| Abstract:
Vitamin D-deficiency rickets among children in Canada.CMAJ.
2007 Jun 28;
BACKGROUND: Based
on regional and anecdotal reports, there is concern that vitamin
Dâdeficiency rickets is persistent in Canada despite guidelines for
its prevention. We sought to determine the incidence and clinical
characteristics of vitamin Dâdeficiency rickets among children living
in Canada. METHODS: A total of 2325 Canadian pediatricians were
surveyed monthly from July 1, 2002, to June 30, 2004, through the
Canadian Paediatric Surveillance Program to determine the incidence,
geographic distribution and clinical profiles of confirmed cases of
vitamin D-deficiency rickets. We calculated incidence rates based on
the number of confirmed cases over the product of the length of the
study period (2 years) and the estimates of the population by age
group. RESULTS: There were 104 confirmed cases of vitamin Dâ
deficiency rickets during the study period. The overall annual
incidence rate was 2.9 cases per 100 000. The incidence rates were
highest among children residing in the the north (Yukon Territory,
Northwest Territories and Nunavut). The mean age at diagnosis was 1.4
years (standard deviation [SD] 0.9, minâmax 2 weeksâ6.3 years).
Sixty-eight children (65%) had lived in urban areas most of their
lives, and 57 (55%) of the cases were identified in Ontario.
Ninety-two (89%) of the children had intermediate or darker skin.
Ninety-eight percent (94%) had been breastfed, and 3 children (2.9%)
had been fed standard infant formula. None of the breast-fed infants
had received vitamin D supplementation according to current guidelines
(400 IU/d). Maternal risk factors included limited sun exposure and a
lack of vitamin D from diet or supplements during pregnancy and
lactation. The majority of children showed clinically important
morbidity at diagnosis, including hypocalcemic seizures (20 cases,
19%). INTERPRETATION: Vitamin Dâdeficiency rickets is persistent in
Canada, particularly among children who reside in the north and among
infants with darker skin who are breastfed without appropriate vitamin
D supplementation. Since there were no reported cases of breast-fed
children having received regular vitamin D (400 IU/d) from birth who
developed rickets, the current guidelines for rickets prevention can
be effective but are not being consistently imple- Abstract mented.
The exception appears to be infants, including those fed standard
infant formula, born to mothers with a profound vitamin D deficiency,
in which case the current guidelines may not be adequate to rescue
infants from the vitamin D-deficient state.
Asymptomatic
rickets in adolescent girls.Indian
J Pediatr. 2007 Jun;74(6):571-5.
OBJECTIVE:
Inadequate sunlight exposure and calcium intake during rapid growth at
puberty lead to hypocalcemia, hypovitaminosis D and eventually to
overt rickets. To determine serum biochemical findings of rickets in
healthy 11-15 yr old girls, the effect of sunlight exposure and oral
vitamin D supplementation on serum 25- hydroxy vitamin D and calcium
administration in girls with abnormal findings during December 2002
through March 2003 in Tehran, Iran. METHODS: Healthy middle school
girls were selected for estimation of vitamin D, calcium and
phosphorus intake by a three-day food recall. And measurement of serum
calcium, phosphorus, parathyroid hormone, alkaline-phosphatase and 25-
hydroxyvitamin D concentration. The girls with abnormal findings
divided in two groups. Hypovitaminosis D girls subdivided into two
groups, supplementary sunlight exposure and vitamin- D administrated
for them and calcium administration for the second group for 20 days.
RESULTS: Of 414 girls, the mean daily vitamin D acquirement and
calcium intake were 119 +/- 52 IU and 360 +/- 350 mg among all girls
respectively. Mean serum 25-hydroxyvitamin D with two or more abnormal
biochemical findings in 15 (3.6%) girls (group I) were 7.8 ng/ml and
alkaline phosphatse with normal or low calcium in 29 (7%) girls (group
II) was 1187 IU/L. Mean serum calcium was 8.2 mg % in 8 of 29 girls.
