NEW YORK (Reuters Health) Nov 21 - Almost 70% of patients taking sunitinib (Sutent) as first-line therapy for metastatic renal cell carcinoma developed hyperparathyroidism, Italian researchers report.
The clinical significance is unclear, however.
Sunitinib, a receptor tyrosine kinase (RTK) inhibitor, was approved by the U.S. Food and Drug Administration in 2006 for treating renal cell carcinoma (RCC) and imatinib-resistant gastrointestinal stromal tumor (GIST).
In a report published online September 28th in Cancer, senior author Dr. Roberto Mazzanti of Istituto Toscano Tumori, Florence and colleagues say the drug's side effect profile isn't clear yet -- and they were starting to notice unexpected elevations of intact plasma parathyroid hormone (PTH) in some patients on sunitinib.
To look for a relationship of sunitinib with phosphorus and calcium homeostasis, the investigators tracked 26 patients receiving treatment in six-week cycles (50 mg daily for four weeks, then two weeks off). Biochemical evaluations were performed at baseline and at the end of each sunitinib treatment period.
Patients completed a mean of 7.2 cycles -- but after an average of roughly 12 weeks, 18 of them (69.2%) developed hyperparathyroidism with normal serum calcium levels and low or undetectable urinary calcium levels. Six developed hypophosphatemia.
25-OH vitamin D3 levels held steady over the course of treatment, but five patients with hyperparathyroidism had elevated 1,25-OH vitamin D3 levels.
"It is noteworthy," say the investigators, "that these biochemical changes persisted, but did not progress, during long-term therapy. Moreover, once treatment was interrupted definitively, PTH plasma levels returned to within the laboratory range in a few months."
They also point out that "increased osteocalcin and bone resorption biomarkers would have been expected but were not observed."
This preliminary work and that by other researchers suggests that "alteration in bone metabolism is the most appropriate explanation for the altered mineral metabolism and parathyroid function," the research team writes, adding that if these findings are confirmed, routine monitoring of serum calcium, phosphate, and vitamin D levels as well as bone mass would be advisable.
Dr. Mazzanti did not respond to requests for comments.
SOURCE: http://bit.ly/tZ8tjg
The clinical significance is unclear, however.
Sunitinib, a receptor tyrosine kinase (RTK) inhibitor, was approved by the U.S. Food and Drug Administration in 2006 for treating renal cell carcinoma (RCC) and imatinib-resistant gastrointestinal stromal tumor (GIST).
In a report published online September 28th in Cancer, senior author Dr. Roberto Mazzanti of Istituto Toscano Tumori, Florence and colleagues say the drug's side effect profile isn't clear yet -- and they were starting to notice unexpected elevations of intact plasma parathyroid hormone (PTH) in some patients on sunitinib.
To look for a relationship of sunitinib with phosphorus and calcium homeostasis, the investigators tracked 26 patients receiving treatment in six-week cycles (50 mg daily for four weeks, then two weeks off). Biochemical evaluations were performed at baseline and at the end of each sunitinib treatment period.
Patients completed a mean of 7.2 cycles -- but after an average of roughly 12 weeks, 18 of them (69.2%) developed hyperparathyroidism with normal serum calcium levels and low or undetectable urinary calcium levels. Six developed hypophosphatemia.
25-OH vitamin D3 levels held steady over the course of treatment, but five patients with hyperparathyroidism had elevated 1,25-OH vitamin D3 levels.
"It is noteworthy," say the investigators, "that these biochemical changes persisted, but did not progress, during long-term therapy. Moreover, once treatment was interrupted definitively, PTH plasma levels returned to within the laboratory range in a few months."
They also point out that "increased osteocalcin and bone resorption biomarkers would have been expected but were not observed."
This preliminary work and that by other researchers suggests that "alteration in bone metabolism is the most appropriate explanation for the altered mineral metabolism and parathyroid function," the research team writes, adding that if these findings are confirmed, routine monitoring of serum calcium, phosphate, and vitamin D levels as well as bone mass would be advisable.
Dr. Mazzanti did not respond to requests for comments.
SOURCE: http://bit.ly/tZ8tjg
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