The so-called thrombocytes (blood platelets) are a type of cell in the blood that is responsible for clotting. They are therefore an important part of hemostasis, as they attach themselves to the damaged tissue in the event of injuries and thus ensure that the wound closes. If one speaks of thrombocytopenia, this means that there are too few thrombocytes in the blood. The opposite of this, i.e. too many platelets, would be called Thrombocytosis describe.
According to the current guidelines of the DGHO, bleeding tendencies are classified according to the extent of the thrombocytopenia. Physiologically, platelet values are in the reference range of 150,000 to 350,000 / µl. Prolonged bleeding times only occur at values below 100,000 / µl; at values above this, no increased bleeding tendency is to be expected. Between 50,000 and 100,000 / µl, bleeding usually only occurs with major injuries. With platelet counts between 30,000 and 50,000 / µl, rather harmless petechial bleeding and a generally prolonged bleeding time can be observed.
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Read more on the subject at: Petechiae
Serious consequences can only be expected at values below 30,000 / µl. This could be spontaneous bleeding into the brain (intracerebral bleeding) or the organ system. Disseminated petechiae on the skin and mucous membranes also occur.
There are several causes of platelet deficiency. However, they can be roughly divided into two areas: either too few functional platelets are produced or the consumption or degradation in the blood is too high.
Like most blood components, platelets are produced in the bone marrow. If there is damage to the bone marrow, this can mean that only a reduced number of platelets can be produced. There are many causes of bone marrow damage, but it is mostly caused by toxins such as Medicines, radiation, lead intoxication, etc., or acquired through cancer, especially leukemia. There are also rare underlying genetic diseases (e.g. Wiskott-Aldrich syndrome) that limit the function of the bone marrow.
$config[ads_text2] not foundA deficiency in vitamin B12 or folic acid can also lead to decreased production, as these are important components of the blood platelets.
If production in the bone marrow is not restricted, the life of the platelets in the bloodstream is likely to be shortened. An abnormally increased breakdown of blood platelets can be responsible for the deficiency. The cause here could be an autoimmune defect, in which our body's own immune system increasingly breaks down the platelets. Examples of diseases for this would be so-called lupus erythematosus or rheumatoid arthritis. Medicines or cancer can also increase the breakdown.
Finally, the consumption of blood platelets can be increased due to damage to artificial heart valves, dialysis or certain infections (e.g. EHEC). Pregnancy can also lead to low blood platelet counts.
Read more on the topic: Causes of Thrombocytopenia
Another cause of a reduced number of blood platelets and an increased tendency to bleed can be the autoimmune disease Werlhof's disease. Find out more at: Werlhof's disease - is it curable?
The HIT syndrome (Heparin-induced thrombocytopenia) is a reaction in the form of thrombocytopenia of a few people to the medication that is given for thrombosis prophylaxis or blood thinning, the heparin. There are two types of HIT syndrome. Type 1 HIT is a harmless variant and is usually not symptomatic. Type 2 HIT, on the other hand, can be life-threatening. An immune reaction occurs in the body and as a result antibodies develop. The antibodies activate the platelets. The active blood platelets lead to increased blood clotting, which can lead to blood clots (Thrombi) arise in arteries and veins. In addition, disturbances can occur in the very small blood vessels and lead to tissue damage due to the impaired blood flow. The consumption of platelets causes the platelet concentration to drop by more than half.
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$config[ads_text3] not foundYou might also be interested in this topic: Heparin-induced thrombocytopenia
Leukemia is called blood cancer in everyday language. In leukemia, the formation of new blood cells is disturbed. There are different types of leukemia caused by different causes. There is a possibility that thrombocytopenia may develop with leukemia. Usually, the formation of leukemia cells leads to a displacement of normal blood formation in the bone marrow, which also affects the formation of platelets in the bone marrow. In addition to the platelets, the formation of the other blood cells is also impaired.
Further information on this topic can be found at: How do you recognize leukemia?
