Thrombocytopenia and platelet dysfunction

The disorder of the blood system, in which circulating insufficient number of platelets - cells that provide hemostasis and play a key role in the process of blood coagulation, is defined as thrombocytopenia (ICD-10 code - D69.6).

Than the thrombocytopenia is dangerous? Reduced concentration of platelets (less than 150 thousand / μl) worsens coagulability of blood so that there is a threat of spontaneous bleeding with significant blood loss with the slightest damage to blood vessels.

Platelet diseases include an abnormal increase in platelet count (thrombocythemia in myeloproliferative diseases, thrombocytosis as a reactive phenomenon), a decrease in platelet counts - thrombocytopenia and platelet dysfunction. Any of these conditions, including a state with an increase in the level of platelets, can cause disruption of the formation of the hemostatic clot and bleeding.

Platelets are fragments of megakaryocytes that provide hemostasis of circulating blood. Thrombopoietin is synthesized by the liver in response to a decrease in the number of bone marrow megakaryocytes and circulating platelets and stimulates the bone marrow to the synthesis of platelets from megakaryocytes. Thrombocytes circulate in the bloodstream for 7-10 days. About 1/3 of the platelets are temporarily deposited in the spleen. Normally, the platelet count is 140,000-440,000 / μL. However, the number of platelets may vary slightly depending on the phase of the menstrual cycle, decrease in late gestation (gestational thrombocytopenia), and increase in response to inflammatory cytokines of the inflammatory process (secondary or reactive thrombocytosis). Eventually, the platelets are destroyed in the spleen.

Causes of thrombocytopenia

The causes of thrombocytopenia include impaired platelet production, increased platelet sequestration in the spleen with their normal survival, increased destruction or consumption of platelets, dilution of platelets and a combination of the above reasons. Increased sequestration of platelets in the spleen suggests the presence of splenomegaly.

The risk of developing bleeding is inversely proportional to the number of platelets. With a platelet count of less than 50,000 / μL, slight bleeding is easily caused and the risk of significant bleeding increases. At a platelet level between 20 000 and 50 000 / μL bleeding may occur, even with a slight injury; with a platelet count of less than 20 000 / μL spontaneous bleeding is possible; with a platelet count of less than 5000 / μL, the development of marked spontaneous bleeding is likely.

Platelet dysfunction can occur with an intracellular platelet abnormality defect or with an external effect damaging the function of normal platelets. Dysfunction can be congenital and acquired. Of congenital disorders, Willebrand's disease is most common and less intracellular platelet defects. Acquired violations of the function of platelets are often due to various diseases, the use of aspirin or other medications.

[1], [2], [3], [4], [5]

Other causes of thrombocytopenia

Platelet destruction can occur due to immune causes (HIV infection, medications, connective tissue diseases, lymphoproliferative diseases, blood transfusion) or as a result of non-immune causes (Gram-negative sepsis, acute respiratory distress syndrome). Clinical and laboratory signs are similar to those available with idiopathic thrombocytopenic purpura. Only a study of the medical history can confirm the diagnosis. Treatment is associated with the correction of the underlying disease.

Acute Respiratory Distress Syndrome

Patients with acute respiratory distress syndrome may develop non-immune thrombocytopenia, possibly due to the deposition of platelets in the capillary bed of the lungs.

[6], [7], [8], [9], [10]

Blood transfusion

Posttransfusion purpura is caused by immune destruction similar to ITP, except for having a history of blood transfusion in the period of 3 to 10 days. Patients mostly women with no platelet antigen (PLA-1), which is available in most people. Transfusions of PLA-1-positive platelets stimulate the production of PLA-1 antibodies that (the mechanism is unknown) can react with PLA-1 negative platelets of the patient. The result is severe thrombocytopenia, which occurs within 2-6 weeks.

[11], [12]

Connective tissue and lymphoproliferative diseases

Connective tissue (eg, SLE) and lymphoproliferative diseases can cause immune thrombocytopenia. Glucocorticoids and splenectomy are often effective.

