Secondary osteoporosis is when another disease or condition or a drug causes osteoporosis. The osteoporosis is called secondary because it comes after the first cause.
Juvenile arthritis often causes osteoporosis, and this can be very detrimental to the child’s physical development. The arthritis itself, the drugs used to control it, and the fact that the person has limited mobility contribute to the lowering of bone density. Osteopenia and osteoporosis happen in all forms of juvenile arthritis. Osteoporosis also occurs in many multiple sclerosis patients.
You might see some people claim all osteoporosis is secondary osteoporosis. It was all caused by some other malady or poor nutrition, so there is no such thing as primary osteoporosis, goes the thinking. This is not the operating philosophy of the medical industry, although most experts would agree that choices in nutrition and exercise made early in life can affect osteoporosis risk. Nevertheless, osteoporosis with no co-morbidity or obvious chemical cause is still considered primary osteoporosis.
Doctors who encounter fragility fractures in younger men or premenopausal women may suspect secondary osteoporosis. There are suggestions that people with secondary osteoporosis are actually at a greater risk for fracture of the hip than those with primary osteoporosis. In fact, one clue doctors use to look for secondary osteoporosis is the occurrence of fractures in people taking treatment for primary osteoporosis.
To look for secondary osteoporosis the doctor considers a person use of drugs (especially steroids, antacids, and other drugs known to cause bone density loss) and may do examinations for gastrointestinal, hematologic, endocrine, and rheumatic diseases. The Academy of American Family Physicians website lists causes of secondary osteoporosis as fitting into several categories: endocrine or metabolic causes, collagen/genetic disorders, medications, and nutritional.
Treatment for other medical conditions can directly lead to development of osteoporosis or contribute to factors that promote its formation. These include:
Thyroid medications such as Levothyroxine LT4 and Armour Thyroid can affect bones, although their contribution to osteoporosis is not clear. The widely used blood thinner Warfarin and the anti-coagulant Heparin both are association with increased risk on thinning bones.
Glucocorticoid drugs slow or stop the increase in bone density that occurs in maturation, resulting in an increased lifetime risk for bone fracture. The antifolate drug methotrexate (Rheumatrex, Trexall), sometimes employed in treatment of arthritis, causes osteopenia when used in high doses, but at the doses used for arthritis, low bone density if usually not observed. Spondyloarthritis, lupus, inflammatory bowel diseases, and chronic obstructive pulmonary disease are often treated with steroid drugs and that increases the risk of low bone density.
Anticonvulsive medications like Valproic acid (Depakote), Phenytoin (Dilantin), and Phenobarbital can affect the skeletal system.
Loop diuretics (e.g. Lasix, Edecrin, Bumex, Demadex, Aldactone, Dyazide, Diamox), increase the production of urine by the kidneys and removes calcium, potassium and magnesium salts from the body. The loss of calcium in the urine increases bone loss and fracture risk. Loop diuretics are given to people with high blood pressure, congestive heart disease, kidney disease and liver disease are often prescribed loop diuretics to reduce swelling, water retention or edema.
For secondary osteoporosis caused by juvenile arthritis, bisphosphonate therapy is common and human growth hormone and teriparatide are used.
Skeletal and connective tissue diseases are primary illnesses that can lead to secondary osteoporosis. These include hypophosphatasia, osteomalacia, avascular necrosis, and osteogenesis imperfecta. Malignant bone diseases including myeloma and leukemia can cause osteoporosis.
Organ transplants appear to increase the odds of developing osteoporosis, even when the organs are not bones. So does Parkinson's Disease.
Diabetes can lead to secondary osteoporosis as hyperglycemia results in nonenzymatic glycosylation of various bone proteins, including type 1 collagen.
Diabetics also end up behaving in ways that increases osteoporosis risk. Insufficient exercise leads to decreased muscle mass. Decreased visual acuity leads to increased more falling down, and incidence of falls, and diabetic angiopathy directly inhibits blood vessels in the bone tissue. In type 2 diabetes there is lower bone formation but the same rate of bone resorption, leading to a slow demineralization. Diabetics have lower levels of PTH and osteocalcin.
One interesting finding is that diabetics with normal or even above average bone density have an increased risk for fracture, and this can be traced to use of the common diabetes drug class, the thiazolidinediones. The drug produces an imbalance in bone formation and resorption. Older people, especially postmenopausal women, are more susceptible to this side effect of thiazolidinediones.
Liver diseases often result in osteoporosis. A meta analysis of other studies found "prevalence of osteoporosis varies between 11% and 58%" among people with chronic liver disease and liver transplants. The authors of the study recommended bone density screening for such patients.
Schizophrenia is co-morbid with osteoporosis in numbers more than would result from chance. This suggests a connection, but the exact reasons are unclear. One possibility is that schizophrenics produce too much prolactin, which results in mineral loss in the bone.
Scientists seem to be moving away from the distinction between Type I and Type II osteoporosis. The idea was that osteoporosis developed after menopause (or younger) was Type I which is related to lower estrogen levels in the body. Type II osteoporosis developed past age 70, although it is more common in women than men also. Type II is aged-related and is also called senile osteoporosis. Type I more often results in vertebrae fractures while Type II most often results in hip fractures.
One possible distinction is that Type I osteoporosis is caused by an increase in bone resorption, while senile osteoporosis is due to a reduction in bone formation.