Chemotherapy is often initiated for various cancers. Chemotherapeutic and cytostatics are powerful drugs that are often associated with side effects. Many chemotherapy drugs can affect blood production in the bone marrow. The formation of different types of blood cells can therefore be affected, including platelets. In addition to thrombocytopenia, there may be a decrease in white blood cells (Leukocytopenia).
You might also be interested in this topic: Chemotherapy side effects
Cirrhosis of the liver is the term used to describe the loss of healthy liver tissue. This is triggered by various liver diseases such as inflammation of the liver (hepatitis) or by long-term alcohol abuse. Cirrhosis of the liver can have numerous consequences, including so-called esophageal varices or cancer of the liver.
Liver cirrhosis can also lead to thrombocytopenia. The liver normally cleanses our blood. For this purpose, it receives an inflow through the so-called portal vein circuit. If the liver function is now restricted, there is a backlog of blood in this venous system. This now also affects the spleen, which becomes larger due to the increased backlog of blood and "temporarily stores" so much blood. This also leads to a rearrangement of the platelets. These are no longer evenly distributed in the bloodstream but are largely stored in the spleen. This is why the symptoms of a platelet deficiency also arise here.
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There are many drugs that can cause thrombocytopenia. Heparins in particular can trigger thrombocytopenia in the context of HIT syndrome. Further active ingredients of drugs that can lead to thrombocytopenia are, for example, the following active ingredients: Abciximab, eptifibatide, tirofiban, penicillamine, linezolid, sulfonamides, vancomycin, carbamazepine or gold salts, valproate, paracetamol, rifampicin or oxalacidine, dinuprofinide, hydrochloride, hydrochloride, dinuprofinide, cimetipliazide, and cimetchloride . There are other drugs that can cause thrombocytopenia. Would you like precise information about possible side effects of a drug, such as thrombocytopenia, you should read the package insert carefully.
The first important step in the diagnosis is the conversation between doctor and patient. The doctor can ask whether the patient has a prolonged bleeding time, e.g. you have noticed a small incision or increased bruising. Current drugs, especially blood-thinning drugs such as heparin, ASA or Marcumar and a possible familial bleeding tendency can reveal possible causes.
This is followed by the physical examination, in which e.g. an enlarged spleen can be felt, but signs of the underlying diseases mentioned above can also be found.
Finally, a laboratory blood test is essential. For example, the shape and quantity of the platelets is assessed through a microscope. This can also provide indications of cancer. Pointing the way to the cause of thrombocytopenia is the so-called "mean platelet volume“, Which can judge whether there is a production disruption or a breakdown via the size of the blood platelets.
If the laboratory shows thrombocytopenia, which does not cause any symptoms and was discovered more or less by chance, a so-called "Pseudothrombocytopenia“Be excluded. The laboratory result is falsified, for example, by the long transport time of the blood sample.
The platelets stop bleeding.If there is a deficiency, there is an increased and prolonged bleeding tendency. This is initially noticeable by small things: a small cut bleeds significantly longer, light bumps cause bruises and frequent nose or gum bleeding occurs. If the platelet count is over 30,000 cells per µl, some patients do not experience any symptoms.
$config[ads_text1] not foundIf the platelet count continues to decrease, so-called petechiae occur, minimal bleeding into the skin, which can be seen as small reddish-purple dots. In addition, there are enlarged bruises and spontaneous bleeding on the mucous membranes.
Further information on the subject can be found at: Petechiae
Petechiae and an increased tendency to bleed can also indicate Werlhof's disease. Find out more at: Werlhof's disease - is it curable?
If the cause is one of the underlying diseases mentioned above, specific accompanying symptoms can occur. Cancer often leads to fever, night sweats and unwanted weight loss.
Rheumatoid arthritis shows up in additional joint problems. If the bone marrow is damaged, however, the production of other blood cells is also often damaged and anemia, anemia, which is often associated with fatigue, tiredness and paleness, can occur.
