Hyperplasia symptoms, treatment, description. Hyperplastic and inflammatory processes of the lymph nodes of the neck

hyperplasia; Old Greek ὑπερ- - super- + πλάσις - education, formation) - an increase in the number of structural elements of tissues through their excessive new formation.

Hyperplasia, which underlies hypertrophy, manifests itself in cell proliferation and the formation of new tissue structures. With rapidly occurring hyperplastic processes, a decrease in the volume of multiplying cellular elements is often observed. New formation of cells during hyperplasia, as well as their normal reproduction, is carried out by direct(amitotic) and indirect(mitotic) divisions. Studies conducted using an electron microscope have established that hyperplasia is not only the proliferation of cells, but also an increase in cytoplasmic ultrastructures (primarily mitochondria, myofilaments, endoplasmic reticulum, ribosomes change). In these cases they talk about intracellular hyperplasia - regeneration.

The term proliferation is also used for cell reproduction.

Pathological physiology

Hyperplasia can develop as a result of a wide variety of influences on tissue that stimulate cell reproduction: disorders of the nervous regulation of metabolic and growth processes, disruption of the correlation of connections in the system of internal secretion organs, increased function of a particular organ (tissue) under the influence of specific tissue growth stimulants, for example, tissue decay products , blastomogenic and carcinogenic substances and many others.

An example of hyperplasia can be the increased proliferation of the mammary gland epithelium during pregnancy and the epithelium of the uterine glands in the premenstrual period. Glandular hyperplasia includes adenomatous polyps of the mucous membrane of the nose, stomach, intestines, uterus, etc.; regenerative hyperplastic processes of myeloid tissue and lymphoid tissue, developing in severe anemia and certain infections - sometimes in such cases, regenerative growths of hematopoietic tissue occur outside the bone marrow, for example in the liver, spleen, lymph nodes (extramedullary hematopoiesis).

Hyperplastic processes in infectious diseases (malaria, relapsing fever, protracted septic endocarditis, tuberculosis, leishmaniasis) are especially pronounced in the spleen. Hyperplastic processes in reticular tissue (lymph nodes, spleen, bone marrow) underlie immunogenic antibody formation during antigenic irritation of any nature. Due to hyperplasia, tissue replacement sometimes occurs ( compensatory nature of hyperplasia), lost as a result of a pathological process, for example, hyperplasia of hematopoietic tissue after blood loss.

Hyperplastic processes are the cause of increased tissue hyperproduction. In some cases, hyperplasia leads to excessive neoplasms of atypical structure and to the development of tumors (for example, malignancy of polypous growths of the mucous membranes with chronic inflammation).

Pathological anatomy

Types of hyperplasia: physiological; pathological

Sources

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Synonyms

See what “Hyperplasia” is in other dictionaries: Hyperplasia...

Spelling dictionary-reference book HYPERPLASIA - (Greek hyper excessively and plasso I create, form), excessive new cell formation (R. Virchow). The process of G., i.e., numerical hypertrophy (see), comes down to cell reproduction and the formation of a whole series of new cell generations. When G.... ...

Great Medical Encyclopedia HYPERPLASIA, an increase in the number of cells in an organ or tissue, leading to an increase in their size. see also HYPERTROPHY...

Scientific and technical encyclopedic dictionary Noun, number of synonyms: 1 proliferation (16) ASIS Dictionary of Synonyms. V.N. Trishin. 2013…

Hyperplasia Synonym dictionary - an increase in the size of an organ or tissue due to an increase in the number of cells... Source: USE OF IODINE CASEIN TO PREVENT IODINE DEFICIENCY DISEASES AS A MEANS OF POPULATIONAL, GROUP AND INDIVIDUAL PREVENTION OF IODINE DEFICIENCY ...

Official terminology hyperplasia - An increase in tissue volume due to an increase in the number of cells, in contrast to hypertrophy, at a rapid pace of growth, a decrease in cell size occurs; G. normally occurs during the regeneration of damaged organs. [Arefyev V.A., Lisovenko L.A. Anglo... ...

