[Risk stratification].
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Biomedical subjects
Publications and source records attributed to P Caselli.
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To investigate whether persistent microalbuminuria is related to altered levels of both lipids and apolipoproteins in Type 2 diabetes mellitus serum total-cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, apolipoprotein A-I, and apolipoprotein B were measured by standard methods in a group of Type 2 diabetic patients affected by persistent microalbuminuria (albumin excretion rate (AER) 20-200 micrograms min-1) as compared with a group of sex- and age-matched non-microalbuminuric patients (AER less than 20 micrograms min-1). The groups were stratified according to a short (less than or equal to 5 years) or a longer (greater than 5 years) duration of diagnosed diabetes. Microalbuminuria was not associated with significant changes of serum total-cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, and apolipoproteins in the group of patients with a duration of disease greater than 5 years, while microalbuminuric patients less than or equal to 5 years from diagnosis (n = 11) had serum total-cholesterol, triglycerides, LDL-cholesterol, and apoprotein B higher than non-microalbuminuric control patients (n = 26) (cholesterol 6.2 +/- 0.9 vs 5.1 +/- 1.0 mmol l-1 (p = 0.003); triglycerides 2.1 +/- 0.7 vs 1.7 +/- 1.3 mmol l-1 (p = 0.03); LDL-cholesterol 4.1 +/- 0.8 vs 3.0 +/- 0.7 mmol l-1 (p less than 0.001); apo-B 1.3 +/- 0.3 vs 1.1 +/- 0.3 g l-1 (p = 0.02). In these patients with shorter duration of diabetes many of the serum lipid measures correlated positively with AER.
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Metabolism of polyamines (spermidine and spermine) is known to be strictly related to the growth processes of eukaryotic cells. Since cell replication processes appear altered in insulin-dependent diabetes mellitus (IDDM), especially when associated with its microvascular complications, the aim of this study was measuring serum spermidine oxidase activity (SOA), a key enzyme in the metabolic pathway of polyamines, in 47 patients with IDDM as compared with 63 healthy control subjects matched for age and sex. Mean SOA levels +/- SD were significantly lower in IDDM patients (177.4 +/- 57.2 mu kat/l) than in controls (247.6 +/- 68.1 mu kat/l; p less than 0.001), being SOA inversely related with daily insulin dose. SOA was moreover significantly higher (but similar to controls) in the group with increased urinary albumin excretion rate (AER persistently greater than 20 micrograms/min); (n = 17; 213.1 +/- 62.6 mu kat/l) in comparison with normoalbuminuric subjects (n = 30; 156.6 +/- 43.5 mu kat/l; F = 21.78; p = 0.0001). SOA was correlated with AER (r = 0.45; p = 0.001), independently of age, duration of disease, serum creatinine, body weight, blood pressure and metabolic control, as shown by a multiple regression analysis model (p = 0.003). Presence of background retinopathy was not associated with modified levels of SOA, which was conversely higher, although not significantly, in the patients with proliferative retinal lesions. In conclusion serum SOA is deeply altered in IDDM patients, being markedly reduced in the whole group of patients and conversely independently increased up to the mean values of controls in presence of increased AER or advanced retinopathy.
Raised levels of plasma fibronectin (PF), an alpha 2-glycoprotein produced by vascular endothelia, have been previously described in diabetic patients with retinopathy and overt nephropathy. The aim of this study was to investigate whether the presence of microalbuminuria is associated with increased PF concentrations. Twenty Albustix-negative diabetic outpatients with microalbuminuria [median albumin excretion rate (AER): 30.2 micrograms/min; range 12.1-194 micrograms/min] were compared with 58 sex- and age-matched patients without microalbuminuria (median AER 3.1 micrograms/min; range 0.8-12 micrograms/min) and 34 control subjects (median AER 2.8 micrograms/min; range 0.8-12.1 micrograms/min). Mean PF was significantly higher in the group with microalbuminuria (406.7 +/- 85.5 micrograms/ml) than in the group without it (325.3 +/- 76.5 micrograms/ml or in control subjects (334.5 +/- 76 micrograms/ml; P less than .05). PF increase associated with microalbuminuria was independent of the presence of retinopathy. Furthermore, in the whole group of diabetic patients, PF was significantly correlated with AER (r = .33; P = .003). Such correlation also remained significant (P = .0002) after covariance analysis by a stepwise discriminant procedure taking into account age, duration of disease, sex, blood pressure, body weight, therapy, and HbA1. In conclusion, PF increase is associated with microalbuminuria independent of the other considered variables; its role as a possible marker for early diabetic nephropathy remains to be fully clarified.
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