Ectopic Calcification: What Do We Know and What Is the Way Forward?

Snijders, Birgitta M G; Peters, M.; Koek, Huiberdina L.

doi:10.3390/jcm12113687

Cited by 4 publications

(1 citation statement)

References 35 publications

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“…In contrast to the described pathogenesis of ectopic mineralization in FD that occurs mainly due to dystrophic calcification, the mineralization FS, such as in the setting of hypoparathyroidism, is thought to be triggered via metastatic calcification as a consequence of systemic mineral imbalance [4,8]. Our patient presented with right hemiparesis, spasticity, and generalized tonic-clonic seizures.…”

Section: Discussionmentioning

confidence: 67%

Fahr’s Syndrome Secondary to Hypoparathyroidism Presenting with Paralysis and Recurrent Seizures: A Case Report

Jihwaprani

Kumara

2023

AJMAH

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Aim: To describe a rare case of Fahr’s syndrome (FS) associated with chronic post-surgical hypoparathyroidism and hypocalcemia. Case Presentation: A 63-year-old female with a previous history of total thyroidectomy and hemiplegia presented to our hospital with altered mentation and recurrent generalized tonic-clonic seizures. Laboratory evaluation revealed hypoparathyroidism, hypocalcemia, and hypokalemia. Head computed tomography (CT) scan was consistent with FS, demonstrating extensive, bilateral, and symmetrical calcified deposits in the brain, predominantly in basal ganglia, corona radiata, and cerebellar hemispheres. The association with post-surgical hypoparathyroidism and relevant biochemical indices determined the suspected etiology of the pathologic process of ectopic calcification. Discussion: FS is a rare, neurodegenerative disorder characterized by abnormal bilateral ectopic calcified deposits in the basal ganglia and other brain structures. FS presents with a wide variety of neurological and psychiatric manifestations. The diagnosis is confirmed by neuroimaging studies such as a head CT scan or magnetic resonance imaging, which displays the calcification of BG and other structures in a bilateral and symmetrical pattern. Biochemical analysis may adjunctively identify the underlying risk factor of the disease. Conclusion: Our case represents a long-term severe consequence of untreated post-surgical hypoparathyroidism, which has consequently led to irreversible secondary FS. Maintenance of eucalcemic and euphosphatemic states is essential to prevent the progression of ectopic cerebral calcification.

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Section: Discussionmentioning

confidence: 67%

Fahr’s Syndrome Secondary to Hypoparathyroidism Presenting with Paralysis and Recurrent Seizures: A Case Report

Jihwaprani

Kumara

2023

AJMAH

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Bacteroides Fragilis Exacerbates T2D Vascular Calcification by Secreting Extracellular Vesicles to Induce M2 Macrophages

Chen,

Liang,

et al. 2024

Advanced Science

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Vascular calcification (VC) in type 2 diabetes (T2D) poses a serious threat to the life and health of patients. However, its pathogenesis remains unclear, resulting in a lack of effective treatment for the root cause. It is found that both intestinal Bacteroides fragilis (BF) and peripheral M2 monocytes/macrophages are significantly elevated in patients with T2D VC. M2 macrophages are identified as a significant risk factor for T2D VC. Both BF and their extracellular vesicles (EV) promote T2D VC and facilitate macrophage M2 polarization. Macrophages clearance significantly antagonized BF EV‐induced T2D VC in mice. Mechanistically, EV‐rich double‐stranded DNA (dsDNA) activates stimulator of interferon response cGAMP interactor 1 (Sting), promotes myocyte enhancer factor 2D (Mef2d) phosphorylation, upregulates tribbles pseudokinase 1 (Trib1) expression, and induces macrophage M2 polarization. Concurrently, Mef2d activated by the EV targets and upregulates the expression of pro‐calcification factor Serpine1, thereby exacerbating T2D VC. Clinical studies have shown that Serpine1 is significantly elevated in the peripheral blood of patients with T2D VC and is closely associated with T2D VC. In summary, this study reveals that intestinal BF promotes Trib1 expression through the EV‐Sting‐Mef2d pathway to induce macrophage M2 polarization and upregulates serpin family E member 1 (Serpine1) expression, thereby aggravating T2D VC. The findings provide a new theoretical and experimental bases for optimizing the strategies for prevention and treatment of T2D VC.

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Optic disc drusen: Dystrophic calcification, a potential target for treatment

Bentin,

Heegaard,

Jørgensen

et al. 2024

Eye

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Ectopic Calcification: What Do We Know and What Is the Way Forward?

Abstract: Ectopic calcification, or ectopic mineralization, is a pathologic condition in which calcifications develop in soft tissues [...]

Cited by 4 publications

References 35 publications

Fahr’s Syndrome Secondary to Hypoparathyroidism Presenting with Paralysis and Recurrent Seizures: A Case Report

Fahr’s Syndrome Secondary to Hypoparathyroidism Presenting with Paralysis and Recurrent Seizures: A Case Report

Bacteroides Fragilis Exacerbates T2D Vascular Calcification by Secreting Extracellular Vesicles to Induce M2 Macrophages

Optic disc drusen: Dystrophic calcification, a potential target for treatment

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