Parathyroid Gland Ultrasound Patterns and Biochemical Findings After One‐year Cinacalcet Treatment for Advanced Secondary Hyperparathyroidism

Abstract

Cinacalcet efficacy is limited in severe secondary hyperparathyroidism (SHPT) and its effect on parathyroid gland (PTG) volume and morphology have not been sufficiently investigated. We evaluated the effect of cinacalcet treatment for one year on the laboratory parameters of calcium-phosphorus metabolism and PTG ultrasound (US) patterns in hemodialysis (HD) patients with severe SHPT and US results indicative of nodular hyperplasia. Thirteen HD patients with severe SHPT (intact parathyroid hormone >700 pg/mL), US/scintigraphic evidence of at least one PTG with a diameter >7 mm, and high surgical risk or refusal of surgery were included. The patients were treated with cinacalcet. The initial dose of 30 mg was increased up to 180 mg once daily. At baseline and after one year of cinacalcet treatment a neck US was performed, providing data on 22 parathyroid glands in eight patients. The mean diameter at baseline and at one year was 12.6 +/- 5.9 and 13.0 +/- 5.3 mm, respectively (P = 0.46). Similarly, the mean volume at baseline and at one year was 513.4 +/- 416.3 and 556.8 +/- 480.8 mm(3), respectively (P = 0.18). The US structural score remained unchanged in 16 parathyroid glands and increased in 6 (P < 0.03), while the vascular score remained unchanged in 16 parathyroid glands and decreased in 6 (P = 0.25). Thus it can be concluded that cinacalcet treatment for one year in HD patients with severe SHPT is not associated with significant changes in parathyroid gland US patterns.

Histology and immunohistochemistry of the parathyroid glands in renal secondary hyperparathyroidism refractory to vitamin D or cinacalcet therapy

“…Conversely, other authors (31,32) failed to detect significant morphological changes after cinacalcet therapy.…”

“…Nevertheless, this study does not allow to determine whether a regression of PTG with DH is possible after cinacalcet therapy. Actually, this hypothesis has been first based on the data obtained in experimental studies (18,19,20,21,22,23) and then by the US evaluation of PTG (28,29,30,31,32).…”

Sonographic Evaluation of Secondary Hyperparathyroidism

“…3 Secondary hyperparathyroidism is a common complication in CKD, characterized by an increase in PTH and disorders of parathyroid cell proliferation. 4 The prevalence of SHPT increases as the GFR decreases. 5 Secondary hyperparathyroidism develops in CKD as an adaptive response to the lowered ionized calcium level that occurs as a result of deteriorating renal function.…”

“…6 Secondary hyperparathyroidism is a significant contributing factor in metabolic bone, multiple cardiovascular complications, fractures, and the increased morbidity and mortality of patients on hemodialysis. 4 Chronic renal failure is best treated with renal transplantation, which should successfully restore vitamin D metabolism and prevent the progression of SHPT. 6 When renal transplantation is not an available option, alternative treatment of SHPT includes oral or intravenous administration of calcium or non-calcium-based phosphate binders to reduce blood serum levels.…”

Parathyroid Nodular Hyperplasia and Responsiveness to Drug Therapy in Renal Secondary Hyperparathyroidism: An Open Question

“…After 12 months, the PTH, diameter and volume of PTG remained substantially unchanged in most of the patients. Vulpio et al , in another retrospective study, compared the echographic parameters of PTG of patient responders (R) and non‐responders (NR) to two different therapies (vitamin D alone: group A, N = 39; vitamin D plus cinacalcet: group B, N = 30). The baseline ultrasound characteristics of PTG (number, maximum diameter and structural and vascular patterns) of R patients were lower than NR ones regardless of the different therapy.…”