RESUMEN
BACKGROUND: Brucellosis is a zoonotic disease transmittable to humans. It is diagnosed either by isolation of Brucella organism in culture of blood or other sample types (e.g., bone marrow or liver biopsy specimens), or by a combination of serological tests and clinical findings. Dialysis patients constitute a special population group with an impaired autoimmune system and a propensity to develop infections, such as brucellosis. This paper presents the high incidence of brucellosis in our dialysis patients during last year, while there was not any zoonotic infection recorded in the previous at least 5 year period. METHODS-RESULTS: This is a retrospective study including 8 dialysis patients, undergoing renal replacement therapies (5 patients were on hemodialysis (HD) and 3 on peritoneal dialysis (PD)), who out of a total of 124 patients developed brucellosis, during the last year. Four patients were male and four female and their mean age was 67 +/- 9 years. Clinical presentation of Brucellosis infection was mild with low-grade fever and symptoms of influenza. All patients were living in places where animal brucellosis was prevalent. Infection was diagnosed on the basis of clinical symptoms and signs and with polymerase chain reaction (PCR) analysis of peripheral blood. The affected patients had consumed fresh unpasteurized milk and cheese and were treated with oral doxycycline and oral rifampicin for 6 weeks. All patients are in follow up for at least 1 year, during which there were no relapses. CONCLUSIONS: Brucellosis is a zoonotic disease that can occur in dialysis patients who are susceptible to infection under certain conditions. Our brucellosis patients lived in agricultural and veterinary areas and had consumed unpasteurized milk and cheese and insufficiently cooked meat derived from infected animals.
Asunto(s)
Brucelosis/epidemiología , Fallo Renal Crónico/terapia , Diálisis Renal , Anciano , Antibacterianos/uso terapéutico , Brucella/aislamiento & purificación , Brucelosis/complicaciones , Brucelosis/tratamiento farmacológico , Doxiciclina/uso terapéutico , Femenino , Humanos , Incidencia , Fallo Renal Crónico/complicaciones , Masculino , Persona de Mediana Edad , Estudios Retrospectivos , Rifampin/uso terapéutico , Resultado del TratamientoRESUMEN
OBJECTIVES: To determine whether the fibrinolytic system is activated and coagulation inhibitors are utilized in sepsis, to compare the findings detected in sepsis with those found in severe sepsis and septic shock, and to compare the role played by different infectious pathogens on fibrinolysis and coagulation inhibitors. DESIGN AND SETTING: Prospective study comparing patients with sepsis, severe sepsis, and septic shock and healthy volunteers in the general intensive care unit of a tertiary university hospital. PATIENTS: Eighty-two consecutive septic patients (47 with sepsis, 18 with severe sepsis, and 17 with septic shock), and 14 healthy volunteers (controls). MEASUREMENTS AND RESULTS: After blood sampling we measured activation markers of fibrinolysis [plasmin/alpha(2)-antiplasmin complexes (PAP), complexes of tissue plasminogen activator/plasminogen activator inhibitor (tPA/PAI), fibrin(ogen) degradation products (FDPs), D-dimmers fibrin degradation products (D-d)], the utilization marker of antithrombin III (ATIII) thrombin/antithrombin complexes (TAT), several factors of fibrinolysis [plasminogen, tissue plasminogen activator (tPA), plasminogen activator inhibitor 1 (PAI-1), alpha(2)-antiplasmin], and the natural coagulation inhibitors [ATIII, protein C (PrC), protein S (PrS)]. In sepsis, PAP, FDPs, D-d, and TAT were increased to 439.8+/-32.35 microg/l, 57% positive, 49% positive, and 3.46+/-0.27 microg/l, respectively, compared with control subjects (205.57+/-28.58 microg/l, 0% positive, 7% positive, and 1.61+/-0.1 microg/l, respectively). These markers further increased in severe sepsis and septic shock. With the exception of a decrease in ATIII and an increase in tPA and PAI-1, coagulation inhibitors and factors of fibrinolysis were not changed in sepsis. In severe sepsis and mainly in septic shock, coagulation inhibitors (ATIII, PrC) and plasminogen were markedly decreased, whereas tPA and PAI-1 were further increased. All changes were independent of the causative infectious pathogen. CONCLUSIONS: Fibrinolysis is strongly activated and ATIII is utilized in sepsis. These findings are further enhanced in severe sepsis and septic shock. In sepsis only ATIII is decreased. In contrast, in severe sepsis and mainly in septic shock plasminogen and the main coagulation inhibitors (i.e., ATIII, PrC) are depleted, indicating exhaustion of fibrinolysis and coagulation inhibitors. Finally, Gram-positive, Gram-negative and other micro-organisms produce identical impairment.
