Hypercalcemia occurs in around 10% of all malignancies.
It's generally seen in solid tumors, especially squamous cell carcinomas (eg, lung, esophagus), renal carcinoma, and breast carcinoma.
Hypercalcemia happens in a lot more than one third of patients with multiple myeloma but is unusual in lymphomas and leukemias.
Solid tumors usually create hypercalcemia by secreting PTHrP, whose properties have been described previously.
This really is humoral hypercalcemia, which mimics primary hyperparathyroidism and results from a diffuse increase in bone resorption induced by higher circulating levels of PTHrP.
The syndrome is exacerbated by the capability of PTHrP to decrease renal excretion of calcium and the capability of hypercalcemia (acting via renal CaSRs) to blunt renal concentrating ability, which results in progressive dehydration.
Several myeloma creates hypercalcemia by a different mechanism; myeloma cells induce local bone resorption or osteolysis in the bone marrow, probably by releasing cytokines with bone-resorbing activity, such as interleukin-1 and tumor necrosis factor.
Rarely, lymphomas create humoral hypercalcemia by secreting 1,25-(OH)2D.
Lastly, even although numerous hypercalcemic sufferers have bone metastases, these might not contribute directly to the pathogenesis of hypercalcemia.
In contrast to sufferers with major hyperparathyroidism, who frequently are minimally symptomatic, patients with hypercalcemia of malignancy are typically really ill.
Hypercalcemia usually occurs in sophisticated malignancy-the average survival of hypercalcemic sufferers is usually a number of weeks to months-and the tumor is nearly invariably obvious on examination of the patient.
In addition, hypercalcemia is often severe and symptomatic, with nausea, vomiting, dehydration, confusion, or coma.
Biochemically, malignancy-associated hypercalcemia is characterized by a decreased serum phosphate along with a suppressed degree of intact PTH.
With most solid tumors, the serum level of PTHrP is increased.
These findings, together with the differences in clinical presentation, usually make the differentiation of this syndrome from primary hyperparathyroidism fairly easy.
It's generally seen in solid tumors, especially squamous cell carcinomas (eg, lung, esophagus), renal carcinoma, and breast carcinoma.
Hypercalcemia happens in a lot more than one third of patients with multiple myeloma but is unusual in lymphomas and leukemias.
Solid tumors usually create hypercalcemia by secreting PTHrP, whose properties have been described previously.
This really is humoral hypercalcemia, which mimics primary hyperparathyroidism and results from a diffuse increase in bone resorption induced by higher circulating levels of PTHrP.
The syndrome is exacerbated by the capability of PTHrP to decrease renal excretion of calcium and the capability of hypercalcemia (acting via renal CaSRs) to blunt renal concentrating ability, which results in progressive dehydration.
Several myeloma creates hypercalcemia by a different mechanism; myeloma cells induce local bone resorption or osteolysis in the bone marrow, probably by releasing cytokines with bone-resorbing activity, such as interleukin-1 and tumor necrosis factor.
Rarely, lymphomas create humoral hypercalcemia by secreting 1,25-(OH)2D.
Lastly, even although numerous hypercalcemic sufferers have bone metastases, these might not contribute directly to the pathogenesis of hypercalcemia.
In contrast to sufferers with major hyperparathyroidism, who frequently are minimally symptomatic, patients with hypercalcemia of malignancy are typically really ill.
Hypercalcemia usually occurs in sophisticated malignancy-the average survival of hypercalcemic sufferers is usually a number of weeks to months-and the tumor is nearly invariably obvious on examination of the patient.
In addition, hypercalcemia is often severe and symptomatic, with nausea, vomiting, dehydration, confusion, or coma.
Biochemically, malignancy-associated hypercalcemia is characterized by a decreased serum phosphate along with a suppressed degree of intact PTH.
With most solid tumors, the serum level of PTHrP is increased.
These findings, together with the differences in clinical presentation, usually make the differentiation of this syndrome from primary hyperparathyroidism fairly easy.
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