Intranasal Calcitonin in the Treatment of Acute Charcot Neuroosteoarthropathy

Abstract

Charcot neuroosteoarthropathy (CNO) can lead to disruption of the bone architecture of the foot (1). Increased osteoclastic activity is believed to be responsible for the bone destruction in CNO (2). Previous studies showed COOH-terminal telopeptide region of type 1 collagen (1CTP) and bone-specific alkaline phosphatase (BALP) as useful markers of bone turnover in patients with CNO (3–5). Presently, only bisphosphonates have been demonstrated to have some benefit in patients with CNO (6). However, bisphosphonates may have potential disadvantages in that they decrease bone remodeling and are contraindicated in patients with renal insufficiency (7). Our previous study (8) showed positive effects of calcitonin on bone resorption in patients with acute CNO. In this study, we set out to assess the effect of calcitonin on bone metabolism and disease activity during a 6-month treatment with intranasal calcitonin in acute CNO. Thirty-two consecutive patients with acute CNO were entered into the study. Subjects were recruited from our diabetic foot clinic during a 17-month period and were followed up for 6 months. The study was approved by the local ethics committee, and all participants gave written informed consent. Acute CNO was defined by clinical signs: warm, swollen foot and skin temperatures ≥2°C at the site of maximum deformity of the affected foot compared with a similar site on the contralateral foot (infrared thermometer) and confirmed by plain X-ray and three-phase technetium bone scan (9). The presence of diabetic neuropathy was determined by measurement of vibration perception …