Extraosseous calcifications correspond to ubiquitous deposits of intra-tissue calcium salts leading to dysfunction of the affected tissue or organ. There are two types: metastatic calcifications and dystrophic calcifications. Their formation mechanism is by mimicking the physiological mineralization process with an "osteoblast-like" cell. The cause of extra-osseous calcification is variable and depends on risk factors. If the subject is young, you will have to think about a genetic syndrome!
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[Calcifications and phosphocalcic metabolism].
Ann Pathol
November 2024
Anatomie et cytologie pathologiques, Institut de cancérologie de l'Ouest, Centre René-Gauducheau, boulevard Jacques-Monod, 44805 Saint-Herblain cedex, France. Electronic address:
Extraosseous calcifications correspond to ubiquitous deposits of intra-tissue calcium salts leading to dysfunction of the affected tissue or organ. There are two types: metastatic calcifications and dystrophic calcifications. Their formation mechanism is by mimicking the physiological mineralization process with an "osteoblast-like" cell.
View Article and Find Full Text PDFHypoparathyroidism Revealed by Unsuccessful Anti-epileptic Therapy.
Cureus
February 2024
Department of Pediatrics, Mohammed VI University of Health Sciences (UM6SS), Casablanca, MAR.
Pediatric hypoparathyroidism is an uncommon endocrine disease that can be either isolated or syndromic. It occurs when the secretion of parathormone is insufficient to maintain normal levels of ionized calcium. Patients with hypoparathyroidism can exhibit cerebral calcifications and metabolic disorders, and the severity of such features is inversely correlated with hypocalcemia.
View Article and Find Full Text PDFLate Presentation of Primary Oxalosis, Microcrystalline Arthropathy, and Tumoral Calcinosis: A Case Report and a Literature Review.
Curr Rheumatol Rev
June 2024
Department of Nephrology, Dialysis, and Transplantation, Hedi Chaker University Hospital, Sfax, Tunisia.
Article Synopsis
- Primary hyperoxaluria is a genetic disorder affecting the glyoxylate pathway, leading to poor oxalate breakdown and complications like kidney and joint diseases, with neonatal oxalosis being the most severe form.
- A 55-year-old male on hemodialysis for end-stage renal failure and diagnosed with primary hyperoxaluria presented with inflammatory joint issues and various calcifications, but his condition continued to worsen despite treatment.
- The case highlights that primary hyperoxaluria can have late-onset symptoms and long-term complications beyond kidney issues, contributing to a complex medical picture.
Hypoparathyroidism and Fahr's Syndrome: A Case Series.
Cureus
June 2023
Department of Endocrinology-Diabetology and Nutrition, Mohammed VI University Hospital Center, Oujda, MAR.
Fahr's syndrome is defined by the presence of striato-pallido-dentate calcifications. It is a rare entity with clinical polymorphism, and it occurs in patients with dysparathyroidism, especially those with hypoparathyroidism. It must be distinguished from Fahr's disease (FD), which is defined by the presence of intracerebral calcifications without phosphocalcic metabolism abnormality.
View Article and Find Full Text PDFCalcification Propensity (T50) Predicts a Rapid Decline of Renal Function in Kidney Transplant Recipients.
J Clin Med
June 2023
Service of Nephrology, Department of Internal Medicine Specialties, University Hospital of Geneva, 1205 Geneva, Switzerland.
Background: Serum creatinine level, proteinuria, and interstitial fibrosis are predictive of renal prognosis. Fractional excretion of phosphate (FEP)/FGF23 ratio, tubular reabsorption of phosphate (TRP), serum calcification propensity (T50), and Klotho's serum level are emerging as determinants of poor kidney outcomes in CKD patients. We aimed at analysing the use of FGF23, FEP/FGF23, TRP, T50, and Klotho in predicting the rapid decline of renal function in kidney allograft recipients.
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