Since thrombocytopenia has a serious cause, symptoms should always be clarified by a visit to the doctor.
In special situations, thrombocytopenia and thrombosis can occur simultaneously. For example, in the case of consumption coagulopathy, a drop in the platelet count is a first diagnostic indicator. While in the acute stage of DIC there may initially be considerable microthrombus formation with vascular occlusion, necrosis and organ infarction, in the advanced stage bleeding due to the consumption of coagulation factors is often characteristic.
There may also be an increased risk of thrombosis in the case of relative heparin-associated thrombocytopenia. This leads to thrombocytopenia after administration of heparin. A distinction must be made between the prognostically favorable type HIT1, which is based on a direct interaction between heparin and platelets, and the more severe type HIT2. This leads to platelet aggregation as a result of the formation of antibodies against the specific complex of the surface protein platelet factor 4 of the platelets and heparin. Even if a reduction in the absolute platelet count can be determined here, thrombocyte aggregations can lead to thromboembolic events. The basic therapeutic rule in the event of HIT2 is to immediately discontinue the existing administration of heparin and to switch the therapy to argatroban or recombinant hirudin. External administration of platelet concentrates is absolutely contraindicated!
Read more on this topic at: Heparin-induced thrombocytopenia
If there is a lack of the formation of blood cells, symptoms of increased fatigue or a decline in performance and poor concentration can definitely occur. In the case of an isolated platelet deficiency, however, symptoms of fatigue are usually not to be expected. Nevertheless, in the special form of pernicious anemia, a decrease in the concentration of all blood cell rows can be determined. It is caused by a lack of vitamin B12 (extrinsic factor) caused. The primarily reduced number of erythrocytes and the associated megaloblastic (hyperchromic / macrocytic) anemia can lead to fatigue.
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The therapy of thrombocytopenia depends on its cause. If an infection or pregnancy is the cause of thrombocytopenia, it usually goes away on its own.
If there is an underlying disease, it must be treated. If there is a deficiency in vitamin B12 and folic acid, it must be compensated for by additional intake. Medicines that lead to a pathological reduction in blood platelets should be re-dosed or discontinued and replaced with better-tolerated preparations. Symptoms caused by autoimmune diseases can be improved by specialists with specific immunosuppressive drugs. Cancer diseases are also assessed and treated by specialists. If the spleen is greatly enlarged, it may have to be removed.
If the platelet deficiency is in a life-threatening range of less than 10,000 platelets per µl of blood, platelet concentrates are given which, like blood transfusions, add foreign platelets to the blood. Here, too, the cause of the platelet deficiency must then be found and treated.
Also read the article: Thrombocytopenia.
There is no general drug therapy for thrombocytopenia because the causes vary widely.
For example, immunosuppressive drugs are used in autoimmune diseases. These suppress the body's immune system and thus prevent the excessive breakdown of blood platelets. Examples from this group of drugs would be glucocorticoids or specific antibodies.
It is also important to check the medication you are currently taking. Strong blood thinners such as Aspirin® or heparin can lead to thrombocytopenia and should be discontinued or re-dosed accordingly.
Read more on this topic at: Heparin-induced thrombocytopenia
The use of cortisone as an immunosuppressant primarily plays a role in autoimmunologically triggered thrombocytopenia. Above all, Werlhof's disease (ITP) described above should be mentioned. The aim of the administration of cortisone is an increase in the absolute platelet count by inhibiting the antibodies directed against the platelets. If this does not happen promptly, a high-dose therapy can possibly lead to an improvement in the form of several cycles. Cortisone therapy (glucocorticoid therapy) can achieve temporary or permanent therapeutic success. This is called a lasting remission.
To support the appropriate therapy for the underlying disease, the patient can increase his platelet count by changing his lifestyle. Moderate exercise or sport is rated as helpful. In addition, there is a healthy diet rich in fiber and vitamins.
