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Biomedical subjects

P L Meroni

Publications and source records attributed to P L Meroni.

At least 199 records · Page 11Linked to original sources
PubMedDate not supplied

Effects of chronic heroin addiction on pituitary-thyroid function in man.

Pituitary-thyroid function has been studied in heroin addicts. Data have been obtained in 10 male addicts, aged 18-24 years, with histories of addiction to heroin alone lasting from 8 months to 4 years, and in 9 controls matched for sex and age. Basal plasma levels of TSH, T4 and T3 were measured. A TRH stimulation test was done, injecting 500 micrograms of TRH iv as a bolus and assaying TSH levels before the injection and at 30 min intervals up to 2 h afterwards. The results revealed no difference between addicts and controls in basal levels of TSH, T4 and T3. The TRH stimulation test induced a blunted TSH rise in 50% of the cases. The possible mechanism of action of heroin on pituitary-thyroid axis is discussed.

Adolescent↗
PubMedDate not supplied

Age-related changes of beta-endorphin and cholecystokinin in human and rat mononuclear cells.

Beta-endorphin (BE) and cholecystokinin (CCK) were measured in fresh PBMC isolated from human subjects and rats. The BE and CCK PBMC contents increased significantly with age both in human and rat models. Moreover, polyclonal stimulation induced a significant decrease of BE but not CCK contents in mononuclear cells from human aged subjects. The time course of changes in BE and CCK concentrations observed in fresh and cultured cells from subjects of different ages did not directly correlate to the time course of age-associated impairment of lectin-induced lymphocyte proliferative response and interleukin-2 synthesis. In fact, the lymphocyte functional defects were significantly observed only in the 71-99 year age group, whereas the neuropeptide changes were already evident in the 31-50 age group. Since BE has been shown to participate in the modulation of the immune system, the age-related modifications of PBMC BE could play a role in the immunodepression observed during aging.

Adult↗
PubMedDate not supplied

Antiphospholipid antibodies cross-reacting with erythrocyte membranes. A case report.

We describe a patient with primary antiphospholipid syndrome (PAPS) and haemolytic anemia with cryoagglutinins, in whom antibodies eluted from red blood cells (RBC) displayed anti-cardiolipin (CL) binding activity. This activity was confined to the IgG isotype and was directed to the negatively-charged phospholipids only. In addition, the patient's IgG fraction displayed a higher binding to RBC in comparison to normal control IgG and this reactivity was inhibited after absorption of the anti-CL activity with CL-micelles. These findings further sustain the association between antiphospholipid antibodies (APA) and Coombs' positivity with or without haemolytic anemia and suggest that APA could be at least in part responsible for anti-RBC activity.

Aged↗
PubMedDate not supplied

The beta-2-glycoprotein I and antiphospholipid antibodies.

Beta 2-GPI is a single chain, 50 kd glycoprotein made up of 326 amino-acids, present in human plasma at concentrations of about 200 micrograms/ml. It has been shown to represent the "serum cofactor" important in determining the binding of aCL to phospholipids both in fluid and in solid phase assays. Its cofactor activity is demonstrable for aPL antibodies from patients with autoimmune but not with infectious diseases. It is immunogenic in heterospecific models, and immunization with beta 2-GPI seems to be able to induce the production not only of anti-beta 2-GPI but also of aPL antibodies. Most probably its binding to CL changes the configuration of phospholipids to a more immunogenic one. The various characteristics of beta 2-GPI are summarized in Table I. beta 2-GPI has been recognized as a natural anticoagulant protein, but its possible role in the pathogenesis of the APLS remains to be determined.

Antiphospholipid Syndrome↗
PubMedDate not supplied

Relationship between anti-phospholipid and anti-endothelial cell antibodies: further characterization of the reactivity on resting and cytokine-activated endothelial cells.

Sera positive for autoimmune anti-phospholipid antibodies were studied by a cell surface radioimmunoassay for their cross-reactivity with resting or activated human endothelial cells. The endothelial cell activation by interleukin 1 beta, gamma-interferon, lipopolysaccharide or phorbol-12 myristate-13 acetate did not affect the cross-reactivity. Comparable findings were also found by testing anti-cardiolipin affinity purified preparations. Taken together these data indicate that endothelial cell activation is not sufficient per se to modulate the expression of antigenic determinants recognizable by the anti-phospholipid antibodies. However, anti-cardiolipin affinity purified preparations displayed enhanced cell binding after cell membrane perturbation by paraformaldehyde fixation, suggesting that an alteration in endothelial cell integrity might further trigger the reaction of circulating anti-phospholipid antibodies with vessel walls in vivo.

