Leukopenia

LEUKOPENIA (leukopenia), a decrease in the number of leukocytes in the blood; this decrease is sometimes called hypoleukocytosis. One usually speaks of leukopenia when there are fewer than 6,000 leukocytes in 1 mm³ of peripheral blood. In rare pathological cases, the number of leukocytes in the blood may drop to 1,000 and even to a few hundred in 1 mm³. There may be a uniform decrease in all types of leukocytes, but more often one particular form decreases. Depending on which form of leukocyte is decreased, one speaks of neutropenia, lymphocytopenia, or eosinopenia. The decrease in the number of monocytes has been studied little; the decrease in the number of basophils usually has no clinical significance. Sometimes, when the total number of leukocytes decreases, there is a relative, and even absolute, increase in the number of lymphocytes (lymphocytosis) and monocytes (monocytosis). The mechanism of the origin of leukopenia differs in different pathological and physiological processes. Leukopenia may be apparent as a result of the redistribution of leukocytes, and real as a result of insufficient formation of leukocytes or increased destruction of the latter. Both factors—the decreased leukopoiesis and the increased leukocytolysis—may play a role simultaneously in the origin of leukopenia. To apparent leukopenia, caused by the redistribution of leukocytes from the periphery to internal organs, one should include leukopenia that often precedes leukocytoses of various origins, for example, digestive leukocytosis after the injection of foreign protein, bacterial toxins. _l One should also include the temporary decrease in leukocytes during the so-called hemoclasic crisis (Widal), observed in some patients after the ingestion of 200 g of milk. Some authors explained this temporary decrease in the number of leukocytes by the destruction of leukocytes (Lowit, Kryukov, etc.); but it has long been proven that during this leukopenic phase one can observe a significant increase in the number of leukocytes in the capillaries of internal organs (Chistovich, Verigo, Goldscheider and Jakob). It was previously thought that this redistribution of leukocytes was caused by negative chemotaxis. In reality, however, it is apparently caused by changes in the vegetative regulation of the vascular system (for more on this, see Leukocytoses, redistribution leukocytosis). Leukopenia due to insufficient formation of leukocytes is observed in some infectious diseases, namely: typhoid fever, influenza, rubella, measles, acute poliomyelitis, protozoal diseases (leishmaniasis, malaria), dengue fever, Papatacci fieber, and often in Malta fever. In typhoid fever, leukopenia is observed from the middle of the first stage to the third stage; the number of leukocytes usually drops to 3–4 thousand. In influenza and rubella, leukopenia is usually observed at the beginning of the disease; in measles—at the height of the disease, especially on the 1st_g and 2nd day of the rash, and in malaria—at the very end of the attack, in the intervals between attacks, and during chronic course. In all these diseases, leukopenia is characterized by neutropenia with an increase in the number of segmented neutrophils, relative, rarely absolute, lymphocytosis; in protozoal diseases (especially malaria), in addition, there is monocytosis. The origin of leukopenia in all the above infectious diseases is connected with their causative agents or, more correctly, with their bacterial toxins _T which inhibit the leukopoietic function of the bone marrow; as a result of this inhibition, there is insufficient production of leukocytes. Thus, there are certain bacterial toxins that lead to the inhibition of the leukopoietic function of the bone marrow. But other bacterial toxins, which usually cause leukocytosis, can cause leukopenia in the case if, under the influence of a large dose of these toxins, the increased regeneration of the bone marrow is replaced by suppression of function. Such leukopenia is observed, for example, in severe lobar pneumonia, severe peritonitis, and other severe purulent processes, miliary tuberculosis, some septic diseases, and severe cholera. Leukopenia in these diseases is usually characterized by relative neutrophilia and lymphocytopenia. In some septic processes, especially those accompanied by necrotic local changes (for example, necrotic angina), the number of leukocytes in the blood may drop to a few hundred in 1 mm³; in this case, neutrophilic polymorphonuclears almost completely disappear, which is why one speaks in these cases of agranulocytosis. Leukopenia due to insufficient formation of leukocytes also occurs in anemia, especially malignant anemia, in myelosis, especially in so-called Banti's disease, in starvation, and sometimes in Basedow's disease. Insufficient production of leukocytes can result not only on a functional basis, but also on an anatomical basis of damage to the hematopoietic tissue. Such leukopenias are those due to anatomical damage to the lymphatic glands in disseminated tuberculosis of the latter, due to the destruction of hematopoietic tissue as a result of long-term exposure to X-rays and radium, and due to necrotic changes in myeloid tissue as a result of septic processes. Leukopenia due to increased destruction of leukocytes can be caused by long-term exposure to X-rays, radium, arsenical preparations, and benzene, which can occur in occupational poisonings. The influence of these factors is limited at first to the destruction of leukocytes in the blood, then the hematopoietic tissue itself, leukopoiesis, is affected, and then the exclusion of globulicidal agents no longer stops the further increase of leukopenia. In diagnostic terms, leukopenia can be used only in conjunction with the general clinical picture of the disease; in this case, it is necessary to pay attention not only to the decrease in the number of leukocytes, but also to the ratio of individual forms. As examples, one can point out that leukopenia with a clearly expressed monocytosis can be significant for the diagnosis of chronic malaria and so-called Banti's disease; leukopenia with lymphocytosis—for typhoid fever and malignant anemia; leukopenia with increasing lymphocytopenia—for miliary tuberculosis (Mathes). And in terms of prognosis, leukopenia can be used with caution only in conjunction with the general clinical picture. It was mentioned above that there are infections that usually run with leukopenia; but even in these infections, a very strong drop in the number of leukocytes (for example, in typhoid fever to 1,000 in 1 mm³) is one of the symptoms of the severity of the infection. The drop in the number of leukocytes is an even worse prognostic symptom in those diseases that usually run with hyperleukocytosis (for example, lobar pneumonia, purulent processes); in this case, a poor prognosis is often indicated by a sharp drop in the number of lymphocytes and sharply expressed nuclear shifts (hyperregenerative, or so-called degenerative) of neutrophils (see Leukocyte formula of blood). But one should not forget that leukopenia reflects the functional state only of the hematopoietic tissue, mostly the bone marrow, the reaction of which is determined not only by the severity of the infection (virulence of the causative agents, their quantity), but also by the individual peculiarities of the given organism.