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1.
J Infect Chemother ; 16(1): 42-4, 2010 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-20054602

RESUMEN

Many hematological abnormalities, such as pancytopenia, anemia, and leukocytosis, can be associated with tuberculosis (TB). Immune thrombocytopenic purpura (ITP) is an extremely rare event in TB. We report a 46-year-old male patient who was admitted to hospital with a history of weight loss, combined with hemoptysis, fever, cough, sputum, general malaise, and night sweats. Physical examination revealed a body temperature of 38.8 °C, and petechiae distributed over the lower extremities. Laboratory findings were as follows: erythrocyte sedimentation rate, 84 mm/h; white blood cells, 7070/mm3; hemoglobin, 11.7 g/dl; and platelet count, 4000/mm3. On Ziehl-Neelsen stain of sputum, acid-fast bacilli were observed. Antituberculosis therapy was started, together with prednisolone, 0.5 mg/kg per day, from the day of admission. He was treated successfully with the steroid and antituberculous drugs.


Asunto(s)
Púrpura Trombocitopénica Idiopática/complicaciones , Tuberculosis Pulmonar/complicaciones , Antiinflamatorios/uso terapéutico , Antituberculosos/uso terapéutico , Humanos , Masculino , Persona de Mediana Edad , Prednisolona/uso terapéutico , Púrpura Trombocitopénica Idiopática/tratamiento farmacológico , Tuberculosis Pulmonar/tratamiento farmacológico
2.
Med Sci Monit ; 15(11): CR583-7, 2009 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-19865058

RESUMEN

BACKGROUND: Anemia is a common finding in dialysis patients. Recent evidence has accrued that hepcidin, an iron regulatory peptide, may play a crucial role in the pathophysiology of this condition. This study investigated the effect of erythropoietin (EPO) therapy on serum levels of prohepcidin, the pro-hormone of hepcidin, in patients with end-stage renal disease (ESRD) undergoing chronic dialysis treatment. MATERIAL/METHODS: A total of 40 ESRD patients with renal anemia receiving either hemodialysis or peritoneal dialysis were included in this study. The patients were randomly allocated to EPO (subcutaneous 2000 microg three times weekly) plus parenteral iron (n=23) or parental iron only (n=17). Serum prohepcidin levels were measured before and at the end of the study. RESULTS: The two groups were comparable in their demographic and laboratory characteristics. No significant differences were found in hemoglobin, hematocrit, iron store indices, or serum levels of prohepcidin at study entry. Significant increases in both hemoglobin and hematocrit as well as a decrease in serum prohepcidin level were evident in the EPO group at the end of the 6-month follow-up in comparison with their values at study entry compared with the control group (P<0.01). CONCLUSIONS: It is concluded that EPO therapy, besides enhancing erythropoiesis, modulates serum prohepcidin levels in dialysis patients.


Asunto(s)
Péptidos Catiónicos Antimicrobianos/sangre , Eritropoyetina/uso terapéutico , Precursores de Proteínas/sangre , Diálisis Renal , Femenino , Estudios de Seguimiento , Hepcidinas , Humanos , Infusiones Parenterales , Hierro/administración & dosificación , Hierro/uso terapéutico , Fallo Renal Crónico/sangre , Fallo Renal Crónico/tratamiento farmacológico , Masculino , Persona de Mediana Edad , Proteínas Recombinantes , Factores de Tiempo
3.
Blood Coagul Fibrinolysis ; 19(3): 243-6, 2008 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-18388507

RESUMEN

We report on a 43-year-old female patient with multiple thrombotic risk factors who, in a few months, developed acute myocardial infarction, an ischemic cerebrovascular event and variceal bleeding due to portal vein thrombosis. The factor V Leiden mutation was carried in heterozygous form, homocysteine was elevated at 19.6 micromol/l, and methylenetetrahydrofolate reductase C677T mutation was carried in homozygous form. Moderately increased plasma homocysteine level and a reduced protein S activity were evident. Anticardiolipin IgG antibodies were mildly positive. We conclude that the presence of multiple genetic and environmental risk factors greatly amplifies the risk of clinical thrombotic events.


Asunto(s)
Factor V/efectos adversos , Predisposición Genética a la Enfermedad/genética , Metilenotetrahidrofolato Reductasa (NADPH2)/genética , Trombofilia/fisiopatología , Trombosis de la Vena/fisiopatología , Adulto , Femenino , Humanos , Infarto del Miocardio/etiología , Vena Porta/fisiopatología , Accidente Cerebrovascular/etiología , Trombofilia/genética , Trombosis de la Vena/etiología , Trombosis de la Vena/genética
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