We agree with Skowroński et al. (1) that the type of diabetes manifested by patients with HCV chronic infection (HCV+) may not be classical type 2 diabetes, and the phenotypic characterization of our patients shows just that. The labeling of HCV+ patients as type 2 diabetes is purely conventional and possibly inaccurate: the lines separating type 1 diabetes, from latent autoimmune diabetes in adults and from type 2 diabetes, are fading away as new pathogenetic information is obtained (2).

HCV chronic infection may be responsible for a constellation of extrahepatic immune-mediated manifestations (3). HCV lymphotropism may trigger lymphocyte expansion followed by the production of different autoantibodies (3). For example, we have previously reported (4) on 229 HCV-related mixed cryoglobulinemia (MC-HCV+) patients without cirrhosis. We found that 1) the prevalence of type 2 diabetes was significantly higher in MC-HCV+ patients without cirrhosis than in control subjects (14.4 vs. 6.9%), 2) MC-HCV+ patients with type 2 diabetes were leaner than type 2 diabetic control subjects (24.2 vs. 30.4 kg/m2) and showed significantly lower LDL cholesterol and systolic and diastolic blood pressure, and 3) MC-HCV+ patients with type 2 diabetes had non–organ-specific autoantibodies more frequently (34 vs. 18%) than nondiabetic MC-HCV+ patients. Thus, in HCV chronic infection, the clinical phenotype of diabetes has been found to be similar across three studies (1,4,5) and different from classical type 2 diabetes. An immune-mediated mechanism for MC-HCV+–associated diabetes has been postulated (4), and a similar pathogenesis might be involved in the diabetes of HCV+ patients. This hypothesis is strengthened by the finding that autoimmune phenomena in type 2 diabetic patients are more common than previously thought (6). Since the prevalence of classic β-cell autoimmune markers in HCV+ patients has not been found to be increased (1), other immune phenomena might be involved, and viral damage to the β-cells may occur by a direct mechanism (7).

1.
Skowroński M, Zozulińska D, Juszczyk J, Wierusz-Wysocka B: Hepatitis C virus infection: evidence for an association with type 2 diabetes (Letter).
Diabetes Care
29
:
750
–751,
2006
2.
Gale EAM: Latent autoimmune diabetes in adults: a guide for the perplexed.
Diabetologia
48
:
2195
–2199,
2005
3.
Ferri C, Mascia MT: Cryoglobulinemic vasculitis.
Curr Opin Rheumato
l 
18
:
54
–63,
2006
4.
Antonelli A, Ferri C, Fallahi P, Sebastiani M, Nesti C, Barani L, Barale R, Ferrannini E: Type 2 diabetes in hepatitis C-related mixed cryoglobulinaemia patients.
Rheumatology
43
:
238
–240,
2004
5.
Antonelli A, Ferri C, Fallahi P, Pampana A, Ferrari SM, Goglia F, Ferrannini E: Hepatitis C virus infection: evidence for an association with type 2 diabetes (Brief Report).
Diabetes Care
28
:
2548
–2550,
2005
6.
Antonelli A, Tuomi T, Nannipieri M, Fallahi P, Nesti C, Okamoto H, Groop L, Ferrannini E: Autoimmunity to CD38 and GAD in type II and type I diabetes: CD38 and HLA genotypes and clinical phenotypes.
Diabetologia
45
:
1298
–1306,
2002
7.
Masini M, Campani D, Boggi U, Menicagli M, Funel N, Pollera M, Lupi R, Del Guerra S, Bugliani M, Torri S, Del Prato S, Mosca F, Filipponi F, Marchetti P: Hepatitis C virus infection and human pancreatic β-cell dysfunction (Brief Report).
Diabetes Care
28
:
940
–941,
2005