Serum 25- hydroxyvitamin D before and after sunlight exposure was 7.1
+/- 1.9 ng/ml and 13.9 +/- 2.4 ng/ml and vitamin D administration was
7.4 +/- 1.8 ng/ml (group Ia) and 27.9 +/- 4.2 ng/ml (group Ib)
respectively. Serum alkaline phosphatase before and after calcium
administration were 1187 IU/L and 666 IU/L respectively. CONCLUSION:
We conclude that low daily calcium intake and vitamin D acquirement
are two important problems in Iranian girls during rapid growth at
puberty; therefore, for prevention of overt rickets calcium and
vitamin D Supplementation appear to be necessary.
Vitamin D
and aging: old concepts and new insights.
J Nutr Biochem. 2007 May 23;
Aging is a
complex biological process driven by a selective class of molecules
and pathways that affect overall deterioration of physiological
functions to increase the risk of age-related diseases. A role of
vitamin D in mammalian aging is well documented. Since vitamin D has
an essential role in bone formation and mineralization, its deficiency
results in impaired bone mineralization, such as rickets in children,
osteomalacia in adults and osteoporosis in the aged population.
Vitamin D replacement therapy therefore is one of the most commonly
prescribed treatments for the elderly. Recent studies using
genetically altered mouse models, such as in Fgf-23(-/-) and klotho
mutant mice, that exhibit altered mineral ion metabolism due to high
vitamin D activities showed features of premature aging that include
atherosclerosis, emphysema, osteopenia/osteoporosis, hypogonadism,
soft tissue calcifications and generalized atrophy of organs; the
pathologic effects of vitamin D in these mouse models are obvious, as
diminution or genetic ablation of the vitamin D pathway ameliorated
most of the above-mentioned phenotypes, by reversing mineral ion
metabolism, and the resultant effect being prolonged survival of the
mutant mice. These in vivo mouse studies, although subject to further
molecular characterization, add new insights into the role of vitamin
D in aging.
Vitamin D
and parathyroid hormone in outpatients with noncholestatic chronic
liver disease.Clin
Gastroenterol Hepatol. 2007 Apr;5(4):513-20.
BACKGROUND &
AIMS: The liver plays a central role in vitamin D metabolism. Our aim
was to determine the prevalence and type of vitamin D-parathyroid
hormone (PTH) disturbance in ambulatory patients with noncholestatic
chronic liver disease (CLD) and its relationship with disease severity
and liver function. METHODS: We studied 100 consecutive outpatients
(63 men, 37 women; mean age, 49.0 +/- 12.1 [SD] y) with noncholestatic
CLD caused by alcohol (n = 40), hepatitis C (n = 38), hepatitis B (n =
12), autoimmune hepatitis (n = 4), hemochromatosis (n = 4), and
nonalcoholic steatohepatitis (n = 2); 51 patients had cirrhosis. Serum
concentrations of 25-hydroxyvitamin D (25[OH]D), PTH, calcium,
phosphate, magnesium, creatinine, and liver function tests were
determined. RESULTS: Serum 25(OH)D levels were inadequate in 91
patients: vitamin D deficiency (<50 nmol/L) was found in 68 patients
and vitamin D insufficiency (50-80 nmol/L) was found in 23 patients.
Secondary hyperparathyroidism (serum PTH, >6.8 pmol/L) was present in
16 patients. The prevalence of vitamin D deficiency was significantly
higher in cirrhotic vs noncirrhotic patients (86.3% vs 49.0%; P =
.0001). In Child-Pugh class C patients, 25(OH)D levels were
significantly lower than in class A patients (22.7 +/- 10.0 nmol/L vs
45.8 +/- 16.8 nmol/L; P < .001). Serum 25(OH)D independently
correlated with international normalized ratio (negatively; P = .018)
and serum albumin (positively; P = .007). Serum 25(OH)D levels of less
than 25 nmol/L predicted coagulopathy, hyperbilirubinemia,
hypoalbuminemia, increased alkaline phosphatase, and anemia and
thrombocytopenia. CONCLUSIONS: Vitamin D inadequacy is common in
noncholestatic CLD and correlates with disease severity, but secondary
hyperparathyroidism is relatively infrequent. Management of CLD should
include assessment of vitamin D status in all patients and replacement
when necessary.
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