Sickle Cell Hemoglobinopathies and Bone Health

Therapuetic Areas:Hematology
Age Range:18 - 45
Start Date:May 2014
End Date:December 2019
Contact:Quratulain Ali, MPH, CCRP

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Sickle Cell Hemoglobinopathies and Bone Heath

This research study has two purposes. The first purpose is to determine whether having sickle
cell trait (SCT) is a risk factor for the development of bone thinning at an earlier age than
expected. Nearly 10% of African Americans (AA) carry sickle cell trait and most of them are
unaware of it. African Americans are less likely to develop thin bones than whites, but if
they sustain a bone fracture, they are more likely to die from it. We believe having sickle
cell trait may lead to bone thinning and predispose a subset of African Americans to
dangerously thin bones. The second purpose is to try to understand why individuals with
sickle cell disease (SCD) have thinner bones than healthy individuals do. Doctors have
already discovered that people with sickle cell disease have very thin bones, but they have
not determined why. Our study will try to identify whether the bone thinning is from the body
not making enough bone or from the body losing bone once it is made.

SCD is a hereditary disease arising only when two parents carrying sickle cell trait (SCT)
conceive a child. SCT is clinically silent but very common in African Americans with a ~10%
prevalence, although most carriers are unaware of their status. There are no data on bone
mineral density (BMD) or vitamin D status in these individuals. Although it is clear that
those with SCD have accelerated bone thinning the effect of SCT on bone metabolism or
fractures has not been studied. Although the incidence of hip fracture in AA women is about
half that of white women, the etiology and risk factors of fractures in AA women are not
clearly defined, and it is intriguing to postulate that SCT may have a relationship to bone
metabolism and fracture risk in this population, and thus contribute to racial disparity. We
hypothesize that the mechanisms underlying altered bone homeostasis in SCD are different than
in the general population but perhaps similar to those with SCT. We also hypothesize that SCT
is a state of reduced bone mineralization which may contribute to racially disparate outcomes
among AAs with bone fractures. Our objectives are (1) to define the mechanisms of bone loss
in SCD and (2) to evaluate parameters of bone metabolism in human subjects with SCT compared
to those with normal hemoglobin and those with SCD. We will investigate the effect of SCD and
SCT on bone homeostasis in premenopausal AA subjects via serum bone turnover markers,
calciotrophic hormones and bone mineral density (BMD) testing. We hypothesize that
premenopausal AA women with SCT will have significantly lower BMD and higher serum bone
turnover markers than race- and age-matched control AA women. In addition, we will explore
Vitamin D status and its relationship to bone turnover and BMD in all three groups. We
further postulate that bone homeostasis in SCT subjects will be intermediate between healthy
controls and subjects with SCD.

Inclusion Criteria:

- Age 18-45 years.

- Female.

- Regular menstrual periods.

- Self-identification of African American race.

Exclusion Criteria:

- Taking oral contraceptives or medications known to influence bone metabolism (e.g.
Glucocorticoids, anti-resorptive or anabolic medications for osteoporosis,
pharmacologic Vit D dosing).

- Known metabolic bone disorder (e.g. uncontrolled thyroid disease,

- Pregnant, breast-feeding, or within 3 months post-partum.

- Taking an investigational drug.
We found this trial at
Farmington, Connecticut 06032
Principal Investigator: Biree Andemariam, M.D
Phone: 860-679-7648
Farmington, CT
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