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Biomedical subjects

M Galli

Publications and source records attributed to M Galli.

At least 163 records · Page 9Linked to original sources
PubMed1996

Reproducibility of histological diagnosis of breast lesions: results of a panel in Italy.

Sixteen pathologists independently examined and classified a series of 81 breast lesions selected from the files of several Italian Pathology Departments in the context of a national task force on breast cancer (FONCAM). A four category classification system was used for analysis; according to the majority diagnosis (MD), simply defined as the most frequently reported in the panel, the series included 37 benign lesions without atypia (45.7%), nine atypical hyperplasias (11.1%), 18 in situ (22.2%) and 17 invasive carcinomas (21.0%). Concordance, estimated for all possible pair-wise comparisons between pathologists, was good (mean kappa value: 0.59). A comparison between the diagnoses of each pathologist and the panel majority diagnosis was also made. Overall, a global kappa value of 0.72 was found (range 0.57-0.85), with category-specific values being excellent for invasive carcinoma (0.89) and benign lesions without atypia (0.77), relatively good for in situ carcinoma (0.69) but poor for atypical hyperplasia (0.38). These results confirm that quality assurance procedures are particularly indicated for large screening programmes for breast cancer, and suggest that for atypical lesions strict diagnostic criteria should be adopted.

Breast Neoplasms↗
PubMed1996

Evidence for type 2 cytokine production and lymphocyte activation in the early phases of HIV-1 infection.

OBJECTIVE: To analyse changes in cytokine production in vitro and T-lymphocyte immunophenotype in the early phases of HIV-1 infection. DESIGN AND METHODS: Mitogen-stimulated in vitro production of interferon (IFN)-gamma, interleukin (IL)-2 (type 1 cytokines), IL-4, and IL-10 (type 2 cytokines) and surface expression of activation and non-activation markers were evaluated in 11 individuals HIV-infected for > 3 but < 12 months (seroconverters). The data were compared to those obtained in 33 asymptomatic HIV-positive individuals infected > 3 years previously and who were stratified according to CD4+ lymphocyte count (group 1: > 500 x 10(6)/l, group 2: < 500 x 10(6)/l CD4 cells) and in 12 HIV-seronegative healthy controls. RESULTS: We observed that the early phase of HIV infection is characterized by (1) reduced mitogen-stimulated IL-2 and IFN-gamma production, (2) increased mitogen-stimulated IL-4 and IL-10 production, (3) a relative decrease in CD4+ and CD4+CD7- as well as an increase in CD4+CD7-CD57+ lymphocytes, and (4) a relative increase in CD8+, CD8+CD38+ and CD8+CD57+ T lymphocytes. In addition, during a 6-month follow-up of six seroconverters we observed a dynamic pattern of changes of these parameters in most individuals, with a resulting profile similar to that observed in group 1 HIV-positive patients. CONCLUSION: The early phase of HIV infection is immunologically characterized by type 2 cytokine secretion and alterations in the expression of phenotypic markers, and closely resembles the more advanced phases of HIV infection. These immunologic alterations are temporally limited by the successive return to a more normal profile. Thus, HIV infection is an immunological complex dynamic process even in its earliest phases.

Acute Disease↗
PubMed1996

High frequency of non-Hodgkin's lymphoma in patients with HIV-associated Kaposi's sarcoma.

OBJECTIVE: To evaluate, with the support of autopsy findings, the frequency of non-Hodgkin's lymphoma (NHL) among patients with AIDS-associated Kaposi's sarcoma (KS) in comparison with that of AIDS patients with other AIDS-defining diseases. METHODS: The study involved 363 consecutive patients with AIDS who were cared for and died at the Clinic of Infectious Diseases in Milan between May 1984 and December 1992. Clinical records and autopsy data of all of the patients were retrospectively reviewed. Kaplan-Meier product-limit estimates of the time to the development of NHL were calculated for all patients and by specific subgroups. Cox proportional hazards analyses were made to determine the factors associated with the development of NHL. RESULTS: In the majority of cases (82%), KS was diagnosed during life, whereas NHL was diagnosed before death in only 41.6% of cases. Taking the autopsy data into account, the cumulative incidence of the two tumours was 16.8% for KS and 16.5% for NHL. Among the 61 patients in whom KS was the index disease of AIDS, 16 also developed NHL. The probability of developing NHL was significantly higher in patients with KS at AIDS diagnosis than in patients with Pneumocystis carinii pneumonia (PCP), oesophageal candidiasis or other AIDS-related diseases (P = 0.004). Multivariate analysis of the factors associated with the development of NHL (such as sex, age, risk factors, AIDS-defining diseases and CD4+ cell counts) showed that the patients with KS as the index disease of AIDS had a 5.3-fold higher risk of developing NHL than the patients with PCP as the primary manifestation of AIDS. CONCLUSIONS: Our results confirm the higher incidence of malignant lymphoma in patients with AIDS-KS than in patients with other AIDS-related diseases. The importance of autopsy in assessing these data is underlined by the high percentage of NHL diagnosed only after death. These observations may support the hypothesis of a common aetiological agent, or of a common pathway, for the two neoplasms.

