Samantha Griffini

Fondazione IRCCS Ca' Granda - Ospedale Maggiore Policlinico, Milano, Lombardy, Italy

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Publications (12)46.19 Total impact

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    ABSTRACT: A 91-year-old woman affected with acquired Von Willebrand (VW) syndrome and intestinal angiodysplasias presented with severe gastrointestinal bleeding (hemoglobin 5 g/dl). Despite replacement therapy with VW factor/factor VIII concentrate qid, bleeding did not stop (eleven packed red blood cell units were transfused over three days). High circulating levels of anti-VW factor immunoglobulin M were documented immunoenzimatically. Heart ultrasound showed abnormalities of the mitral and aortic valves with severe flow alterations. When intravenous immunoglobulins were added to therapy, prompt clinical and laboratory responses occurred: complete cessation of bleeding, raise in hemoglobin, VW factor antigen, VW ristocetin cofactor and factor VIII levels as well as progressive reduction of the anti-VWF autoantibody levels.
    Experimental hematology & oncology. 01/2014; 3:15.
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    ABSTRACT: Thrombolysis with recombinant tissue-type plasminogen activator (rt-PA) is successfully used in acute myocardial infarction with ST elevation (STEMI). Reocclusions follow rt-PA treatment in up to 30% of patients within one year. The infusion of rt-PA may induce the production of anti-t-PA antibodies which could interfere with the function of the native t-PA molecule. In order to detect and characterise anti-t-PA antibodies, plasma samples were collected from 30 STEMI patients (20 treated and 10 not treated with rt-PA) at baseline before rt-PA infusion and then 15, 30, 90 and 180 days after STEMI and from 40 healthy subjects at baseline only. Immunoenzymatic, chromatographic and chromogenic methods were employed. An increase of anti-t-PA antibodies was observed 15 days (IgM, p=0.0001) and 30 days (IgG, p=0.0001) after rt-PA infusion. Six patients had large increases of anti-t-PA IgG which bound the catalytic domain of t-PA (two cases) or kringle 2 domain (four cases), were of IgG1 or IgG3 subclasses and interacted with the t-PA molecule in fluid phase. The infusion of rt-PA may induce the production of specific antibodies that bind active sites of t-PA, thus potentially reducing its in vivo function.
    European Journal of Internal Medicine 02/2010; 21(1):25-9. · 2.05 Impact Factor
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    ABSTRACT: Cl-inhibitor (C1-INH) deficiency leads to recurrent attacks of mucocutaneous edema and may be inherited (hereditary angioedema [HAE]) or acquired (acquired angioedema [AAE]), which have the same clinical picture characterized by angioedema involving the skin, gastrointestinal tract, and larynx. Although cutaneous swelling is evident, abdominal angioedema is still a diagnostic challenge and attacks can mimic surgical emergencies. There is currently no laboratory marker for identifying angioedema attacks. As coagulation and fibrinolysis are activated during angioedema attacks, we assessed if plasma measurements of prothrombin fragment F1 + 2 (marker of thrombin generation) and D-dimer (marker of fibrin degradation) can be useful for the diagnosis of angioedema because of C1-INH deficiency, especially in case of hidden locations as abdominal attacks. Methods: In addition to complement, we measured plasma levels of F1 + 2 and D-dimer in 28 patients with C1-INH deficiency during acute attacks and remission, 35 patients without C1-INH deficiency during abdominal colics, and 20 healthy subjects. Plasma F1 + 2 levels were higher in patients with C1-INH deficiency during remission than in healthy controls (P = 0.001), and further increased during cutaneous and abdominal attacks (P = 0.0001); patients without C1-INH deficiency had normal F1 + 2 levels during abdominal colics. Plasma D-dimer levels were higher in patients with C1-INH deficiency during remission than in controls (P = 0.012) and increased during angioedema attacks, reaching higher levels than in patients without C1-INH deficiency during colics (P = 0.002). During acute angioedema attacks, patients with C1-INH deficiency have high prothrombin fragment F1 + 2 and D-dimer levels, the measurement of which may have an important diagnostic value.
