Charcot arthropathy of the diabetic foot. Current concepts and review of 36 cases.

BACKGROUND AND AIMS: The incidence of diabetic Charcot neuroarthropathy has increased. The purpose here was to study the current diagnostics and treatment of the Charcot foot. MATERIALS AND METHODS: During a time period from 1994 to 2000, a total of 36 feet were diagnosed as cases of diabetic Charcot neuroarthropathies. A retrospective analysis of patient records and radiographs was undertaken. A review of the recent literature is presented. RESULTS: 29 cases were diagnosed in the dissolution stage, 2 in coalascence, and 5 in the resolution stage. The diagnostic delay averaged 29 weeks. Treatment with cast immobilisation ranged from 4 to 37 weeks (mean 11 weeks). A total of 14 surgical procedures were carried out on 10 patients: six exostectomies, four midfoot arthrodeses, one triple arthrodesis, one tibiocalcaneal arthrodesis and two below-knee amputations. A radiological fusion was achieved in two thirds of the attempted arthrodeses. CONCLUSIONS: A physician should always consider the Charcot neuroarthropathy when a diabetic patient has an inflamed foot. In the absence of fever, elevated CRP or ESR, infection is a highly unlikely diagnosis, and a Charcot process should primarily be considered. The initial treatment of an inflamed Charcot foot consists in sufficiently long non-weightbearing with a cast, which should start immediately after the diagnosis. The prerequisites of successful reconstructive surgery are correct timing, adequate fixation and a long postoperative non-weightbearing period. In the resolution stage most Charcot foot patients need custom-molded footwear.

High frequency of coeliac disease in adult patients with type-I diabetes.

Anti-reticulin antibodies were measured by an indirect immunofluorescence method in 195 consecutive patients with insulin-dependent diabetes mellitus, and positive titres were found in 8 patients. A jejunal biopsy was performed in these patients, all of whom had small-intestinal atrophy. Thus the frequency of coeliac disease in adult diabetes patients was 4.1%. The patients had no signs of malabsorption or of significant abdominal complaints. We conclude that coeliac disease is commoner in type-I diabetes than in the normal population, and measurement of anti-reticulin antibodies seems to be a suitable screening method.

Metabolic control in adolescent insulin-dependent diabetics referred from pediatric to adult clinic.

The metabolic control of 61 consecutive cases of adolescent diabetes was followed 1 year before and 1 year after the patients were referred from a pediatric to adult clinic. The level of control of the disease was determined by measurements of haemoglobin A1 made on visits to the out-patient clinic. No significant deterioration of the disease was noted on the first visit to the adult clinic. Boys and patients with a shorter disease history coped better with the transition period. During the first year of treatment at the adult clinic the metabolic control of the disease improved significantly (p less than 0.001). Girls and diabetics with a long disease history should be well-prepared for referral to adult clinics.

Comparison of acute and prolonged effects of glibenclamide and chlorpropamide in patients with non-insulin-dependent diabetes.

The effects of single oral dose of glibenclamide (Gilemid 5 mg) and chlorpropamide (250 mg) on serum insulin and glucose levels and electrolyte (sodium, potassium) balance were studied, in a cross-over double-blind manner, in 11 patients with non-insulin-dependent diabetes. Both drugs increased serum insulin for more than 8 h but less than 24 h. The effect of glibenclamide was slightly stronger than that of chlorpropamide. Serum glucose concentration was significantly decreased by glibenclamide only. Glucose excretion in urine was declined for a longer time by glibenclamide than by chlorpropamide. Neither of the drugs essentially effected on sodium and potassium excretion. After the acute study, all the above patients and 5 additional ones were treated in open care with glibenclamide (2.5-10 mg daily) and chlorpropamide (125-500 mg daily) for 8 weeks in a cross-over manner. Both drugs showed practically similar efficacy; 5 mg of glibenclamide corresponded to 250 mg of chlorpropamide. One patient under chlorpropamide treatment exhibited hyponatraemia. Eight weeks after the commencement of therapy, serum potassium concentration was lower under chlorpropamide than under glibenclamide treatment. The results suggest that, in non-insulin-dependent diabetes, a single oral dose of glibenclamide acts as long as that of chlorpropamide, and that in long-term therapy 5 mg of glibenclamide is equipotent with 250 mg of chlorpropamide.