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Current Opinion in Pediatrics Apr 2022Although vitamin A deficiency (VAD) is rare in well resourced countries, there is a growing trend of VAD in at-risk pediatric populations. Early diagnosis is critically... (Review)
Review
PURPOSE OF REVIEW
Although vitamin A deficiency (VAD) is rare in well resourced countries, there is a growing trend of VAD in at-risk pediatric populations. Early diagnosis is critically important to prevent its associated morbidity and mortality. This review highlights key lessons for evaluation, diagnosis, and management of children with xerophthalmia in the United States. It synthesizes the latest findings from the literature on the pathophysiology, epidemiology, risk factors, evaluation, and management of VAD in low-prevalence areas.
RECENT FINDINGS
Vitamin A is crucial for maintaining the functional integrity of the eye, immune system, skin, and mucous membranes. Despite the scarcity of VAD in developed countries, there are increasing reports of VAD in at-risk children, including those with autism spectrum disorder and gastrointestinal conditions. There is a broad range of manifestations of VAD, posing a diagnostic challenge. Familiarity with the variable presentations of VAD and having a high index of suspicion in at-risk populations can aid in its early diagnosis. Systemic vitamin A supplementation and a multidisciplinary approach are important components of the management of VAD.
SUMMARY
Even in well resourced countries, VAD should remain on the differential in patients with risk factors who present with relevant signs and symptoms. Early diagnosis and appropriate involvement of a multidisciplinary care team can help prevent morbidity and mortality associated with VAD.
Topics: Autism Spectrum Disorder; Child; Humans; Prevalence; Vitamin A; Vitamin A Deficiency; Xerophthalmia
PubMed: 35125379
DOI: 10.1097/MOP.0000000000001110 -
Nutrients Apr 2022Pernicious anemia is still a neglected disorder in many medical contexts and is underdiagnosed in many patients. Pernicious anemia is linked to but different from... (Review)
Review
Pernicious anemia is still a neglected disorder in many medical contexts and is underdiagnosed in many patients. Pernicious anemia is linked to but different from autoimmune gastritis. Pernicious anemia occurs in a later stage of autoimmune atrophic gastritis when gastric intrinsic factor deficiency and consequent vitamin B deficiency may occur. The multifaceted nature of pernicious anemia is related to the important role of cobalamin, which, when deficient, may lead to several dysfunctions, and thus, the proteiform clinical presentations of pernicious anemia. Indeed, pernicious anemia may lead to potentially serious long-term complications related to micronutrient deficiencies and their consequences and the development of gastric cancer and type 1 gastric neuroendocrine tumors. When not recognized in a timely manner or when pernicious anemia is diagnosed with delay, these complications may be potentially life-threatening and sometimes irreversible. The current review aimed to focus on epidemiology, pathogenesis, and clinical presentations of pernicious anemia in an attempt to look beyond borders of medical specialties. It aimed to focus on micronutrient deficiencies besides the well-known vitamin B deficiency, the diagnostic approach for pernicious anemia, its long-term complications and optimal clinical management, and endoscopic surveillance of patients with pernicious anemia.
Topics: Anemia, Pernicious; Gastritis; Humans; Micronutrients; Precancerous Conditions; Stomach Neoplasms; Vitamin B 12; Vitamin B 12 Deficiency; Vitamins
PubMed: 35458234
DOI: 10.3390/nu14081672 -
Annals of Nutrition & Metabolism 2020Vitamin D supplementation is known to both prevent and treat rickets, a disease of hypomineralized bone. Childhood is a period of great bone development and, therefore,... (Review)
Review
BACKGROUND
Vitamin D supplementation is known to both prevent and treat rickets, a disease of hypomineralized bone. Childhood is a period of great bone development and, therefore, attention to the vitamin D needed to optimize bone health in childhood is imperative.
