Expression of Osteogenic Molecules in the Caudate Nucleus and Gray Matter and Their Potential Relevance for Basal Ganglia Calcification in Hypoparathyroidism

Goswami, Ravinder; Millo, Tabin; Mishra, Shruti; Das, Madhuchhanda; Kapoor, M M; Tomar, Neeraj; Saha, Soma; Roy, Tara Shankar; Sreenivas, Vishnubhatla

doi:10.1210/jc.2013-3863

Cited by 34 publications

(19 citation statements)

References 36 publications

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“…Вероятнее всего, именно низкий уровень ПТГ запускает процесс отложения кальция в базальных ганглиях [13], поэтому заместительная терапия препаратами ПТГ представляется патогенетически обоснованной в комплексном лечении идиопатического гипопаратиреоза.…”

Section: Discussionunclassified

Treatment of severe idiopathic hypoparathyroidism: a case report

et al. 2018

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Hypoparathyroidism is a rare disorder characterized by parathyroid hormone (PTH) insufficiency, the development of hypocalcemia and alteration of bone tissue remodeling. The goal of treatment is to normalize the indicators of calcium-phosphorus metabolism and leveling of clinical manifestations. Standard treatment of hypoparathyroidism consists of oral calcium and active forms of vitamin D, in doses necessary to maintain calcium levels at the lower limit of the reference interval. Nevertheless, treatment of the disease exerts certain difficulties in clinical practice. At the same time, compensation of the hypoparathyroidism is necessary to prevent ectopic calcification. Daily subcutaneous delivery of PTH (1–84) and PTH (1–34) has emerged as a promising therapeutic tool. However, its use should be restricted to patients insufficiently controlled with the standard treatment with active vitamin D and calcium. We present a clinical case of idiopathic hypoparathyroidism with severe clinical presentation of hypocalcaemia and ectopic calcification. Idiopathic hypoparathyroidism is a consequence of autoimmune destruction of the parathyroid glands and is exhibited by excluding all known causes of hypoparathyroidism. PTH (1–34) treatment allowed reducing the dose of calcium and vitamin D and achieving compensation of the disease.

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Section: Discussionunclassified

Treatment of severe idiopathic hypoparathyroidism: a case report

et al. 2018

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“…In the case of our patient, more than 60 years after surgery, severe hypocalcaemia resulting from non-adherence to the prescribed therapy was responsible for confusion, seizures and loss of consciousness that led to hospitalization. Irregular monitoring and control of calcaemia and phosphoremia enabled the formation of calcium deposits in the central nervous system, in particular in the basal ganglia, where several osteogenic molecules are expressed [6]. Chronic deficiency in active vitamin D, along with the absence of PTH, contributed to subperiosteal thickening and bone marrow fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Hypoparathyroidism, Brain Calcifications and Seizures

Bertoli¹,

Valentini²,

Mauriello³

et al. 2017

IJMPCR

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Background: The most common cause of hypoparathyroidism is iatrogenic in the context of surgical procedures to the neck and commonly the thyroid gland. Hypoparathyroidism is characterized by hypocalcaemia, hyperphosphatemia and low or inappropriately normal levels of parathyroid hormone (PTH) and may be associated with multiorgan complications and variable clinical presentation. Seizures may be the only presenting symptom and may result in antiepileptic therapy. Knowledge of all possible consequences of hypoparathyroidism is essential for correct patient management.

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“…Two PTH receptors are expressed in the brain: parathyroid hormone receptor 1 and 2, the latter having the highest expression (Goswami et al, 2014). Both receptors, in response to PTH binding, can increase cAMP production and [Ca 2+ ]I, and this can lead to activation of protein kinase A and phosphorylation of proteins, including P450s (Swarthout et al, 2002;Bisello et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Effects of Chronic Renal Failure on Brain Cytochrome P450 in Rats

Naud

Harding

Lamarche

et al. 2016

Drug Metabolism and Disposition

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Chronic renal failure (CRF) impedes renal excretion of drugs and their metabolism by reducing the expression of liver cytochrome P450 (P450). Uremic serum contains factors, such as parathyroid hormone (PTH), that decrease liver P450s. The P450s are also involved in the metabolism of xenobiotics in the brain. This study investigates: 1) the effects of CRF on rat brain P450, 2) the role of PTH in the downregulation of brain P450s in CRF rats, and 3) the effects of PTH on P450s in astrocytes. Protein and mRNA expression of P450s were assessed in the brain of CRF and control (CTL) rats, as well as from CTL or CRF rats that underwent parathyroidectomy (PTX) 1 week before nephrectomy. CYP3A activity was measured using 3-[(3, 4-difluorobenzyl) oxy]-5, 5-dimethyl-4-[4-methylsulfonyl) phenyl] furan-2(5H)-1 metabolism in brain microsomal preparation.CYP3A protein expression was assessed in primary cultured astrocytes incubated with serum obtained from CRF or CTL rats or with PTH. Significant downregulations ( ‡40%) of CYP1A, CYP2C11, and CYP3A proteins were observed in microsomes from CRF rat brains. CYP3A activity reduction was also observed. CYP3A expression and activity were unaffected in PTX-pretreated CRF rats. Serum of PTX-treated CRF rats had no impact on CYP3A levels in astrocytes compared with that of untreated CRF rats. Finally, PTH addition to normal calf serum induced a reduction in CYP3A protein similar to CRF serum, suggesting that CRF-induced hyperparathyroidism is associated with a significant decrease in P450 drugmetabolizing enzymes in the brain, which may have implications in drug response.

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Expression of Osteogenic Molecules in the Caudate Nucleus and Gray Matter and Their Potential Relevance for Basal Ganglia Calcification in Hypoparathyroidism

Cited by 34 publications

References 36 publications

Treatment of severe idiopathic hypoparathyroidism: a case report

Treatment of severe idiopathic hypoparathyroidism: a case report

Hypoparathyroidism, Brain Calcifications and Seizures

Effects of Chronic Renal Failure on Brain Cytochrome P450 in Rats

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