    Allergy 01/2009; 64(2):254-7. · 5.88 Impact Factor
  • Digestive and Liver Disease - DIG LIVER DIS. 01/2009; 41.
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    ABSTRACT: Increased cardiovascular (CV) risk is a rheumatoid arthritis (RA) hallmark and it has been mainly related to chronic systemic inflammation. Since inflammation is linked to coagulation perturbation, both may play a role in increasing CV risk. Treatment with tumor necrosis factor (TNF)-alpha blocking agents is effective in RA and reduces local and systemic inflammation but there is little information on its effect on coagulation. We therefore investigated inflammation and coagulation plasma biomarkers before and after infliximab treatment in RA patients. We studied 20 patients with active RA and 40 healthy controls. Patients were treated with: a stable dose of methotrexate (10mg/week), and infliximab (3mg/kg) at weeks 0, 2, 6 and 14. At baseline and week 14, we determined: disease activity score (DAS-28), visual analogue scale pain, erythrocyte sedimentation rate (ESR), and plasma levels of C-reactive protein (CRP), TNF-alpha, interleukin (IL)-6, prothrombin fragment 1+2 (F1+2) and D-dimer. The same inflammation and coagulation parameters were evaluated 1h after infliximab infusion in 10 patients. At baseline, ESR, CRP, TNF-alpha, IL-6, F1+2 and D-dimer levels were significantly higher in RA patients than in controls (P=0.0001). After 14weeks of infliximab treatment, there was a significant clinical improvement and ESR and CRP, IL-6, F1+2 and D-dimer level decrease (P=0.001-P=0.008). The levels of TNF-alpha, IL-6, F1+2 and D-dimer significantly decreased 1h after infliximab infusion (P=0.005). Infliximab decreases inflammation and coagulation biomarkers in RA patients. Such a combined effect may be pivotal in reducing the whole thrombotic risk in these patients.
    Journal of Autoimmunity 10/2008; 31(2):175-9. · 8.15 Impact Factor
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    ABSTRACT: Patients with chronic urticaria (CU) frequently show signs of thrombin generation as a result of the activation of the extrinsic pathway of coagulation and signs of fibrinolysis as shown by slightly increased mean D-dimer plasma levels. Here, we studied patients with severe CU to see whether the activation of coagulation and fibrinolysis parallels the severity of the disease. Eight consecutive patients with severe exacerbations of CU and 13 with slight CU were studied. Plasma prothrombin fragment F(1+2) as well as D-dimer were measured by ELISA. Serum histamine-releasing activity was assessed by basophil histamine release assay. Seventy-four normal subjects were used as controls. In patients with severe CU, median levels of both D-dimer (11.20 nmol/l) and F(1+2) (592 pmol/l) largely exceeded those found in patients with slight CU [D-dimer: 2.66 nmol/l (P = 0.001) and F(1+2): 228 pmol/l (P = 0.003)] and in normal subjects [D-dimer: 1.41 nmol/l (P = 0.0001) and F(1+2): 159 pmol/l (P = 0.0001)]. Sera from 25% of patients with severe CU and 31% of those with slight CU, but from none of normal subjects, showed in vitro histamine-releasing activity. D-dimer and F(1+2) levels were significantly correlated each other (r = 0.64, P = 0.002) and with CU severity score (r = 0.80-0.90, P = 0.0001), but no correlation was observed between serum histamine-releasing activity and coagulation parameters or severity score. Severe exacerbations of CU are associated with a strong activation of coagulation cascade and fibrinolysis. Whether this activation is the cause of CU or acts as an amplification system is still a matter of debate.
