Cascading vertebral fractures: an osteoporosis odyssey

5 minute read

Early use of an anabolic bone agent might have been beneficial, but PBS restrictions ruled this out.

A 73-year-old female presented seeking management for osteoporosis, having experienced four painful vertebral fractures in just six months.

The fractures occurred in rapid succession at L1, T9, T12 and L4. The T9 and T12 fractures exhibited marked anterior wedging, while L1 and L4 had endplate fractures. All fractures resulted from minimal trauma, such as lifting her grandson, twisting to get out of bed or lifting a chair.

There had been no prior osteoporotic fractures and no family history of osteoporosis. She had a hysterectomy at 42, making it uncertain when she entered menopause. She maintained adequate dairy intake. No history of bariatric surgery or eating disorders was reported and her BMI is 28. Vitamin D levels were slightly low at 40 at the time of the first fracture, but this level increased to 75 with supplementation.

At 70, she had a bone density scan revealing a lumbar spine T-score of -2.9 and femoral neck T-score of -1.5, yet no osteoporosis treatment was initiated due to the absence of fractures at that time.

After the initial fracture she was prescribed oral risedronate, which was discontinued after five weeks due to gastrointestinal side effects. She subsequently had one injection of denosumab and was referred for further management.

The patient’s inactivity, combined with fear of moving or lifting objects, prompted rehabilitation through physiotherapy and hydrotherapy. Symptom relief was achieved with paracetamol and amitriptyline, as she showed marked intolerance to stronger opioids.

Her case is characterised by severe osteoporosis with four successive vertebral fractures. Concerns about secondary causes and high fracture risk led to consideration of an anabolic bone agent, with teriparatide (recombinant PTH) the only agent available at the time. However, she did not meet PBS authority criteria, as the criteria stipulate a new osteoporotic fracture after more than one year of continuous anti-resorptive therapy.   

A comprehensive work-up for secondary causes of osteoporosis included FBC, UEC, LFT, CMP, Vitamin D levels, TFT, PTH, coeliac serology, EPG/IEPG, ACTH, morning cortisol, and 24-hour urinary calcium and cortisol.

This extensive investigation was justified by the number of fractures and lack of identifiable causes in her history. However, the work-up did not reveal a secondary cause, leading to the conclusion that fractures were due to post-menopausal osteoporosis. A cascade of vertebral fractures stemming from altered spinal biomechanics due to a wedge fracture, could explain the rapid succession.

The patient continued denosumab, which she tolerated well. A bone density scan one year after starting treatment showed a 2% increase in the lumbar spine T-score and 6% in the femoral neck.  Three years later, another bone scan showed a 12% increase in lumbar spine T-score and 6% increase in the femoral neck, with no interval fractures.

Four years after her initial fractures, she developed classic symptoms of polymyalgia rheumatica (PMR) with shoulder and pelvic girdle joint pain and an increased ESR of 46mm/hr (N<20). Treatment for PMR typically involves corticosteroids, which are detrimental to bone health.

A modified treatment course was recommended, involving early introduction of methotrexate and a rapid six-month taper of prednisone. This approach proved effective for her, though a typical prednisone taper for PMR usually lasts 18 months. She was maintained on methotrexate for a total of 18 months before this was able to be ceased. The patient was noted to have a positive rheumatoid factor of 40 (N<20), but never developed typical rheumatoid arthritis symptoms. 

After five years of treatment with denosumab, a switch to a different mode of action was considered, though this decision is not evidence-based. She was prescribed annual intravenous zoledronic acid infusions, but unfortunately experienced a new T8 vertebral osteoporotic fracture after two infusions.

Her bone density at the time indicated lumbar spine T-score of -3.1. An abbreviated work-up for further secondary causes revealed an IgA kappa paraprotein of 2.6 g/L. A skeletal survey did not show any lytic lesions and calcium, renal function and beta-2 microglobulin were within normal range.

A bone marrow biopsy and haematology review determined this to be monoclonal gammopathy of uncertain significance (MGUS), unrelated to her osteoporosis. The paraprotein may have caused a false positive rheumatoid factor.

The patient experienced a new interval fracture after taking more than one year of continuous anti-resorptive therapy, so she qualifies for a PBS-subsidised anabolic bone agent. At this point, romosozumab (an anti-sclerostin agent) was available on the PBS, offering a more convenient monthly injection compared to teriparatide’s daily injection.

Unfortunately, after two months of this treatment she had another fracture, this time at T9. She now had a total of six fractures! Extensive investigations and multidisciplinary reviews yielded no clear secondary cause for her severe osteoporosis. The consideration of a bone biopsy with double tetracycline labelling was ultimately abandoned due to its invasive nature and low yield.   

She received one year of treatment with romosozumab and then switched to maintenance intravenous zoledronate infusions, with two infusions since. Fortunately, she has not experienced any further fractures. Her IgA kappa paraprotein has been monitored for three years without any increase, and the diagnosis remains MGUS.

This case underscores the challenges of managing severe osteoporosis.

A cascade of vertebral fractures can result from altered spinal biomechanics, placing increased load on adjacent vertebrae. Early use of an anabolic bone agent might have been beneficial in hindsight, although cost constraints limited this at the time. Despite her clear thoracic kyphosis from the fractures, she remains relatively active. Lifelong osteoporosis treatment will be necessary.

Dr Andrew Jordan is a rheumatologist based in Parramatta, Sydney, with a special interest in inflammatory arthritis, gout and PRP injections.

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