Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Hypercalcemia”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMedDate not supplied

Humoral hypercalcemia of hepatocellular carcinoma associated with elevated levels of parathyroid-hormone-related-peptide.

Parathyroid-hormone-related-peptide (PTHrP) has been shown to be important in the pathogenesis of hypercalcemia of malignancy. The malignancies most commonly associated with hypersecretion of PTHrP include squamous cell carcinoma and breast cancer. The pathogenesis of hypercalcemia associated with hepatocellular carcinoma was evaluated in this study. Two male patients with hepatocellular carcinoma were found to have severe hypercalcemia at initial presentation. PTHrP was measured with radioimmunoassay in these two patients before treatment as well as in nine other patients with hepatocellular carcinoma but without hypercalcemia. The levels were markedly elevated in the two patients with hypercalcemia (29.3 and 32.1 pM), but were less than 5 pM in the nine patients without hypercalcemia. These results suggest that PTHrP was important in the pathogenesis of hypercalcemia associated with hepatocellular carcinoma in these men.

Journal Article↗
PubMed1978

Hypercalcemia and head and neck cancer. Bony metastases from tongue cancer.

Hypercalcemia causes lethargy and coma in patients with head and neck cancer. It is important to realize that coma may be due to hypercalcemia and need not be a terminal event in the progress of the tumor. Also, the development of hypercalcemia in a previously normocalcemic patient requires investigation as to the cause of the hypercalcemia. I report two cases of comatose patients, hypercalcemic from bony metastases from tongue cancer, in whom treatment by furosemide and intravenous fluid diuresis, prednisone, sodium phosphate, and mithramycin produced worthwhile remissions. Hypercalcemia may be due to (1) bony metastases, (2) pseudohyperparathyroidism, (3) unrelated associated parathyroid tumors, or (4) a second primary tumor. Even with treatment, hypercalcemia is a bad prognostic sign in patients with head and neck cancer.

Bone Neoplasms↗
PubMed1991

Frequency of the hypercalcemia-leukocytosis syndrome in oral malignancies.

There have been a number of reports over the last 15 years of patients with cancer who develop both leukocytosis and hypercalcemia, particularly in patients with cancers of the oral cavity. In this study, the authors report the frequency of hypercalcemia and leukocytosis in 225 patients with oral malignancies. Ten patients (4.4%) had hypercalcemia, 11 patients (4.9%) had leukocytosis, and five (2.2%) had both hypercalcemia and leukocytosis. The occurrence of these two distinct paraneoplastic syndromes in the same patients was greater than could have been expected from chance alone (chi-square = 45.8, P less than 0.0001). This study demonstrates that although hypercalcemia and leukocytosis are relatively uncommon in oral cancers, when they do occur they are frequently associated. To the knowledge of the authors, this is the first report in which the frequency of the association hypercalcemia and leukocytosis is studied in detail in large numbers of patients with oral cancer.

Adenocarcinoma↗
PubMed1992

Humoral hypercalcemia in seminomas.

Seminomas are germ cell tumors that are rarely associated with hypercalcemia. In this report, four cases of seminoma with concomitant hypercalcemia are presented and another three from the literature are reviewed. All seven patients exhibited hypercalcemia with a normal serum concentration of inorganic phosphorus and no evidence of skeletal metastases. The peripheral venous level of parathyroid hormone (PTH) was normal in four of the five patients in whom it was measured. The serum concentration of calcitriol was elevated in the two patients in whom it was measured. After systemic chemotherapy, the serum "corrected" total calcium concentration returned to normal and remained normal; the decrease in the levels temporally paralleled the decrease in tumor volume. Both patients with elevated calcitriol levels remained eucalcemic after treatment of the malignancy, suggesting that the increased serum calcitriol level was linked to the development of hypercalcemia as this humoral agent was inappropriately elevated by patients with this syndrome. In contrast to many forms of malignancy, the development of hypercalcemia did not adversely affect the prognosis of the patients with seminoma, since all seven patients entered complete remission. Hypercalcemia appears to be heretofore unrecognized paraneoplastic syndrome associated with seminoma.

Adult↗
PubMed2000

Hypercalcemia due to parathyroid hormone-related protein produced by primary ovarian clear cell adenocarcinoma: case report.

