Secondary Osteoporosis: Are You at Risk?

By Cory Wilczynski , MD

Osteoporosis [os'tē-ō-pō-rō'sis] is a common condition, affecting nearly 8 million women and 2 million men in the United States. The condition is one in which the bones become fragile and is due to an inherited, poor quality of bone structure combined with the effects of estrogen deficiency in women, testosterone and estrogen deficiency in men, and the results of the aging process. However, there are other conditions, not truly disorders of bone, which make the bones more fragile and increase your fracture risk. When this occurs it is referred to as secondary osteoporosis, which may arise at any age and affect men and women equally.

In order to determine if secondary osteoporosis is present, the diagnosis of osteoporosis first needs to be established. This can be achieved through several methods of testing. A T score compares your bone density to that of young people who are at their peak (best) bone density and lowest fracture risk. The more your score differs from their score, the more you are at risk for fracture. A score of less than or equal to a -2.5 on a dual-energy x-ray (DEXA) – which is a means of measuring bone mineral density – or clinical assessment and use of a fracture risk assessment tool (FRAX)–a diagnostic tool used to evaluate the 10-year probability of bone fracture risk–are used to establish the diagnosis of osteoporosis and judge the risk of fracture. FRAX scores are calculated based on your medical history and include such factors as your gender, whether you smoke, alcohol intake, personal history of fracture, parents’ history of fracture, steroid use and most recent T score; a score greater than or equal to 20 percent for major risk and greater than or equal to three percent in the hip would also help identify if you are at risk for a fracture. A FRAX score is only applicable for patients not currently on drugs that reduce the excessive removal of old, hardened bone (some removal of bone happens normally when bones repair wear-and-tear damage) or other medications for treatment of osteoporosis.

Sixty percent of men and 50 percent of premenopausal women diagnosed with osteoporosis will have at least one secondary cause. This article provides an overview of secondary causes of osteoporosis such as endocrine disorders, blood cell disorders, connective tissue disorders, medications, malabsorptive disorders (difficulty absorbing nutrients from food), genetic disorders and others.

Endocrine Disorders

Endocrine disorders that can be linked to secondary osteoporosis include: hyperparathyroidism [hi-per-para-thi-royd-ism], an overproduction of a hormone that can lead to high calcium levels; Cushing’s [kush-ings] syndrome, a condition that is associated with high levels of steroid; hyperthyroidism [hi-per-thi-royd-izm], a condition in which the thyroid gland produces too much thyroxine hormone; hypogonadism [hi-po-go-nad-izm], a condition in which the body doesn't produce enough of the male hormone testosterone; prolactinoma [pro-lakti- no-ma], a non-cancerous tumor of the pituitary gland which produces a hormone called prolactin; diabetes mellitus, a condition in which the pancreas no longer produces enough insulin or cells stop responding to the insulin that is produced, so that glucose in the blood cannot be absorbed into the cells of the body; acromegaly [ak-row-meg-a-le], a long-term condition in which there is too much growth hormone and the body tissues get larger over time; and other causes of estrogen deficiency (chemotherapy or primary ovarian failure).

In men, hypogonadism is still the most common cause of osteoporosis. The exact relationship between testosterone, estrogen and bone mineral density is unclear, but it is known that the depletion of either hormone is related to a decrease in body mass density (BMD) in both men and women. For men with proven hypogonadism (a testosterone level of less than 200 nanograms per deciliter), testosterone replacement therapy will improve bone mineral density.

Uncontrolled hyperthyroidism is another example where, if treated early and controlled, there is only a small loss in bone mineral density. Similarly, identification and treatment of hyperparathyroidism through surgery can also reduce the risk of fracture.

Blood Cell Disorders

Multiple myeloma [mi-e-lo-ma], a cancer of plasma cells, a type of white blood cell normally responsible for producing antibodies; mastocytosis [mas-toe-sitoe- sis], a disorder caused by too many mast cells in your body; leukemia [lu-ke-me-a], cancer of the blood or bone marrow; lymphoma [lim-fo-ma], cancer of the lymphatic system; sickle cell disease, an inherited blood disorder that turns normal, round blood cells into crescent-shaped cells; lipidoses [lip-id-sez], harmful amounts of fats accumulating in some of the body’s cells; and polycythemia [pol-e-si-the-me-a], a blood disorder in which your bone marrow makes too many red blood cells, all represent disorders in the blood cell lines that are also related to osteoporosis. There is some suggestion that chronic blood loss is also related to osteoporosis.

