Inmunoterapia en el asma / Immunotherapy in asthma

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[The influence of the arterio-alveolar gradient of carbonic dioxide and of the real value of respiratory gas exchange on the estimation of alveolo-arterial gradient of oxygen]. / El influjo del gradiente arterio-alveolar de anhídrido carbónico y del valor real del intercambio gaseoso respiratorio en el cálculo del gradiente alveolo-arterial de oxígeno.

In 46 patients with diverse respiratory alterations, the alveolus-arterial gradient for oxygen (PA-aO2) was calculated from a simplified equation and from the complete equation of alveolar gas. In order to be able to apply the latter, the composition of expired air, ventilation, and capnogram was measured in each patient upon taking an arterial blood sample. These values are later used in determining the alveolar fraction of carbon dioxide (CO2) and thus, calculate the PA-aO2 from the complete equation for alveolar gas. The values for PA-aO2 estimated from this equation were greater than those derived from the simplified equation. With the latter, the PA-aO2 was underestimated in 36 percent of the patients with abnormal respiratory function. This underestimate is due to the fact that, in the simplified equation, both the possible variability of respiratory exchange (R) as well as increases in the arterio-alveolar gradient of CO2 (Pa-ACO2), as commonly found in patients with bronchopulmonary problems are taken into account. The high percentage of falsely normal gradients for O2 found in our study, we believe, may justify, at least in some cases, the calculation of PA-aO2 from the complete equation, and thus, the measurement of alveolar pressure for CO2 upon arterial blood sample extraction for gasometry.

[Sea-blue histiocyte syndrome (author's transl)]. / Síndrome del histiocito azul marino.

The literature published before October, 1977 on the so-called sea-blue histiocyte syndrome is reviewed. This is a new lipid thesaurismosis, and from a morphological point of view it is characterized by the appearance of large histiocytes in the organs of the reticuloendothelial system with numerous intracytoplasmic granules which take on a typical sea-blue or greenish color with Wright's or Giemsa stain. The exact nature of the accumulated substance has not yet been specifically determined, though it appears to be gluco- and/or phosphosphingolipid, essentially sphingomyelin. The specific biochemical alteration responsible for this chronic deposit has not been established, though a partial sphingomyelinase deficiency has been detected. Sea-blue histiocytes have been observed in two different situations, either as an acquired phenomenon or as a primary condition. Of the latter there have been sporadic cases and cases with a definite familial incidence. The clinical manifestations include enlargement of the liver and spleen, neurological symptoms, cirrhosis of the liver, hemorrhagic diathesis and purpura, chronic pneumopathies, eye or cutaneous disturbances, or no symptoms at all. The disease has a benign clinical course, and the prognosis is less favourable when clinical manifestations appear early in life. These cases have a greater tendency to develop neurological alterations. The final definition of the syndrome must await the clear identification of the accumulated material and the altered enzyme or metabolic pathway.

[Hematologic aspects of alcoholism (author's transl)]. / Aspectos hematológicos del alcoholismo.

Alcohol causes different hematologic alterations on each of the three bone marrow cellular series. Its effect on the red series leads to the appearance of megaloblastic disturbances, erythroblastic vacuolization, iron metabolism abnormalities, and hemolytic syndromes. Megaloblastic disturbances may arise as a consequence of folic acid or vitamin B12 deficiency or of a direct toxic effect of ethanol on the erythroblasts. Iron metabolism alterations include reversible sideroblastic anemia, and hemosiderosis. The three hemolytic syndromes related to the consumption of ethanol are: acanthocytosis, stomatocytosis, and Zieve's syndrome. Alcohol induces leukopenia and functional deffects of the leukocytes; these facts explain the frequent susceptibility of chronic alcoholics to infection. Ethanol may act upon the megakaryocytic series to produce reversible thrombopenia and various alterations in platelet function. Thus alcohol exerts toxic effects on bone marrow, which interfere with the proliferation, maturation, release and survival of the three cellular series, either directly or by means of complex mechanisms related to the metabolism of folic acid, vitamin B12, pyridoxine, or iron. Alcoholism should therefore be considered as a possible cause whenever an obscure hematological condition comes under scrutiny.