OBJECTIVE: Amongovarian carcinomas, clear cell adenocarcinoma is one of the most common histologic subtypes associated with hypercalcemia. However, the mechanisms of hypercalcemia in clear cell adenocarcinoma are still unclear. In the following case report, we tried to determine the etiology of hypercalcemia and also to demonstrate the management of hypercalcemia diagnosed preoperatively. CASE: A 49-year-old woman was diagnosed as having a malignant ovarian tumor with hypercalcemia caused by elevated serum parathyroid hormone-related protein (PTHrP) prior to her primary surgery. Treatment with disodium incadronate promptly normalized the serum calcium level. An immunohistochemical study demonstrated PTHrP expression in the primary ovarian lesion, but not in the metastatic lesion. A Northern blot analysis of the cancer cells from the ovarian tumor confirmed the presence of PTHrP mRNA. CONCLUSION: Humoral hypercalcemia of malignancy in this case has been conclusively shown to be due to the production of PTHrP at the primary ovarian tumor, based on both immunohistochemical and molecular analyses.

Adenocarcinoma, Clear Cell↗
PubMed2000

Immunohistochemical detection of parathyroid hormone-related protein in a squamous cell carcinoma arising from mature cystic teratoma causing humoral hypercalcemia of malignancy.

BACKGROUND: Humoral hypercalcemia of malignancy is a cancer-related hypercalcemia caused by the production of humoral factors by malignant cells in patients without bone metastases. Squamous cell carcinomas are the tumors most frequently associated with humoral hypercalcemia of malignancy, and parathyroid hormone-related protein (PTH-rP) is the main humoral factor implicated. Squamous cell carcinoma arising from mature cystic teratoma is a rare diagnosis itself, much less the description of associated hypercalcemia, despite the fact that the normal keratinocytes produce parathyroid hormone-related protein. CASE: We present a well-documented case of squamous cell carcinoma arising from mature cystic teratoma of the ovary, complicated by hypercalcemia in a patient with high levels of plasma parathyroid hormone-related protein and immunohistochemical evidence of parathyroid hormone-related protein expression by the tumor cells. CONCLUSION: In this case, the carcinoma cells had already produced PTH-rP in the primary tumor although the serum calcium levels had not been significantly high at surgery. It is therefore suggested that hypercalcemia may have occurred after PTH-rP production had overcome the homeostatic level during the terminal stage.

Aged↗
PubMed1989

Humoral hypercalcemia complicating adenosquamous carcinoma of the proximal colon.

Hypercalcemia as a complication of carcinoma of the colon is uncommon (1). It usually occurs in the presence of anorectal or rectal carcinoma that metastasizes to the lumbosacral vertebrae (2-4). Hypercalcemia complicating colon carcinoma in the absence of bone metastases--so-called humoral hypercalcemia of malignancy or paraneoplastic hypercalcemia--is rare. Only two such cases associated with adenocarcinoma of the colon (5,6) and two cases associated with adenosquamous carcinoma of the distal colon (rectum and sigmoid) (7) have been reported. We describe the first reported case of an adenosquamous carcinoma of the cecum and ascending colon that was accompanied by severe humoral hypercalcemia. The hypercalcemia was associated with a parathyroid hormone (PTH)-like substance.

Adenocarcinoma↗
PubMedDate not supplied

Electrocardiographic evidence for a cardioprotective effect of nifedipine during experimental hypercalcemia.

To investigate the effect of nifedipine on hypercalcemic electrocardiographical alterations, steadily increasing hypercalcemia was induced in guinea-pigs by continuous calcium gluconate infusion until cardiac arrest occurred. During the experimental time the electrocardiograms were continuously recorded and compared in animals with and without pretreatment by nifedipine (Adalat). The hypercalcemia-induced electrocardiographical alterations intensified during increasing serum calcium levels. Ascending serum potassium and magnesium levels indicated increasing cell damage with a leak of these mainly intracellular ions. Pretreatment by nifedipine did not significantly influence the hypercalcemia-induced bradycardia and augmentation of the P-Q interval except a small and transient effect during relatively low calcium levels. The drug, however, exerted a distinct normalizing effect on hypercalcemic reduction of the S-T segment and the Q-T interval despite of an unaltered development of hypercalcemia. Accordingly, the cellular potassium and magnesium leaks were markedly reduced and the survival time during calcium infusion was significantly prolonged after nifedipine pretreatment. These electrophysiological data are in agreement with our previous cytochemical studies, which showed a protective effect of nifedipine against hypercalcemia-induced overloading of the cellular calcium depots in myocardial cells. Whether this cardio-protective effect of nifedipine during hypercalcemia can be used therapeutically in hypercalcemic crisis, has to be examined in clinical studies.

