An elite Kenyan runner presented with a tibial fracture sustained during an international cross-country race. There was no clear history of symptoms suggestive of preceding overload and no radiological features of stress fracture. He was found to have sustained an osteoporotic, insufficiency fracture. There are no previous case reports of an osteoporotic fracture in a male athlete. Possible aetiologies and directions for future investigation are presented.
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A 21-year-old Kenyan male athlete was running uphill, after 2 km of a 10-km cross-country race, when he felt a sudden onset of right lower leg pain and collapsed. He was unable to bear weight on that leg, and subsequent radiographs showed a transverse, undisplaced, comminuted fracture of the right tibia at the junction of the proximal two-thirds and distal third of the bone (fig 1). There was no evidence of sclerosis and the appearance was not of a stress fracture.
The athlete had no history of previous tibial injuries or any stress fracture. He had been training consistently at 160 km/week for 3 months and had completed a full summer track season before this training phase. He replaced his training shoes monthly and his training terrain consisted of paths and trails. He competed regularly on the international circuit. There was no history of an eating disorder and he ate the same meals as other members of the squad. This consisted of meat, vegetables and large amounts of low-glycaemic carbohydrates in the form of ugali, a Kenyan maize dish, and appeared adequate to supply his energy requirements. There was no systemic, medical or family history of note. On further questioning, the patient reported noticing some medial tibial discomfort 5 days previously, during a run. The pain settled throughout the run and did not return before the race.
On examination, the patient was not pyrexic and appeared well. A full physical examination was within normal limits, with the exception of the immobilised transverse fracture of the tibia.
A full range of blood tests were performed (full blood count, urea and electrolytes, calcium, phosphate and alkaline phosphatase, liver function tests, plasma protein electrophoresis and immunoglobulins, erythrocyte sedimentation rate, C-reactive protein, parathyroid hormone, total morning testosterone and vitamin D), and results were all within normal limits. An MRI scan showed an area of increased signal intensity at the fracture site, as expected, but no evidence of bone destruction or soft-tissue mass.
A dual-energy X-ray absorptiometry (DEXA) scan showed that the bone mineral density (BMD) within the lumbar spine was 0.894 g/cm2, giving a T-score of −2.9; a diagnosis of osteoporosis was made based on the World Health Organization classification.
The patient was immobilised in a below-knee lightweight non-weight-bearing cast for 8 weeks. He declined treatment with low-intensity ultrasonography. He was started on calcium 1 g and vitamin D 800 IU. At 8 weeks, he was free of pain at the fracture site, and there was evidence of good callus formation. He was advised to wear a high Aircast boot for a further 4 weeks and to commence flexibility and proprioceptive exercises. At 12 weeks, the leg was weight-bearing with no pain and had a full range of movement at the knee, ankle and subtalar joints. Strengthening and proprioceptive rehabilitation was progressed at this stage.
What is already known on this topic
Osteoporosis in female endurance athletes is a well-recognised condition.
Osteoporosis in male athletes is less well understood, but may result from hormonal insufficiency, negative energy balance, genetic predisposition, micronutrient deficiencies, or misuse of drugs or alcohol.
Endurance running in itself does not have a deleterious effect on bone metabolism.
What this study adds
This is the first case report, to our knowledge, of an elite male athlete with an osteoporotic insufficiency fracture.
Clinicians should consider the diagnosis of osteoporosis in male athletes with bony injuries and address predisposing factors.
The management of osteoporosis in the young athlete raises medical, ethical and research challenges for sports physicians.
Review of the literature reveals one previously reported case of osteoporosis in a male athlete.1 There are no reported cases of an osteoporotic insufficiency fracture in a young male athlete. Although osteoporosis has a genetic component, there is no evidence of increased prevalence in African men. It is recognised that male osteoporosis may result from hormonal imbalances, such as low testosterone. Although endurance athletes in heavy training can suffer from suppression of testosterone levels,2 this has not been associated with reduced BMD in athletes.3 The athlete we report had a normal testosterone level.
Poor nutrition has been identified as a potential cause of secondary osteoporosis. A low serum vitamin D level has been implicated in osteoporosis and stress-fracture aetiology.4 Bone formation also requires an appropriate balance of calcium, zinc, vitamin C and magnesium among other micronutrients.5 It is not known whether this athlete had micronutrient deficiencies, but calcium, magnesium and vitamin D levels were normal. Interestingly, this Kenyan athlete’s diet was largely based on maize, which has been implicated in limiting the absorption of calcium, zinc and iron.6
It is well recognised that female endurance athletes can develop osteoporosis, probably secondary to a negative energy balance.7 Our patient had not made any recent dietary changes and was eating the same meals as the other squad members but, although his energy intake seemed adequate, it is possible that he had a similar negative energy balance. There is some evidence that endurance running, when in negative energy balance, can reduce insulin-like growth factor-1 and type 1 collagen synthesis.8 This would negatively effect bone formation but does require further research, particularly in male athletes.
Weight-bearing exercise has repeatedly been shown to enhance BMD in males and females.9 Endurance running in itself does not have a deleterious effect on bone parameters, and a study on elite marathon runners identified significantly higher BMD at loaded sites compared with those in non-training controls.10
We started our patient on calcium and vitamin D. Bisphosphonates were not prescribed due to concern over the long–term effect on bone remodelling. Nasal calcitonin was considered but not taken further due to cost implications. A repeat DEXA scan at 1 year was recommended.
There is a recognised incidence of osteoporosis in female endurance athletes but this case was of osteoporosis in a male athlete presenting with an insufficiency fracture. Micronutrient deficiencies or genetic predisposition may be implicated, and hormonal insufficiency or negative energy balance should be considered, but the aetiology and management of male osteoporosis in athletes is not fully understood.
Competing interests: None.
Patient consent: Obtained.
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