Vitamins C, D, K and B12 are particularly helpful here. There is a lot of vitamin C in citrus fruits (lemons, kiwi, oranges) or in some vegetables (cabbage, tomatoes, broccoli). Vitamin B12 and folic acid can of course be supplemented with dairy products, fish, eggs and spinach. Of course, there are also corresponding supplements for the vitamins, which can be purchased in consultation with the family doctor in the pharmacy.
The healthy omega-3 fatty acids, which are increasingly found in fish, vegetable oils and nuts, are also said to have a positive influence on the platelet count.
Finally, a positive effect of herbal ingredients from green tea, white giseng, olive leaves and piperine is also discussed.
It is important to note that such therapy should never be carried out on its own and should always be done in consultation with the family doctor!
A slight decrease in platelets can be compensated for by making certain adjustments in food intake. Basically, a diet containing vitamin B and vitamin C has shown a productive effect on increasing platelet counts. Foods that are particularly rich in these two vitamins are tomatoes, citrus fruits and green leafy vegetables. Other important supports in platelet formation are vitamin D, folic acid and vitamin B12. Foods containing omega-3 such as linseed oil, rapeseed oil, nuts, seeds and sea fish should also play a supporting role. Basically, in addition to a balanced diet with a vitamin-rich intake, the intake of alcohol, caffeinated drinks and refined sugars should be avoided.
In principle, a permanently low platelet count can lead to bleeding events with the following complications. However, bleeding due to thrombocytopenia or thrombocytopathy (e.g. due to ASA therapy) is mostly limited to petechial skin bleeding. Rather, these symptoms are indicative of a diagnostic intervention than that this petechial skin haemorrhage has far-reaching prognostic value. However, thrombocytopenias can occur in combination with various serious diseases such as certain anemias (e.g. pernicious anemia) and leukemia as well as other bone marrow diseases. A broader diagnostic spectrum such as Use laboratory diagnostics or apparatus diagnostics in order to prevent possible complications.
In around 5-10% of all pregnancies, women have a slight drop in their platelet count. This means a decrease in platelets by 15% (so-called pregnancy thrombopenia). This slight decrease in platelets is the second most common pathological change in the blood count after manifest pregnancy anemia. The slight platelet deficiency occurs primarily in the last trimester (third of pregnancy) of pregnancy.
In general, if the platelet count drops, there is an increased tendency to bleeding complications in the form of petechiae (small punctiform bleeding of the skin). However, it is important to differentiate between a weak and a strong drop. If the decrease is relatively weak, as in most cases of pregnancy thrombopenia, bleeding is not to be expected in some cases, since the organism only shows a decompensation of blood coagulation at very low platelet counts.
A distinction must also be made between thrombocytopenia in terms of the cause of the disease. In the most common form of pregnancy thrombocytopenia (Gestational thrombocytopenia) there is usually no risk to mother and child in the form of bleeding complications. With autoimmune thrombocytopenia, on the other hand, the mother may have an increased tendency to bleed during the period of birth. In the case of newborns, severe bleeding can also occur due to the passage of autoantibodies against platelets through the placenta. In principle, when bleeding occurs in mother and child in the form of cerebral haemorrhage or all organ haemorrhages, several forms of manifestation are possible.
In terms of differential diagnosis, it is very important to differentiate these typical, complication-free pregnancy thrombocytopenias from other clinical pictures. Above all, the complication that often develops during pregnancy, the HELLP syndrome and eclampsia (pregnancy poisoning). HELPP chronologically means an occurring hemolysis (destruction of blood cells of different origins), an increase in liver enzymes and a decrease in platelet counts. While the first two diagnostic abnormalities in particular can lead to symptomatic complications, normal gestational thrombocytopenia usually turns out to be an asymptomatic phase of pregnancy. Symptoms are not expected after the birth either. On the contrary, the laboratory diagnostic thrombocytopenia disappears within a short time.
