Search

Unstimulated whole saliva was collected from 21 HIV-positive men and women before and after dental treatment. The frequency of HIV detection did not increase after dental treatment. Infectious HIV was recovered from only one patient. Study findings raise the possibility that, in most cases, salivary inhibitors render the virus non-infectious.

In four patients with cold agglutinins, erythrocyte mean corpuscular volume was increased. Erythrocyte volume histograms showed that in each case macrocytosis was due entirely to doublet erythrocytes counted as single cells. For two of the four patients, macrocytosis was reported intermittently, when the blood had been allowed to cool to room temperature during laboratory processing. For these two patients, macrocytosis due to doublet erythrocytes could be elicited in vitro proportionate to the degree of cooling of the blood and could be abolished to rewarming to 37 C. Two other patients had macrocytosis constantly during the acute illness. Otherwise unexplained macrocytosis may reflect cold agglutinin activity without overt hemolysis, particularly if the macrocytosis is intermittent.

We measured the complete blood cell count, including the index of RBC size heterogeneity (RBC distribution width [RDW]), in 181 subjects without anemia to determine whether RDW became abnormal earlier in the development of iron deficiency than did other variables. In 163 subjects selected only for otherwise normal blood cell counts, an increased RDW was 66% specific (48/73) and 100% sensitive (48/48) for decreased serum iron saturation. Stool guaiac testing was equally specific but less sensitive. In 13 subjects with polycythemia, as iron deficiency developed, RDW increased a minimum of four weeks before mean cell volume changed. In one apparently normal young woman, an abrupt isolated rise in RDW revealed a newly developed low serum transferrin saturation; all values remained normal during serial testing of four other normal subjects. We conclude that RDW is the part of the routine blood cell count that first becomes abnormal during the development of iron deficiency.

Sixteen adults with chronic acquired aplastic anemia had abnormally large RBCs and abnormally small platelets before chemotherapy. During their therapy, transfusion initially obscured these macrocytic RBCs. In the eight who had erythropoietic recovery, endogenous RBCs again were macrocytic, and platelets remained small whether or not the platelet count increased. The percentage of cells containing hemoglobin F changed in only one of the eight subjects. In contrast, the eight who did not have erythropoietic recovery had no reappearance of macrocytes. Of 19 other previously treated patients whose hemoglobin level had recovered to normal for seven to 196 months, 16 had increased mean corpuscular volume (101 to 133 femtoliters) and abnormally small platelets. We conclude that in aplastic anemia the appearance of macrocytes reliably and easily predicts RBC recovery. Furthermore, even in treated, apparently recovered subjects, an abnormality of blood cell size remains.

To permit quantitative study of red cell volume heterogeneity, the coefficient of variation (CV) of erythrocyte volume was determined in blood samples from 868 subjects, including normal individuals and those with various hematologic disorders. In groups of subjects with various hemoglobinopathies, CV increased above normal in parallel with the presence and degree of anemia. However, all subjects with iron, folate, or vitamin B12 deficiency showed marked increase in CV (anisocytosis): increased CV accompanied even early iron deficiency not yet associated anemia or microcytosis. Effects of other conditions on CV also were studied.

We measured whole-blood mean platelet volume (MPV) and platelet count, determined by the Coulter Counter model S-Plus, in 683 normal subjects. There was nonlinear, inverse relation between MPV and platelet count throughout the normal range of platelet count: the change in MPV was most pronounced at the lower platelet counts. Because of this non-linear relation, "platelet-crit," the product of platelet count and MPV, was not constant, but varied directly with platelet count. Thus, the definition of "normal" values for MPV requires simultaneous reference to platelet count. In the whole blood of 13 patients, non-platelet cell fragments spuriously increased the automated platelet count. Seven patients with erythrocyte fragmentation had spuriously high MPV also: correct MPV and platelet count could be obtained from platelet rich plasma (PRP). In five patients with leukemic blast fragmentation, MPV remained spuriously low and platelet count spuriously high in PRP: only phase count allowed correct count. A patient with megakaryoblastic leukemia had megakaryoblast fragments confused for platelets.

Coefficient of variation (C.V.) of red cell volume is inversely proportional to red cell mass in hemoglobinopathies and thalassemias. Even a subject with markedly reduced red cell survival and abnormal hemoglobin had a normal C.V. associated with normal hemoglobin level. In contrast are patients with nutritional deficiency, who have increased C.V. whether or not there is anemia, and patients with hypoplastic anemia, who have normal to near-normal C.V. independent of anemia.