[13], [14], [15], [16], [17], [18]

Drug-induced immune destruction

Quinidine, quinine, sulfonamides, carbamazepine, methyldopa, aspirin, oral antidiabetics, gold salts and rifampicin can cause thrombocytopenia, usually caused by an immune reaction, in which the drug binds to a platelet to form a new "foreign" antigen. This disease is indistinguishable from ITP, except for the history of taking the drug. When the medication is stopped, the amount of platelets rises within 7 days. Gold-induced thrombocytopenia is an exception, since gold salts can be found in the body for many weeks.

5% of patients receiving unfractionated heparin develop thrombocytopenia, which is possible even with the administration of very low doses of heparin (for example, when washing an arterial or venous catheter). The mechanism is usually immune. There may be bleeding, but more often platelets form aggregates that cause vessel occlusion with the development of paradoxical arterial and venous thromboses, sometimes life-threatening (eg, thrombotic occlusion of arterial vessels, stroke, acute myocardial infarction). Heparin should be abolished in all patients with developed thrombocytopenia or a decrease in the number of platelets by more than 50%. Since 5 days of heparin use is sufficient to treat venous thrombosis, and most patients start taking oral anticoagulants concomitantly with heparin, heparin can usually be safely discontinued. Low molecular weight heparin (LMWH) is less immunogenic than unfractionated heparin. However, LMWH is not used in heparin-induced thrombocytopenia, since most antibodies cross-react with LMWH.

[19], [20], [21]

Gram-negative sepsis

Gram-negative sepsis often causes non-immune thrombocytopenia, which corresponds to the severity of the infection. Caused thrombocytopenia can be many factors: disseminated intravascular coagulation, the formation of immune complexes that can interact with platelets, activation of complement and deposition of platelets on the damaged endothelial surface.

HIV infection

Patients infected with HIV can develop immune thrombocytopenia, similar to ITP, except for association with HIV. The number of platelets can be raised by the appointment of glucocorticoids, which are often abstained from use until the platelet count drops below 20,000 / μl, as these drugs can further reduce immunity. The number of platelets is also usually increased after the use of antiviral drugs.

Pathogenesis of thrombocytopenia

The pathogenesis of thrombocytopenia is found either in the pathology of the hematopoietic system and in the reduction of platelet production by myeloid bone marrow cells (megakaryocytes), or in disorders of hemodiereza and increased destruction of platelets (phagocytosis), or in sequential pathologies and platelet retention in the spleen.

In the bone marrow of healthy people, an average of 10 ¹¹ platelets are produced daily , but not all of them circulate in the systemic circulation: reserve platelets are stored in the spleen and released if necessary.

When a patient's examination does not reveal diseases that caused a decrease in platelet counts, a diagnosis of thrombocytopenia of an unknown genesis or idiopathic thrombocytopenia is made. But this does not mean that the pathology arose "just like that."

Thrombocytopenia, associated with a decrease in platelet production, develops with a lack of vitamins B12 and B9 (folic acid) and aplastic anemia in the body.

Combined with leukopenia and thrombocytopenia in the violation of bone marrow function associated with acute leukemia, lymphosarcoma, cancerous metastases from other organs. Suppression of platelet production may be due to changes in the structure of hematopoietic stem cells of the bone marrow (the so-called myelodysplastic syndrome), congenital hypoplasia of hematopoiesis (Fanconi syndrome), megakaryocytosis or bone marrow myelofibrosis.

Also read - Causes of thrombocytopenia

Symptoms of thrombocytopenia

Thrombocyte disorders lead to a typical pattern of bleeding in the form of multiple petechiae on the skin, usually more on the legs; scattered small ecchymoses in places of light injuries; bleeding of the mucous membranes (nasal bleeding, bleeding in the gastrointestinal tract and genitourinary tract, vaginal bleeding), marked bleeding after surgical interventions. Severe bleeding in the gastrointestinal tract and the central nervous system can be life threatening. However, manifestations of severe bleeding in the tissue (for example, deep visceral hematoma or hemarthrosis) are not typical for the pathology of platelets and suggest the presence of secondary hemostasis (for example, hemophilia).