Animals↗
PubMed1984

A model for malignancy-associated humoral hypercalcemia.

Tumor tissue from a patient with squamous cell carcinoma of the lung and hypercalcemia has been serially implanted into athymic mice. Tumor-bearing mice develop cachexia, hypercalcemia without bone metastases, hypophosphatemia, increased urinary cyclic adenosine monophosphate (cAMP) to creatinine ratio, and undetectable human immunoreactive parathyroid hormone levels. Radiographs of spines in the tumor-bearing mice demonstrate demineralization, suggesting skeletal resorption as the source of the hypercalcemia. Within 4-8 hours following tumor removal, hypercalcemia is reversed, suggesting that a relatively short-acting humoral substance is responsible for the hypercalcemia. The animals gain weight and become essentially normal within 4 days following tumor removal. The studies demonstrate that this animal model is similar in many aspects to human malignancy-associated humoral hypercalcemia (MAHH) and can provide a useful tool for further investigation of the pathogenesis and treatment of this syndrome.

Animals↗
PubMed2000

[Differential diagnosis of hypercalcemia in adults].

BACKGROUND: Increases in serum calcium are often detected by chance. They warrant a prompt diagnostic work-up to identify the underlying cause. DIAGNOSIS: Measurement of intact parathyroid hormone (PTH) is the first step to further evaluate confirmed hypercalcemia. With few exceptions, marked increases in PTH confirm primary hyperparathyroidism. Mildly elevated PTH levels may also be observed in familial hypocalciuric hypercalcemia. Low-normal or decreased PTH levels are mostly associated with clinically evident malignancies or granulomatous diseases. A careful history will often be sufficient to make the diagnosis of drug-related hypercalcemia. Clinical presentation, measurements of 1,25-dihydroxyvitamin D, PTH-related peptide and efforts to localize the underlying disease are successful in over 90% in finding the cause of hypercalcemia with low PTH. CONCLUSION: Hypercalcemia in adults can have many different causes. Identification of the underlying disease is important, since the corresponding treatment is very different for the different causes of hypercalcemia. In most cases, medical history, clinical presentation, and a few carefully directed laboratory measurements are sufficient to differentiate between the most important hypercalcemic disorders.

Adult↗
PubMed2000

[Immobilization hypercalcemia as a complication of polyneuropathy].

Prolonged immobilization or physical inactivity has been shown to produce increased bone resorption due to enhanced osteoclastic activity and diminished bone formation. These skeletal changes are a typical complication in tetraplegic patients, who are at risk of developing hypocalcemia. Hypercalciuria is the most characteristic symptom. However, some patients develop hypercalcemia, which is infrequent in these patients, and the hypercalcemia can become a life-threatening complication. Until now, it has been unclear why a small percentage of immobilized patients develop hypercalcemia. Here we present a case of symptomatic hypercalcemia (serum calcium: 3.5 mM/l) following immobilization due to a critical illness polyneuropathy. The diagnosis could be established after malignant hypercalcemia, primary hyperparathyroidism, and other causes of hypercalcemia were excluded. Treatment with intravenous saline, furosemide, and calcitonin was not effective in lowering serum calcium. Treatment with pamidronate (Aredia) was successful and reduced the serum calcium to normal values.

Anti-Inflammatory Agents↗
PubMed2005

Humoral hypercalcemia complicating adenocarcinoma of the sigmoid colon: report of a case.

Humoral hypercalcemia can arise from a variety of malignancies, but its association with primary colorectal carcinoma is rare, with only 20 such cases documented in the English-language literature to date. We report an additional case to clarify the clinicopathologic features of colorectal carcinoma with humoral hypercalcemia. A 54-year-old woman was admitted with symptomatic hypercalcemia of 14.2 mg/dl and multiple hepatic metastases, 2 years after resection of sigmoid colon cancer. The hypercalcemia was caused by the circulating parathyroid hormone-related peptide (PTHrP) produced by poorly differentiated adenocarcinoma in the liver. The PTHrP level on admission was 13.5 pmol/l. Despite systemic chemotherapy, the patient died of disease progression 3 weeks after the humoral hypercalcemia was diagnosed. A review of the 21 reported cases, including ours, suggests that colorectal carcinoma associated with humoral hypercalcemia is characterized by a poorly differentiated tumor with or without squamous or neuroendocrine features, distant metastases, and a dismal prognosis.