SUMMARY
Observational studies have pointed to a vitamin D status, as indicated by a 25-hydroxyvitamin D concentration, of 50 nmol/L to ensure avoidance of rickets and of 75 nmol/L to optimize health. However, the benefits of achieving these levels of vitamin D status are less evident when pediatric randomized, controlled trials are performed. In fact, no specific pediatric vitamin D supplementation has been established by the existing evidence. Yet, study of vitamin D physiology continues to uncover further potential benefits to vitamin D sufficiency. This disconnection between vitamin D function and trials of supplementation has led to new paths of investigation, including establishment of the best method to measure vitamin D status, examination of genetic variation in vitamin D metabolism, and consideration that vitamin D status is a marker of another variable, such as physical activity, and its association with bone health. Nevertheless, vitamin D supplementation in the range of 10-50 μg/day appears to be safe for children and remains a promising intervention that may yet be supported by clinical trials as a method to optimize pediatric health. Key Message: Pediatric vitamin D status is associated with avoidance of rickets. Randomized, controlled trials of vitamin D supplementation for pediatric bone health are limited and equivocal in their results. Beyond bone, decreased risk for autoimmune, infectious, and allergic diseases has been associated with higher vitamin D status. The specific vitamin D supplementation to optimize toddler, child, and adolescent outcomes is unknown, but doses 10-50 μg/day are safe and may be beneficial.
Topics: Adolescent; Bone Density; Bone Development; Child; Child Nutritional Physiological Phenomena; Child, Preschool; Dietary Supplements; Female; Humans; Infant; Male; Nutritional Status; Rickets; Vitamin D; Vitamin D Deficiency
PubMed: 33232959
DOI: 10.1159/000505635 -
The Indian Journal of Medical Research Oct 2020Defective mineralization of the growth plate and preformed osteoid result in rickets and osteomalacia, respectively. The leading cause of rickets worldwide is solar... (Review)
Review
Defective mineralization of the growth plate and preformed osteoid result in rickets and osteomalacia, respectively. The leading cause of rickets worldwide is solar vitamin D deficiency and/or dietary calcium deficiency collectively termed as nutritional rickets. Vitamin D deficiency predominates in high-latitude countries in at-risk groups (dark skin, reduced sun exposure, infants and pregnant and lactating women) but is emerging in some tropical countries due to sun avoidance behaviour. Calcium deficiency predominates in tropical countries, especially in the malnourished population. Nutritional rickets can have devastating health consequences beyond bony deformities (swollen wrist and ankle joints, rachitic rosary, soft skull, stunting and bowing) and include life-threatening hypocalcaemic complications of seizures and, in infancy, heart failure due to dilated cardiomyopathy. In children, diagnosis of rickets (always associated with osteomalacia) is confirmed on radiographs (cupping and flaring of metaphyses) and should be suspected in high risk individuals with the above clinical manifestations in the presence of abnormal blood biochemistry (high alkaline phosphatase and parathyroid hormone, low 25-hydroxyvitamin D and calcium and/or low phosphate). In adults or adolescents with closed growth plates, osteomalacia presents with non-specific symptoms (fatigue, malaise and muscle weakness) and abnormal blood biochemistry, but only in extreme cases, it is associated with radiographic findings of Looser's zone fractures. Bone biopsies could confirm osteomalacia at earlier disease stages, for definitive diagnosis. Treatment includes high-dose cholecalciferol or ergocalciferol daily for a minimum of 12 wk or stoss therapy in exceptional circumstances, each followed by lifelong maintenance supplementation. In addition, adequate calcium intake through diet or supplementation should be ensured. Preventative approaches should be tailored to the population needs and incorporate multiple strategies including targeted vitamin D supplementation of at-risk groups and food fortification with vitamin D and/or calcium. Economically, food fortification is certainly the most cost-effective way forward.
