metastatic disease. Although still unclear, the mechanism by which colon cancer causes cutaneous metastases and hypercalcemia, in light of current theories presented in the literature, is discussed.

Adult↗
PubMed2003

Parathyroid hormone-related protein and hypercalcemia in patients with metastatic melanoma: case report and review.

Hypercalcemia associated with malignancy has been attributed to osteolytic processes secondary to bony metastases and to humoral factors causing increased bone resorption and decreased renal excretion of calcium. Parathyroid hormone-related protein (PTH-rP) is a humoral factor that has been associated with hypercalcemia in renal cell carcinoma, squamous cell carcinoma, and bladder carcinoma. Hypercalcemia does occur in patients with melanoma; however, few studies have reported on hypercalcemia in these patients, and even fewer have described a direct connection to PTH-rP. We here report a patient with stage IV malignant melanoma presenting with severe hypercalcemia associated with elevated PTH-rP levels. Immunohistochemistry showed strong expression of PTH-rP in biopsy of the patient's subcutaneous masses. In addition, we found a 4.9% incidence of hypercalcemia in 1,146 consecutive patients treated for metastatic melanoma at the Surgery Branch of the National Cancer Institute between January 1, 1988 and March 31, 2000. Thus, PTH-rP may play a significant role in severe hypercalcemia in patients with metastatic melanoma. The discovery of PTH-rP and relevant literature will also be reviewed.

Adult↗
PubMed2006

Hypercalcemia in the emergency department.

BACKGROUND: Severe hypercalcemia can be life-threatening. However, its incidence and the underlying causes in the emergency department (ED) have not been determined. In the present study, we investigated these issues and the impacts on renal function and patients' survival. METHODS: We performed a retrospective study to analyze the patients with hypercalcemia in the ED for 1 year. Serum total calcium level greater than 10.3 mg/dL was defined as hypercalcemia. RESULTS: During the study period, 321 of 4293 patients (7.5%) were found to have hypercalcemia (serum calcium 11.7 +/- 1.6 mg/dL). Most of them had mild hypercalcemia (calcium level < 12.0 g/dL, 70.7%). Malignancy (36.4%) and uremia (32.4%) were the most common underlying causes. Normal renal function was observed in only 75 (23.4%) of all patients with hypercalcemia. The total mortality rate was 23.1%, and death was associated with male gender, higher calcium level, lower hemoglobin, and malignancy (all P < 0.05). Logistic analysis found that serum calcium and hemoglobin levels were independent risk factors for mortality. CONCLUSIONS: Severe hypercalcemia is frequently and life-threatening in the ED. Therefore routine determination of serum calcium level is recommended, and immediate therapy should be initiated to treat the patients at high risk.

Adult↗
PubMed2005

Hypercalcemia and childhood cancer: a 7-year experience.

Hypercalcemia is a rare but potentially fatal complication during the management of childhood cancer. The treatment of severe hypercalcemia in children has not been clearly defined. The authors present a retrospective series of 16 children (11 boys and 5 girls) with severe hypercalcemia (>/=2.9 mmol/L) treated between 1997 and 2004 for malignancy. Median serum calcium level was 3.14 mmol/L. Hypercalcemia was present at the initial diagnosis of cancer (eight patients) or occurred during treatment (five patients) or during relapse (three patients). Three children had several episodes of hypercalcemia. All children were treated by hydration for a median of 7 days (range 2-12 days). Eight patients received intravenous pamidronate. The other treatments were adapted to the mechanism of hypercalcemia. Serum calcium levels were lowered to below 3 mmol/L after a median of 2 days and to below 2.7 mmol/L after a median of 4 days after starting treatment. Pamidronate was well tolerated apart from one case of multifactorial renal failure. Intravenous pamidronate is a safe and effective treatment for severe cancer-related hypercalcemia in children. Specific therapy must be initiated as soon as possible. Serum calcium levels must be monitored for a fortnight after administration of pamidronate due to the risk of hypocalcemia.

Adolescent↗