Asunto(s)
Inhibidores de Factor de Coagulación Sanguínea/sangre , Fibrinólisis/inmunología , Sepsis/sangre , Choque Séptico/sangre , Adolescente , Adulto , Anciano , Anciano de 80 o más Años , Análisis de Varianza , Biomarcadores , Estudios de Casos y Controles , Femenino , Humanos , Masculino , Persona de Mediana Edad , Estudios Prospectivos , Sepsis/inmunología , Choque Séptico/inmunologíaRESUMEN
OBJECTIVE: To test the hypothesis that the coagulation system and platelets are activated in sepsis, the uncomplicated and usually earliest stage of the septic process, and to compare the findings detected in sepsis with those found in severe sepsis and septic shock. DESIGN: Prospective study comparing patients with sepsis, severe sepsis, and septic shock, and healthy volunteers. SETTING: General intensive care unit in a tertiary university hospital. PATIENTS: Seventy-four consecutive septic patients (45 with sepsis, 15 with severe sepsis, and 14 with septic shock). Fourteen healthy volunteers served as control subjects. INTERVENTION: None. MEASUREMENTS AND MAIN RESULTS: After blood sampling, molecular activation markers of coagulation (prothrombin fragments 1 and 2, fibrinopeptide A, thrombin-antithrombin complexes, and monomers of fibrin) and of platelets (beta-thromboglobulin and platelet factor 4), several coagulation factors, global tests of coagulation (prothrombin time and activated partial thromboplastin time), and platelet count (PTL) were measured. In sepsis, prothrombin fragments 1 and 2, fibrinopeptide A, thrombin-antithrombin complexes, and monomers of fibrin were increased to 2.52+/-0.21 nmol/L, 20.88+/-2.52 ng/mL, 33.8+/-2.9 microg/L, and 69% positive, respectively, compared with control subjects (0.86+/-063 nmol/L, 1.14+/-0.15 ng/mL, 16.07+/-1.01 microg/L, and 0%, respectively). Beta-Thromboglobulin and the beta-thromboglobulin-to-platelet factor 4 ratio were also increased to 107.87+/-11.87 IU/mL and 8.86+/-1.06, compared with controls (18.36 +/-2.99 IU/mL and 2.67+/-0.52, respectively). With the exception of a decrease in factor XII and an increase in fibrinogen, coagulation factors, global coagulation tests, and PTL were not changed in sepsis. In severe sepsis and mainly in septic shock, coagulation factors were markedly decreased, global coagulation tests were prolonged, and PTL was reduced. All changes were independent of the causative infectious pathogen. CONCLUSION: Coagulation system and platelets are strongly activated in sepsis. In this stage, only factor XII is decreased. In contrast, in severe sepsis and mainly in septic shock, most of the coagulation factors are depleted, PTL is decreased, and global coagulation tests are prolonged, indicating exhaustion of hemostasis. Finally, Gram-positive, Gram-negative, and other microorganisms produce identical impairment of coagulation.
Asunto(s)
Trastornos de la Coagulación Sanguínea/sangre , Trastornos de la Coagulación Sanguínea/microbiología , Activación Plaquetaria , Sepsis/sangre , Sepsis/complicaciones , Choque Séptico/sangre , Choque Séptico/complicaciones , Adolescente , Adulto , Anciano , Antitrombina III/metabolismo , Biomarcadores/sangre , Pruebas de Coagulación Sanguínea , Estudios de Casos y Controles , Femenino , Fibrinopéptido A/metabolismo , Humanos , Masculino , Persona de Mediana Edad , Fragmentos de Péptidos/sangre , Fragmentos de Péptidos/metabolismo , Péptido Hidrolasas/metabolismo , Recuento de Plaquetas , Estudios Prospectivos , Precursores de Proteínas/sangre , Precursores de Proteínas/metabolismo , Protrombina/metabolismo , Sepsis/microbiología , Índice de Severidad de la Enfermedad , Choque Séptico/microbiologíaRESUMEN
The aim of this prospective study was to determine whether treatment with a combination of GM-CSF and erythropoietin (rhEpo) can improve the anemia associated with low risk myelodysplastic syndrome (MDS), namely refractory anemia (RA), RA with ring sideroblasts (RAS), and RA with excess of blasts (RAEB) with bone marrow blasts less than 10%. Eligibility criteria included an Hb level of less than 10.5 g/dl for newly diagnosed patients, or symptomatic anemia. GM-CSF was given at a dose of 3 microg/kg s.c. on days 1-2, rhEpo at a dose of 60 U/kg s.c. on days 3-5. No treatment was given on days 6-7. Patients were followed-up with full blood count on a weekly basis. The treatment was repeated for a total of 6 weeks. At that time, if a rise in Hb above 1.5 g/dl had not been achieved, the dose of rhEpo increased to 120 U/kg. Post-treatment evaluation was performed at the completion of 12 weeks. Erythroid response was defined as good (GR), if an increase in untransfused Hb values above 2 g/dl or a 100% decrease in red blood cell transfusion requirements, over the treatment period was observed, while an increase in untransfused Hb values 1-2 g/dl or a >50% decrease in transfusion requirements, were considered as partial response. Responders continued to receive the same treatment until disease progression. Nineteen patients (13 male and six female) with a median age of 69 years were enrolled in the study. The FAB subtypes were: RA one case, RAS eight cases and RAEB 10 cases. Ten of 19 patients (52.6%) responded to the treatment: 7/19 (36.8%) achieved a GR and 3/19 (15.8%) a PR. Six of eight (75%) patients with RAS, one case with RA and 3/10 (30%) of cases with RAEB responded to treatment. Pretreatment serum epo levels were generally low (less than 200 Mu/ml) in responding patients. At the completion of the initial 12 weeks, 8/12 responding patients (5 RAS, 2 RAEB and 1 RA) continued to receive the same treatment. All responding patients with RAS continued to show an erythroid response in a time period from 3 to 24 months, whilst one patient with RA and two with RAEB did not have a continuing response at 2, 4 and 12 months, respectively. The above data suggest that the combination of rhEpo and GM-CSF should be recommended in all cases with RARS. However, the clear indication of this combination for other patients with MDS remains to be determined.