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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.

Hematocrit,% Reticulocytes, % Erythrocyte porphobilinogen deaminase and uroporphyrinogen decarboxylase were measured as previously described (5, 6) by using porphobilinogen and pentacarboxylporphyrinogen I, respectively, as substrates. CV5 for these assays in this laboratory are 8.3% and 14.2%, respectively. rocytes,it is possible that detection of these diseases could be compromised when coexisting conditions or interventions stimulate erythropoiesis. It will be of interest, for example, to determine if erythrocyte uroporphyrinogen decarboxylase increases during therapeutic phlebotomy in patients with porphyria cutanea tarda. The intent of this therapy, which is effective in both inherited and acquired forms of porphyria cutanea tarda, is to stimulate erythropoiesis and thereby utilize and reduce iron stores. If phlebotomy does increase erythrocyte uroporphyrinogen decarboxylase, it might be recommended that the enzyme activity be measured before institution of phlebotomy.

In 26 patients with severe iron deficiency and microcytic anemia (MCV less than 70 fl), serial red cell size distribution histograms (erythrograms) were taken before and during iron therapy. Initially all patients had a single population of red cells, all microcytes. With the first reticulocytosis after iron therapy, a new population of cells appeared, larger in volume than the original. In 23 of 26 patients the new population of cells was of normal size (82–96 fl). In 3 of 26, the new population was macrocytic (MCV greater than 98 fl). Of these 3, 1 had folate deficiency; after folate was given, normocytes were produced. The other 2, both taking phenytoin and 1 a heavy alcohol using, had persistent macrocytosis despite folate administration. Erythrograms allowed quantitative, rapid evaluation of erythropoietic response to iron repletion. Abnormal macrocytic responses could be identified and seemed to occur with some frequency.

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.

New automated blood cell analyzers provide an index of red cell volume distribution width (RDW) or heterogeneity and a histogram display of red cell volume distribution. We have developed a classification of red cell disorders, based on mean corpuscular volume (MCV) or red cell size, heterogeneity, and histograms, to guide diagnosis from the peripheral blood analysis. The distinction of iron deficiency anemia from heterozygous thalassemia or the anemia of chronic disease and the detection of early iron and folate deficiency is improved. Red cell volume distribution histograms identify red cell fragmentation or agglutination, dimorphic populations, and artifactual counting of lymphocytes as red cells. We recommend the use of these new variables in the initial classification of anemia by the practicing physician.

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.

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.

To the Editor. —The message of the article by Hansen et al1and Howe's2accompanying editorial in the January issue of theArchivesis sobering. During the last decade, not only have electronic counters made the traditional red blood cell counts and indices more reliable for detecting iron deficiency and thalassemia3,4but new indices, such as the red blood cell distribution width (RDW), are now widely available. The RDW improves the distinction between iron deficiency and heterozygous thalassemia when mean corpuscular volume (MCV) is low5-7and between iron-deficient and normal subjects when MCV is normal.8However, in view of the data of Hansen et al, it is unlikely that physicians who do not use the long-established MCV will do much better with the additional information given by the RDW. We share the view that the diagnostic approach to microcytic anemias needs to be improved. Incidentally