Autoimmune thrombocytopenia

The pathogenesis of increased destruction of platelets is divided into immune and non-immune. And the most common is autoimmune thrombocytopenia. The list of immune pathologies in which it manifests itself includes: idiopathic thrombocytopenia (immune thrombocytopenic purpura or Verlhof disease ), systemic lupus erythematosus, Sharp or Sjogren's syndromes, antiphospholipid syndrome, etc. All these states are united by the fact that the body produces antibodies attacking its own healthy cells, including platelets.

It should be borne in mind that when the antibodies of a pregnant woman with immune thrombocytopenic purpura enter the fetal blood flow in a child in the neonatal period, transient thrombocytopenia is revealed.

According to some reports, antibodies against platelets (their membrane glycoproteins) can be detected in almost 60% of cases. Antibodies have immunoglobulin G (IgG), and as a result, platelets become more vulnerable to increased phagocytosis with splenic macrophages.

[22], [23], [24], [25], [26], [27], [28], [29], [30], [31]

Congenital thrombocytopenia

Many abnormalities and their result - chronic thrombocytopenia - have a genetic pathogenesis. Stimulates megakaryocytes, a protein synthesized in the liver, thrombopoietin encoded on chromosome 3p27, and is responsible for the effect of thrombopoietin on the specific receptor protein encoded by the C-MPL gene.

As expected, congenital thrombocytopenia (in particular, amygakaryocytic thrombocytopenia), as well as hereditary thrombocytopenia (with familial aplastic anemia, Wiskott-Aldrich Syndrome, Meia-Hegglin, etc.) is associated with a mutation of one of these genes. For example, the inherited mutant gene forms permanently activated thrombopoietin receptors, which causes hyperproduction of abnormal megakaryocytes incapable of forming a sufficient number of platelets.

The average life span of circulating platelets is 7-10 days, their cell cycle is regulated by the anti-apoptotic membrane protein BCL-XL, which is encoded by the BCL2L1 gene. In principle, the function of BCL-XL is to protect cells from damage and induced apoptosis (death), but it turned out that when the gene is mutated, it acts as an activator of apoptotic processes. Therefore, the destruction of platelets can occur faster than their formation.

But hereditary disaggregation thrombocytopenia, characteristic for hemorrhagic diathesis (Glanzman's thrombasthenia) and Bernard-Soulier syndrome, has a slightly different pathogenesis. Because of a gene defect, thrombocytopenia is observed in young children due to a disorder in the structure of platelets, which prevents them from "sticking together" to form a blood clot, which is necessary to stop bleeding. In addition, such inferior platelets are disposed of in an accelerated manner in the spleen.

[32], [33], [34], [35], [36],

Secondary thrombocytopenia

By the way, about the spleen. Splenomegaly - an increase in the size of the spleen - develops for various reasons (due to liver pathologies, infections, hemolytic anemia, hepatic vein obstruction, tumor cell infiltration in leukemia and lymphomas, etc.), and this leads to the fact that it can delayed to a third of the total platelet mass. As a result, there is a chronic disturbance of the blood system, which is diagnosed as symptomatic or secondary thrombocytopenia. With an increase in this organ in many cases, splenectomy is indicated for thrombocytopenia or, more simply, removal of the spleen with thrombocytopenia.

Chronic thrombocytopenia can also develop due to hypersplenic syndrome, which means hyperfunction of the spleen, as well as premature and too rapid destruction of blood cells by its phagocytes. Hyperplenism is secondary in nature and most often due to malaria, tuberculosis, rheumatoid arthritis or a tumor. So, in fact, secondary thrombocytopenia becomes a complication of these diseases.

Secondary thrombocytopenia is associated with a bacterial or systemic viral infection: the Epstein-Barr virus, HIV, cytomegavirus, parvovirus, hepatitis, varicella-zoster virus (causative agent of chicken pox), or rubivirus (causing measles rubella).

When exposed to the body (directly on the bone marrow and its myeloid cells) of ionizing radiation and the use of large amounts of alcohol, secondary acute thrombocytopenia may develop.

