Combining three different sources as a valid tool to identify known diabetic patients: use in a prevalence study in an Italian local health unit.

This study was carried out to validate the prevalence of known diabetes estimated from three different simultaneous sources (medical records from out-patient departments, registers and pharmaceutical prescriptions) as against the diagnosis of family doctors who had received ad hoc training before the study. To this effect, a selected Local Health Unit (Unità Sanitaria Locale or USL) in Bari, southern Italy, was examined. 2917 diabetic patients were found, with a 2.82% prevalence. The prevalence of known diabetes estimated from separate sources was 1.41% from medical records, 1.52% from the registers and 1.59% from prescriptions. With reference to the family doctor's conclusions, sensitivity, positive predictive value and efficiency of medical records were 49.8%, 92.5% and 57.4% of USL registers 53.8%, 95.6% and 61.8% of prescriptions 56.3%, 71.2% and 47.9%. 46% of the diabetic subjects were only identified from one source. In conclusion, by combining several sources of information together, a higher number of diabetic patients are identified than would be done by using separate sources; also, active cooperation from the family practitioners seems to be needed to correct the large number of false positive patients (n = 798) mostly identified from prescriptions.

In vitro secretion of interleukin-1 beta and interferon-gamma by peripheral blood lymphomononuclear cells in diabetic patients.

There is evidence that cytokines, in particular interleukin-1 beta (IL-1 beta) and interferon-gamma (IFN-gamma) might mediate beta cell destruction in type 1 diabetes. Therefore the secretion of these cytokines by peripheral blood lymphomononuclear cells (PBMNC) was investigated in basal conditions and 48 h after stimulation with T-cell mitogen phytohaemagglutinin (PHA) in 33 diabetic patients and in 10 normal controls. The patients were divided in 4 groups (Group 1, 10 controls; Group 2, 13 newly diagnosed type 1 diabetics, the onset had occurred from 5 days to 3 months before the study; Group 3, 10 Long Standing (LS) type 1 diabetics with duration of the disease between 2 years and 10 years; and Group 4, 10 type 2 diabetics). No difference was found among the 4 groups considered in IL-1 beta secretion by unstimulated cultures, although the percentage of TAC+ cells was significantly higher in type 1 newly diagnosed diabetic patients with respect to the LS, the type 2 diabetics and the controls. After PHA stimulation a significant increase of IL-1 beta was found in newly diagnosed type 1 diabetic patients in comparison with the control subjects, the LS and type 2 diabetic patients (P < 0.001). The supernatants of newly diagnosed type 1 diabetics also showed a significant reduction in IFN-gamma production both in basal (P < 0.01) and in stimulated conditions (P < 0.001) in comparison with the controls, the LS (P < 0.002 in basal, and P < 0.001 in stimulated conditions) and the type 2 diabetic patients (P < 0.001 both in basal and stimulated conditions).(ABSTRACT TRUNCATED AT 250 WORDS)

In search of predictive markers of remission from insulin dependence in type 1 diabetes: a preliminary report.

We studied 18 newly diagnosed diabetic patients (8 males and 10 females, aged 18-26 years, within 10-120 days from the onset of symptoms) who were submitted for 15 days to intensive insulin therapy performed via subcutaneous insulin infusion (CSII). We investigated some metabolic and immunological parameters in order to identify a possible marker to predict the selection of patients potentially more responsive to CSII treatment for the remission of type 1 diabetes. In accordance with the International Diabetes Immunology Group we considered clinical remission as being the withdrawal of insulin therapy for at least 3 months. In order to assess beta-cell function a fasting and post-prandial serum C-peptide, blood glucose and HbA1c were performed on all patients before, and 3 days after, the discontinuation of CSII. Islet cell antibodies were determined in all sera by indirect immunofluorescence. Analysis of T-lymphocyte subpopulations was carried out before starting the therapy. The following monoclonal antibodies were used: CD4, CD8, CD57, CD25, HLA-DR. The levels of C3 and C4 and serum IgG, IgA and IgM were also evaluated. After CSII, 11 of 18 patients showed remission. At the beginning of the study we observed no major difference in metabolic parameters between the two groups. Interestingly, the patients who exhibited remission presented a statistically higher percentage of positive cells for CD57, HLA-DR and CD25 surface antigens, significantly lower C4 levels and CD4/CD8 ratio and significantly higher IgG levels compared with patients who did not show any remission.(ABSTRACT TRUNCATED AT 250 WORDS)

Somatomedin-C (SM-C). Study in diabetic patients with and without retinopathy.

In the present study we evaluated somatomedin-C (Sm-C) plasma levels in diabetic patients, with and without retinopathy. One hundred and thirty four diabetic patients (65 type I and 69 type II) and 90 controls, strictly matched for age and sex, were enrolled in the study. Ophthalmoscopy and fluorescein angiography allowed to distinguish: 49 patients without retinopathy, 45 patients with background retinopathy, and 40 with proliferative retinopathy. Growth hormone (GH) and Sm-C plasma levels were measured using a pool of 20-24 blood samples over 24h. Sm-C levels in type I (0.62 +/- 0.11 U/ml) and type II (0.56 +/- 0.09 U/ml) patients were significantly decreased (p less than 0.01) when compared to controls (0.89 +/- 0.30 U/ml). The mean daily secretion of GH was significantly (p less than 0.01) greater in diabetic patients (7.8 +/- 2.6 ng/ml) than in controls (4.1 +/- 1.5 ng/ml), but no correlation was found between Sm-C and GH (r = 0.15; p = n.s.). Our findings did not show any correlation between Sm-C plasma levels and either the existence of retinopathy, regardless of the degree of microvascular damage, or duration of the disease, or degree of metabolic control, as evaluated by HbA1c.