Hyperplasia Technical Translator's Guide - an increase in the size of an organ or tissue due to an increase in the number of cells. Source …

Spelling dictionary-reference book Dictionary-reference book of terms of normative and technical documentation - English hyperplasie German Hyperplasie French hyperplasie see > …

I Hyperplasia (hyperplasia; Greek hyper + plasis formation, formation) an increase in the number of structural elements of a tissue or organ due to cell division. Develops as a result of various influences that stimulate cell reproduction... ... Medical encyclopedia

Lymphadenopathy- enlargement of lymph nodes in infectious, systemic non-tumor and oncological diseases or local inflammatory processes. During the inflammatory process in the orofacial region, the submandibular, parotid, lingual, preglottic, as well as superficial (later deep cervical) lymph nodes may enlarge.

Reactive lymph node hyperplasia- hyperplasia of lymphoid tissue of lymph nodes during an immune response. It develops in the lymph nodes that drain the inflammatory focus, and they increase in size to 2 cm or more and have a soft-elastic consistency. Types of reactive hyperplasia: follicular hyperplasia (B-zones), paracortical hyperplasia (T-zones), sinus-histiocytic hyperplasia (reactive sinus histiocytosis). In the practice of dentists, regional forms of hyperplasia of the cervical lymph nodes and inflammatory lesions of the latter in the presence of an infectious process in the oral cavity, dental system, organs and soft tissues of the neck are more common.

Special clinical and morphological variants of lymphadenopathy/hyperplasia: Castleman's disease (Morbus Castleman, angiofollicular hyperplasia), Rosai-Dorfman disease (sinus histiocytosis with massive lymphadenopathy); dermatopathic

sky lymphadenopathy (dermatopathic lymphadenitis).

Clinical and morphological classification of lymphadenitis: acute lymphadenitis, adenophlegmon; necrotizing lymphadenitis Kikuchi-Fujimoto; chronic lymphadenitis (nonspecific and specific), lymphadenitis/lymphadenopathy in viral, bacterial, mycotic and protozoal infections.

The introduction of pyogenic microorganisms into the lymph node can cause purulent melting of the node tissue with the involvement of perinodular tissue in the process (adenophlegmon). Concept "chronic lymphadenitis" has not yet been clearly defined. It is believed that its microscopic manifestations are primarily atrophy of lymphoid tissue and sclerosis.

Damage to the cervical lymph nodes in tuberculosis is a consequence of lymphogenous dissemination of mycobacteria from elements of the primary pulmonary tuberculosis complex or hematogenous dissemination (in hematogenous tuberculosis).

Damage to the cervical lymph nodes with syphilis, if the primary chancre is localized on the mucous membrane of the mouth or lips, it is typical for the submandibular lymph nodes. Typical morphological manifestations of syphilitic lymphadenitis are vasculitis and diffuse infiltration of all zones of the lymph node

plasma cells, hyperplasia of lymphoid follicles with a decrease in the number of lymphocytes in the paracortical zone, sinus histiocytosis, the appearance of epithelioid cells and Pirogov-Langhans cells in the pulpy cords.

Cat scratch disease (felinosis), caused by a bacterium of the genus Bartonella, characterized by follicular hyperplasia and proliferation of monocytoid B cells. Subsequently, in the accumulations of these cells, usually near the germinative center or subcapsular sinus, small foci of necrosis appear in which neutrophil granulocytes accumulate, which then disintegrate. These areas increase in size, the number of leukocytes increases, and histiocytes accumulate around the lesions. This leads to the formation of a characteristic picture abscess granulomatosis.

Lymphadenopathy in HIV infection(see chapter 7, 19). At the onset of the disease, due to follicular-paracortical hyperplasia, an increase in all groups of lymph nodes occurs (generalized lymphadenopathy as a manifestation of the hyperplastic stage of changes in lymphoid tissue). Morphological examination reveals thinning or destruction of the mantle of lymphoid follicles; the latter looks as if “moth-eaten” (due to the focal disappearance of lymphocytes); an increase in the number of plasma cells in the tissue of the lymph node, proliferation and swelling of the vascular endothelium are also possible. At the end of HIV infection (AIDS stage), atrophy of the lymph nodes is observed (involutive stage of changes in lymphoid tissue). As HIV infection progresses, the number of follicles decreases and the paracortical zone thins due to a decrease in the level of lymphocytes. Between the follicles the number of blast forms of lymphoid cells, plasma cells and macrophages increases. The development of histiocytosis of the sinuses and exposure of the reticular stroma are characteristic. Diffuse fibrosis often develops.

