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Biomedical subjects

M Galli

Publications and source records attributed to M Galli.

405 records · Page 23Linked to original sources
PubMedDate not supplied

[Pre-therapeutic management and surveillance of menopausal hormone replacement therapy].

Pre-therapeutic evaluation of menopausal hormone replacement therapy (HRT) requires certain measures in addition to a standard gynecological assessment. It is important to identify any possible breast or endometrial disorder which might require specific treatment or an adjustment of standard HRT. Skeletal status is assessed by history and, if necessary, by double-photon absorptiometry. Following such evaluation, absolute contra-indications are few in number, by virtue of the use of natural estradiol and non-androgenic progestogens. They essentially concern breast cancer and a thrombo-embolic history. The first follow-up visit, at three months, enables confirmation of the acceptability and efficacy of treatment and its adjustment if required. A monitoring calendar is then suggested.

Absorptiometry, Photon↗
PubMedDate not supplied

Family history and risk of stomach cancer in Italy.

One thousand sixteen gastric cancer (GC) patients and 1623 population controls, interviewed in a multicentric study in Italy, reported their family history for gastric, esophageal, and colorectal cancer. A significant association was found only with a history of GC in a sibling or in a parent [odds ratio (OR), 2.6 and 1.7, respectively], which persisted after adjusting for potential confounders including nutrient intake. Adjusted GC risk was higher for subjects having an affected mother than an affected father (OR, 2.3 and 1.3) and showed a further increase for subjects reporting both parents (OR, 3.0) or two or more siblings affected with GC (OR, 8.5). The proportion of patients with an affected first-degree relative was higher among females, in the elderly, and in high-risk areas. Among adult siblings of controls and cases, GC prevalence reported at interview was 1 and 2.7%, respectively; a further increase was shown in families with at least one parent affected (1.4 and 5.7%). GC risk associated with a positive family history was greater among residents of low-risk areas where risks were increased about two-fold. Among cases, family history of GC was not related to blood group A or to histological type according to the Lauren classification. These findings are discussed in terms of the contributions of genetic and environmental risk factors and their possible interactions.

ABO Blood-Group System↗
PubMedDate not supplied

Viruses and cryoglobulinemia.

Circulating cryoglobulins have been reported in association with several acute and chronic viral diseases. In all of the reported cases, the viruses involved have been hepatotropic, lymphocytotropic or both. Among the hypotheses concerning the causes of cryoglobulinemia, two possible pathways have been more frequently debated: an impairment of the macrophagic system of the liver, with the consequent impairment of the clearance of gut antigens and immunoglobulins, as the first ring of a chain of events including the activation of the B cell compartment with increased production (and decreased clearance) of cryoglobulins; and a low-grade malignant lymphomatous process involving rheumatoid factor producing clones. Recent evidence of a close association between hepatitis C virus (HCV) and "essential" mixed cryoglobulinemia has focused the attention of several researchers on the mechanisms by which the virus is capable of causing cryoglobulin synthesis. The open questions include: (1) Why do only a minority of chronically HCV-infected people (mainly "sporadically" infected elderly women) develop a cryoglobulinemic syndrome? (2) What kind of mechanisms can up- or down-regulate cryoglobulin production? (3) Are immunoregulatory mechanisms involved? (4) Is there a connection between HCV infection and the low-grade malignant lymphoma hypothesis identifying cryoglobulinemias as the consequence of the slow proliferation of CD5+ B cells? and (5) Are particular HCV genotypes specifically involved in causing cryoglobulinemias? Several of these questions still remain unanswered. HCV has been detected in the peripheral blood mononuclear cells of both cryoglobulinemic and non-cryoglobulinemic infected subjects; on the other hand, the detection of viral RNA in the bone marrow cells of virtually all cryoglobulinemic patients suggests that this might be related to the pathogenesis of the disease.

Cryoglobulinemia↗
PubMedDate not supplied

HCV genotypes in bone marrow and peripheral blood mononuclear cells of patients with mixed cryoglobulinemia.

OBJECTIVE: The association of the hepatitis C virus (HCV) with the cryoglobulinemic syndrome is well known, but its pathogenetic mechanism still remains to be clarified. HCV-RNA has been found in the peripheral blood mononuclear cells (PBMC) of infected subjects. We investigated the presence of the HCV genome in bone marrow cells (BMC), and the distribution of different HCV genotypes in individuals with mixed cryoglobulinemia (MC) and in noncryoglobulinemic controls. METHODS: 15 anti-HCV positive subjects with MC, 7 non-cryoglobulinemic patients with type C chronic active hepatitis (CAH) and 2 anti-HCV negative controls were studied. HCV-RNA was detected by nested PCR of the highly conserved 5'-NCR sequence. HCV typing was carried out by means of the hybridization of the same amplified region with specific probes. RESULTS: HCV-RNA was present in the PBMC of a large proportion of the MC patients and controls without any significant differences. On the contrary, HCV-RNA was present in the bone marrow cells of all the patients with MC and in 43% of the CAH controls. The HCV 1b and 2a genotypes seem to be the most prevalent among MC patients. Nevertheless, the patients with type II MC had a very high prevalence of the 2a genotype (77%). CONCLUSION: The results suggest that the presence of HCV-RNA in bone marrow cells may be correlated to the pathogenetic mechanism of MC. Other studies are needed to confirm the frequent association of HCV genotype 2 with MC.

Aged↗
PubMedDate not supplied

HCV-RNA detection using different PCR methods in sera, cryoglobulins and peripheral blood mononuclear cells of patients with mixed cryoglobulinemia.

