Timars (Sweden)

To estimate the prevalence of non-healed and healed chronic leg ulcers in an elderly rural population. All persons 70 years or older were asked about present and previous leg ulcers. A rural village in mid-west Sweden with 4000 inhabitants. 541 persons aged 70 years and above. The prevalence of healed or non-healed chronic leg ulcers in the population aged > or = 70. Healed or non-healed leg ulcers were reported by 53 persons (9.8%). Examination of these patients and also 100 individuals who had negated present or previous leg ulceration, giving the total prevalence of 12.6%. The result indicates a certain risk for overestimation of prevalence, as well as underestimation and decreased reliability when basing the figures only on telephone interviews or posted questionnaires.

A woman born in 1949 was diagnosed in 1990 with systemic lupus erythematosus. She was treated with prednisolone, and < 1 year later she presented with marked hyperglycemia. Large doses of insulin were given four times per day. Even though the patient was thin (BMI 17.4 kg/m2), very little improvement was seen. Serum insulin levels were high, and a euglycemic clamp investigation confirmed severe insulin resistance. The patient's serum contained insulin receptor antibodies inhibiting insulin binding, and thus the patient had a type B syndrome of insulin resistance. After diet and exercise, glycemic control stabilized and insulin treatment was withdrawn. However, in late 1993 she was in a catabolic and hyperglycemic state even though prednisolone doses were increased and azathioprin was added. In early 1994 she was treated with plasmapheresis and cyclophosphamide i.v. Subsequently, cyclosporin A was started as a maintenance therapy in addition to azathioprin. There was a rapid and sustained clinical improvement. Since late 1994 and onward, there is no sign of diabetes or glucose intolerance and there are no demonstrable insulin receptor antibodies in the patient's serum. Severe type B insulin resistance may respond favorably to treatment with plasmapheresis and cyclophosphamide followed by cyclosporin A in combination with azathioprin.