Thrombocytopenia in children

According to the research, in the second trimester of pregnancy the platelet count in the fetus exceeds 150 thousand / mkl. Thrombocytopenia in newborns is present after 1-5% of births, and severe thrombocytopenia (when platelets are less than 50 thousand / μL) occurs in 0.1-0.5% of cases. In this case, a significant proportion of infants with this pathology are born prematurely or placental insufficiency or hypoxia of the fetus took place. U15-20% of newborn thrombocytopenia are alloimmunic - as a result of receiving antibodies from the mother against platelets.

Other causes of thrombocytopenia, neonatologists consider genetic defects of bone marrow megakaryocytes, congenital autoimmune pathologies, the presence of infections, as well as the DIC syndrome (disseminated intravascular coagulation).

In most cases, thrombocytopenia in children older is symptomatic, and among the possible pathogens are fungi, bacteria and viruses, for example, cytomegalovirus, toxoplasma, rubella or measles virus. Especially often, acute thrombocytopenia occurs with fungal or gram negative bacterial infection.

Vaccinations in patients with thrombocytopenia are done with caution, and in severe forms of pathology, preventive vaccination by injection and cutaneous applications (with skin scarification) may be contraindicated.

For more details see - Thrombocytopenia in children, as well as - Thrombocytopenic purpura in children

Thrombocytopenia in pregnancy

Thrombocytopenia during pregnancy can have many causes. However, one must take into account that the average number of platelets during pregnancy decreases (up to 215 thousand / μl), and this is normal.

First, in pregnant women, the change in the number of platelets is associated with hypervolemia - a physiological increase in blood volume (an average of 45%). Secondly, platelet consumption during this period is increased, and the megakaryocytes of the bone marrow produce not only platelets, but also significantly more thromboxane A2, which is necessary for platelet aggregation during coagulation (coagulation) of blood.

In addition, the dimeric glycoprotein PDGF - platelet-derived growth factor, which regulates cell growth, division and differentiation, is also synthesized intensively in α-granules of platelets of pregnant women, and plays an important role in the formation of blood vessels (including the fetus).

As noted by midwives, asymptomatic thrombocytopenia is observed in about 5% of pregnancies with normal course of gestation; in 65-70% of cases there is a thrombocytopenia of an unknown genesis. 7.6% of pregnant women have a moderate degree of thrombocytopenia, and 15-21% of women with preeclampsia and gestosis develop severe thrombocytopenia during pregnancy.

Classification of thrombocytopenia

Cause	Conditions
Disruption of platelet production Reduction or absence of megakaryocytes in the bone marrow. Decreased platelet production, despite the presence of megakaryocytes in the bone marrow	Leukemia, aplastic anemia, paroxysmal nocturnal hemoglobinuria (in some patients), myelosuppressive medications. Alcohol-induced thrombocytopenia, thrombocytopenia in megaloblastic anemia, HIV-associated thrombocytopenia, myelodysplastic syndrome
Sequestration of platelets in the enlarged spleen	Cirrhosis with congestive splenomegaly, myelofibrosis with myeloid metaplasia, Gaucher's disease
Increased destruction of platelets or immune destruction of platelets	Idiopathic thrombocytopenic purpura, HIV-associated thrombocytopenia, posttransfusion purpura, drug-induced thrombocytopenia, neonatal alloimmune thrombocytopenia, connective tissue diseases, lymphoproliferative diseases
Destruction not caused by immune mechanisms	Disseminated intravascular coagulation, thrombotic thrombocytopenic purpura, hemolytic-uremic syndrome, thrombocytopenia in acute respiratory distress syndrome
Breeding	Massive blood transfusions or exchange transfusions (loss of platelet viability in stored blood)

[37], [38], [39], [40], [41]

Thrombocytopenia due to sequestration in the spleen

Increased sequestration of platelets in the spleen occurs with various diseases accompanied by splenomegaly. It appears in patients with congestive splenomegaly caused by far-reaching cirrhosis. The number of platelets is usually greater than 30,000 μl, until the disease causing splenomegaly leads to a disruption in platelet production (eg, myelofibrosis with myeloid metaplasia). Under stress, platelets are released from the spleen after exposure to adrenaline. Therefore, thrombocytopenia, caused only by the sequestration of platelets in the spleen, does not lead to increased bleeding. Splenectomy normalizes thrombocytopenia, but its conduct is not shown, until there is severe thrombocytopenia, additionally due to impaired hematopoiesis.

