Thrombocytopenia

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Thrombocytopenia is a condition characterized by low platelet levels, also known as platelets, in the blood.

Normal human platelet counts range from 150,000 to 450,000 platelets per microliter of blood. This limit is determined by the lower and upper 2nd percentile, so values ​​outside this range do not necessarily indicate illness. One common definition of thrombocytopenia requiring emergency care is the platelet count below 50,000 per microliter.

Video Thrombocytopenia

Signs and symptoms

Thrombocytopenia usually has no symptoms and is picked up in a complete full blood count (or full blood count). Some individuals with thrombocytopenia may experience external bleeding such as nosebleeds, and/or bleeding gums. Some women may experience more severe or longer periods or have severe bleeding. Bruises, especially the purpura in the forearm and petechiae in the legs, feet, and mucous membranes, may be caused by spontaneous bleeding under the skin.

Requesting a complete medical history is essential to ensure low platelet counts are not secondary to other disorders. It is also important to ensure that other types of blood cells, such as red blood cells and white blood cells, are also not suppressed. Without pain, round and precise (1 to 3 mm in diameter) petechiae usually appear and fade, and sometimes groups to form ecchymoses. Larger than petechiae, ecchymoses are areas of purple, blue or yellow-green skin that vary in size and shape. They can occur anywhere in the body.

A person with this disease may also complain of malaise, fatigue and general weakness (with or without accompanying blood). The acquired thrombocytopenia may be associated with a history of drug use. Inspection usually shows evidence of bleeding (petechiae or ecchymoses), along with slow and persistent bleeding from any injury or injury. An adult may have a large bull, full of blood in the mouth. If a person's platelet count is between 30,000 and 50,000/mm ³ , bruising with minor trauma can be expected; if between 15,000 and 30,000/mm ³ , spontaneous bruises will be visible (mostly on the arms and legs).

Maps Thrombocytopenia

Cause

Thrombocytopenia can be inherited or acquired.

Production decreased

The production of abnormal platelets may be caused by:

• Dehydration, Vitamin B ₁₂ or folic acid deficiency
• Leukemia or myelodysplastic syndrome or aplastic anemia
• Decreased thrombopoietin production by the liver in liver failure
• Sepsis, virus or systemic bacterial infection
• Leptospirosis
• Hereditary syndrome
  • Congenital amegacaryocytic thrombocytopenia
  • Thrombocytopenia absent radius syndrome
  • Fanconi Anemia
  • Bernard-Soulier Syndrome (associated with large platelets)
  • May-Hegglin's anomaly
  • Gray platelet syndrome
  • Alport Syndrome
  • Wiskott-Aldrich Syndrome

Increased destruction

High levels of platelet destruction may be caused by immune or non-immune conditions, including:

• Immune thrombocytopenic purpura
• Thrombotic thrombocytopenic purpura
• Hemolytic-uremic syndrome
• Disseminated intravascular coagulation Paroxysmal nocturnal hemoglobinuria
• The antiphospholipid syndrome
• Systemic lupus erythematosus
• Purpura post-transfusion
• Neonatal alloimmune thrombocytopenia
• Hipersplenism
• Dengue fever
• Gaucher's Disease
• Zika virus

Drug induced

The following medications can induce thrombocytopenia through direct myelosuppression.

• Valproic acid
• Methotrexate
• Carboplatin
• Interferon
• Isotretinoin
• Panobinostat
• H ₂ blocker and proton pump resistor

Other causes

• Lab error, probably because of EDTA anticoagulants in the CBC specimen tube; platelet count citrate is a useful follow-up study
• Snakebite
• Niacin toxicity
• Lyme disease
• Thrombocytapheresis (also called Plateletpheresis)

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Diagnosis

Laboratory tests for thrombocytopenia may include complete blood count, hepatic enzyme, renal function, vitamin B ₁₂ levels, folic acid level, blood sedimentation rate, and peripheral blood smear. If the cause of low platelet counts remains unclear, bone marrow biopsy is usually recommended to differentiate cases of platelet production decline from cases of peripheral platelet destruction.

Thrombocytopenia in hospitalized alcoholics can be caused by enlarged spleen, folate deficiency, and, most often, direct toxic effects of alcohol on production, survival time, and platelet function. Platelet count begins to increase after 2 to 5 days do not drink alcohol. The condition is generally benign, and significant clinical bleeding is rare.

In severe thrombocytopenia, bone marrow studies can determine the number, size and maturity of megakaryocytes. This information can identify ineffective platelet production as the cause of thrombocytopenia and rule out malignant disease at the same time.