For practical gynecology, the processes of endometrial hyperplasia, which range from 15 to 40% and occupy second place after infectious pathology in the structure of all gynecological diseases, are a multifaceted and complex problem.

This is explained by their tendency to have a recurrent long-term course, the absence of specific symptoms, the difficulty of carrying out timely differential diagnosis and difficulties in choosing adequate treatment. Why is hyperplasia dangerous and what are its causes?

Endometrial hyperplasia - what is it?

Endometrial hyperplasia is a morphofunctional pathological condition of the uterine mucosa, consisting of diffuse or focal growth (proliferation) of glandular and stromal structures with predominant damage to the glandular component in the functional (superficial) layer, much less often in the basal layer of the endometrium. The thickness of the endometrium with hyperplasia exceeds the norm depending on the phase of the menstrual cycle - up to 2-4 mm in the early proliferation phase and up to 10-15 mm during the secretory phase.

In recent decades, there has been a steady increase in the number of pathological hyperplastic processes in the uterine mucosa, due to an increase in the average age of life of the female part of the population, an unfavorable environment, an increase in the number of somatic chronic diseases, many of which are to one degree or another associated with the hormonal system or have influence on her.

The frequency of pathology is 10-30% and depends on its form and age of women. It occurs in girls and women of childbearing age, but most often between 35 and 55 years of age, and according to some authors, in half of women who are in the late reproductive or menopausal period.

In recent years, there has been an increase in the number of cases of the disease. Moreover, this growth occurs in parallel with the increase in the number of diseases of uterine cancer, which ranks 4th among all malignant tumors in women, and 1st among malignant neoplasms of the genital organs.

Various forms of hyperplasia of the uterine mucosa - is it cancer or not?

Pathological changes in the endometrium are benign, but at the same time it is noted that against their background, malignant tumors develop much more often. Thus, simple endometrial hyperplasia without atypia in the absence of treatment accompanies uterine cancer in 1% of cases, with atypia - in 8-20%, complex atypical form - in 29-57%. The atypical form is considered a precancerous condition.

How is endometrial hyperplasia different from endometriosis?

If the first is localized only within the uterine mucosa, then it is a chronic progressive recurrent benign disease, which in its growth and spread resembles a malignant tumor.

The cells of endometrioid tissue are morphologically and functionally similar to endometrial cells, however, they grow into the wall of the uterus, spread and grow beyond it - in the fallopian tubes and ovaries. They can also affect neighboring organs (peritoneum, bladder, intestines) and be transported by blood flow (metastasize) to distant organs and tissues.

Causes of endometrial hyperplasia and its pathogenesis

Due to the presence of a specific receptor apparatus in the uterine mucosa, it is a tissue that is highly sensitive to changes in the endocrine status in the female body. The uterus is the “target organ” for the effects of sex hormones.

Periodic cyclic changes in the endometrium are caused by a balanced hormonal effect on the receptors of the nuclei and cytoplasm of cells. Menstruation occurs as a result of rejection of only the functional layer of the endometrium, and restoration of glandular structures occurs due to the proliferation of glands of the basal layer, which is not rejected.

Therefore, the occurrence of hormonal imbalance in a woman’s body can cause disruption of the differentiation and growth of endometrial cells, which leads to the development of their limited or widespread excessive growth, that is, local or diffuse endometrial hyperplasia develops.