Topics: Adolescent; Calcium; Child; Female; Humans; Infant; Lactation; Osteomalacia; Pregnancy; Rickets; Vitamin D; Vitamin D Deficiency; Vitamins
PubMed: 33380700
DOI: 10.4103/ijmr.IJMR_1961_19 -
Medicina (Kaunas, Lithuania) Mar 2021There are numerous risk factors for stress fractures that have been identified in literature. Among different risk factors, a prolonged lack of vitamin D (25(OH)D) can... (Review)
Review
There are numerous risk factors for stress fractures that have been identified in literature. Among different risk factors, a prolonged lack of vitamin D (25(OH)D) can lead to stress fractures in athletes since 25(OH)D insufficiency is associated with an increased incidence of a fracture. A 25(OH)D value of <75.8 nmol/L is a risk factor for a stress fracture. 25(OH)D deficiency is, however, only one of several potential risk factors. Well-documented risk factors for a stress fracture include female sex, white ethnicity, older age, taller stature, lower aerobic fitness, prior physical inactivity, greater amounts of current physical training, thinner bones, 25(OH)D deficiency, iron deficiency, menstrual disturbances, and inadequate intake of 25(OH)D and/or calcium. Stress fractures are not uncommon in athletes and affect around 20% of all competitors. Most athletes with a stress fracture are under 25 years of age. Stress fractures can affect every sporty person, from weekend athletes to top athletes. Stress fractures are common in certain sports disciplines such as basketball, baseball, athletics, rowing, soccer, aerobics, and classical ballet. The lower extremity is increasingly affected for stress fractures with the locations of the tibia, metatarsalia and pelvis. Regarding prevention and therapy, 25(OH)D seems to play an important role. Athletes should have an evaluation of 25(OH)D -dependent calcium homeostasis based on laboratory tests of 25-OH-D, calcium, creatinine, and parathyroid hormone. In case of a deficiency of 25(OH)D, normal blood levels of ≥30 ng/mL may be restored by optimizing the athlete's lifestyle and, if appropriate, an oral substitution of 25(OH)D. Very recent studies suggested that the prevalence of stress fractures decreased when athletes are supplemented daily with 800 IU 25(OH)D and 2000 mg calcium. Recommendations of daily 25(OH)D intake may go up to 2000 IU of 25(OH)D per day.
Topics: Aged; Dietary Supplements; Female; Fractures, Stress; Humans; Vitamin D; Vitamin D Deficiency; Vitamins
PubMed: 33804459
DOI: 10.3390/medicina57030223 -
Nutrients Apr 2020Vitamin D and calcium have different biological functions, so the need for supplementation, and its safety and efficacy, need to be evaluated for each separately.... (Review)
Review
Vitamin D and calcium have different biological functions, so the need for supplementation, and its safety and efficacy, need to be evaluated for each separately. Vitamin D deficiency is usually the result of low sunlight exposure (e.g., in frail older people, those who are veiled, those with dark-skin living at higher latitudes) and is reversible with calciferol 400-800 IU/day. Calcium supplements produce a 1% increase in bone density in the first year of use, without further increases subsequently. Vitamin D supplements do not improve bone density in clinical trials except in analyses of subgroups with baseline levels of 25-hydroxyvitamin D <30 nmol/L. Supplementation with calcium, vitamin D, or their combination does not prevent fractures in community-dwelling adults, but a large study in vitamin D-deficient nursing home residents did demonstrate fracture prevention. When treating osteoporosis, co-administration of calcium with anti-resorptive drugs has not been shown to impact on treatment efficacy. Correction of severe vitamin D deficiency (<25 nmol/L) is necessary before use of potent anti-resorptive drugs to avoid hypocalcemia. Calcium supplements cause gastrointestinal side effects, particularly constipation, and increase the risk of kidney stones and, probably, heart attacks by about 20%. Low-dose vitamin D is safe, but doses >4000 IU/day have been associated with more falls and fractures. Current evidence does not support use of either calcium or vitamin D supplements in healthy community-dwelling adults.
Topics: Adult; Aged; Bone Density; Calcium; Calcium, Dietary; Female; Fractures, Bone; Humans; Male; Vitamin D; Vitamin D Deficiency
PubMed: 32272593
DOI: 10.3390/nu12041011 -
Blood May 2020
Topics: Adult; Anemia, Pernicious; Female; Humans; Prognosis; Vitamin B 12; Vitamin B 12 Deficiency; Vitamin B Complex
PubMed: 32379881
DOI: 10.1182/blood.2020005344 -
CMAJ : Canadian Medical Association... Feb 2020
Topics: Adult; Alcoholism; Female; Humans; Magnetic Resonance Imaging; Thiamine; Thiamine Deficiency; Treatment Outcome; Vitamin B Complex; Wernicke Encephalopathy
PubMed: 32041699
DOI: 10.1503/cmaj.190998 -
Clinical Nutrition (Edinburgh, Scotland) Jun 2020Maternal vitamin D deficiency has been associated with an increased risk for preeclampsia. Despite this, the current evidence regarding the efficacy of vitamin D... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Maternal vitamin D deficiency has been associated with an increased risk for preeclampsia. Despite this, the current evidence regarding the efficacy of vitamin D supplementation in preventing preeclampsia is controversial. To assess the impact of vitamin D supplementation on the risk of preeclampsia, we performed a systematic review of the literature and a meta-analysis of the available randomized clinical trials (RCTs).
