RESUMO
Acute mesenteric ischemia (AMI) is a rare condition that may be associated with a variety of congenital prothrombotic disorders (PDs). The purpose of this study was to assess the prevalence of these disorders in 28 AMI patients compared with 103 healthy individuals from the northeastern region of Turkey. They were screened for protein C, antithrombin III, and protein S deficiencies; and gene analysis was performed using the polymerase chain reaction. A PD was revealed in 16 (57%) patients and 33 (32%) controls (p = 0.020). Factor V Leiden (FVL), prothrombin G20210A mutation, and TT677 homozygous mutation of methylenetetrahydrofolate reductase was detected in 10 (36%) patients versus 16 (15%) controls (p = 0.035), 3 (11%) patients versus 10 (9%) controls (p = 1.00), and 1 (3%) patient versus no controls, respectively. Consistent with caucasian ethnic groups, there was high prevalence of PDs, especially FVL; and these abnormalities might be a significant predisposing factor in the pathogenesis of AMI.
Assuntos
Transtornos da Coagulação Sanguínea/diagnóstico , Transtornos da Coagulação Sanguínea/epidemiologia , Isquemia/epidemiologia , Veias Mesentéricas , Trombose/diagnóstico , Trombose/epidemiologia , Doença Aguda , Idoso , Idoso de 80 Anos ou mais , Antitrombina III/metabolismo , Transtornos da Coagulação Sanguínea/genética , Estudos de Casos e Controles , Ensaio de Imunoadsorção Enzimática , Fator V/genética , Feminino , Humanos , Masculino , Metilenotetra-Hidrofolato Redutase (NADPH2)/genética , Pessoa de Meia-Idade , Mutação , Reação em Cadeia da Polimerase , Prevalência , Deficiência de Proteína C/diagnóstico , Deficiência de Proteína C/epidemiologia , Deficiência de Proteína C/genética , Deficiência de Proteína S/diagnóstico , Deficiência de Proteína S/epidemiologia , Deficiência de Proteína S/genéticaRESUMO
Mesenteric vein thrombosis (MVT) is uncommon condition. The purpose of this study was to assess prevalence of prothrombotic disorders in these patients. Eleven patients with MVT were screened for protein C, protein S, and antithrombin III deficiencies. Gene analysis was performed by polymerase chain reaction. A prothrombotic disorder was detected in 9 (81.8%) patients. Factor V Leiden, methylenetetrahydrofolate reductase TT677, and prothrombin G20210A mutations were found in 2 (18.2%), 2 (18.2%), and 5 patients (45.4%), respectively. Protein S, protein C, and antithrombin III deficiencies were present in 1, 1, and 2 patients, respectively. Four patients (36.3%) had combined defects. Thus, prothrombotic disorders may have a causative role in the pathogenesis of MVT, and these patients must be screened for these disorders.
Assuntos
Transtornos da Coagulação Sanguínea/diagnóstico , Transtornos da Coagulação Sanguínea/epidemiologia , Veias Mesentéricas , Protrombina/genética , Trombose/diagnóstico , Trombose/epidemiologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Transtornos da Coagulação Sanguínea/genética , Fator V/genética , Feminino , Humanos , Metilenotetra-Hidrofolato Redutase (NADPH2)/genética , Pessoa de Meia-Idade , Prevalência , Deficiência de Proteína C/diagnóstico , Deficiência de Proteína C/epidemiologia , Deficiência de Proteína C/genética , Deficiência de Proteína S/diagnóstico , Deficiência de Proteína S/epidemiologia , Deficiência de Proteína S/genéticaRESUMO
BACKGROUND: The purpose of this study was to demonstrate the effect of oral nifedipine on maximal resting anal pressure (MRAP) in healthy volunteers and to evaluate its role in the treatment of chronic anal fissure (CAF). METHODS: MRAP was measured in 10 healthy volunteers and 10 patients with CAF before and after oral nifedipine (20 mg b.i.d.). Patients were assessed on the first visit and every fortnight for measurement of MRAP, pain scores, blood pressure, pulse rate, healing of the fissure and adverse effects. Treatments were continued until healing had occurred or for up to 8 weeks. RESULTS: MRAP values before and after nifedipine were 73.2 and 49.3 cm H2O, respectively, in healthy volunteers (p < 0.001). Nifedipine caused a reduction in mean MRAP from 105.2 to 74.0 cm H2O (p < 0.001) in patients with CAF. Pain scores were significantly reduced after 2 weeks of treatment with nifedipine (p < 0.001) and continued throughout the treatment period. At the end of the study 6 of the 10 patients treated with nifedipine were deemed to be healed (n = 5) or improved (n = 1). Headache occurred in 1 patient. CONCLUSION: We conclude that oral nifedipine is effective in reducing MRAP and should become the first-line treatment for CAF.