Risk factors for the occurrence of pathological processes of cell proliferation in the endometrium are:

hypothalamic-pituitary syndrome or Itsenko-Cushing disease;
chronic;
the presence of hormonally active;
Tamoxifen therapy (an antitumor and antiestrogenic drug) and estrogen replacement therapy;
chronic inflammatory processes of the internal genital organs, frequent abortions and diagnostic curettages (occur in 45-60% of women with hyperplasia);
fasting and psycho-emotional stress conditions;
diseases of the thyroid gland, the hormones of which modulate the influence of female sex hormones (estrogens) at the cellular level;
violation of the metabolism of fats and carbohydrates, in particular diabetes mellitus and obesity;
pathology of the liver and biliary system, the result of which is a slowdown in the processes of estrogen utilization in the liver, which leads to hyperplastic processes in the uterine mucosa;
hypertonic disease;
postmenopausal period - due to increased hormonal activity of the adrenal cortex;
immune changes, which are especially pronounced in women with metabolic disorders.

Hormones play a major role in the development of endometrial tissue proliferation. Among them, the primary role belongs to estrogens, which, through their participation in the metabolic processes of cells, stimulate the division and growth of cells. At different periods of life, absolute or relative hyperestrogenism can be provoked by one or another of the above factors.

During puberty

Hyperplastic processes in this period are caused mainly by anovulation cycles, and they, in turn, are associated with a disorder in the activity of the hypothalamic-pituitary system. The latter is accompanied by unstable frequency and amplitude of GnRH (gonadotropin-releasing hormone) emissions that persist for a long time, which is the cause of inadequate secretion of follicle-stimulating hormone (FSH) by the pituitary gland.

The result of all this is premature (before reaching the stage that corresponds to ovulation) follicular atresia in many menstrual cycles. In this case, a relative excess of estrogen occurs (as a result of the monotony of its production) with the secretion of progesterone (deficiency), which does not correspond to the stages of the menstrual cycle, which causes defective growth of the endometrium. Predominantly glandular epithelium grows while the growth of the stromal component lags. Thus, adenomatous or cystic endometrial hyperplasia is formed.

During the reproductive period

Excessive levels of estrogen during the reproductive period can occur as a result of:

hypothalamic disorders, hyperprolactinemia, frequent stressful conditions, fasting, chronic somatic diseases, etc., leading to dysfunction of the hypothalamus-pituitary gland system;
disturbances in the hormonal feedback mechanism, as a result of which in the middle of the menstrual cycle the secretion of luteinizing hormone is not activated, which means there is no ovulation;
changes directly in the ovaries themselves with the growth of their stroma, ovarian polycystic disease, etc.

During the periods of premenopause and perimenopause

Cycles of non-ovulation are caused by age-related changes in the activity of the hypothalamic-pituitary system, resulting in changes in the intensity and frequency of GnRH release. According to these cycles, both the secretion of FSH by the pituitary gland and the effect of the latter on ovarian function change.

Insufficient estrogen levels in the middle of the menstrual cycle, which causes a decrease in stimulation of luteinizing hormone secretion, as well as depletion (by this age) of the ovarian follicular apparatus lead to anovulation. In postmenopausal women, the activity of the adrenal cortex increases, which also plays a role in the development of endometrial hyperplasia.

In addition, recent studies indicate the primacy of tissue resistance to insulin, which is caused by hereditary or immune factors, for example, insufficiency of insulin receptors in tissues, the presence of specific antibodies against insulin receptors or blockade of the latter by growth factors similar to insulin and inherited, etc.

These genetic and immune disorders can cause metabolic disorders (carbohydrate metabolism disorders and diabetes mellitus, male obesity, atherosclerosis, etc.), as well as functional and structural changes (hypertension, coronary heart disease, etc.). They are considered secondary to the tissues' inability to respond to the action of insulin, which automatically leads to increasing secretion of insulin in the body.

An increased concentration of insulin, acting on the corresponding ovarian receptors and growth factors, stimulates multiple follicles, causing the development of polycystic disease, excessive production of androgens in the cysts, which are transformed into estrogens. The latter cause a lack of ovulation and hyperplastic processes in the endometrium.

Along with this, the condition of the uterine hormonal receptors is also of no small importance, which is not least influenced by mechanical damage (abortion, curettage) and inflammatory processes. Due to a deficiency of receptors, very often hormonal treatment of endometrial hyperplasia (in 30%) is ineffective, since its sensitivity to hormonal drugs is insufficient.

