Home     Consultations     Peri Menopause     Symptoms     Nurturing Products     About Us     Site Map     Bone Health      
 

 

 

 

 

Selective Estrogen Receptor Modulators (SERM's)


Select estrogen receptor modulators attach to the estrogen receptors within bone while blocking the action of estrogen on the breast and uterus. Below is an overview of how selective estrogen receptor modulators reduce postmenopausal bone loss.

 

Select estrogen receptors are indicated for the prevention and treatment of osteoporosis in postmenopausal women. Select estrogen receptor modulators produce estrogen like effects is some estrogen sensitive tissues while blocking the effect of estrogen in other tissues. Raloxifene is a select estrogen receptor modulator that attaches to the estrogen receptor within bone while blocking the action of estrogen on the breast and uterus.

 

Resorption is a process when old bone is dissolved. Raloxifene reduces resorption of bone and decreases overall bone turnover. These positive effects on bone are indicated by reductions in serum (blood) and urine levels of bone turnover markers.

 

Raloxifene is a prescription anti-resorptive agent that works by reducing bone remodeling it does not cause a sustained increase in bone formation.

In a study that included more than 7000 women, mean age 67 years, with osteoporosis, raloxifene reduce the incidence of new vertebral (spine) fractures by 30-50%. In this study group, raloxifene increased bone mineral density at the hip and spine by 3% and 2% and decreased markers for bone turnover. Vertebral fracture reduction is evident at one year and sustained for up to four years in woman remaining on continuous therapy. When therapy is discontinued, bone turnover returns to its previous state, resulting in bone loss.The women in this study group also received 500 mg of calcium and between 400 to 600 IU of vitamin D per day.


A number of changes that occur in the lipid profile after menopause are associated with increased cardiovascular risk. Raloxifene favorably alters biochemical markers of cardiovascular risk by lowering total cholesterol and LDL-cholesterol. Raloxifene is neutral on overall HDL cholesterol, however it does elevate HDL-2, the subpartical considered the most active in sending cholesterol to the liver, to be removed from the body (reverse cholesterol transport).

Raloxifene is also neutral in regard to triglycerides, C reactive protein and PAI-1. Additional encouraging findings regarding raloxifene include the lowering of lipoprotein (a), homocysteine and plasma fibrinogen.

 

Lipoprotein (a) hinders the body's ability to dissolve blood clots. Fibrinogen is a protein in blood plasma that is essential for the clotting (coagulation) of blood.


Homocysteine is an amino acid in the blood. Studies have shown that too much homocysteine is related to a higher risk of coronary heart disease, stroke and peripheral vascular disease. Homocysteine is thought to damage the inner lining of arteries (endothelial cells) and promote blood clots.

The Raloxifene Use in The Heart (Ruth) study which has over 10,000 women enrolled will further clarify the effect of SERM's in regard to cardiovascular health. The data from this study is a few years away.

SERM's help reduce risk of breast cancer.
Women taking raloxifene were shown to have a 75% reduction of the incidence of breast cancer.

 

 

 

 

 

 

Calcium supplementation improves

the efficacy of hormone replacement therapy,

selective estrogen receptor modulators

and bisphosphonates in

reducing postmenopausal bone loss.

 

 

The site map page has a listing of additional osteoporosis overviews.  



Sources:
Reduction of Vertebral Fracture Risk in Postmenopausal Women with Osteoporosis treated with Raloxifene:
Results from a three year randomized clinical trail.
Multiple Outcomes of Raloxifene Evaluation Investigators.
JAMA 1999;282(7);637-645.
Ettinger B Black, Mittlak BH

Raloxifene: A Selective Estrogen Receptor Modulator
Janine A. Scott MD
American Family Physician: Clinical Pharmacology 1999

 

State of the Art Management of Osteoporosis

American Medical Association 2004

revised Jan 2008

 

 

 

 

 

 

 

 

 

 

 

Postmenopausal women who
do not take preventive measures
to maintain bone mass,
loss bone.

 

   

  

 

 

 

A Silent Disease

 

Osteoporosis is a silent disease,
typically there are no symptoms

until a fracture occurs.

By the time a fracture occurs, the osteoporosis is

usually advanced and the individual is

then susceptible to more vertebral fractures.

 Osteoporosis is a main
cause of vertebral fractures.

It is estimated that approximately 25 percent of
postmenopausal women in the United States
have had a vertebral compression fracture.

______________


Osteoporosis causes bones to thin
and become brittle and weak.
When the bones in the spine (vertebrae) weaken
they can break or cave in under normal pressure.
The thinning bones can collapse during
normal activity, leading to a spinal fracture.


The type of break in the spine that
is typically caused by osteoporosis is
called a compression fracture, and is defined
as a vertebral bone in

the spine that has decreased
at least 15 to 20% in height.


Compression fractures can occur in
vertebrae anywhere in the spine, but they
tend to occur most commonly in
the upper back (thoracic spine), particularly
in the lower vertebrae of

this section of the spine.


The vertebrae are the box-shaped bones
that make up the spine.
Compression fractures occuring from
osteoporosis usually effect

the front of the vertebra,
collapsing the bone in the front of the spine
and leaving the back of

the same bone unchanged.
This results in a wedge shaped vertebra.


If several vertebrae are compressed,
a rounded or hunched back may be noticed.
This is called kyphosis.


Cervical Kyphosis
is an outward curvature (kyphosis) of
the cervical vertebrae

(the bones of the neck),
creating a hump at

the back of the neck.


Thoracic kyphosis is commonly
referred to as a dowager's hump.