    Allergy 03/2008; 63(2):176-80. · 5.88 Impact Factor
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    ABSTRACT: Previous studies have shown that patients with multiple-drug allergy syndrome (MDAS) frequently have positive autologous serum skin test results, similar to patients with chronic urticaria (CU). Recent investigations have found that patients with CU show signs of thrombin generation and activation of the tissue factor pathway of the coagulation cascade. To study thrombin generation and fibrinolysis in patients with MDAS. Nine patients with MDAS underwent autologous plasma skin testing (APST) and measurement of plasma prothrombin fragment F(1 + 2) and D-dimer levels. Furthermore, the basophil histamine-releasing activity of plasma from patients with MDAS was evaluated. Plasma samples from 74 healthy control subjects and 13 patients with CU were used as negative and positive controls, respectively. All 9 patients with MDAS had positive APST results, and 7 showed elevated plasma levels of fragment F(1 + 2). In patients with MDAS, the median F(1 + 2) level (339 pmol/L; interquartile range [IQR], 250-401 pmol/L) significantly exceeded that in healthy controls (159 pmol/L; IQR, 123-196 pmol/L) (P = .001) but did not significantly differ from that in controls with CU (292 pmol/L; IQR, 182-564 pmol/L; P = .38). Plasma D-dimer levels were normal in all the patients with MDAS and were significantly lower than in controls with CU (P = .009). Finally, the histamine-releasing activity of plasma from patients with MDAS was significantly increased and correlated with F(1+ 2) levels (r = 0.68; P = .04). Positive APST results and thrombin generation indicate a common physiopathologic background in MDAS and CU. The lower D-dimer levels suggest that fibrinolysis occurs less intensely in MDAS than in CU.
    Annals of allergy, asthma & immunology: official publication of the American College of Allergy, Asthma, & Immunology 02/2008; 100(1):44-8. · 3.45 Impact Factor
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    ABSTRACT: In patients with chronic urticaria (CU), plasma shows signs of thrombin generation and autologous plasma skin tests score positive in as many as 95% of cases. To evaluate the initiators of blood coagulation that lead to thrombin generation and fibrinolysis in CU. Activated factor VII, activated factor XII, fragment F(1+2), and D-dimer plasma levels were measured in 37 patients with CU and 37 controls. Skin specimens from 10 patients with CU and 10 controls were tested for tissue factor immunohistochemically. Mean F(1+2) levels were higher in patients than controls (2.54 [SD 2.57] nmol/L vs 0.87 [0.26] nmol/L; P < .001); disease activity was moderate or severe in 9 of 11 (82%) and 9 of 26 (35%) patients showing high or normal F(1+2) levels, respectively (P < .025). Mean D-dimer plasma levels were higher in patients than controls (329 [188] ng/mL vs 236 [81] ng/mL; P < .01); disease activity was moderate or severe in 6 of 8 (75%) and 11 of 29 (38%) showing elevated or normal plasma D-dimer levels (P = NS). Factor VIIa levels were higher in patients than controls (2.86 ng/mL [0.66] vs 1.97 ng/mL [0.65]; P < .001). Activated factor VII and F(1+2) levels were correlated (r = 0.529; P = .008). Tissue factor reactivity was observed only in CU skin specimens. The extrinsic pathway of clotting cascade is activated in CU. Disease severity is associated with the activation of the coagulation cascade. The involvement of the coagulation pathway in CU opens new perspectives for a better understanding of the pathogenesis and, possibly, for the treatment of this disease.
    Journal of Allergy and Clinical Immunology 04/2007; 119(3):705-10. · 12.05 Impact Factor
  • Molecular Immunology - MOL IMMUNOL. 01/2007; 44(16):3969-3970.
  • Journal of Allergy and Clinical Immunology - J ALLERG CLIN IMMUNOL. 01/2007; 119(1).