An important role in the development of pathological proliferation is played not only by the intensification of the processes of proliferation of the endometrial cells themselves, but also by gene dysregulation of their apoptosis (programmed timely cell death).

Thus, the mechanism of proliferative processes in the uterine mucosa is determined by the complex interaction of many factors, both systemic (neurondocrine, metabolic, immune) and local (cellular receptor and genetic apparatus of the uterine mucosa) nature.

This mechanism is implemented mainly as a result of:

excessive influence of estrogens with insufficient counteraction of progesterone;
abnormal reaction of the glandular structures of the uterine mucosa in response to normal estrogen levels;
due to the high activity of insulin growth factors in insulin resistance, accompanied by high insulin concentrations (metabolic syndrome, type II diabetes mellitus, polycystic ovary syndrome).

Classification of endometrial hyperplasia

Pathomorphologically and cytologically, the following forms of hyperplasia are distinguished:

simple glandular - cystic expansion of the glands is mostly absent; if proliferative processes are pronounced, then cystic expansion is possible in some areas of the mucous membrane; this form, in this case, is called glandular-cystic and is a stage of a single process;
glandular-stromal, characterized by proliferation of both glandular and stromal structures; depending on the severity of this process, the glandular-stromal form is divided into active and resting; thickening of the endometrium occurs due to the superficial layer;
atypical, which is also called atypical glandular and adenomatous; This form is characterized by the severity of proliferative changes and a wide variety of morphological patterns.

Depending on the severity of changes of a proliferative and atypical nature, mild, moderate and severe degrees of the pathological condition are distinguished, and on its prevalence - diffuse and focal forms.

In 1994, the World Health Organization (WHO) proposed a classification that is generally followed today. However, in practical gynecology and oncology, the terminology of other authors is often used in parallel.

According to the WHO classification, endometrial proliferation can be:

Without cytologically detectable atypical cells (non-atypical).
With atypical cells (atypical).

The first, in turn, differs as:

Simple endometrial hyperplasia, which corresponds to the previously accepted term “glandular cystic hyperplasia”. In this form, the volume of the mucous membrane is increased, there is no atypia of cell nuclei, the structure of the endometrium differs from its normal state in the activity and uniform growth of the glandular and stromal components, the uniform distribution of vessels in the stroma, the uneven location of the glands and the moderate cystic expansion of some of them.
Complex or complex hyperplasia, or grade I. Corresponds to adenomatosis (in other classifications). In this form, proliferation of the glandular epithelium is combined with a change in the structure of the glands, in contrast to the previous form. The balance between the proliferation of glands and stroma is disturbed in favor of the former. The glands have a structurally irregular shape, and there is no cellular-nuclear atypia.

Atypical proliferation is divided into:

Simple, which corresponds (according to other classifications) to atypical hyperplasia of the second degree. It differs from the simple non-atypical form by the significant proliferation of glandular epithelium and the presence of atypical cells. Cellular and nuclear polymorphism is absent.
Atypical complex (complex), in which changes in the endometrium are of the same nature as in non-atypical, but, unlike the latter, atypical cells are present. Signs of their atypia are a violation of cell polarity, irregular stratification of the epithelium and its change in size, nuclear cell polymorphism, enlarged cell nuclei and their excessive staining, expanded cytoplasmic vacuoles.

In the WHO classification, local hyperplasia (single or multiple polyps) is not distinguished as an independent variant. This is explained by the fact that polyps (polypous hyperplasia is a term sometimes used by practitioners) are considered not as a variant of endometrial hyperplasia as a result of hormonal disorders, but as a variant of a productive process in chronic disease, which requires appropriate bacteriological examination and anti-inflammatory and antibacterial treatment.

Clinical picture

In the vast majority of cases, the main symptom in women of different ages is either/or bloody discharge from the genital tract. The nature of menstrual disorders does not depend on the severity of proliferative processes in the endometrium.

