Infarction of mediastinal parathyroid gland causing spontaneous remission of secondary hyperparathyroidism

Tanaka, Motoko; Tominaga, Yoshihiro; Sawatari, Eizou; Itoh, Kazuko; Matsushita, Kazunori; Matsushita, Kazutaka; Matsuoka, Susumu; Ueki, Tsuneo; Goto, Norihiko; Sato, Tetsuhiko; Katayama, Akio; Haba, T; Uchida, Kazuharu

doi:10.1053/j.ajkd.2004.06.023

Cited by 14 publications

(18 citation statements)

References 25 publications

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“…High blood flow signals evaluated by power Doppler ultrasonography are associated with pathological features of nodular hyperplasia [27]. To date, however, there have been no reports showing a reduction in the parathyroid gland vasculature in CKD patients, except for rare cases associated with spontaneous infarction of the glands [6,7]. Conceptually, it is possible that the reduced vascularity observed in this study was secondary to enhanced apoptosis of parathyroid cells.…”

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confidence: 37%

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Regression of parathyroid hyperplasia by calcimimetics--fact or illusion?

Komaba

Fukagawa

2008

Nephrology Dialysis Transplantation

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Secondary hyperparathyroidism is one of the most common and serious complications of chronic kidney disease (CKD). The main factors responsible for excessive synthesis and secretion of parathyroid hormone (PTH) include phosphate retention, hypocalcaemia and calcitriol deficiency resulting from decreased kidney function [1,2]. Sustained hypersecretion of PTH is associated with an increase in the parathyroid gland size, initially leading to diffuse parathyroid hyperplasia. Subsequently, some cells in the parathyroid glands proliferate in a monoclonal growth pattern, and the enlarged glands exhibit an advanced type of nodular hyperplasia [3]. In the course of parathyroid hyperplasia, both calcium-sensing receptors (CaSR) and vitamin D receptors (VDR) are progressively down-regulated [4,5], which results in diminished responsiveness of parathyroid glands with nodular hyperplasia to active vitamin D treatment.Conversely, whether regression of parathyroid hyperplasia can occur has remained a matter of discussion. Regression of parathyroid hyperplasia has been reported in rare cases of spontaneous infarction of the glands [6,7]. In addition, enhanced apoptosis of parathyroid cells has been observed in diffuse hyperplasia after kidney transplantation, suggesting the possibility of regression in the long term [8].In the past, the capacity of calcitriol therapy to induce regression of parathyroid hyperplasia had been a matter of debate. In a study of oral calcitriol pulse therapy, given to chronic haemodialysis patients, we observed a significant decrease in the mean ± SD volume of parathyroid glands (from 0.87 ± 0.32 to 0.51 ± 0.23 cm 3 ) after 12 weeks of treatment, with a concomitant significant reduction in intact PTH levels [9]. In contrast, Quarles et al. failed to observe a decrease in the parathyroid gland size after 36 weeks of intermittent intravenous or oral calcitriol treatments [10]; the mean ± SD gland volume was 1.9 ± 0.6 and 2.1 ± Correspondence and offprint requests to:

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confidence: 37%

“…Regression of parathyroid hyperplasia has been reported in rare cases of spontaneous infarction of the glands [6,7]. In addition, enhanced apoptosis of parathyroid cells has been observed in diffuse hyperplasia after kidney transplantation, suggesting the possibility of regression in the long term [8].…”

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confidence: 94%

Regression of parathyroid hyperplasia by calcimimetics--fact or illusion?

Komaba

Fukagawa

2008

Nephrology Dialysis Transplantation

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“…Lately, neck ultrasound examination has become a more beneficial and specific method for the diagnosis of enlarged parathyroid glands, in contrast to classic diagnostic techniques such as computed tomography (CT), magnetic resonance imaging (MRI) and scintigraphy [1,2]. The diagnosis of parathyroid infarction reported in previous studies, however, was often based on CT, MRI and scintigraphy findings and only a few studies have reported such diagnosis by emergency power Doppler ultrasonography of the neck.…”

Section: Introductionmentioning

confidence: 74%

“…Spontaneous remission due to parathyroid infarction of secondary hyperparathyroidism (SHPT) [1,2] is very rare compared to that of primary hyperparathyroidism [3,4]. It is possible that the diagnosis of parathyroid infarction is missed in patients with SHPT because parathyroid infarction often occurs in only one of the enlarged glands.…”

Section: Introductionmentioning

confidence: 99%

Autoinfarction of the parathyroid gland diagnosed by power Doppler ultrasonography in a patient with secondary hyperparathyroidism

Tanaka

Tominaga²,

Itoh³

et al. 2005

Nephrology Dialysis Transplantation

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“…The CaSR play a key role in the excessive cell proliferation in PTG hyperplasia (17,18,19,20,21,22,23). In humans, the regression of PTG hyperplasia has been reported rarely, in cases of spontaneous infarction of the glands (24,25) and in cases of DH after kidney transplantation (26,27).…”

Section: Introductionmentioning

confidence: 99%

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

Vulpio

Bossola

Stasio

et al. 2013

European Journal of Endocrinology

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Background: Cinacalcet is a new effective treatment of secondary hyperparathyroidism (SHPT) in hemodialysis patients (HP), but the alterations of parathyroid gland (PTG) hyperplasia determined by cinacalcet and vitamin D have not been extensively investigated in humans. Methods: We performed histological analyses of 94 PTGs removed from 25 HP who underwent parathyroidectomy (PTx) because of SHPT refractory to therapy with vitamin D alone (group AZ13 HP and 46 PTGs) or associated with cinacalcet (group BZ12 HP and 48 PTGs). The number, weight, the macroscopic cystic/hemorrhagic changes, and type of hyperplasia of PTG (nodularZNH, diffuseZDH) were assessed. In randomly selected HP of group A (4 HP and 14 PTGs) and group B (4 HP and 15 PTGs), the labeling index of cells positive to Ki-67 and TUNEL and the semiquantitative score of immunohistochemistry staining of vitamin D receptor, calcium-sensing receptor, and vascular endothelial growth factor-a (VEGF-a) were measured in the entire PTGs and in the areas with DH or NH. Results: The number and weight of single and total PTG of each HP were similar in the two groups as well as the number of PTG with macroscopic cystic/hemorrhagic areas. TUNEL, Ki-67, and VEGF-a scores were higher in NH than in DH areas. Conclusion: This observational study of a highly selected population of HP, submitted to PTx because SHPT refractory to therapy, shows that the macroscopic, microscopic, and immunochemistry characteristics of PTG in HP who received or did not receive cinacalcet before PTx did not differ significantly.

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Infarction of mediastinal parathyroid gland causing spontaneous remission of secondary hyperparathyroidism

Cited by 14 publications

References 25 publications

Regression of parathyroid hyperplasia by calcimimetics--fact or illusion?

Regression of parathyroid hyperplasia by calcimimetics--fact or illusion?

Autoinfarction of the parathyroid gland diagnosed by power Doppler ultrasonography in a patient with secondary hyperparathyroidism

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

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