METHODS
The primary outcome was preeclampsia. Subgroup analyses were carried out considering the timing of the supplementation, type of intervention and the study design. Meta-regression analysis, including the amount of vitamin D and maternal age, were planned to explore heterogeneity (PROSPERO database registration number: CRD42019119207).
RESULTS
Data were pooled from 27 RCTs comprising 59 arms, which included overall 4777 participants, of whom 2487 were in the vitamin D-treated arm and 2290 in the control arm. Vitamin D administration in pregnancy was associated with a reduced risk of preeclampsia (odd ratio [OR] 0.37, 95% confidence interval [CI]: 0.26, 0.52; I = 0%). If the vitamin D supplementation was started up to 20 weeks' gestation, the odds was a little lower (OR 0.35, 95% CI: 0.24, 0.50, p < 0.001). The effect was largely independent of the supplementation cessation (until delivery or not), type of intervention (vitamin D alone or in association with calcium), and study design. Increasing dose of vitamin D was associated with reduced incidence of preeclampsia (slope of log OR: -1.1, 95% CI: -1.73, -0.46; p < 0.001).
CONCLUSIONS
Results suggest that vitamin D supplementation may be useful in preventing preeclampsia. These data are especially useful for health-care providers who engage in the management of pregnant women at risk for preeclampsia. Our findings are a call for action to definitively address vitamin D supplementation as a possible intervention strategy in preventing preeclampsia in pregnancy.
Topics: Adolescent; Adult; Avitaminosis; Dietary Supplements; Female; Humans; Incidence; Middle Aged; Pre-Eclampsia; Pregnancy; Protective Factors; Randomized Controlled Trials as Topic; Risk Assessment; Risk Factors; Treatment Outcome; Vitamin D; Young Adult
PubMed: 31526611
DOI: 10.1016/j.clnu.2019.08.015 -
Indian Journal of Pediatrics Jun 2023Nutritional rickets, caused by vitamin D and/or calcium deficiency is by far the most common cause of rickets. In resource-limited settings, it is therefore not uncommon... (Review)
Review
Nutritional rickets, caused by vitamin D and/or calcium deficiency is by far the most common cause of rickets. In resource-limited settings, it is therefore not uncommon to treat rickets with vitamin D and calcium. If rickets fails to heal and/or if there is a family history of rickets, then refractory rickets should be considered as a differential diagnosis. Chronic low serum phosphate is the pathological hallmark of all forms of rickets as its low concentration in extracellular space leads to the failure of apoptosis of hypertrophic chondrocytes leading to defective mineralisation of the growth plate. Parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) control serum phosphate concentration by facilitating the excretion of phosphate in the urine through their action on the proximal renal tubules. An increase in PTH, as seen in nutritional rickets and genetic disorders of vitamin D-dependent rickets (VDDRs), leads to chronic low serum phosphate, causing rickets. Genetic conditions leading to an increase in FGF23 concentration cause chronic low serum phosphate concentration and rickets. Genetic conditions and syndromes associated with proximal renal tubulopathies can also lead to chronic low serum phosphate concentration by excess phosphate leak in urine, causing rickets.In this review, authors discuss an approach to the differential diagnosis and management of refractory rickets.
Topics: Humans; Calcium; Fibroblast Growth Factors; Rickets; Vitamin D; Parathyroid Hormone; Vitamins; Phosphates; Familial Hypophosphatemic Rickets
PubMed: 37074534
DOI: 10.1007/s12098-023-04538-4