Adenocarcinoma↗
PubMed1988

Hypercalcemia.

The approach to the patient with hypercalcemia requires a solid understanding of the principles of calcium homeostasis, knowledge of its differential diagnosis and the associated pathophysiologies, and the clinical judgment to know when and how to administer appropriate therapy. Recent advances in our understanding of the regulation of mineral metabolism have led to new insights into these areas and have improved our ability to deal with this rather common clinical entity. The purpose of this monograph is to give a current view of hypercalcemia as it is appreciated in the outpatient and the inpatient setting. It is designed to focus the evaluation of the hypercalcemic patient in a way that is both expedient and accurate as well as to take advantage of available therapies. A summary of the underlying physiological principles of calcium homeostasis is followed by a consideration of the complete differential diagnosis of hypercalcemia. The two most important causes of hypercalcemia, primary hyperparathyroidism and malignancy, are emphasized. Signs and symptoms of hypercalcemia are discussed with particular attention to those factors that are influential in accentuating or masking these features. Finally, an approach to the therapy of hypercalcemia is presented within a pathophysiological framework.

Humans↗
PubMed1992

Parathyroid hormone-like peptide in pancreatic endocrine carcinoma and adenocarcinoma associated with hypercalcemia.

Parathyroid hormone-like peptide (PLP) is produced by a number of tumors commonly associated with hypercalcemia as well as by nontumorous tissue, including some endocrine organs. We applied immunohistochemistry using the avidin-biotin-peroxidase technique to localize PLP in formalin-fixed, paraffin-embedded tissues of two human pancreatic carcinomas associated with hypercalcemia and normal blood parathyroid hormone levels. One tumor was endocrine and one was exocrine in differentiation. There was no evidence of bone metastasis in either case. We documented normalization of serum calcium level after removal of the pancreatic endocrine tumor. These observations support the suggestion that PLP production by pancreatic carcinoma may play a role in the development of hypercalcemia. However, the presence of PLP in tumors not associated with hypercalcemia indicates that other factors in addition to PLP are necessary for the manifestation of hypercalcemia. Hypercalcemia associated with exocrine pancreatic tumor has rarely been reported. Our exocrine pancreatic tumor appears to be the first reported case in which immunohistochemistry localized PLP. Since PLP has been localized to cells of exocrine ducts and ductules of normal pancreas, our results provide insight into the cell of origin of this tumor type.

Adenocarcinoma↗
PubMed1995

Hypercalcemia of malignancy in the palliative care patient: a treatment strategy.

Hypercalcemia of malignancy is most commonly due to the effects of parathyroid hormone-related peptide, which acts as a humoral factor to cause generalized osteoclast-mediated bone resorption and reabsorption of calcium by the kidney tubule, and may also act as a local resorptive factor adjacent to bone metastases. Local resorptive mechanisms are less common causes of malignant hypercalcemia than previously believed. Treatment begins with intravenous fluid rehydration, followed by a furosemide diuresis and the bisphosphonate pamidronate, 60-90 mg, intravenously. Gallium nitrate is an efficacious but inconvenient alternative to pamidronate. Calcitonin combined with pamidronate is a reasonable initial therapy for severe hypercalcemia to hasten normalization of the serum calcium. Steroids should be reserved for hypercalcemia due to tumor production of 1,25 dihydroxyvitamin D, or for steroid-responsive malignancies. Oral or parenteral bisphosphonates can be used to maintain normocalcemia. In addition to improving the morbidity of acute hypercalcemia, bisphosphonate therapy has been shown to reduce bone pain and pathological fractures in patients with bone metastases, and calcitonin also has a potent analgesic effect in these patients. Treatment for hypercalcemia should therefore be considered in the majority of patients in the palliative care setting.

Aged↗
PubMed1994

Determination of circulating parathyroid hormone levels and differential diagnosis of hypercalcemia.