Drug thrombocytopenia

Drug-induced or drug-induced thrombocytopenia is due to the fact that many common pharmacological drugs can affect the blood system, and some can suppress the production of megakaryocytes in the bone marrow.

The list, including drugs that cause thrombocytopenia, is quite extensive, and included antibiotics and sulfonamides, analgesics and NSAIDs, thiazide diuretics and protieepileptic drugs based on valproic acid. Transient, i.e. Transient thrombocytopenia, may be caused by interferons, as well as proton pump inhibitors (used in the therapy of stomach and duodenal ulcers).

Thrombocytopenia after chemotherapy is also a side effect of antitumor drugs-cytostatics (methotrexate, carboplatin, etc.) due to their inhibition of the functions of the hematopoietic organs and myelotoxic effects on the bone marrow.

And heparin-induced thrombocytopenia develops because heparin is used to treat and prevent deep vein thrombosis and pulmonary embolism, it is an anticoagulant of direct action, that is, it reduces platelet aggregation and prevents blood clotting. The use of heparin induces an idiosyncratic autoimmune reaction that manifests itself in the activation of platelet factor-4 (a protein-cytokine PF4) that is released from the α-granules of activated platelets and binds to heparin to neutralize its effect on the endothelium of blood vessels.

[42], [43], [44], [45], [46], [47], [48], [49],

Degrees of thrombocytopenia

It should be remembered that the number of platelets from 150,000 / μL to 450,000 / μL is normal; and there are two pathologies associated with platelets: the present thrombocytopenia and thrombocytosis, in which the platelet count exceeds the physiological norm. Thrombocytosis has two forms: reactive and secondary thrombocythemia. The reactive form can develop after removal of the spleen.

The degree of thrombocytopenia varies from mild to severe. With a moderate degree, the level of circulating platelets is 100,000 / μL; at moderately severe - 50-100 thousand / mkl; at severe - below 50 thousand / mkl.
According to hematologists, the lower the level of thrombosis in the blood, the more severe the symptoms of thrombocytopenia. At an easy degree the pathology can show nothing, and at moderate on a skin (especially on legs or foots) there is an eruption at a thrombocytopenia are a dot hypodermic hemorrhage (petechia) of red or violet color.

If the number of platelets is below 10-20 thousand / μl. Spontaneous formation of hematomas (purpura), bleeding from the nose and gums.

Acute thrombocytopenia is often a consequence of infectious diseases and has a spontaneous resolution within two months. Chronic immune thrombocytopenia persists longer than six months, and often its specific cause remains unexplained (thrombocytopenia of an unknown genesis).

With an extremely severe degree of thrombocytopenia (with a platelet count of <5000 / μl.), Serious, fatal complications are possible: subarachnoid or intracerebral hemorrhages, gastrointestinal or other internal bleeding.

[50], [51], [52], [53], [54]

Diagnosis of thrombocytopenia

The pathology of platelets is suspected in patients with the presence of petechiae and bleeding of the mucous membranes. A general blood count is performed with platelet count, a study of hemostasis and a smear of peripheral blood. Increased number of platelets and thrombocytopenia are determined by counting the number of platelets; Coagulogram tests are usually normal, if there is no coagulopathy at the same time. At normal values of the general blood test, platelet count, MHO and normal or slightly elongated TTV, the presence of platelet dysfunction can be suspected.

In patients who have thrombocytopenia, a smear of peripheral blood may indicate a possible cause of it. If there are other abnormalities in the smear than thrombocytopenia, such as the presence of nucleated red blood cells and young leukocytes, bone marrow aspiration is indicated.

