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Biomedical subjects

H A Pearson

Publications and source records attributed to H A Pearson.

At least 91 records · Page 5Linked to original sources
PubMed1980

Fever in young children with sickle cell disease.

Bacterial septicemia and meningitis are major causes of death in young children with sickle cell anemia. We report a prospective study of 182 episodes of fever among 22 children with sickle cell diseases identified at birth. The majority of patients with fever exceeding 39.5 degrees C were treated with antibiotics intravenously until results of blood cultures were known. Infectious diseases were documented in 38% of all febrile events. Six episodes of bacterial septicemia, two associated with meningitis, were successfully treated with no mortality or residual morbidity. These data form the basis of suggestions for management of the young child with sickle cell disease and fever.

Anemia, Sickle Cell↗
PubMed1979

Accuracy of cord blood screening for sickle hemoglobinopathies. Three- to five-year follow-up.

The strategic advantages of neonatal diagnosis of sickle hemoglobinopathies depend on an accurate cord blood screening procedure. One hundred thirty-eight black children in whom a range of normal and abnormal hemoglobin genotypes was identified by agar gel and cellulose acetate hemoglobin electrophoresis at birth were retested by cellulose acetate three to five years later. The original cord blood diagnoses were verified in all 138, including all 26 with major sickle syndromes (SS, S-beta thalassemia, and SC). Cord blood hemoglobin electrophoresis using these techniques permits accurate neonatal diagnosis of major and minor sickle hemoglobinopathies.

Anemia, Sickle Cell↗
PubMed1979

A new syndrome of refractory sideroblastic anemia with vacuolization of marrow precursors and exocrine pancreatic dysfunction.

In the past decade, we have studied four unrelated children with what we believe is a previously unreported disorder affecting the bone marrow and exocrine pancreas. During infancy these patients had the onset of severe, transfusion-dependent, macrocytic anemia plus a variable degree of neutropenia and thrombocytopenia. Their bone marrows had normal cellularity but were characterized by remarkable vacuolization of erythroid and myeloid precursors, hemosiderosis, and ringed sideroblasts. The vacuoles probably represented manifestations of cellular degeneration and death. In two patients, in vitro bone marrow cultures showed abnormal erythroid and myeloid progenitor cell growth and, in one child, abnormal vacuolated erythroid colonies. Family histories were unrevealing, parents were hematologically normal, and both sexes were involved. There was no evidence of specific nutritional deficiencies or exposure to agents associated with marrow vacuolization. A number of therapeutic interventions produced no effect. One child had clinical malabsorption. This child and one other had extensive pancreatic fibrosis at autopsy. The other two patients had findings indicating exocrine pancreatic dysfunction. Two children had splenic atrophy. This new syndrome, with associated bone marrow and exocrine pancreatic dysfunctions, differs in several respects from the syndrome of pancreatic liposis and neutropenia described by Shwachman et all and Bodian et al, and from other conditions with vacuolization of the marrow or sideroblastosis.

Anemia, Sideroblastic↗
PubMed1979

Antibody-mediated acquired sideroblastic anemia: response to cytotoxic therapy.

A 5 1/2-yr-old child developed severe anemia with erythroid hypoplasia and 50% ringed sideroblasts in his bone marrow. A serum inhibitor of erythropoiesis was demonstrated, utilizing syngeneic and autologous bone marrow in a plasma-clot culture system. The IgG fraction of the patient's serum effected similar suppression of erythroid colony formation. Prednisone therapy was ineffective, but following treatment with cyclophosphamide, normal erythropoiesis was established, ringed sideroblasts disappeared, and his serum no longer inhibited erythropoiesis in vitro. Cyclophosphamide was discontinued, and the patient has remained hematologically normal. This patient is an example of antibody-mediated sideroblastic anemia successfully treated with a cytotoxic drug.

Anemia, Sideroblastic↗
PubMed1978

Growth and development in children with sickle-cell trait. A prospective study of matched pairs.

To ascertain if sickle-cell trait (Hb AS) impairs physical growth and cognitive development, we prospectively investigated 50 matched pairs of black children. For each child with Hb AS, an Hb AA child was matched at birth for sex, birth date, birth weight, gestational age, five-minute Apgar score and socioeconomic status. Between the ages of three and five years, the members of each matched pair were evaluated, with one month of one another, by persons "blind" to the hemoglobin genotype. Twelve outcome measurements were obtained at evaluation: height, weight, head circumference, skin-fold thickness, cross-sectional area of arm muscle, bone age, five scores of the McCarthy Scales of Children's Abilities, and the Peabody Picture Vocabulary Test. There were no statistically significant differences in these measurements favoring the AA group. The results show that children with sickle-cell trait in this age group have no deficits in standard measurements of growth and development and emphasize the importance of rigorous methods when clinical groups are assembled and compared.

Anemia, Sickle Cell↗
PubMed1978

The born-again spleen. Return of splenic function after splenectomy for trauma.

We assessed splenic activity after splenectomy by interference phase microscopical examination of circulating red cells. Normal eusplenic children had a low number (less than 1 per cent) of red cells with surface indentations or "pits". About 20 per cent of red cells of children who had electively been subjected to splenectomy for hematologic indications were "pitted". Thriteen of 22 children who had had emergency splenectomy because of traumatic injury had a low percentage of "pitted" red cells, suggesting a return of splenic function. In five of these children a 99mTc sulfur colloid scan demonstrated multiple nodules of recurrent splenic tissue. In contrast to the prevailing opinion that splenosis is rare, we have found it to be a frequent occurrence. Return of splenic function may, in part, account for the low frequency with which overwhelming bacterial sepsis and meningitis have been documented after splenectomy for traumatic indications.

Adolescent↗
PubMed1978

Comparative effects of aspirin and acetaminophen on hemostasis.

Aspirin, even in small doses, has a profound and relatively long-lasting effect on platelet function and hemostasis. This usually produces few clinical problems. However, if a patient has an underlying hemostatic defect, undergoes surgery or sustains an injury, or is a newborn, severe hemorrhage is a potential risk. Aspirin is contraindicated in these clinical contexts. In contrast, acetaminophen has no effect on the hemostatic mechanism unless massive overdose results in hepatic necrosis with depression of synthesis of coagulation factors. Acetaminophen can be used when indicated in clinical situations where the use of aspirin may be potentially dangerous.

Acetaminophen↗
PubMed1977

Methotrexate hepatotoxicity in children with leukemia.

Percutaneous liver biopsy was performed on seven children with acute lymphocytic leukemia who had received maintanance chemotherapy with high-dose intravenous methotrexate for 1 1/2 to 2 1/2 years. Portal fibrosis was found in four of the seven children and in an additional patient treated with oral methotrexate. Serial tests of liver function and 99mtechnetium-sulfur-colloid scans did not accurately identify children with hepatic fibrosis. Clinical evidence of liver disease was not seen.

Adolescent↗