Menstrual irregularities are possible in the form of delayed menstruation for up to 1–3 months, which is subsequently replaced by bleeding or spotting (in 60–70% of women with endometrial hyperplasia). Somewhat less often, cyclic bleeding lasting more than 1 week, corresponding to menstrual days, is possible. They are more common among women who do not have metabolic disorders.

Menstruation with endometrial hyperplasia is usually long. Their intensity can vary - from moderate bleeding to heavy bleeding, with large blood loss (profuse). On average, in 25% of cases, bleeding occurs due to anovulatory menstrual cycles or absence of menstruation (in 5-10% of women with hyperplasia).

In menopausal women, menstruation is irregular, followed by ongoing bleeding or spotting. During menopause, short-term or long-term scanty discharge of blood is possible.

Other, less significant and uncharacteristic signs of uterine endometrial hyperplasia are pain in the lower abdomen and bleeding after sexual intercourse, heavy lifting, and long walking (contact bleeding).

In addition, there may be general complaints that are caused by both blood loss over a long period of time and metabolic and/or neuroendocrine disorders. These may be headaches, thirst, palpitations, high blood pressure, sleep disorders, decreased performance and fatigue, psycho-emotional instability, excessive weight gain, the appearance of pink stretch marks and pathological hair growth, development, psycho-emotional disorders, decreased quality of life.

A small percentage of patients have no symptoms. Pathological changes in their mucous membrane are detected during random examinations, sometimes not even related to gynecological diseases.

Hyperplasia and pregnancy

Is it possible to get pregnant if this pathology develops?

Considering the etiology and pathogenesis of the development of the pathological condition under consideration, it becomes clear that endometrial hyperplasia and pregnancy are practically incompatible. Infertility is associated not only with the fact that the altered mucous membrane does not allow the fertilized egg to implant. The reasons, predominantly hormonal in nature, that caused these pathological changes are also the causes of infertility.

Therefore, endometrial hyperplasia and IVF are also incompatible. However, a preliminary course of necessary treatment at the stage of preparation for pregnancy most often contributes to conception and successful resolution of pregnancy.

In some cases, when there is moderate hyperplasia, implantation of a fertilized egg is possible in a relatively healthy area of the uterine mucosa. But this usually leads to spontaneous abortion or fetal development disorders.

Endometrial hyperplasia after childbirth develops relatively rarely. However, its relapse is quite possible, even in the form of an atypical form. Recurrent endometrial hyperplasia, especially its atypical forms, is dangerous due to its tendency to transform into a malignant hyperplastic process. Therefore, in the postpartum period, it is necessary to be under the supervision of a gynecologist, conduct additional examinations and, if necessary, undergo a course of prescribed therapy.

Diagnostics

The diagnosis is made based on various methods, the results of which are specific to the corresponding age period.

Among the diagnostic methods, the main ones are:

Ultrasound examination using a transvaginal probe

According to various sources, its information content ranges from 78 to 99%. The thickness of the endometrium during hyperplasia in the secretory phase exceeds 15 ± 0.4 mm (up to 20.1 ± 0.4 mm); in the postmenopausal period, a thickness of more than 5 mm indicates a hyperplastic process. Exceeding the value of 20.1 ± 0.4 mm already raises suspicion of the possibility of adenocarcinoma. Other M-echo signs of hyperplasia are the heterogeneous structure of the uterine mucosa, inclusions similar to small cysts, or other ECHO-positive formations of varying sizes.

Separate diagnostic curettage of the mucous membrane of the cervix and uterine cavity

The study is most informative on the eve of menstruation. Further histological examination of the obtained material allows us to more accurately determine the nature of the morphological changes occurring. Cytological examination reveals the presence of cellular atypia. Indications for repeated curettage are recurrent bleeding in the postmenopausal period and monitoring the effectiveness of the course of hormonal treatment.

Hysteroscopy

Being a fairly informative technique (informativeness ranges from 63 to 97.3%), the study significantly increases the diagnostic value of separate curettage. It is advisable to carry it out on days 5-7 of the menstrual cycle. Hysteroscopy for endometrial hyperplasia makes it possible to differentiate the morphological forms of transformation of the uterine mucosa. Hysteroscopic signs are:

with simple hyperplasia - the thickness of the endometrium is more than 15 mm, its uneven surface with the presence of multiple folds of pale pink or, less often, bright red color, pronounced vascular pattern, uniform arrangement of the excretory ducts of the glands;
with cystic - folded bright red surface, increased thickness, unevenness of the vascular network, in the projection of superficial vessels - a large number of cysts.

