Case of The Month

A 62-year-old woman of normal body size came to my attention for severe progressive osteoporosis. She had 3 previous vertebral fractures (T10, T11, L1). DEXA scan revealed a BMD T-score of -4.1 on lumbar spine and -3.9 on hip.

Her clinical history pointed to an ordinary post-menopausal osteoporosis. She entered physiological menopause at 52 years and never used HRT. At age 58 she suffered her first vertebral fracture (T10) simply carrying a shopping bag. Osteoporosis was then discovered by spine DEXA scan. She started bisphosphonate therapy (Clodronate at the daily dose of 400 mg per os). 2 years later she had a second crush fracture (L1) and a new spine DEXA scan showed a persistent decrease in BMD (-2.3% yearly). In this occasion, her doctor performed some lab tests: serum calcium was low-normal (8.9 mg/dl) and alkaline phosphatase (AP) moderately increased (358 U/l). He changed therapy to another bisphosphonate (alendronate 10 mg/day) and added 500 mg of calcium supplement daily.

10 months later - after a flu episode with prolonged cough - she had a new vertebral fracture. There was persistent thoracic pain in the thorax and X-rays showed a clear reduction in median height of T11. She was completely discouraged and stopped any therapy.

After 5 months she arrived at my Bone Metabolic Unit for recurrent back pain. Clinical examination did not reveal significant signs, apart from a painful thoracic and lumbar spine and kyphosis. The clinical history revealed that her mother had an important kyphosis. The patient was regularly consuming dairy products and the calculated calcium intake was 1g/day. She had never used corticosteroids and her thyroid function was normal. Lab tests showed: moderate sideropenic anemia, slight increase in GOT and GPT, without previous hepatitis or liver diseases, low serum calcium, normal-low serum phosphate, normal-high AP, increased urinary N-terminal telopeptide, slight PTH increase.

Evaluating the general lab tests occasionally performed in the past, anemia and GOT and GPT increase appeared as persistent alterations. A more detailed anamnesis was performed and frequent episodes of severe bloating, flatulence and bowel irregularities were revealed. On this basis, intestinal malabsorption was suspected. Specific lab tests revealed high levels of antibodies against gliadine and endomysium and endoscopical biopsy confirmed the diagnosis of celiac disease. The intestinal absorption of calcium, evaluated with stable strontium as a tracer, showed a marked reduction. Reduced levels of serum 25-vitamin D were also found.

At this point, a gluten-free diet and therapy with parenteral vitamin D (ergocalciferol, 400.000 IU i.m. weekly) were started. 4 months later, after complete normalization of PTH and 25-vitamin D levels, therapy was changed to alendronate per os plus 25-OH vitamin D at a low oral dose.

After 2 years, there were no further fractures and back pain was much reduced. BMD increased significantly (+ 7.8% year on spine, and + 5.6% year on hip). All lab tests were normal.

A few comments may be indicated. This patient presented an intestinal disease relatively common in Italy, where a reduction of 25-vitamin D and intestinal calcium absorption are present, with the consequence of secondary hyperparathyroidism. Untreated celiac disease in the adult is often accompanied by reduced bone mass, and certainly may worsen post-menopausal bone loss. Common features of the disease are anemia and increased serum aminotransferase values. Restoring of vitamin D levels induce calcium absorption and, as a consequence, normalization of PTH: the full effect of bisphosphonate therapy can then be achieved.

In my opinion, this is a quite interesting history of secondary osteoporosis, and two points must be stressed:

• The importance to always look for a cause, beyond the simple diagnosis of a condition. A thorough history is essential to gather a full picture of the patient, beyond a condition such as menopause or the results of DEXA scan.
• In the specific case of osteoporosis, especially when standard therapy fails to induce the expected changes, a thorough clinical evaluation is indicated to ascertain the possibility of secondary osteoporosis.