Peripheral blood with thrombocytopenic diseases

Blood changes	Conditions
Normal red blood cells and leukocytes	Idiopathic thrombocytopenic purpura, thrombocytopenia of pregnant women, HIV-associated thrombocytopenia, drug-induced thrombocytopenia, posttransfusion purpura
Fragmentation of erythrocytes	Thrombotic thrombocytopenic purpura, hemolytic-uremic syndrome, preeclampsia with ICE, metastatic carcinoma
Abnormal leukocytes	Immature cells or a large number of mature lymphocytes in leukemia. Low number of granulocytes in aplastic anemia. Hypersegmented granulocytes in megaloblastic anemia
Giant platelets (similar in size to erythrocytes)	Bernard-Soulier syndrome and other congenital thrombocytopenia
Erythrocyte anomalies, nucleated erythrocytes, immature granulocytes	Myelodysplasia

The study of bone marrow aspirate allows estimating the number and appearance of megakaryocytes, and can also determine other causes of bone marrow hemopoiesis deficiency. If there are no abnormalities in the myelogram, but there is splenomegaly, the most likely cause of thrombocytopenia is the sequestration of platelets in the spleen; if the bone marrow and the size of the spleen are normal, the most likely cause of thrombocytopenia is increased destruction. However, the definition of antiplatelet antibodies is not of significant clinical significance. An HIV test is performed in patients with suspected HIV infection.

In patients with platelet dysfunction and the presence of a prolonged history of increased bleeding after extraction of teeth, other surgical procedures or with easy formation of subcutaneous hemorrhage, there are grounds for suspecting congenital pathology. In this case, it is necessary to determine the antigen and activity of the von Willebrand factor. If there is no doubt in the presence of congenital pathology, no further tests are performed.

[55], [56], [57], [58], [59], [60],

Treatment of thrombocytopenia

Patients with thrombocytopenia or platelet dysfunction should avoid drugs that can disrupt the function of platelets, especially aspirin and other non-steroidal anti-inflammatory drugs. Patients may need platelet transfusions, however only in certain situations. Prophylactic transfusions are rarely used, as repeated transfusions can be ineffective due to the production of antiplatelet allo-antibodies. With platelet dysfunction or thrombocytopenia caused by impaired platelet production, transfusions are prescribed with active bleeding or severe thrombocytopenia (eg, platelet count <10,000 / μL). In thrombocytopenia, caused by the destruction of platelets, transfusions are prescribed only with life-threatening hemorrhages or hemorrhages of the central nervous system.

In modern hematology, etiological treatment of thrombocytopenia is carried out, taking into account the severity of the disease and the causes of its occurrence.

Practice is the introduction of corticosteroids, which suppress the immune system and block the antibodies of platelets. Prednisolone in thrombocytopenia of an autoimmune nature (inside or injectively) is used for mild to moderate thrombocytopenia; However, after a dose reduction or discontinuation, 60-90% of patients have relapses.

Lithium carbonate or folic acid in thrombocytopenia can be used to stimulate the production of platelets by the bone marrow. Patients with idiopathic thrombocytopenia are treated with plasmapheresis and immunosuppressive drugs are prescribed (Imuran, Mycophenolate mofetil, etc.).

Chronic idiopathic thrombocytopenia, especially with relapses in patients with a distant spleen, is treated with the injectable preparation Romiplostim, which is a thrombopoietin receptor agonist that stimulates the formation of platelets.

Dicycinum with thrombocytopenia (tablets and solution for injection) can be used to treat capillary bleeding, since it is a drug of the haemostatic group. Its hemostatic effect is based on local activation of the tissue factor of blood coagulation III (thromboplastin).

Ascorutin, Couantil and Sodecor in thrombocytopenia

These three drugs are not separately isolated. Complex antioxidant vitamins-ascorbic acid and routine - Ascorutinum with thrombocytopenia does not appear in the list of recommended medications, although it has angioprotective properties, that is, increases the impermeability of small vessels. Ascorutin is commonly used in the complex therapy of varicose veins and thrombophlebitis of the veins, chronic venous insufficiency, hypertonic microangiopathies, increased permeability of capillaries during hemorrhagic diathesis. Rutin provides a more valuable effect of ascorbic acid, but, on the other hand, reduces platelet aggregation, it prevents blood coagulation.