Antibodies↗
PubMedDate not supplied

[SLE: Extra-renal clinical manifestations and lupus nephritis].

Systemic Lupus Erythematosus (SLE) is a chronic inflammatory autoimmune disease affecting multiple organ systems, skin and joints the most involved. Lupus Nephritis occurs in Approximately 50% of patients, sometimes it may be the first manifestation of SLE. Clinical features range from asymptomatic urinary abnormalities to full-blown nephrotic syndrome or rapidly progressive renal failure. Because of the heterogeneity of clinical renal manifestations, renal biopsy plays an important role in the management of patients with SLE: it provides information about the class, severity, activity and chronicity of the renal disease that cannot be accurately predicted on the basis of clinical parameters. The complexity of protean renal manifestation of SLE can be approached using the original WHO classification (1982), recently revised (2004).

Humans↗
PubMedDate not supplied

The pathophysiology of anti-phospholipid antibodies.

Anti-phospholipids represent a heterogeneous family of antibodies able to react with the negatively charged phosphodiester groups of phospholipids. It includes the antibodies directed against the cardiolipin moiety of the VDRL antigen, the antibodies reacting with the phospholipids of the prothrombin activator complex and the antibodies able to react with solid phase cardiolipin. Data are reported indicating that reagins share distinct characteristics in comparison to the autoimmune anti-cardiolipin antibodies (ACA). On the contrary anti-phospholipid antibodies responsible for lupus-like anticoagulant activity display a quite similar reactivity with ACA, even if a complete overlapping cannot be demonstrated. The relationships between ACA and anti-DNA antibodies are also reported. The biological and clinical significance of these crossreactivities are discussed.

Autoantibodies↗
PubMedDate not supplied

Antinuclear antibodies in progressive systemic sclerosis.

Sera from 84 patients with progressive systemic sclerosis (PSS) were tested for the presence of antinuclear antibodies by immunofluorescence on HEp2 cells and gel immunodiffusion. Fluorescent antinuclear antibodies were detected in 80 subjects with PSS (95%). Ninety-three percent of patients with CREST syndrome and 3% of those with diffuse scleroderma had a centromere staining. Precipitating antibodies were found in 57% of PSS sera and identified as anti-Scl 70 in 42 cases (50%). This specificity was found in 42 of 70 subjects with diffuse scleroderma (60%); another patient was positive for anti-nRNP antibodies, and 5 more sera from PSS patients showed precipitin lines of unknown specificity. No serum from 14 patients with CREST syndrome was positive for anti-Scl 70 antibodies. Significant relationships have been found between centromere staining and CREST syndrome (p less than 0.0005) and between the presence of anti-Scl 70 antibodies and the diffuse form of scleroderma (p less than 0.0005). The latter specificity is strongly associated with grainy speckled pattern on HEp2 fluorescence (p less than 0.0005). These data suggest that anti-Scl 70 antibodies and anti-centromere antibodies are useful markers for different subgroups of patients with PSS.

Adult↗
PubMedDate not supplied

Anti-phospholipid and anti-mitochondrial type M5 antibodies in systemic lupus erythematosus.

Fifty-one sera from patients with systemic lupus erythematosus (SLE) were studied in order to evaluate the prevalence of anticardiolipin (ACA) and anti-mitochondrial antibodies (AMA) type M5, and also to explore their relationship with the main serological and clinical features of the disease. A group of 25 (49.0%) patients was found to be ACA positive (IgG or IgG and IgM); in this group we found a significantly higher prevalence of false positive VDRL (p less than 0.01), lupus-like anticoagulant (p less than 0.05), and AMA type M5 (p less than 0.01), but not of anti-ds or ss-DNA antibodies. Three sera positive for ACA, AMA-M5 and anti ss-DNA were absorbed with cardiolipin liposomes. Anti-DNA and AMA-M5 showed only a minimal decrease. Central nervous system involvement and especially seizure syndrome was demonstrated with a higher prevalence in ACA-positive groups (p less than 0.05). Despite the results of absorption experiments, the close relationship between AMA-M5 and ACA, false positive VDRL or lupus-like anticoagulant (LLAC) might justify a speculation on the antiphospholipid nature of this antimitochondrial activity.

Adolescent↗
PubMedDate not supplied

[Idiopathic pulmonary hemosiderosis: report of a case with a favorable response to cyclophophamide therapy].