Primary hyperparathyroidism is the most frequent cause of hypercalcemia in outpatients. In contrast, this electrolyte disorder is very often associated with cancer when detected in hospital, particularly in the frame of tumors of breast, lung or lympho-hematopoietic system. Hypercalcemia results from an imbalance between the fluxes of calcium entering and leaving the extracellular space. Theses fluxes, mainly those at the levels of bone and kidney, are the main regulators of calcium homeostasis. Depending on the etiology, increases in either bone resorption or renal tubular calcium reabsorption can predominate as the cause of elevated calcemia. Thus, an increment of renal tubular reabsorption of calcium plays a prominent role in hypercalcemia resulting from increased serum concentrations of parathyroid hormone, but can also be detected in 50% of malignant hypercalcemias. The ectopic production of authentic parathyroid hormone has convincingly been demonstrated in very few cases. The syndrome of pseudohyperparathyrodism encountered in malignant hypercalcemia can be accounted for by the tumoral secretion of an analog of parathyroid hormone, parathyroid hormone-related protein. Both proteins, which are produced by different genes located on different chromosomes, interact with the same cell membrane receptors and display identical spectrum of actions. Since they are immunologically quite distinct, there is no cross-reactivity in the various competitive or radiometric immunoassays actually available. The determination of circulating levels of parathyroid hormone is an essential step in the differential diagnosis of hypercalcemias, provided the assays offer adequate sensitivity and specificity. Nowadays, this appears to be generally the case.

Calcium↗
PubMed2005

Hypercalcemia produced by parathyroid hormone suppresses experimental autoimmune encephalomyelitis in female but not male mice.

Besides its role in regulating serum levels of calcium and phosphorus, 1alpha, 25-dihydroxyvitamin D3 (1,25-(OH)2D3) has potent effects on the immune system and suppresses disease in several animal models of autoimmune disorders including experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis. While the amount of 1,25-(OH)2D3 needed to prevent EAE is dependent on the gender of the mouse and amount of calcium available in the diet, the minimum levels of 1,25-(OH)2D3 sufficient to prevent disease cause hypercalcemia. To test if hypercalcemia independent of high levels of 1,25-(OH)2D3 can suppress EAE, we used a 25-hydroxyvitamin D3-1alpha-hydroxylase (1alpha-hydroxylase) knockout mouse strain. Because these 1alpha-hydroxylase knockout mice lack the parathyroid hormone (PTH)-regulated enzyme that synthesizes 1,25-(OH)2D3, hypercalcemia from increased bone turnover was created by continuous administration of PTH without changing the circulating levels of 1,25-(OH)2D3. This PTH-mediated hypercalcemia generated after EAE induction prevented disease in female mice but not male mice. When hypercalcemia was prevented by diet manipulation, PTH administration no longer prevented EAE. We conclude that hypercalcemia is able to prevent EAE after disease induction in female mice.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed2006

Persistent hypercalcemia is a significant risk factor for graft dysfunction in renal transplantation recipients.

Hypercalcemia is a common problem in renal transplant recipients, although in most cases, spontaneous resolution occurs within 1 year after renal transplantation. This condition may persist in some patients producing effects on renal function which are not well understood. In this study, we sought to analyze the effect of persistent hypercalcemia in the posttransplantation period on the function of renal transplants. A total of 121 recipients (31 women, 90 men; mean age, 34.1 +/- 9.9 years) underwent renal transplantation between 1999 and 2002. All patients underwent prospective evaluation of their serum calcium levels at 6-month intervals. A sustained corrected mean serum calcium level higher than 10.2 mg/dL was defined as "persistent hypercalcemia." Patients who had a gradual increase in their serum creatinine levels to >2 mg/dL or a 50% rise above the baseline were considered to display chronic allograft dysfunction (CAD). Among 121 recipients, 52 patients (43%) developed CAD and 37 patients (30.6%) had persistent hypercalcemia. Among the CAD patients, 22 suffered persistent hypercalcemia, while the other 15 patients were without CAD, a difference that was statistically significant (42.3% vs 21.7%, P = .01). The mean calcium levels were lower among patients without than with CAD, a difference that did not reach statistical significance (9.9 +/- 0.4 mg/dL vs 10.1 +/- 0.6 mg/dL, P = .1). In conclusion, persistent hypercalcemia in the posttransplantation period may significantly contribute to the development of chronic allograft nephropathy.

Adult↗