Vitamin deficiencies such as scurvy and Wernicke's encephalopathy are poorly recognized in Western populations. Inadequate intake of these micronutrients and low levels when measured are more frequent than expected. Cases of combined vitamin deficiencies such as that of ascorbic acid and thiamine are seldom reported. Two patients with clinical and biochemical evidence of vitamin deficiencies are described. Signs and symptoms rapidly responded to vitamin replacement. Neither patient was overtly malnourished, but nutritional histories and physical examination were strongly suggestive. Vitamin replacement may require large intravenous doses but is inexpensive and potentially of great benefit.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4318664 | PMC |
http://dx.doi.org/10.4088/PCC.14br01649 | DOI Listing |
PLoS One
January 2025
Department of Encephalopathy, The First Affiliated Hospital of Henan University of Traditional Chinese Medicine, Zhengzhou, China.
Background: Vitamin D is thought to play a role in the development of migraine, but the nature of the relationship is still not fully understood. Although some studies have shown an association between vitamin D deficiency and migraine, other studies have had inconsistent or inconclusive results. Therefore, further research is needed to better understand the relationship between vitamin D and migraine headaches.
View Article and Find Full Text PDFCalcif Tissue Int
January 2025
Department of Paediatric Endocrinology, Alder Hey Children's Hospital, Liverpool, UK.
Autosomal recessive hypophosphatemic rickets type 2 (ARHR2) is an uncommon hereditary form of rickets characterised by chronic renal phosphate loss and impaired bone mineralisation. This results from compound heterozygous or homozygous pathogenic variants in ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1), a key producer of extracellular inorganic pyrophosphate (PPi) and an inhibitor of fibroblast growth factor23 (FGF23). ENPP1 deficiency impacts FGF23 and increases its activity.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Indiana University School of Medicine, Stark Neurosciences Research Institute, Department of Neurology, Indianapolis, IN, USA.
Background: Diagnosis of Alzheimer's disease (AD) via MRI is costly and can be limited by regional availability. With the recent advancements and discovery of amyloid in the retina, diagnosis of AD and the effect of AD pathology on the retina is becoming well characterized. However, the prevalence of vascular contributions to cognitive impairment and dementia (VCID) and its effects on the retina are less well known.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Alzheimer's Center at Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Background: Brain endothelial cell (EC) stress, including that induced by vascular amyloid β (Aβ) deposits in cerebral amyloid angiopathy (CAA) and Alzheimer's disease (AD), contributes to cerebral blood flow impairment, blood brain barrier (BBB) damage, neurovascular unit dysfunction, microhemorrhages and hypoperfusion, precipitating neurodegeneration and neuroinflammation processes. Epidemiological and experimental evidence suggests that hyperhomocysteinemia (Hhcy) contributes to increasing AD risk as well as CAA pathology. However, the cellular and molecular mechanisms through which Aβ and Hhcy drive EC and BBB dysfunction, whether the molecular effects of these challenges are additive or independent, and possible therapeutic strategies, remain to be determined.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Alzheimer's Center at Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Background: Over the years, Alzheimer's Disease (AD) has been identified as a multifactorial disease, with cerebral vascular dysfunction being one of the most common and early pathological features. Vascular risk factors (VRF) are thought to further increase AD risk and pathology. Cerebral Amyloid Angiopathy (CAA) is defined as the accumulation of amyloid-beta (Aβ) on the vascular wall.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!