A 13-years old boy who presented a severe degree of iron-deficiency anemia and diffuse parenchimal infiltrates on the chest roentgenogram is reported. The clinical picture and the presence of hemosiderin laden macrophages in bronchial washing suggest Idiopathic Pulmonary Hemosiderosis (I.P.H.): open lung biopsy confirmed the diagnosis. Immunofluorescence studies showed no deposition of IgG, IgA, IgM and B1C in the lung. The most striking abnormality observed at electron microscopy was hemosiderin deposition in the alveolar-capillary basement membrane. One year after cyclophosphamide therapy was both in complete hematologic and pulmonary remission.

Adolescent↗
PubMedDate not supplied

Relationship between anti-phospholipid and anti-endothelial cell antibodies III: beta 2 glycoprotein I mediates the antibody binding to endothelial membranes and induces the expression of adhesion molecules.

OBJECTIVE: To investigate the role of antibodies reacting with beta 2 glycoprotein I (beta 2GPI) in the antiendothelial cell binding activity present in sera from patients with the anti-phospholipid syndrome. METHODS: Sera positive for anti-phospholipid, anti-endothelial and anti-beta 2 GPI antibodies were studied for their binding activity on endothelial monolayers cultured in the presence or absence of media containing bovine serum as a source of beta 2GPI. Anti-endothelial activity was also evaluated on endothelial cells cultured without serum and supplemented with exogenous human purified beta 2GPI. Affinity purified anti-beta 2 GPI antibodies were investigated under the same experimental conditions. Finally, the effect of the incubation of these affinity purified fractions on the expression of adhesion molecules (ELAM-1) was studied. RESULTS: The reactivity of the sera decreased on endothelial cells incubated in serum-free medium, while endothelial cell binding was restored in a dose dependent manner after the addition of exogenous purified human beta 2 GPI. Affinity purified anti-beta 2 GPI antibodies obtained from the same sera retained their endothelial cell binding and were able to activate endothelial cells by inducing the ex novo surface expression of adhesion molecules (ELAM-1). CONCLUSIONS: These findings indicate that the close association between anti-endothelial and anti-phospholipid antibodies is sustained by antibodies which recognize beta 2 GPI adhering to the endothelial cells, and can promote their activation.

Antibodies, Antiphospholipid↗
PubMedDate not supplied

What is the pathogenetic role of antiphospholipid antibodies?

The association between antiphospholipid antibodies (aPL) and arterial or venous thrombosis, fetal loss and thrombocytopenia defines the so-called "antiphospholipid syndrome" (APS). Despite serial studies in recent years, a clear pathogenetic mechanism(s) has not yet been demonstrated. Several authors have investigated the interaction between aPL and the membranes of blood cells (endothelial cells and platelets) involved in coagulation. aPL is also thought to affect the balance between the procoagulant and anticoagulant states by interacting with plasma or tissue cofactors. Finally, the strong association between aPL and experimental animal models of fetal loss supports a direct pathogenetic role for aPL in inducing a poor pregnancy outcome in APS women.

Abortion, Spontaneous↗
PubMedDate not supplied

Anti-neutrophil cytoplasmic antibodies in patients with chromomycosis.

OBJECTIVE: Antineutrophil cytoplasmic antibodies (ANCA) are a family of antibodies that react to proteins within neutrophil granules and monocyte lysosomes, and occur prominently in sera from patients with systemic necrotizing vasculitis. The cytoplasmic staining pattern (c-ANCA) is very sensitive and specific for Wegener's granulomatosis (WG), and most commonly results from reactivity with proteinase 3 (PR3). The features of tissue damage in the fungal infection chromomycosis, in particular polymorphonuclear neutrophil (PMN) infiltration and granuloma formation, bear a resemblance to that seen in WG. METHODS: We tested sera from 25 patients with clinical and histologic diagnosis of chromomycosis for the presence of ANCA by indirect immunofluorescence. These same sera were analyzed for reactivity to neutrophil primary granule extracts and PR3 by ELISA. RESULTS: Five of the 25 patients (20%) had detectable c-ANCA, without central accentuation, at serum dilutions of at least 1:40. Three of these 5 ANCA-positive patients reacted with neutrophil primary granule extracts by ELISA; however, none of them reacted with PR3. CONCLUSIONS: These results demonstrate that fungal infection should be included among the conditions, unrelated to necrotizing vasculitis, that can trigger autoreactivity against myeloid lysosomal antigens.

Adult↗