Monocytosis is a pathological condition in which there is an increase in the content of monocytes more than 1000 in 1 µl of blood. The causes are infectious, inflammatory, and oncohematological diseases. In children, infectious mononucleosis is the most common cause. There are no specific symptoms. The clinical picture is determined by the underlying pathology. The level of monocytes is examined in capillary or venous blood when calculating the leukocyte formula. To return monocytes to reference values (from 1 to 10%), the disease that served as a background for the occurrence of monocytosis is treated.
There are no clear digital divisions of monocytosis. Conditionally distinguish between moderate and severe monocytosis. According to the pathogenetic mechanism, there are:
From the moment of birth, a slight increase in monocytes is observed in children, it reaches a maximum by the end of 1 week of life (up to 15%), then slowly decreases and by the 12th month it becomes like in adults.
Despite the wide variety of pathological causes, most often monocytosis indicates recovery after an acute infectious disease. As a rule, it is mainly observed in children. An increase in the level of monocytes after infection means that the infectious agent has been completely eliminated. Monocytosis is usually mild and may persist for up to 2 weeks, after which monocyte levels return to normal.
Monocytes are the first line of defense against infection. Migrating into tissues, they turn into mononuclear phagocytes (macrophages). When a microorganism (bacteria, virus) penetrates, macrophages absorb it (phagocytize), and also present foreign pathogen antigens on their surface for recognition by T- and B-lymphocytes. In addition, macrophages secrete a wide range of different mediators and cytokines, causing neutrophil chemotaxis to the focus of infectious inflammation. Often, viral infections, in addition to monocytosis, also become the cause of an increase in lymphocytes (lymphomonocytosis).
Monocytosis is characteristic of chronic bacterial infections accompanied by epithelioid cell proliferation with the formation of granulomas. First of all, they include tuberculosis, brucellosis, syphilis. Monocytosis also occurs in subacute bacterial endocarditis, rickettsiosis. The pathogenesis of an increase in the content of monocytes in the blood in these diseases is somewhat different from that of viral infections.
The cause is believed to be inefficient phagocytosis. Macrophages, having absorbed bacteria, are not able to destroy them inside themselves, since many of these bacteria are resistant to the destructive action of lysosomal macrophage enzymes. As a result, they act as a refuge for bacteria, protecting them from other immune cells, and, allowing them to multiply, participate in the formation of the granuloma. By releasing cytokines, macrophages stimulate the formation of new monocytes in the bone marrow, providing bacteria with new "shelters".
Thus, the chronic course of the disease is maintained. The increase in the concentration of monocytes is moderate, due to the chronic course of the pathology, it can persist for months, years, drops to normal numbers only after etiotropic treatment. Scarlet fever is recognized as the only acute bacterial infection that causes monocytosis in children.
Monocytosis often occurs against the background of infectious diseases
Chronic non-infectious systemic inflammatory diseases are also accompanied by monocytosis, the development mechanism of which is as follows. For unknown reasons, a cell-mediated immune response is triggered. Macrophages (tissue monocytes), along with lymphocytes and mast cells, begin to accumulate in various organs, gradually forming giant cell granulomas. By secreting interleukins, cytokines, and other mediators, macrophages maintain chronic inflammation.
In adults, the cause is sarcoidosis, Langerhans cell histiocytosis, Wegener's granulomatosis. Of the systemic granulomatous pathologies in children, inflammatory bowel diseases (ulcerative colitis, Crohn's disease) are more common. Moderate monocytosis, but somewhat higher than in bacterial and viral infections, decreases under the influence of pathogenetic treatment.
The causes of monocytosis in collagenoses are not exactly known. There is a theory that under the influence of autoantibodies to various components of the connective tissue and cytokines, bone marrow maturation of monocytes is stimulated. The role of monocytes in the induction and maintenance of chronic inflammation has also been studied. The cause of monocytosis in adults is systemic lupus erythematosus, systemic scleroderma, in children, dermato- and polymyositis is mainly observed. The degree of monocytosis correlates with the activity of the disease, during remission it is within the reference values.
A fairly common cause of monocytosis are oncohematological diseases. The mechanism for increasing the number of monocytes is the tumor transformation of bone marrow stem cells. Monocytosis is very high, cells can account for more than 50% of the total number of leukocytes. Monocytosis persists for a long time, decreasing only after treatment with chemotherapy drugs or bone marrow transplantation.
For adults, chronic myeloid leukemia is more common. In children, the causes of monocytosis are often lymphogranulomatosis (Hodgkin's lymphoma), acute monoblastic (monocytic) leukemia. In addition to quantitative changes, in acute leukemia, there is such a phenomenon as a leukemic failure, which implies the presence of only mature forms of leukocytes and a large number of blast cells, the absence of intermediate forms.
Another cause of monocytosis, often observed in children, is recognized as diseases accompanied by a decrease (mainly genetically determined) in the production of neutrophilic granulocytes - neutrophils - by the bone marrow. These include cyclic neutropenia, Kostman's syndrome (children's agranulocytosis), chronic neutropenia with a violation of the release of granulocytes from the bone marrow (myelocahexia). The exact mechanism of monocytosis in these pathologies is unknown. Moderate monocytosis is usually observed in combination with eosinophilia.
The level of monocytes is measured during the calculation of the leukocyte formula in a clinical blood test. The detection of monocytosis requires the advice of a medical specialist, preferably a general practitioner. The doctor must conduct a survey of the patient's complaints, collect anamnestic data, perform a general examination to identify signs of a particular disease. The obtained data serve as a support for the appointment of an additional examination to determine the cause of monocytosis:
Laboratory diagnosis of monocytosis
It is impossible to bring the level of monocytes to normal values directly. To do this, it is necessary to deal with the cause, i.e. treat the underlying pathology, against which monocytosis developed. If monocytosis is found in the blood of a person who has recently had an acute infectious disease, then treatment is not required. This is absolutely normal, the concentration of monocytes normalizes on its own after a few days. In the case of prolonged and, especially, high monocytosis, medical intervention is necessary:
There is a surgical method for the treatment of oncohematological diseases and some types of congenital neutropenia, which makes it possible to achieve complete recovery from the disease - this is a transplantation of donor hematopoietic stem cells. For this operation, it is necessary to perform HLA typing (a genetic test that determines histocompatibility antigens) in order to select a suitable donor. However, this method of treatment is resorted to as a last resort when conservative therapy is unsuccessful, as it is associated with a high risk of death.
Monocytosis itself is not an indicator of prognosis. The outcome is directly determined by the cause of monocytosis. For example, physiological monocytosis in children does not affect life expectancy in any way. Some chronic granulomatous diseases, in particular sarcoidosis, sometimes even without any treatment end in self-remission. Oncohematological pathologies and hereditary neutropenia in children, on the contrary, are characterized by an unfavorable prognosis and a high probability of death.