OBJECTIVE: The hepatitis C virus (HCV) is frequently associated with mixed cryoglobulinemia (MC), and a number of authors have reported the presence of anti-HCV antibodies and HCV-RNA in the blood of MC patients. The presence of the HCV genome in the blood cells of individuals infected by HCV may correlate with the etiopathology of MC. We investigated the presence of HCV-related sequences in the sera, cryoglobulins and peripheral blood mononuclear cells (PBMC) of patients with MC and of individuals with type C chronic active hepatitis (CAH). METHODS: 39 patients with MC, 11 non-cryoglobulinemic HCV-positive individuals with CAH, and 2 anti-HCV negative controls were included in the study. The presence of HCV-RNA was detected by nested RT-PCR and by a commercial kit. The PCR was performed by amplifying the 5'-non coding region (5'-NCR) of HCV. RESULTS: HCV-RNA was detected in the sera and cryoglobulins of about 90% of the patients; the commercial kit showed a higher sensitivity than nested PCR. One MC patient showed HCV-RNA only in the cryoglobulins. HCV-RNA was present in the PBMC of 14 of the 20 (70%) MC patients analyzed. No differences in serum and PBMC HCV-RNA positivity were found between MC patients and controls. CONCLUSION: Our results confirm the spread of HCV infection among patients with MC. HCV-RNA is present in the serum, cryoglobulins and PBMC of a large proportion of MC patients. The prevalence of HCV-RNA in the PBMC of MC patients and controls did not differ significantly; this may suggest a tropism of HCV for PBMC regardless of the presence of cryoglobulinemia.

Base Sequence↗
PubMedDate not supplied

Disappearance of cryoglobulins and remission of symptoms in a patient with HCV-associated type II mixed cryoglobulinemia after HIV-1 infection.

OBJECTIVE: We report the case of a woman with long-lasting mixed cryoglobulinemic syndrome, who experienced clinical and laboratory remission of her cryoglobulinemia after becoming infected with human immuno-deficiency virus and developing HIV-1 induced immunosuppression. METHODS: Serum cryoglobulin concentrations and the CD4+ cell count were monitored every three months. RESULTS: After the diagnosis of HIV-1 infection, the immunological status of the patient was constantly depressed (CD4+ cell count dropping from 337/microL in January 1991 to 21/microL in June 1994). Serum cryoglobulins were persistently absent over 43 months of follow-up, despite the presence of HCV-RNA. CONCLUSION: In this case, HIV-1 induced immunodeficiency seems to be responsible for the remission of the cryoglobulin syndrome and the disappearance of serum cryoglobulins. These findings indicate that CD4+ T lymphocytes may play a role in regulating the activity of cryoprecipitating rheumatoid factor secreting B cell clones.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Severe bleeding due to acquired hypoprothrombinemia-lupus anticoagulant syndrome. Case report and review of literature.

A 17-year-old girl was admitted to our department with a hemorrhagic syndrome due to a serious coagulopathy; prothrombin time (PT) INR was 2.46 and the activated partial thromboplastin time (aPTT) ratio 3.46. Coagulation tests with pooled normal fresh plasma did not correct aPTT because of a coagulation inhibitor, and only partially corrected PT. Factor II activity reached only 5%. Diluted Russell viper venom tests (dRVVT) and kaolin clotting time (KCT) of patient plasma (PP) and of a mixture of PP/normal plasma (NP) detected the lupus anticoagulant (LA). The level of factor II antigen was 10%. We diagnosed systemic lupus erythematosus (SLE) with a rare acquired hypoprothrombinemia-LA syndrome (HLAS). The patient was treated with corticosteroids and high-dose Ig and a normal PT value was re-established.

Adolescent↗
PubMedDate not supplied

[Clinical significance and predictive value of laboratory tests in thrombosis associated with antiphospolipid antibodies].

Antiphospholipid antibodies are a wide ranging, heterogeneous family of autoantibodies, formerly believed to be directed to anionic phospholipids. Recent research, however, has confirmed that they are directed to plasma proteins bound to suitable (phospholipid) anionic surfaces. The most well-known and best characterized antigens are beta 2-glycoprotein I, recognized by anticardiolipin antibodies, and prothrombin, recognized by most lupus anticoagulants. Lupus anticoagulants are generally identified on the basis of their capacity to prolong the phospholipid-dependent coagulation tests. Two types of lupus anticoagulants, anticardiolipin-type A, and antiprothrombin antibodies, whose presence is associated with different coagulation profiles, have been identified. Anticardiolipin-type A and antiprothrombin antibodies may be detected also by specific immunoassays. The capacity of several methodologies to detect antiphospholipid antibodies reflects chiefly their immunological and functional heterogeneity. Since most of the laboratory methods have not yet been standardized, the results of studies on the clinical relevance of antiphospholipid antibodies must be analyzed with caution. The association between antiphospholipid antibodies with peculiar clinical manifestations such as venous and arterial thrombosis, recurrent miscarriage, and thrombocytopenia, characterizes the so-called "antiphospholipid syndrome". Retrospective and cross-sectional studies have confirmed the role of anticardiolipin antibodies and lupus anticoagulants as risk factors for both venous and arterial thrombosis, the most common clinical manifestations of the antiphospholipid syndrome. Prospective studies performed in different patient populations have confirmed the association between anticardiolipin antibodies and lupus anticoagulants with venous, and possibly, arterial thrombosis, although information on the predictive value of the various laboratory tests with respect to thrombosis is still limited. It is hoped that the development and standardization of assays that selectively identify antiphospholipid antibodies associated with increased risk of thrombosis will lead to therapeutic strategies able to prevent thromboembolic complications of the antiphospholipid syndrome.

Adult↗