AIDS-Related Opportunistic Infections↗
PubMed1996

No evidence of a higher risk of progression to AIDS in patients with HIV-1-related severe thrombocytopenia.

The prognostic role of platelet (PLT) counts was evaluated in a cohort of 1,533 HIV-1-infected subjects followed for a median of 21 months. Thrombocytopenia (TCP), defined as a PLT count < or = 100 x 10(9)/L was present at enrollment in 11.2% of cases, with counts < or = 50 x 10(9)/L (severe TCP) in 5.3%. With the subjects with normal PLT counts (PLT >150 x 10(9)/L) as the reference group, the relative risk of developing acquired immunodeficiency syndrome (AIDS) was 0.8 [95% confidence interval (CI) 0.5-1.3, p = 0.4] for subjects with severe TCP, 2.1 (95% CI 1.4-3.1, p = 0.002) for those with PLT counts ranging from 51 to 100 x 10(9)/L (moderate TCP), and 1.6 (95% CI 1.2-2.1, p = 0.0004) for those with borderline PLT values (PLT ranging from 101 to 150 x 10(9)/L). Most of the risk increase associated with moderate TCP and borderline PLT values was explained by a higher prevalence of subjects with an older age and lower CD4+ cell counts. However, at multivariable analysis considering age, sex, risk group, and zidovudine (ZDV) treatment, the risk for subjects with severe TCP remained significantly lower than that for subjects with moderate TCP and borderline values. These results suggest the existence of different types of HIV-1-associated TCP and also suggest that severe TCP (which often arises in the early phases of infection) is not related to disease progression.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Non beta 2-glycoprotein I cofactors for antiphospholipid antibodies.

The Antiphospholipid Syndrome is defined by the association between peculiar clinical manifestations, namely arterial and/or venous thrombosis, recurrent abortions and thrombocytopenia, and the antiphospholipid antibodies. These antibodies are directed to plasma proteins bound to anionic phospholipids or other anionic surfaces: so far, beta 2-glycoprotein I is the best known and characterized antiphospholipid 'cofactor' (this issue is specifically treated in other parts of this journal). In recent years, such a role has been reported also for prothrombin, activated Protein C, Protein S, Annexin V, Thrombomodulin, high- and low-molecular weight kininogens. Anti-prothrombin antibodies are detected in approximately 50% of the antiphospholipid-positive patients; conversely, limited data are available regarding the prevalence the other antibodies. 'Cofactors' are necessary for the expression of both the immunological and the functional properties of their respective antiphospholipid antibodies. In particular, the recognition of the calcium-mediated prothrombin/lipid complex by anti-prothrombin antibodies hampers prothrombin activation, thus causing the prolongation of the phospholipid-dependent coagulation reactions. The interaction between antiphospholipid antibodies and natural inhibitors of coagulation such as activated Protein C, its non-enzymatic accessory protein Protein S or Thrombomodulin might increase the risk to develop thromboembolic events. Similarly, the presence of antibodies to surface-bound Annexin V has been hypothesized to play a role in recurrent abortions and fetal deaths. However, to clearly establish whether and which antiphospholipid antibodies represent risk factors for the thromboembolic events of the antiphospholipid syndrome, further studies of their behaviour and properties as well as the identification and characterization of (possibly) other antibodies are required.

Antibodies, Antiphospholipid↗
PubMed1996

A population-based study of inflammatory bowel disease in Florence over 15 years (1978-92).