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Treatment

Treatment is guided by the severity and specific causes of the disease. Treatment focuses on removing the underlying problem, whether it means stopping the drug that is suspected of causing or treating the underlying sepsis. Serious diagnosis and treatment of thrombocytopenia is usually directed by a hematologist. Corticosteroids can be used to increase platelet production. Lithium carbonate or folate can also be used to stimulate platelet production in the bone marrow.

Thrombotic thrombocytopenic purpura

Treatment of thrombocytopenic purpura (TTP) is a medical emergency, because hemolytic anemia and associated platelet activation can lead to renal failure and altered levels of consciousness. TTP treatment underwent a revolution in 1980 with the application of plasmapheresis. According to the Furlan-Tsai hypothesis, this treatment works by removing antibodies to protease-forming proteins ADAMTS-13 von Willebrand. The plasmapheresis procedure also added ADAMTS-13 active protease proteins to the patient, restoring normal levels of von Willebrand factor multimers. Patients with persistent antibodies to ADAMTS-13 do not always show TTP, and these antibodies alone are not sufficient to explain how plasmapheresis treats TTP.

Purpura thrombocytopenic idiopathic

Many cases of ITP can be left without treatment, and spontaneous remission (especially in children) is not uncommon. However, numbers under 50,000 are usually monitored with regular blood tests, and those with numbers under 10,000 are usually treated, because the risk of serious spontaneous bleeding is high with low platelet counts. Any patient who experiences symptoms of severe bleeding is also usually treated. The threshold for treating ITP has declined since the 1990s; hematologists admitted that patients rarely spontaneously bleed with a platelet count of more than 10,000, although there were documented exceptions for this observation.

Analog thrombopoetin has been extensively tested for the treatment of ITP. These agents have previously shown promise but have been found to stimulate antibodies to endogenous thrombopoietin or cause thrombosis. Romiplostim (trade name Nplate, formerly AMG 531) was found safe and effective for the treatment of ITP in refractory patients, especially those who relapsed after splenectomy.

Heparin-induced thrombocytopenia

The termination of heparin is very important in the case of heparin-induced thrombocytopenia (HIT). Beyond that, however, doctors generally treat to avoid thrombosis. Treatment may include direct thrombin inhibitors, such as lepirudin or argatroban. Other blood thinners sometimes used in this setting include bivalirudin and fondaparinux. Platelet transfusions are not routinely used to treat HIT because thrombosis, not bleeding, is a major problem. Warfarin is not recommended until the platelets return to normal.

Congenital amegacaryosytic thrombocytopenia

Bone marrow transplantation/stem cells is the only known cure for this genetic disease. Platelet transfusion is often necessary to keep patients from bleeding to death before transplantation can be performed, although this is not always the case.

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Neonatal thrombocytopenia

Thrombocytopenia affects several percent of newborns, and their prevalence in neonatal intensive care units (NICUs) is high. Usually, it's light and resolves without consequences. Most cases affect premature birth and results from fetal placental insufficiency and/or fetal hypoxia. Other causes, such as aloimities, genetics, autoimmunities, and infections, are rare.

Thrombocytopenia that begins after the first 72 hours of birth is often the result of underlying sepsis or necrotizing enterocolitis (NEC). In the case of infection, PCR testing may be useful for rapid identification of pathogens and the detection of antibiotic resistance genes. Possible pathogens include viruses (eg Cytomegalovirus (CMV), rubella virus, HIV), bacteria (eg Staphylococcus sp. , Enterococcus sp. , Streptococcus agalactiae (GBS), Listeria monocytogenes , Escherichia coli , Haemophilus influenzae , Klebsiella pneumoniae , Pseudomonas aeruginosa , Yersinia enterocolitica ), fungi (eg Candida sp. ), and Toxoplasma gondii . The severity of thrombocytopenia may be correlated with the type of pathogen; several studies have shown that the most severe cases are associated with fungal or gram-negative bacterial infections. Pathogens can be transmitted during or before birth, through breastfeeding, or during transfusion. Interleukin-11 is being investigated as a drug for managing thrombocytopenia, especially in cases of sepsis or necrotizing enterocolitis (NEC).

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References

src: www.bloodadvances.org

External links

• 11-133b. in Merck Manual Diagnosis and Therapy Professional Edition
• Thrombocytopenia Forum
• Fluorouracil/5-FU Toxicity & amp; DPD Deficiency Education - DPD-Deficiency.com

Source of the article : Wikipedia