Based on the most significant histological features lymphadenopathy, we have developed a classification of this heterogeneous group. This classification is somewhat arbitrary, since some lymphadenopathies have common features that can vary at different stages of the disease. Most often, a biopsy in patients with persistent lymphadenopathy is performed to exclude malignancy.

In such cases Properly taken, well-fixed whole lymph node biopsies are preferred because a number of reactive lymphadenopathy may closely resemble malignant lymphoma.

Follicular hyperplasia is probably the most common type of lymph node reaction, characterized by enlargement of follicles and expansion of reproductive centers. Often these changes are combined with the appearance of plasma cells in the brain cords and interfollicular parenchyma. Reactive follicular hyperplasia is usually associated with the entry of antibodies into the body that stimulate a B-cell response.

Using auxiliary Diagnostic methods make it possible to identify many pathogens. However, in the absence of evidence of infection by microorganisms and no specific histological features indicating an etiology, this reaction is called “nonspecific hyperplasia.” Such nonspecific reactions are more common in children and young people, and are also more often detected in nodes that collect lymph from sites of infection (such as the tonsils, skin and gastrointestinal tract).

In reactive lymphadenopathy, follicles retain a distinct mantle zone consisting of small lymphocytes; in the centers of reproduction, the polarization of centroblasts and centrocytes can be determined. They are usually distributed predominantly in the cortex of the ganglion and often have unequal shape and size. In the reactive centers of reproduction, a large number of mitotic figures and numerous apoptotic bodies are detected, which are often phagocytosed by “macrophages of colored bodies.”

Rheumatoid lymphadenopathy.

Lymphadenopathy in rheumatoid arthritis is not limited to the lymph nodes that collect lymph from the affected joints, but as a component of this systemic disease can often be generalized. Severe follicular hyperplasia develops. Enlarged reproductive centers may contain amorphous PHIK-positive hyaline inclusions; occasionally, follicular hyperplasia may be accompanied by the appearance of sarcoid-like granulomas.

Large quantities plasma cells, often with Russell bodies, infiltrate the medullary cords and can also be detected in the reproductive centers.

Complication of long-term intramuscular injections of drugs colloidal gold in the treatment of rheumatoid arthritis is “golden lymphadenopathy”. Changes in the lymph nodes are similar to those seen in rheumatoid lymphadenopathy.

Hearing the unfamiliar word “hyperplasia” in the doctor’s office should not fall into despair. It’s not so scary if you understand the cause of the disease and start treatment on time.

What is it and why did it appear?

Hyperplasia means that in any tissue of the body (not related to a tumor) or organ, the number of cells has increased and this has led to an increase in the volume of the formation or organ.

After such an explanation, it is reasonable to ask the reason for such changes. But it’s not easy to answer unequivocally, because there are many reasons. The stimulus for cell growth can be tissue growth stimulants, any antigenic stimulus, various oncogenic substances, or previous operations to remove an entire organ or part of it.

If we talk about the symptoms of physiological hyperplasia, then we will talk about the proliferation of the mammary gland epithelium that occurs during pregnancy. There is also such a thing as glandular hyperplasia, which occurs before the onset of menstruation. Only a doctor can understand all the intricacies, and our task is to give general concepts about the disease. Because although it refers to benign formations, there is still a possibility that the process of degeneration into a malignant form may begin.

If we talk about glandular hyperplasia, there are several types of proliferation - cell multiplication, causing tissue growth, which are determined by the degree of disturbance. For example, epithelial separation may have cytologic atypia or may not be found. They observe whether there is invasive growth - penetration of cells into surrounding tissues; with hyperplasia it is not observed.

When the thickness of the endometrium, the inner mucous layer of the uterus, increases, they speak of endometrial hyperplasia.