BACKGROUND: In the group of inflammatory bowel disease (IBD), ulcerative colitis (UC) and Crohn's disease (CD) are considered to be more frequent in Western countries and in areas with a high socioeconomic development but relatively infrequent in southern Europe. Sporadic reports have indicated a lower incidence and a milder course of the disease in Mediterranean countries. Although conclusive data on this point are still lacking, recent reports suggest an increase in both incidence and prevalence rates. METHODS: The incidence of UC and CD during the period January 1978 to December 1992 and their prevalence on 31 December 1992 were estimated in the 15-year-old population of the metropolitan area of Florence. Clinical, demographic, and follow-up information was collected for all identified IBD patients. RESULTS: A total of 796 residents (345 females and 454 males) were newly diagnosed as having IBD during the study period. Of these 593 had UC and 203 CD. The age-standardized incidence rates, calculated for each of five 3-year consecutive periods, rose from 3.8 (in 1978-80) to 9.6 per 100,000 person-years (in 1990-92) for UC and from 1.9 (in 1978-80) to 3.4 (in 1990-92) for CD. Both trends were statistically significant. The prevalence estimated on 31 December 1992 was 121.0 and 40.0 per 100,000 inhabitants for UC and CD, respectively. CONCLUSIONS: Our results confirm that IBD incidence rates and prevalence in this area of central Italy are currently comparable with those reported in northern Europe. These data are necessary for planning adequate health care services for IBD patients.

Adolescent↗
PubMed1996

Viral load, viral phenotype modification, zidovudine susceptibility and reverse transcriptase mutations during the first 6 months of zidovudine monotherapy in HIV-1-infected people.

We studied 14 zidovudine-naive, HIV-1-infected patients attending an infectious diseases clinic in Milan during zidovudine therapy for 6 months. We monitored CD4 cell counts, immune complex-dissociated p24 antigen, viral phenotype and viral load in plasma. The virus infecting a subset of patients was examined for zidovudine susceptibility and zidovudine resistance-associated mutations. A significant correlation was established between the increase in the CD4 cell count and the decrease in viral load (Spearman's coefficients < -0.5). Patients who were p24 antigen positive had a higher viral load (P < 0.005 at baseline and after 6 months of therapy). Patients with non-syncytium-inducing (NSI) virus had higher CD4 cell counts over time than those with syncytium-inducing (SI) virus. We also examined the viral load in relation to viral phenotype. The median viral load in patients with NSI virus was higher than in SI controls at baseline, but not after 3 and 6 months of therapy. Sequential isolates of HIV-1 were obtained from nine patients and tested for resistance to zidovudine by monitoring the drug susceptibility and the reverse transcriptase-encoding sequence. Amino acid changes at codons 70 and 215 were present in some but not all isolates with zidovudine-resistant phenotype in vitro. It was possible to perform a correlation between zidovudine susceptibility and zidovudine-associated pol gene mutations only at the 6-month time point (Spearman's coefficient = 0.076). SI phenotype was associated with the development of a decreased zidovudine susceptibility. A correlation between zidovudine-associated pol gene mutations and SI phenotype was detected at the 6-month time point.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Platelet-derived microvesicles in thrombotic thrombocytopenic purpura and hemolytic uremic syndrome.

Thrombotic thrombocytopenic purpura (TTP) and the related hemolytic uremic syndrome (HUS) are disorders characterized by thrombocytopenia, microangiopathic hemolytic anemia, a variable degree of impairment of renal function and fluctuating neurological symptoms, which are thought to be due to platelet activation and subsequent formation of thrombi in the microcirculation. Since platelet activation is accompanied by the generation of microvesicles (PMPs), we determined their presence in patients with TTP and HUS by flow cytometry. The analysis was performed in whole blood, using FITC-conjugated monoclonal antibodies (CD 42b and/or CD 61a). PMPs were discriminated from platelets on the basis of size and fluorescence profiles. Their levels in 21 normal controls ranged between 2.4% and 9.4% (mean +/- SD: 5.2 +/- 1.99%). No correlations were found with platelet number. PMPs were then evaluated in 13 patients with TTP and 2 cases of HUS. In all patients they were found higher than in controls, ranging from 11.0 to 91.1% (45.0 +/- 26.0%; p = 0.0001 vs controls). PMPs were serially measured in patients with TTP: at diagnosis a correlation between PMPs and platelet number was found (R]2 = 0.669) and the time-course showed that the improvement of both microangiopathy and clinical manifestations of cerebral and renal involvement was accompanied by a progressive normalization of PMP levels and platelet count. PMP levels were measured also in patients suffering from other forms of thrombocytopenia: they were 17 patients with idiopathic thrombocytopenic purpura and 10 patients with acute leukemias and severe thrombocytopenia during the aplastic phase following chemotherapy. PMP ranges were: 2.0-79.6% (21.6 +/- 20.8%; p = 0.001 vs controls) and 4.6-12.5% (8.8 +/- 2.4%; p = 0.0001 vs controls), respectively. No correlations were found between platelet number and the absolute number of PMPs in these 2 groups of patients. These findings show that increased levels of PMPs may be found in peripheral thrombocytopenias and suggest that their presence may be clinically relevant, particularly in the microangiopathic forms.

