These findings suggest a possible role of leptin in the recovery of neuromuscular response to hypercapnia obtained during long-term nocturnal NIMV in OHS patients without OSAH.

Alterations of the lipid profile are a well known phenomenon in thyroid dysfunction. Thyroid hormones regulate lipid metabolism through various mechanisms, but a key role is played by the LDL receptor pathway. Thyroid hormone influence on Lipoprotein (a) (Lp[a]) metabolism is unknown; therefore we studied Lp(a) concentrations in a group of 29 hypothyroid patients with post-surgical hypothyroidism and in a group of 14 hyperthyroid subjects with Graves' disease before and after the thyroid function was normalized by treatment. In hypothyroid patients total and LDL-cholesterol markedly decreased after T4 treatment (342 +/- 78 mg/dl before and 193 +/- 46 mg/dl after; 225 +/- 72 mg/dl before, 111 +/- 43 mg/dl after respectively, p < 0.001). Also HDL-cholesterol and triglycerides decreased (from 75 +/- 22 mg/dl to 56 +/- 18 mg/dl and from 182 +/- 87 mg/dl to 112 +/- 42 mg/dl respectively, p < 0.001). Lp(a) showed minor but not significant variations (median values 80 mg/l before 55 mg/l after treatment, p: N.S.). In hyperthyroid patients total and LDL-cholesterol increased after methimazole treatment (from 148 +/- 49 mg/dl before to 254 +/- 67 mg/dl after and from 87 +/- 38 mg/dl before to 178 +/- 51 mg/dl after, p < 0.001). HDL-cholesterol increased (from 39 +/- 9 to 50 +/- 15, p < 0.01) while triglycerides were unchanged. Lp(a) levels slightly rose (median values 57 mg/l before 84 mg/l after treatment, p < 0.05). These data suggest that the influence of thyroid hormones on Lp(a) metabolism is of minor entity and probably does not operate through the LDL receptor pathway.

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In order to evaluate if residual B-cell function is a protecting factor against the development of diabetic retinopathy in type I diabetics we measured C-peptide levels before and after glucagon stimulation (1 mg i.v.) in 74 type I diabetics. In all patients retinopathy was assessed by fluorescein angiography and retinal lesions were classified as: grade 0, normal; grade 1, background retinopathy; grade 2, proliferative retinopathy. We then correlated the degree of retinopathy to sex, age, duration of diabetes, smoking, percentage of ideal body weight, systolic and diastolic blood pressure, serum cholesterol, triglycerides, creatinine and C-peptide by means of multiple linear regression analysis. Twenty-three out of 74 type I diabetics had retinopathy. In all 7 subjects with proliferative retinopathy duration of diabetes exceeded 10 years. There was significant correlation between retinopathy and duration of diabetes (r = 0.373, p less than 0.001). No correlation was found between retinopathy and all the other variables, in particular between retinopathy and basal C-peptide or C-peptide increment (delta). An inverse correlation was found between the increment of C-peptide and duration of diabetes (r = -0.404, p less than 0.01). Our data show that residual B-cell function cannot be considered a protecting factor against the development of diabetic retinopathy.