Anemia, some of its forms, can cause proliferation of the components of myeloid (blood-forming) tissue. Infectious diseases sometimes cause hyperplastic processes in the lymphoreticular tissue that makes up the lymph nodes and the spleen.

Between us women

Although the name of the disease is the same, common to all, nevertheless, it also has its own characteristics. Therefore, it is better to conduct the conversation in this direction.

The mucous membrane of a woman's uterus is called the endometrium. Hyperplasia and its growth are classified as benign processes. The endometrium enlarges monthly when, under the influence of estrogen, it prepares to receive a fertilized egg. In the absence of conception, excess endometrium is shed, which is expressed by menstrual bleeding. If the process is disrupted, the mucous membrane begins to grow stronger. The type of disease depends on how much the thickness of the endometrium has increased.

With glandular hyperplasia, the lumen between the endometrial glands is disrupted. But the tissue has a homogeneous structure, the thickness of the endometrium is no more than 1.5 cm.

If cysts are found among the tissues, then the diagnosis already sounds like glandular cystic hyperplasia.

The atypical form of the disease is characterized by a structural change in tissue, the mucous membrane grows up to 3 cm; this condition of the uterus is also called adenomatosis.

Focal hyperplasia means that polyps have formed in the endometrium in the form of separate foci. They are also divided into glandular, fibrous and adenomatous. In the focus of hyperplasia, the thickness of the endometrium can be up to 6 cm.

What is the risk of each type of disease? The danger in terms of degeneration into a malignant formation is represented by atypical and focal hyperplasia. As for glandular and cystic endometrial hyperplasia, doctors consider them benign and not prone to degeneration.

The first sign that endometrial hyperplasia may have appeared is a menstrual irregularity. Menstruation becomes painful and most often occurs as heavy bleeding. There is also amenorrhea - their absence for up to six months or more. In general, endometrial hyperplasia primarily indicates hormonal disorders, which can result in a number of other diseases, such as endometriosis, polycystic ovary syndrome, and infertility.

There are several treatment options for hyperplasia, it all depends on its type, how much the tissue has grown and how old the patient is. In reproductive age, treatment is conservative: therapy using hormonal drugs. With the right treatment, the growth of the endometrium stops. But if hyperplasia has reached a significant size or relapses, then you have to turn to surgeons.

This disease is often accompanied by endocrine disorders - diabetes, obesity. Women over 50 years of age, overweight and suffering from hypertension are susceptible to the disease.

And men suffer too

After the age of 50, about 85% of men come to a urologist with benign prostatic hyperplasia (adenoma). The disease indicates that a nodule or several have appeared in the prostate; they grow, compress the urethra and cause problems with urination. The more the cells grow, the more serious the problem becomes.

The cause of the disease is said to be hormonal changes, the so-called male menopause. But there is no exact data on how much sexual activity, sexual orientation, bad habits, and inflammatory diseases of the genital organs affect the appearance of adenoma.

Symptoms of hyperplasia in men primarily manifest themselves in the form of problems with urination - the bladder does not completely empty. Then everything becomes more complicated: a sluggish stream, frequent urges at night, and the abdominal muscles have to be very strained. Delaying a visit to the doctor can result in a number of troubles - chronic renal failure, urinary incontinence. And then complications follow in the form of cystitis, hematuria (blood in the urine), urolithiasis and a number of others.

If the process is not stopped and treatment is not started, the outcome can be quite sad: the urethra will be completely compressed. Only suprapubic puncture will help alleviate the patient’s condition.

Treatment of adenoma hyperplasia depends on the extent of the disease. Medicines can help only in the first stages, when the bladder is still completely emptied.

Non-operative methods, in particular the use of a catheter, are used when a man cannot be operated on for health reasons.

The most effective method of treating hyperplasia remains surgery. If the disease is not advanced, transuretal resection is proposed - the adenoma is removed through the urethra. This operation is more gentle than abdominal surgery.

In general, I would like to say that one article cannot cover all the nuances and symptoms of hyperplasia. The goal was to give general information about it, to show that a diagnosis made at an early stage gives every chance of a complete cure.

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