Lactnet Journal Club
Please review the following summary of a recent article from the
medical literature. Optimally, one has also been able to review the
article itself (article posted on Lactnet 10/6).
Interested parties are invited to post, on Lactnet, either objective
comments or criticisms of the article as well as questions related to
the article itself or relevant subject matter.
The periodic publication, over the last 25 years, of a number of
similar case reports (of nutritional rickets) raises the question:
ought all or selected groups of healthy term exclusively breastfed
infants be supplemeneted with vitamin ?
In light of this and other case reports what 'should' pediatric health
care providers (this includes colleagues in the field of lactation)
recommend to their patients/clients ? Where do we 'go' from here ?
What is your objective opinion of this report (strengths &
weaknesses)?
We look forward to a lively and stimulating discussion: ...
October 2000
NUTRITIONAL RICKETS IN AFRICAN AMERICAN BREAST-FED INFANTS
JOURNAL OF PEDIATRICS AUGUST 2000;137:153-7. Shelley Kreiter et al.
(NOTE: also read the accompanying editorial)
INTRODUCTION:
Recently, there has been an increase in reports of nutritional rickets
(rickets secondary to vitamin D deficiency) in the United States. The
increase in cases of nutritional rickets referred to two university
medical centers in North Carolina in recent years prompted the
question as to what changes might be occurring in the care of infants
living in the area.

METHODS:
Records were reviewed on all patients with a diagnosis of nutritional
rickets between 1990 and 1999. All patients were seen by at least one
of the authors at one of three pediatric subspecialty clinics. Both
clinical and biochemical data were obtained.

RESULTS:
Between 1990 and June 1999, 30 patients with nutritional rickets were
referred to the two medical centers. 57% of the patients presented in
1998 and the first half of 1999. 57% were male and 43% were female.
All patients were of African-American background.
Dietary history (provided at time of diagnosis): all were breastfed,
mean duration of breastfeeding: 12.5 months, all children in whom the
diagnosis was made after 1 year of age had a history of poor intake of
fortified cow's milk or other dietary products.
Age at diagnosis: mean =3D 14.9 months, median =3D 15.5 months, range of
5-25 months.
*One-third presented at 12 months of age or younger.
Presenting signs: skeletal abnormalities: 16, failure to thrive: 13,
seizures (secondary to hypocalcemia): 2, developmental delay: 1
Radiologic findings: all had classic radiologic changes consistent
with rickets.
Growth abnormalities: Length measurements were available for 26 of the
patients. In 17, length was noted to be less than or equal to the 5
percentile.
Laboratory abnormalities: 25-hydroxy vitamin D levels were obtained in
23 patients, 19 had abnormally low levels.

DISCUSSION (from the article):
Several possible causes for the increase in the number of cases of
nutritional rickets at the 2 institutions:
1. increase in incidence of breastfeeding amongst the African-American
population
2. decrease in the number of infants receiving vitamin D
supplementation
3. decreased exposure to sunlight, also compared to light-skinned
individuals, dark-skinned individuals require more sunlight exposure
4. nutritional rickets was improperly diagnosed
Conclusion: "We support breastfeeding as the ideal nutrition for
babies and children but recommend supplementation of all dark-skinned,
breastfed infants and children with 400 IU of vitamin D per day,
starting at least by 2 months of age."

The following information is provided to enhance the understanding of
and provide a conceptual framework for the article. =85
*************************
VITAMIN D PHYSIOLOGY
What is vitamin D?
Vitamin D is actually not a vitamin. Rather it is a steroid hormone.
Like a hormone, vitamin D is transported into the cell. Upon
reaching specific receptors in the nucleus, it causes the expression
of ("turns on") vitamin D-sensitive genes. The expression of these
vitamin D-sensitive genes results in the production of various
proteins. One such protein is a calcium-binding protein.
How is vitamin D obtained? Can the body make its own?
Sunlight, specifically ultraviolet B light, catalyzes the synthesis of
a form of Vitamin D in the skin. Until relatively recently, this
constituted the principal source of D for man-and womankind. This is
because very few foods naturally contain D (fish liver, visceral oils
from some fish including cod and tuna and egg yolks). Both human and
cow's milk contain low amounts of D (20-50 IU per liter). Note: the
recommended daily intake of D for an infant is 300 IU per day (ages 0
- 6 months) and 400 IU per day (ages 6 - 12 months).
After being ingested or synthesized in the skin, D is then modified by
the liver and finally the kidney. The final conversion by the kidney
results in the biologically active form of D (1,25-dihydroxy vitamin
D).
What are the functions of D?
Stimulates intestinal absorption of calcium and phosphorous
Promotes renal reabsorption of calcium and phosphorous
Maintains serum calcium levels via its mobilization from the bone
Excess D results in hypercalcemia
What happens when a child does not ingest or synthesize enough D?
In the mid-17th century, it was noted that children living in cities
developed a severe bone disease. In North America and Northern
Europe, the incidence of this disorder increased dramatically during
the industrial revolution.
In vitamin D-deficient rickets, formerly referred to as 'common'
rickets, the following physiologic, biochemical and clinical changes
are affected:
-low phosphorous levels
-high alkaline phosphatase levels
-high parathyroid hormone levels
-low 25 hydroxy vitamin D levels
-reduced intestinal calcium absorption
-leading to decreased serum calcium levels
-in turn, leading to defective bone mineralization
-thus, bones have reduced density and strength
-because one's calcium and phosphorous requirements are greatest
during the first year of life, most patients diagnosed with vitamin
D-deficient rickets are less than 18 months old
-CLINICALLY: knobby deformities of arms and legs, as well as the rib
cage, chest wall deformities, an enlarged fontanelle (the soft spot on
an infant's skull), a soft skull, fractures, seizures from low serum
calcium levels, decreased growth and delayed development



Kathleen B. Bruce, BSN, IBCLC co-owner Lactnet, Indep. Consultant
mailto:[log in to unmask]
http://homepages.together.net/~kbruce/kbblact.html
LACTNET Archives http://peach.ease.lsoft.com/archives/lactnet.html

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