Context: Clinical manifestations of vitamin D deficiency rickets are widely described; however cardiorespiratory arrest is an extremely rare presentation.
Objective: The aim of this paper is to present the symptoms of severe vitamin D deficiency rickets and to highlight the importance of vitamin D prophylaxis in infants.
Results: We report a case of a 16-month-old infant who presented to emergency room with a stridor that evolved into a full cardiorespiratory arrest secondary to hypocalcemia. Medical history revealed that the infant was exclusively breastfed without vitamin D supplementation until the age of 10 months. Due to cultural habits, his diet was also grossly deficient in dairy products. Physical exam revealed clinical signs of rickets. Laboratory test showed severe hypocalcemia, elevated alkaline phosphatase, normal serum phosphorous, decreased 25(OH) cholecalciferol, increased intact parathyroid hormone level, and normal urine calcium excretion. The radiography of the wrist showed evidence of cupping, fraying, metaphyseal widening, and demineralization of the distal radial and ulnar metaphyses. The bone mineral density of the lumbar spine measured by dual x-ray absorptiometry showed a Z-score below -2 SD. His cardiorespiratory arrest secondary to hypocalcemia was therefore attributed to severe nutritional rickets.
Conclusion: Vitamin D deficiency rickets can be life threatening. Vitamin D supplementation is therefore crucial, especially in breastfed infants and some ethnic minorities (dark-skinned people, poor sun exposure), more at risk for developing severe rickets if not supplemented.
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http://dx.doi.org/10.1210/jc.2011-1112 | DOI Listing |
PLoS One
January 2025
Department of Epidemiology, Epidemiology Biostatistics and Prevention Institute, University of Zurich, Zurich, Switzerland.
Background: Multiple sclerosis (MS) onset is caused by genetic and environmental factors. Vitamin D has been identified as contributing environmental risk factor, with higher prevalence at latitudes further from the equator. Mongolia, at 45°N, has limited sunlight exposure, increasing the population's risk for vitamin D deficiency.
View Article and Find Full Text PDFIndian J Pediatr
January 2025
Department of Medicine, Institute Gesünder Leben, Vienna, Austria.
Rev Med Chil
September 2024
Hospital de Niños Dr. Roberto del Río, Santiago, Chile.
Hereditary tyrosinemia type 1 (HT-1) is an inborn error of metabolism caused by a defect in tyrosine (tyr) degradation. This defect results in the accumulation of succinylacetone (SA), causing liver failure with a high risk of hepatocarcinoma and kidney injury, leading in turn to Fanconi syndrome with urine loss of phosphate and secondary hypophosphatemic rickets (HR). HT-1 diagnosis is usually made in infants with acute or chronic liver failure or by neonatal screening programs.
View Article and Find Full Text PDFDiseases
January 2025
Department of Internal Medicine, College of Medicine, Taibah University, Madinah 42353, Saudi Arabia.
Background/objectives: Vitamin K2 analogs are associated with decreased vascular calcification, which may provide protective benefits for individuals with coronary artery disease (CAD) by stimulating anti-calcific proteins like matrix Gla protein and adjusting innate immune responses. This study addresses a significant gap in understanding the association between serum levels of vitamin K2 analogs in different CAD types and examines their correlations with clinical risk parameters in CAD patients.
Methods: This case-control study enrolled CAD patients and healthy controls to assess and compare serum concentrations of two vitamin K2 analogs including menaquinone-4 (MK-4) and menaquinone-7 (MK-7) via ultra-performance liquid chromatography with tandem mass spectrometry (UPLC-MS/MS).
Discov Med
January 2025
Faculty of Medicine, Institute of Anatomy, University of Belgrade, 11000 Belgrade, Serbia.
Two billion people worldwide suffer from anemia, which can lead to the onset of cardiac disorders; nevertheless, the precise mechanisms remain unclear. There are at least three distinct mechanisms by which iron deficiency (ID) contributes to the development of cardiac disorders. First, ID increases concentrations of intact fibroblast growth factor-23 (iFGF-23), which promotes left ventricular hypertrophy.
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