Connective Tissue Disorders

Osteogenesis imperfecta [os-t-eh-jen-i-sis im-per-fekte] is a disorder that causes secondary osteoporosis due to a high level of calcium, the same as hyperparathyroidism, as discussed above. Other connective tissue diseases include Ehler-Danlos syndrome, a condition of skin and tissues having a lot of flexibility, and vitamin C deficiency. Most of these conditions are related to genetic disorders that weaken formation of bone by associated effects with connective tissue.

Medications

Glucocorticoids [glu-ko-kor-ti-koids], often referred to as steroids, are the most common cause of secondary osteoporosis. Conditions that require frequent exposure to steroids, such as rheumatoid arthritis, organ transplants, chronic pulmonary disease and inflammatory bowel disease, have strong associations with osteoporosis as well. Steroids are known to inhibit formation of osteoblasts and osteoclasts over time as well as decrease the lifespan of these cells. Osteoblasts and osteoclasts are the two cells involved in bone formation. The duration of glucocorticoid use is not well defined, but it is known that short bursts of taking the medication such as those seen in treatment of COPD (chronic obstructive pulmonary disease) and asthma exacerbations do not have the same detrimental effects on bone such as the long-term effects of bone metabolism resulting from lifelong immunosuppression for transplant patients.

Other medications associated with increased risk of osteoporosis include some anti-seizure medications, some anticoagulants (an agent used to prevent the formation of blood clots), immune system-suppressing medications, some hormones, some antidepressants and aluminum-containing antacids.

Malabsorptive and Nutritional Disorders

Calcium and vitamin D supplementation is the key component to the prevention of progression from osteopenia [os-te-eh-pe-ne-eh], a condition where bone mineral density is lower than normal, to osteoporosis. Calcium and vitamin D deficiencies alone are risk factors for osteoporosis. The problem with malabsorption syndromes such as inflammatory bowel disease, chronic liver disease, alcoholism, celiac [se-le-ak] disease (an autoimmune digestive disease that interferes with absorption of nutrients from food), eating disorder anorexia nervosa [an-uh-RECK-see-uh nur-VOH-suh], chronic use of total parenteral nutrition (feeding of a person intravenously), and patients that have had a gastrectomy [gas-trek-to-mee] , a partial or total surgical removal of the stomach, is that they absorb vitamin D poorly. The same was thought to be true even of steroid-related osteoporosis. Vitamin D deficiency is exceedingly common, with an overall prevalence of 46.1 percent in the U.S. population. Though not always caused by a gastrointestinal disease, vitamin D deficiency should be treated aggressively to maintain a normal level.

Additional Disorders

Other disorders associated with increased risk of osteoporosis include some listed above that require the use of medications that affect osteoblast or osteoclast function or inhibit the body’s absorption of calcium and vitamin D, which are essential for bone health. These conditions include rheumatoid arthritis, chronic obstructive pulmonary disease, organ transplantation, immobilization, idiopathic hypercalciuria [hi-per-kalse-yu-ree-a] (high calcium concentrations in the urine), multiple sclerosis, mastocytosis and end-stage kidney disease. In conditions involving defects in the body’s ability to eliminate calcium, the risk to bones actually originates from the kidneys’ inability to reabsorb calcium.

There are many conditions and medications that can contribute to the development of osteoporosis. A careful history and medication list can exclude many of the above causes. Most women of postmenopausal age will have primary osteoporosis, but in men, premenopausal women and perimenopausal women, other conditions should be evaluated as the discovery would change medical management options.

Cory Wilczynskiwas born in Moline, IL. She was diagnosed with type 1 diabetes at the age of 3. She started going to a diabetes camp, Camp Hertko Hollow in Boone, Iowa. She eventually became a camp counselor and acting physician when in medical school. Cory finished her undergrad at Knox College in Galesburg, IL. She then went to Rush Medical College and graduated in 2010. She finished her Internal Medicine residency at Saint Louis University in 2013. Currently she is an Endocrinology Fellow at Loyola University in Maywood, IL.