RESUMEN
Five cases of megakaryoblastic leukemia, presenting as "de novo" acute leukemias are reported. They represented 7.2% of all cases of adult acute non-lymphoblastic leukemias (ANLL) seen in our Hematology Service during the past 30 months. These cases showed features of predominantly blast proliferation with a marked increase of reticulin fibres in the bone marrow. One case had features of acute leukemia with trilineage myelodysplasia and one had a more chronic evolution with splenomegaly initially resembling a myeloproliferative syndrome. In all cases, the definitive diagnosis was made on bone marrow histology as cytology was poor and the blast cells were positive for factor VIII with the immunoperoxidase technique. The importance of bone marrow histology is emphasized.
RESUMEN
The kidney is involved in virtually all individuals who inherit the sickle cell form of hemoglobin. Though asymptomatic and relatively common, proteinuria in patients with sickle cell anemia (SS) over 40 years old is associated with reduced creatinine clearance. The subclinical increase in urinary albumin is termed microalbuminuria and is a marker of preclinical glomerular damage. The aim of the present study was to determine the presence of microalbuminuria measured by radioimmunoassay in patients with sickle cell disease. The study included 41 patients with SS, 11 patients with hemoglobin SC disease, 4 subjects with S beta-thalassemia and 10 normal controls. All subjects were teenagers or adults. Sixteen SS patients (40%) and 1 SC (9%) and 1 S beta (25%) patient presented mean urinary albumin excretion (UAE) above normal values (30 mg/l. No correlation was observed between UAE and age, creatinine clearance, hemoglobin level or %HbF. These parameters, as well as the presence of leg ulcers, were not significantly different between SS patients with and without UAE above 30 mg/dl. The high prevalence of microalbuminuria in patients with sickle cell anemia indicates that glomerular damage is common. The connection between microalbuminuria and clinical nephropathy has been demonstrated in diabetes and may indicate a sign of early disease rather than a marker for susceptibility. Thus, microalbuminuria may be an early indicator of glomerular damage for patients with sickle cell disease.
Asunto(s)
Albuminuria/orina , Anemia de Células Falciformes/orina , Enfermedad de la Hemoglobina SC/orina , Talasemia/orina , Adolescente , Adulto , Albuminuria/etiología , Anemia de Células Falciformes/complicaciones , Femenino , Enfermedad de la Hemoglobina SC/complicaciones , Humanos , Masculino , Radioinmunoensayo , Talasemia/complicacionesRESUMEN
The kidney is involved in virtually all individuals who inherit the suckle cell form of hemoglobin. though asymptomatic and relatively common, proteinuria in patients with sickle cell anemia (SS) over 40 years old is associated with reduced creatinine clearance. The subclinical incrase in urinary albumin is termed microalbuminuria and is a marker of preclinical glomerular damage. The aim of the present study was to determine the presence of microalbuminuria measured by radioimmunoassay in patients with sickle cell disease. The study inclused 41 patients with SS, 11 patients with hemoglobin SC disease, 4 subjects with Sß-thalassemia and 10 normal controls. All subjects were teenagers or adults. Sixteen SS patients (40%) and 1 SC (9%) and 1 Sß (25%) patient presented mean urinary albumin excretion (UAE) above normal values (30 mg/l). No correlation was observed between UAE and age, creatinine clearance, hemoglobin level or %HbF. These parameters, as well as the presence of ulcers, were not significantly differente between SS patients with and without UAE above 30 mg/dl. The high prevalence of microalbuminuria in patient with sickle cell anemia indicates that glomerular damage is common. The connection between microalbuminuria and clinical neplhropathy has been demonstrated in diabetes and may indicate a sign of early disease rather than a marker for susceptibility. Thus, microalbuminuria may be an early indicator of flomerular damage for patients with sickle cell disease