Read more on this topic at: HELLP syndrome
A basic distinction must be made between congenital and acquired thrombocytopenias in the newborn. Thrombocytopenia occurs before birth or from the first days of life (congenital) or in the course of the first few weeks to months (acquired). Most thrombocytopenias in humans occur as a result of e.g. Infections or as a side effect of medication.
An important form is idiopathic immune thrombocytopenic purpura (ITP). Werlhof's disease is synonymous with ITP. With this clinical picture, there is typically an isolated drop in platelets in childhood (only affecting the platelets) with numbers below 100,000 / ul. The cause of ITP is still unknown, although previous viral infections of the upper respiratory tract are assumed. Werlhof's disease is the most common cause of bleeding tendencies in childhood. There are two possible diagnostic signs that indicate ITP. On the one hand, IgG antibodies can be detected in the blood plasma which are directed against the platelets and are often formed in the non-enlarged spleen. In addition, there is an isolated thrombocytopenia due to a shortened lifetime with reactively increased megakaryopoiesis in the bone marrow punctate.
As congenital forms of thrombocytopenia, various diseases may be the cause. As a rule, however, these are very rare and are divided into the presence of a reduced formation of platelets or the formation of defective platelets, which are subsequently broken down prematurely. Mention should be made here of congenital amegakaryocytic thrombocytopenia (CAMT). This shows a reduced formation of the precursor cells of the platelets, the megakaryocytes in the bone marrow. The problem here is an impairment in the formation of other blood cell rows that becomes more difficult. A bone marrow transplant should be considered as a form of therapy here.
In addition, the Wiskott-Aldrich syndrome (WAS) is another disease of the congenital thrombocytopenia. This syndrome is associated with an immunodeficiency. Therefore, the affected patients suffer from a tendency to bleed as well as a possible increased susceptibility to infections. Eczema (inflammation of the skin with itching and the formation of papules and reddening of the skin) and inflammatory bowel diseases are also common here. Male individuals are almost exclusively affected, as the WAS is inherited in an x-linked manner.
In Bernard-Soulier syndrome (BSS), pathologically enlarged platelets are noticeable, which are subject to a severe functional defect and are therefore rejected. In addition, among the congenital thrombocytopenias, the X-linked macrothrombocytopenia with disruption of the formation of platelets and erythrocytes (red blood cells) and the MYH9-associated diseases with complex defects in the MYH9 gene should be mentioned.
A connection between thrombocytopenia and increased alcohol consumption can certainly be established. The red bone marrow, in which all blood cells are formed, is very sensitive to various toxic influences. In addition to exposure to radiation (e.g. during radiotherapy), this also includes chemotherapy or substances containing benzene. A prolonged elevated blood level of alcohol can also have a toxic effect on the bone marrow and lead to impaired formation of platelets, because alcohol is classified as a potent cell poison in the broader sense. Strict alcohol restrictions must therefore be observed when performing chemotherapy or radiotherapy.
Read more on this topic at: Consequences of alcohol
HIV-associated thrombocytopenia can also occur in the case of HIV infection. It is one of the most common pathological blood count changes in HIV. In the absence of antiretroviral therapy, the frequency increases significantly with the duration of the infection. HIV-associated thrombocytopenia is based on two mechanisms below. On the one hand, there is an increased, immunologically induced degradation of platelets.
On the other hand, platelet production in the bone marrow in the form of the precursor cells megakaryocytes is also reduced. Most affected patients initially experience bleeding without complications such as mucosal bleeding, ecchymosis, epistaxis (nosebleeds) and gingival bleeding (bleeding gums). However, intracerebral and gastrointestinal bleeding (cerebral haemorrhage and gastrointestinal bleeding) can occur rarely. However, in this case the platelets must drop to values below 30,000 / µl. Diagnostically distinguishable e.g. HIV-associated thrombocytopenia from ITP is primarily due to moderate splenomegaly and enlarged lymph nodes.
You can find more information on this topic here: HIV
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