Current perspectives of therapeutic patient education in Italy.

Therapeutic patient education is a well-defined branch of health education aimed at patient empowerment. It consists of helping the patient to understand his own disease and its treatment, actively collaborating to its fulfillment and to take care of his own health status in order to maintain and improve his life quality. The correct implementation of both communication and therapeutic patient education involves the mastery of specific professional skills by healthcare personnel. In Italy, institutional therapeutic patient education is delivered mainly to diabetic patients. However, other activities and projects aimed at therapeutic education of chronic patients are gradually appearing. An overview of current situation and perspective of therapeutic patient education practice in Italy are presented.

[Raynaud's phenomenon. Practical considerations on the forms secondary to immunomediated systemic diseases]. / Fenomeno di Raynaud. Considerazioni pratiche sulle forme secondarie a malattie sistemiche immunomediate.

Raynaud's phenomenon is a frequent asphyxial vascular syndrome interesting the 4% of general population. In most of cases it is a functional problem (Raynaud's disease). Less frequently it has an organic cause (Raynaud's syndrome). The pathogenesis of primitive Raynaud's phenomenon remains an enigma. In secondary Raynaud phenomenon the attacks of vasospasm can be explained by the physiopathologic events characterizing the underlying disease. For example, multiple cytokines, transforming grow factor beta, serum immunocomplexes are of great importance in the contest of connective diseases. Clinical examination, some usual laboratory and roentgenographic investigations and nailfold capillary microscopy are of particular importance in orientating the diagnosis.

Antiphospholipid antibodies (aPL) in systemic lupus erythematosus. Are they specific tools for the diagnosis of aPL syndrome?

OBJECTIVE: Antiphospholipid antibody (aPL) specificity for aPL-related events was evaluated in systemic lupus erythematosus (SLE). METHODS: A study was carried out on 105 patients affected with SLE comparing the prevalence of lupus anticoagulant (LA) and IgG and IgM anticardiolipin antibodies (aCL) between patients with and without features of antiphospholipid syndrome (APS). Antiphospholipid antibody profile was subsequently evaluated in the aPL positive patients with and without aPL-related events, thus excluding the patients with complications of APS possibly due to factors other than aPL. RESULTS: LA showed a strong association with thrombosis and livedo reticularis, and IgG aCL with thrombosis and neurological disorders, while no clinical features were associated with IgM aCL. A considerable number of aPL positive patients with no aPL-related manifestations was also observed, suggesting the low specificity of aPL assays (54.4%). When studying the 60 aPL positive patients, LA was specific (91.3%) for the diagnosis of aPL-related thrombosis, whereas aCL were not specific, although IgG aCL mean levels were higher in patients with arterial thrombosis than in those without APS features. CONCLUSIONS: LA but not aCL positivity is a specific tool for the diagnosis of thrombotic complications due to aPL in SLE.

Long-term follow-up of acute and chronic non-A, non-B post-transfusion hepatitis: evidence of progression to liver cirrhosis.

The long-term outcome of non-A, non-B post-transfusion hepatitis was evaluated in 21 patients who developed the illness after open-heart surgery and could be followed thereafter up to five years. Histological chronic sequelae were documented in 13 patients, and consisted of chronic persistent hepatitis in one case, chronic lobular hepatitis in two and chronic active hepatitis in 10, five of whom also developed superimposed cirrhosis. Progression to these chronic states was in most cases symptomless, independently of the severity of liver lesions; one patient, however, died of gastrointestinal bleeding due to cirrhosis of the liver. During follow-up the biochemical pattern of chronic non-A, non-B hepatitis was unique, while striking fluctuations of transaminase levels. Liver histology proved essential to identify the severity of chronic liver lesions, as clinical and biochemical features were uniform and not indicative of it. Our results suggest that cirrhosis may develop, often with an asymptomatic course, in a significant number of patients who do not recover after acute post-transfusion non-A, non-B hepatitis.

Expression of HBsAg on the membrane of hepatocytes in chronic carriers of hepatitis B virus infection.

Liver cell membrane localization of hepatitis B surface antigen (HBsAg) was investigated in 31 asymptomatic chronic carriers by a direct immunofluorescence technique. A close relationship was found between absence of inflammatory liver disease, presence of large amounts of HBsAg in the liver and expression of the antigen at the hepatocyte surface. Capping of HBsAg after the addition of anti-HBs serum could be inhibited by factors (temperature, metabolic inhibition) that are known to influence viral antigenic mobility at the cell surface. In two patients with chronic active hepatitis as well as in some cases showing histological features of focal parenchymal necrosis, HBsAg could be detected in the cytoplasm of a few scattered hepatocytes but never at the surface of the cells. Both the cases with CAH and one with focal parenchymal necrosis had IgG bound to the liver cell membrane. These findings are in agreement with the hypothesis that the absence of liver damage in HBsAg healthy chronic carriers is related to immune tolerance to the antigen. In chronic active liver disease the presence of IgG on the membrane of hepatocytes suggests a possible role of blocking antibodies directed against viral antigens expressed at the hepatocyte surface.

T-lymphocyte cytotoxicity to HBsAg-coated target cells in hepatitis b virus infection.

The cytotoxic effect of peripheral lymphocytes on chicken red blood cells (ChRBC) coated with purified hepatitis B surface antigen (HBsAg) has been studied as an in vitro parameter of cell-mediated immunity in acute and chronic infection with hepatitis B virus. Using this technique, the mean cytotoxic index of lymphocytes from patients with acute hepatitis B (29.13 +/- 20.88) was significantly higher than that obtained with lymphocytes from control subjects (6.53 +/- 3.75). Only 33.3% of the patients with HBsAg-positive chronic active hepatitis exhibited lymphocyte cytotoxicity to HBsAg-coated target cells and the mean cytotoxic index (11.66 +/- 6.60) was in these cases significantly lower than that found in acute hepatitis B. Healthy chronic carriers of HBsAg failed to show lymphocyte cytotoxicity to target cells. The effector cells detected in acute hepatitis B by this in vitro assay have been demonstrated to be T-lymphocytes, as T-cell depleted subpopulations lacked cytotoxic activity. Target cell lysis could be blocked by addition of HBsAg-coated unlabelled ChRBC as well as of purified HBsAg in the culture tubes. It is suggested that damage to the liver cells in acute hepatitis B is related to the presence of cytotoxic T-lymphocytes reacting with HBsAg on the surface of infected hepatocytes. An inadequate lymphocyte response to the antigen may be responsible for the persistence of the infection in the liver with varied clinical manifestations and associated hepatic lesions.

[Lymphocytotoxic antibodies and systemic lupus. Clinical correlations and prognostic significance]. / Anticorpi linfocitotossici e lupus sistemico. Correlazioni cliniche e significato prognostico.

The present prospective study was designed to examine the diagnostic and prognostic value of lymphocytotoxins in 20 patients with Systemic Lupus Erythematosus both in active stage and in remission. Lymphocytotoxic antibodies were present in 79% of all the sera examined, in 100% of the sera of patients with active disease and in 52% of those in remission. The different frequency in the two groups is significant as well as the correlation of these antibodies with anti-DNA antibodies, hypocomplementaemia and leukopenia. In spite of their diagnostic value, lymphocytotoxins do not appear as sensible parameter as complementaemia and anti-DNA antibodies in monitoring the disease, since they are still detectable in the sera for several months after the disappearance of clinical signs of activity.