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    ABSTRACT: Background: Patients with inflammatory bowel disease (IBD) have an increased prevalence of thromboembolic events. The pathogenetic mechanisms of these events include reduced fibrinolysis, which may be caused by antibodies to tissue-type plasminogen activator (t-PA). Objectives: To evaluate anti-t-PA antibodies in patients with IBD, considering clinical, biochemical and functional characteristics. Patients and methods: We immunoenzymatically measured anti-t-PA antibodies in plasma from 97 consecutive IBD patients and 97 ageand sex-matched healthy controls. We also assessed the antibody interactions with different epitopes of t-PA, the antibody inhibition on t-PA activity and the correlations with clinical features and other serum antibodies. Results: IBD patients had higher median anti-t-PA antibody levels (5.4 U/mL vs. 4.0 U/mL; P Keywords: antibodies; inflammatory bowel disease; tissue type plasminogen activa Document Type: Research Article DOI: http://dx.doi.org/10.1111/j.1538-7836.2006.00201.x Affiliations: 1: Department of Internal Medicine, University of Milan, IRCCS Fondazione Ospedale Policlinico, Mangiagalli and Regina Elena, Milan, Italy 2: Gastroenterology and Gastrointestinal Endoscopy Service, IRCCS Fondazione Ospedale Policlinico, Mangiagalli and Regina Elena, University of Milan, Milan, Italy 3: Gastroenterology and Gastrointestinal Endoscopy Unit, Istituto Policlinico San Donato, San Donato Milanese, Milan, Italy Publication date: October 1, 2006 $(document).ready(function() { var shortdescription = $(".originaldescription").text().replace(/\\&/g, '&').replace(/\\, '<').replace(/\\>/g, '>').replace(/\\t/g, ' ').replace(/\\n/g, ''); if (shortdescription.length > 350){ shortdescription = "" + shortdescription.substring(0,250) + "... more"; } $(".descriptionitem").prepend(shortdescription); $(".shortdescription a").click(function() { $(".shortdescription").hide(); $(".originaldescription").slideDown(); return false; }); }); Related content In this: publication By this: publisher In this Subject: Allergy & Immunology By this author: Cugno, M. ; Saibeni, S. ; Ciscato, C. ; Vecchi, M. ; Boscolo Anzoletti, M. ; Griffini, S. ; de Franchis, R. GA_googleFillSlot("Horizontal_banner_bottom");
    Journal of Thrombosis and Haemostasis 01/2006; 4:90-90. · 6.08 Impact Factor
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    ABSTRACT: Rheumatoid arthritis (RA) is associated with increased cardiovascular risk and involvement of inflammation, coagulation and fibrinolysis. Treatment with infliximab, a tumour necrosis factor-alpha (TNF-alpha) blocking chimeric monoclonal antibody, induces a long-term reduction of inflammation and coagulation, but its effect on fibrinolysis is still unknown. We carried out an observational study investigating plasma biomarkers of inflammation and fibrinolysis in RA patients before and after 14 weeks of infliximab treatment given according to the therapeutic guidelines for RA. We studied 20 selected patients with active RA and without any other atherosclerosis risk factor as well as 40 healthy controls. Patients, treated with a stable dose of methotrexate, received infliximab (3 mg/kg) at week 0, 2, 6 and 14. At week 0 and 14, we assessed clinical, inflammatory and fibrinolyitic parameters. At baseline, plasminogen activator inhibitor (PAI-1) antigen, PAI-1 activity and tissue-type plasminogen activator (t-PA) antigen were significantly higher in RA patients than in controls (p=0.01, p=0.001 and p=0.0001 respectively). After 14 weeks of infliximab treatment, the levels of PAI-1 antigen, PAI-1 activity and t-PA antigen significantly decreased till normalization (p=0.0001). Plasma levels of C reactive protein (CRP) and interleukin-6 (IL-6) were directly correlated with levels of PAI-1 antigen (p=0.011 and p=0.0001), PAI-1 activity (p=0.013 and p=0.027) and t-PA antigen (p=0.017 and p=0.040). This study provides evidence that TNF-alpha blockade by infliximab not only decreases inflammation, but also reduces the inhibition of fibrinolysis. Such a combined effect may be pivotal in reducing the whole thrombotic risk in these patients.
    Clinical and experimental rheumatology 28(2):254-7. · 2.66 Impact Factor