Adolescent↗
PubMed1996

Thrombocytopenia in the antiphospholipid syndrome: pathophysiology, clinical relevance and treatment.

The antiphospholipid syndrome (APS) is characterized by the association of antiphospholipid antibodies with venous and/or arterial thrombosis, recurrent abortions and thrombocytopenia. With respect to this latter clinical manifestation, a variable degree of thrombocytopenia occurs in approximately 20-40% of the patients with APS, it is generally mild and does not modify the policy for treatment of thrombosis. Severe thrombocytopenia is relatively uncommon and seldom associated with bleeding complications. When required, its treatment is similar to that of idiopathic thrombocytopenic purpura. Finally, uncertainties still exist as to the interaction between aPL antibodies and platelets and to the role of platelets and these antibodies on the pathogenesis of the thrombotic complications of the APS.

Antiphospholipid Syndrome↗
PubMed1996

[Exertion-induced myocardial ischemia has little influence on ventricular remodeling in post-infarction patients with preserved systolic function].

BACKGROUND: The effects of acute and recurrent ischemia on ventricular function are well documented. However, the role of residual exertional ischemia in the remodelling process after infarction has not yet been established. In this study, we investigated whether exercise-induced myocardial ischemia influences left ventricular remodelling in patients with recent myocardial infarction and preserved left ventricular function and volumes. METHODS: Sixty-four patients with a first anterior Q wave myocardial infarction were studied at 5 weeks by rest echocardiography and exercise scintigraphy; the echocardiographic examination at rest was repeated 6 months later. Based on the presence and extent of reversible perfusion defects on exercise scintigraphy, patients were classified as having no exertional ischemia (group 1, n = 13 [20%]), mild to moderate ischemia (group 2, n = 32 [50%]) and severe exertional ischemia (group 3, n = 19 [30%]). RESULTS: At 5 weeks after infarction left ventricular volumes, ejection fraction, percent wall motion abnormalities and regional dilatation were similar in the three groups. After 6 months, end-diastolic and end-systolic volumes and regional dilatation did not change in patients in all groups, while ejection fraction and percent wall motion abnormalities showed a slight but significant (p < 0.01) improvement in all groups. CONCLUSIONS: Exercise-induced myocardial ischemia, either mild or severe, does not affect ventricular remodelling and function after myocardial infarction in patients with preserved ejection fraction.

Adult↗
PubMed1996

Thallium-201 reverse redistribution at reinjection imaging correlated with coronary lesion, wall motion abnormality and tissue viability.

UNLABELLED: Previous studies based on standard stress-redistribution 201TI scintigraphy provided conflicting results about the clinical significance 201Tl reverse redistribution. Recent observations indicate that the majority of these defects normalize following reinjection reflecting viable myocardium. METHODS: In this study, the meaning of reverse redistribution occurring at reinjection imaging, its relation to standard 4-hr redistribution, coronary lesion, abnormal wall motion and tissue viability were assessed. A region with normal activity in the stress image was considered as having reverse redistribution if 201Tl activity at reinjection imaging was definitely abnormal with a decrease in relative tracer uptake >15% of the peak. From a series of 270 patients, 29 showed reverse redistribution. Of these 29 patients, 27 had evidence of previous myocardial infarction. Coronary lesions were detected in all but 1 patient. Average ejection fraction was 0.38 +/- 0.11. RESULTS: On a segmental basis, 50/377 regions showed the pattern of reverse redistribution. A significant coronary lesion (> or = 50%) was found in 78% of these regions; occlusion rate was 50%, and collateral circulation was found in 35% of occluded vessels. Hypokinesis or akinesis was present in 72% of segments. Tissue viability, defined as an uptake >55% of the peak, was found in 44% of these segments. The 50 segments showing reverse redistribution were divided into two groups according to an abnormal uptake also at 4-hr redistribution (group 1, 25 segments) or appearing only following reinjection (group 2,25 segments). Despite segments of group 1 showing a higher degree of coronary stenosis (80 +/- 32 versus 59 +/- 43%, p < 0.01), a similar rate of coronary occlusion, ventricular dysfunction and maintained viability was found in the two groups. CONCLUSION: Reverse redistribution in chronic coronary artery disease is frequently associated with significant coronary lesion, collateral-dependent dysfunctioning myocardium and preserved tissue viability. The occurrence of reverse redistribution following reinjection expands the indication for viability imaging to all patients with known coronary artery disease and regional wall motion abnormalities who undergo diagnostic and prognostic 201TI scintigraphy.

Coronary Angiography↗