It is spread that Quarantil in thrombocytopenia can be used to "restore immunity", prevent thrombosis and eliminate blood circulation disorders. However, this drug has nothing to do with immunity. Curantil is an angioprotective agent that is used to prevent blood clots and activate peripheral circulation. The antithrombotic effect of the drug is that it increases the ability of prostaglandin E1 (PgE1) to inhibit the aggregation of platelets. Among its side effects are thrombocytopenia and increased bleeding.

Also, some sites report that it is possible to normalize the platelet level by taking Sodekor tincture in thrombocytopenia. The water-alcohol solution contains extracts of rhizomes and roots of elecampane; roots of dandelion, licorice and ginger; fruits of sea-buckthorn; pine nuts, as well as cinnamon bark, cardamom and coriander seeds, carnation buds.

Pharmacodynamics of this product of plant origin is not represented, but, according to the official description, the drug (quoted verbatim): "has anti-inflammatory, restorative effect, improves the nonspecific resistance of the organism, improves mental and physical performance." That is, about the use of Sodecor in thrombocytopenia is not a word.

How do the components of the tincture work? Devyasil is used as an expectorant, antimicrobial, diuretic, choleretic and antihelminthic. The root of the dandelion is used for gastrointestinal disorders and constipation. The licorice root (licorice) is used for dry cough, and also as an antacid for gastritis and diuretic for cystitis.

Cinnamon is useful for colds and nausea; cardamom has a tonic effect, and also increases the secretion of gastric juice and helps with flatulence. Ginger is very useful, the root of which is included in Sodecor, but with thrombocytopenia, ginger will not help, because it reduces blood clotting. Seeds of coriander, containing flavonoid rutozid, act similarly.

Alternative agents for thrombocytopenia

There are some alternative agents for thrombocytopenia. So, shark fat is an alternative for thrombocytopenia in the Scandinavian countries, where it is sold in pharmacies in the form of capsules (take 4-5 capsules per day for a month). At us it with success can replace usual cod-liver oil which too contains polyunsaturated fatty acids (ω-3) - on 1-2 capsules in day.

It is recommended to use sesame oil, wrung out raw, in case of thrombocytopenia - on a tablespoon twice a day. It is claimed that this oil has properties that increase the level of platelets. Obviously, this is possible due to the content of polyunsaturated fats (including ω-9), folic acid (25%) and vitamin K (22%), as well as amino acids such as L-arginine, leucine, alanine, valine, etc. Aggregates, these biologically active substances promote normal metabolism and proliferation of bone marrow tissues and, thus, stimulate hemopoiesis.

Also phytotherapists recommend herbal treatment of thrombocytopenia, as detailed in the separate publication - Treatment of thrombocytopenia

[61], [62], [63], [64], [65]

Diet with thrombocytopenia

A special diet of thrombocytopenia does not require, but it is necessary to organize proper nutrition with thrombocytopenia. What does this mean?

It is enough to introduce into your diet more fruits and vegetables, especially green: cabbage, lettuce, parsley, onion, laminaria. They contain chlorophyll, and therefore, a lot of vitamin K.

Useful products for thrombocytopenia: vegetable oils; low-fat dairy products (containing calcium, which works together with vitamin K); almonds and dried figs; oranges and orange juice (they have enough vitamin B9); cereals, peas, lentils and kidney beans (a source of vegetable protein); seafood and beets (rich in zinc).

Undesirable products in thrombocytopenia include white rice, white sugar, as well as foods that contain few nutrients, contribute to obesity and do not give the body vitamins and minerals. And, of course, alcohol should be excluded.

[66], [67], [68], [69], [70]

Prevention of thrombocytopenia

Specific methods of preventing thrombocytopenia do not exist. Do not forget about the importance of vitamins (they were discussed above).

But in the presence of this pathology doctors recommend to be cautious in everyday life and at work when using everything that can be accidentally injured. Men should shave better with an electric shaver and avoid contact sports and other activities that can lead to injuries. Children with a low level of platelets in the blood require special attention.

Forecast

The prognosis of thrombocytopenia depends on the underlying cause and progression of the disease.

[71], [72]