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Do you have any of these 25 diseases? If you do, you need to be on the lookout for early signs of the brittle bone disease called osteoporosis, so you and your doctors may be able to stop bone fractures before they start.

Osteoporosis is a disease of brittle bones. Secondary osteoporosis is a condition triggered by another disease process, or by the medications used to treat it. Here are some of the most common conditions associated with secondary osteoporosis. (Because some of the definitions of these diseases overlap, you may count more than 25.)

Autoimmune diseases such as ankylosing spondylitis, rheumatoid arthritis, multiple sclerosis, and systemic lupus erythramatosus generate inflammation that can destroy bone, and their treatments can make the problem worse.

  • About 25 percent of people who have ankylosing spondylitis develop osteoporosis. Another 50 percent have reduced bone mineral density. The inflammation generated by the condition stimulates osteoclasts, cells that break down bone.
  • Rheumatoid arthritis patients have a two- to three-fold greater risk of hip and spine fractures. Bisphosphonate treatments (drugs like Fosamax and Reclast) help preserve bone in this form of arthritis.
  • Multiple sclerosis patients almost always have low vitamin D. The body needs this vitamin to absorb calcium from food and supplements, and to keep the kidneys from "stealing" calcium from bones to maintain pH. 
  • Lupus patients often avoid sun. As a result, most people who have lupus have low vitamin D levels. The disease itself generates inflammation that degrades bone, and the immunosuppressant drugs used to control it compound the problem. Lupus patients have about a 10 to 12 percent greater risk of bone fractures than people who do not have the disease.

Diseases of malabsorption deprive the bones of the nutrients they need.

  • Gastric bypass surgery patients often experience osteoporosis because of malnutrition after the procedure. The weight of the patients makes monitoring bone with DXA testing difficult.
  • Anorexia patients don't get the calcium, magnesium, vitamins, and protein they need for healthy bones. Just taking supplements will not restore normal metabolic function in anorexia. It is also necessary to get carbs and protein.
  • Celiac disease is often complicated by bone disease. The problem is absorbing calcium, magnesium, and vitamins, especially fat-soluble vitamins such as D and K.
  • Inflammatory bowel disease such as Crohn's disease and ulcerative colitis generates inflammation that destroys bones. The corticosteroids used to treat the condition make bone destruction worse. And the disease itself interferes with the body's ability to absorb vitamins D and K.
  • About 25 percent of people who have end-stage liver disease experience bone fractures. The causes of osteoporosis in liver disease are complex and include malnutrition, the liver's processing of estrogen and testosterone, and side effects of medication. 
  • Hepatitis C can cause osteoporosis even when it does not progress to cirrhosis.

Iron overload diseases such as hereditary hemochromatosis and beta-thalassemia damage bone by depositing iron. Medically directed chelation therapy (the kind of "chelation" promoted in natural health clinics, with DMSO, won't help) removes iron and stops damage to bone.

Kidney disease and osteoporosis often go together. However, the treatments for brittle bones in kidney disease are not necessarily what you would expect.

  • Chronic kidney disease is a double-whammy on bone health. The kidneys remove calcium from circulation so that bones don't develop properly, and the condition leads to muscle weakness that leads to falls. Treatment of osteoporosis in chronic kidney disease is a complicated process that requires medical supervision.
  • Idiopathic hypercalciuria is a condition in which the kidneys excrete too much calcium so that bones weaken. In this condition, vitamin D levels are typically too high. The treatment is thiazide "pee pills" that keep the kidneys from sending too much calcium into the urine. When osteoporosis is already present, patients are given bisphosphonates to encourage bones to absorb calcium.

Multiple myeloma causes lesions in bone that move calcium into the bloodstream. Bones ache and break. It is possible to stop some of the damage with conventional osteoporosis treatments. Monoclonal Gammopathy of Uncertain Significance (MGUS) and systemic mastocytosis also result in unusually high numbers of fractures.

There are also a number of diseases for which treatment complicates bone health.

  • The drugs phenytoin, carbamazepine and phenobarbital, used to treat seizures, interfere with the body's processing of vitamin D and greater risk of fractures. There are alternatives to these drugs that do not have this side effect.
  • Loop diuretics used to treat congestive heart failure often deplete calcium and cause loss of bone mineral density. Thiazide diuretics conserve calcium but deplete potassium, sometimes causing severe fatigue and irregular heart rhythms.
  • Proton pump inhibitors used to esophagitis, esophageal reflux disease, and chronic heartburn interfere with the stomach's ability to digest calcium from food.
  • Treatments for HIV may increase the risk of fractures. Tenofovir (Viread and Vemlidy) alters kidney function so that calcium is sent into the urine. Non-nuclease reverse transcription inhibitors (NNRTIs) can deplete vitamin D. This group of HIV drugs includes Truvada, AZT, ddl, ddC, d4T, 3TC, ABC, FTC, and ETV.
  • Some of the above-listed medications that are used to treat both HIV and hepatitis B can cause bone issues in hep B patients.
  • Heparin for hypercoagulation disorders is associated with decreased bone mineral density, but there is no conclusive evidence that long-term heparin treatment causes fractures.

  • Barbour KE, Lui LY, Ensrud KE, Hillier TA, LeBlanc ES, Ing SW, Hochberg MC, Cauley JA Study of Osteoporotic Fractures Research G. Inflammatory markers and risk of hip fracture in older white women: the study of osteoporotic fractures. J Bone Miner Res. 2014.29:2057–2064.
  • Mirza F, Canalis E. Management of endocrine disease: Secondary osteoporosis: pathophysiology and management. Eur J Endocrinol. 2015 Sep
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  • Sheu A, Diamond T. Secondary osteoporosis. Aust Prescr. 2016 Jun. 39(3):85-7. doi: 10.18773/austprescr.2016.038. Epub 2016 Jun 1. Review. PMID: 27346916.
  • Photo courtesy of SteadyHealth

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