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 = 14.9 months, median = 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. …

*************************

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

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