A collaborative study of nutritional anemia in third trimester pregnancy was performed in seven Latin American countries. Laboratory measurements included hemoglobin level, mean corpuscular hemoglobin concentration (MCHC), serum iron and iron-binding capacity, serum folate, vitamin B12 and albumin. Iron deficiency (transferrin saturation below 15%) was found in 48% of pregnant women, as compared with 21% of nonpregnant females and 3% of male controls of comparable age. The prevalence of folate deficiency (serum folate below 3 ng/ml.) was 10%, 10% and 9% in these three groups, respectively. Vitamin B12 deficiency (serum level below 80 pg/ml.) was found in 15% of pregnant women, but in less than 1% of both control groups. Anemia, as defined by current WHO criteria, was found in 38.5% of pregnant women, 17.3% of nonpregnant women and 3.9% of men. Analysis of the frequency distribution for hemoglobin levels, based on a Gaussian distribution in normal subjects, suggested that a large portion of subjects considered anemic by WHO criteria were normal and that the true incidence of anemia in pregnant and nonpregnant females was 22 and 12% respectively. Correlation analysis indicated that iron deficiency was of major importance as a cause of anemia, while folate lack was contributory only in pregnancy; no relationship could be demonstrated between vitamin B12 deficiency and anemia.

Foram estudados 17 casos de ancilostomose e determinados alguns parâmetros hematológicos como: dosagem de hemoglobina, do ferro sérico e da transferrina, contagem de hemácias, hematócrito, volume corpuscular médio (VCM) e hemoglobina corpuscular média (HCM). O estudo incluiu também a obtenção de alguns dados eritrocinéticos, como a determinação da velocidade de decaimento do ferro plasmático (T1V2 do 59Fe) e da incorporação do ferro à hemoglobina. O estudo radioisotópico permitiu ainda determinar o volume de sangue e a quantidade de hemoglobina perdida nas fezes, bem como o teor de ferro reabsorvido dessa hemoglobina. Estabeleceram também o grau de infecção através da contagem de ovos e de vermes nas fezes. Os doentes não apresentaram evidente alteração nutricional. A carência de ferro foi o fator comum a todos os casos que exibiram anemia, constituindo a base fisiopatológica da anemia ancilostomótica. O verme fixado à mucosa duodenal suga o sangue do hospedeiro e esta espoliação de sangue a longo prazo provoca a anemia. O volume de sangue perdido é geralmente proporcional ao grau de infecção, mas a quantidade de hemoglobina perdida mostrou ser independente do volume de sangue espoliado. A reabsorção de grande parte do ferro da hemoglobina perdida na luz intestinal concorre para que a anemia se estabeleça mais tardiamente que em outras hemorragias como a vaginal. Os indivíduos anêmicos foram submetidos a transfusões de sangue e com isso apresentaram melhora clínica e laboratorial, imediata mas temporária. A cura clínica foi estabelecida somente após tratamento adequado com vermífugos.

3 patients with renal transplantation who developed polycythemia presented normalization of the hemoglobin levels immediately after nephrectomy of the native kidneys. This observation induced the authors to study the role of the native kidneys in the genesis of polycythemia in recipients of renal allografts. Comparison was made among 32 patients submitted to renal transplantation, with maintenance of native kidneys (group I) and among 31 under the same conditions, but without the native kidneys (group II). Both groups were comparable according to age, sex, rejection crisis incidence and immunosuppressive therapy. It was observed that the hemoglobin levels of group I were significantly higher (p < 0.05 to p < 0.005) than those observed in group II, from the 3rd to the 30th posttransplantation month, becoming comparable from the 36th to the 54th months. The hemoglobin production, measured by the kinetics of labeled iron (⁵⁹Fe), was higher in patients of group I. The authors concluded that the native kidneys are responsible for the observed polycythemia after a kidney transplantation.

INTRODUÇÃOA anemia ancilostomótica é uma anemia ferropriva que se instala de modo insidioso tem um organismo parasitado, e geralmente é decorrente de várias reinfecções. Esta é a conseqüência natural do meio ambiente em que vivem os indivíduos de baixa classe sócio-econômica e da zona rural. A anemia desenvolve-se lenta e progressivamente, embora a espoliação de sangue ocorra diariamente e em quantidades até consideráveis.Isto assim se estabelece porque parte do ferro da hemoglobina perdida pela hemorragia é reabsorvida e reaproveitada para a formação de novas hemácias 5,9,13 .Sem esta reabsorção, certamente a anemia seria mais grave e a sua instalação mais rápida, o que obrigaria o indivíduo a procurar o auxílio médico mais precocemente. Desse modo, até que os estoques de ferro do organismo sejam depletados, os doentes portadores de grande parasitose conseguem manter-se por período de tempo relativamente longo sem exibir qualquer sintomatologia.Para demonstrar este importante aspecto da patogenia da anemia ancilostomótica, propusemo-nos a efetuar o presente trabalho.O estudo foi realizado através da

Ferrokinetic studies were made in 16 patients before and after kidney transplantation. The Fe clearance decreased in 9 of 11 patients, the plasma iron turnover showed no variation in six patients, while it increased in three and decreased in one, the production of hemoglobin increased significantly after transplantation. The nonnephrectomized patients showed more erythropoiesis after transplantation, manifested by higher hemoglobin level, shorter Fe clearance, and lower serum iron. Uremic patients, including the anephric, had significant responses in erythropoiesis both to stimulation by phlebotomy and to inhibition by blood transfusion. After transplantation, however, the response to phlebotomy was greater and the blockade by blood transfusion smaller, than during uremia.

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