What is Thrombocytopenia?

Thrombocytopenia (thrombopenia in short) is the presence of relatively few platelets in blood.

Generally speaking, in human beings a normal platelet count ranges from 150,000 to 450,000 platelets per microliter of blood.These limits are determined by the 2.5th lower and upper percentile, so values outside this range do not necessarily indicate disease. One common definition of thrombocytopenia is a platelet count below 50,000 per microliter.


Often, low platelet levels do not lead to clinical problems; rather, they are picked up on a routine full blood count (or CBC, complete blood count). Occasionally, there may be bruising, particularly purpura in the forearms, petechia (pinpoint hemorrhages on skin and mucous membranes), nosebleeds and/or bleeding gums.

It is vital that a full medical history is elicited, to ensure the low platelet count is not due to a secondary process. It is also important to ensure that the other blood cell types, such as red blood cells and white blood cells, are not also suppressed. Painless, round and pinpoints (1 to 3 mm in diameter), petechiae usually appear and fade, and sometimes group to form ecchymoses. Another type of blood leakage (and larger than petechiae), ecchymoses are purple, blue or yellow-green bruises that vary in size and shape. They can occur anywhere on the body from a traumatic injury.

A person with thrombocytopenia may also complain of malaise, fatigue and general weakness (with or without accompanying blood loss). In acquired thrombocytopenia, the patient’s history may include the use of one or several offending drugs.

Inspection typically reveals evidence of bleeding (petechiae or ecchymoses), along with slow, continuous bleeding from any injuries or wounds. Adults may have large, blood-filled bullae in the mouth. If the person’s platelet count is between 30,000 and 50,000/mm3, bruising with minor trauma may be expected; if it is between 15,000 and 30,000/mm3, spontaneous bruising will be seen (mostly on the arms and legs).

What are the Causes of  Thrombocyptopenia?

Decreased platelet counts can be due to a number of disease processes:

Decreased production

  • Vitamin B12 or folic acid deficiency
  • Leukemia or myelodysplastic syndrome
  • Decreased production of thrombopoietin by the liver in liver failure.
  • Sepsis, systemic viral or bacterial infection
  • Dengue fever can cause thrombocytopenia by direct infection of bone marrow megakaryocytes as well as immunological shortened platelet survival
  • Hereditary syndromes
    • Congenital amegakaryocytic thrombocytopenia (CAMT)
    • Thrombocytopenia absent radius syndrome
    • Fanconi anemia
    • Bernard-Soulier syndrome, associated with large platelets
    • May Hegglin anomaly, the combination of thrombocytopenia, pale-blue leuckocyte inclusions, and giant platelets
    • Grey platelet syndrome
    • Alport syndrome
    • Wiskott–Aldrich syndrome

Increased destruction

  • Idiopathic thrombocytopenic purpura (ITP)
  • Thrombotic thrombocytopenic purpura (TTP)
  • Hemolytic-uremic syndrome (HUS)
  • Disseminated intravascular coagulation (DIC)
  • Paroxysmal nocturnal hemoglobinuria (PNH)
  • Antiphospholipid syndrome
  • Systemic lupus erythematosus (SLE)
  • Post-transfusion purpura
  • Neonatal alloimmune thrombocytopenia (NAITP)
  • Splenic sequestration of platelets due to hypersplenism
  • Dengue fever has been shown to cause shortened platelet survival and immunological platelet destruction
  • HIV-associated thrombocytopenia


Thrombocytopenia-inducing medications include:

  • Direct myelosuppression
    • Valproic acid
    • Methotrexate
    • Carboplatin
    • Interferon
    • Isotretinoin
    • Other chemotherapy drugs
    • H2 blockers and Proton-pump inhibitors have shown increased Thrombocytopenia symptoms, such as red dots near the bottom of the legs.
  • Immunological platelet destruction
    • Drug binds Fab portion of an antibody. The classic example of this mechanism is the quinidine group of drugs. The Fc portion of the antibody molecule is not involved in the binding process.
    • Drug binds to Fc, and drug-antibody complex binds and activates platelets. Heparin induced thrombocytopenia (HIT) is the classic example of this phenomenon. In HIT, the heparin-antibody-platelet factor 4 (PF4) complex binds to Fc receptors on the surface of the platelet. Since Fc portion of the antibody is bound to the platelets, they are not available to the Fc receptors of the reticulo-endothelial cells, so therefore this system cannot destroy platelets as usual. This may explain why severe thrombocytopenia is not a common feature of HIT.
    • Abciximab induced thrombocytopenia.

More extensive lists of thrombocytopenia-inducing medications are available.

Other causes

  • Snakebites, particularly by pit vipers.
  • Onyalai, a disease of unknown etiology seen only in parts of Africa, but suspected of being caused by poor nutrition or consumption of tainted food

How to Diagnose?

Laboratory tests might include: full blood count, liver enzymes, renal function, vitamin B12 levels, folic acid levels, erythrocyte sedimentation rate, and peripheral blood smear.

If the cause for the low platelet count remains unclear, a bone marrow biopsy is usually recommended, to differentiate whether the low platelet count is due to decreased production or peripheral destruction.

Thrombocytopenia in hospitalized alcoholics may be caused by splenomegaly, folate deficiency, and, most frequently, a direct toxic effect of alcohol on production, survival time, and function of platelets. Platelet count begins to rise after 2 to 5 days’ abstinence from alcohol. The condition is generally benign, and clinically significant hemorrhage is rare.

Lab tests to determine the platelet count and clotting function may also be done. In severe thrombocytopenia, a bone marrow study can determine the number, size and maturity of the megakaryocytes (the bone marrow cells that release mature platelets). This information may identify ineffective platelet production as the cause of thrombocytopenia and rule out a malignant disease process at the same time.


Treatment is guided by etiology and disease severity. The main concept in treating thrombocytopenia is to eliminate the underlying problem, whether that means discontinuing suspected drugs that cause thrombocytopenia, or treating underlying sepsis. Diagnosis and treatment of serious thrombocytopenia is usually directed by a hematologist.

Corticosteroids may be used to increase platelet production. Lithium carbonate or folate may also be used to stimulate the bone marrow production of platelets. Platelet transfusions may be used to stop episodic abnormal bleeding caused by a low platelet count. However, if platelet destruction results from an immune disorder, platelet infusions may have only a minimal effect and may be reserved for life-threatening bleeding.

Specific treatment plans often depend on the underlying etiology of the thrombocytopenia.

Condition Treatment
Thrombotic thrombocytopenic purpura Treatment of thrombotic thrombocytopenic purpura is a medical emergency, since the hemolytic anemia and platelet activation can lead to renal failure and changes in the level of consciousness. Treatment of TTP was revolutionized in the 1980s with the application of plasmapheresis. According to the Furlan-Tsai hypothesis,[9][10] this treatment theoretically works by removing antibodies directed against the von Willebrand factor cleaving protease, ADAMTS-13. The plasmapheresis procedure also adds active ADAMTS-13 protease proteins to the patient, restoring a more physiological state of von Willebrand factor multimers. Patients with persistent antibodies against ADAMTS-13 do not always manifest TTP, and these antibodies alone are not sufficient to explain the how plasmapheresis treats TTP.
Idiopathic thrombocytopenic purpura Many cases of ITP can be left untreated, and spontaneous remission (especially in children) is not uncommon. However, counts of under 50,000 are usually monitored with regular blood tests, and those with counts of under 10,000 are usually treated, as the risk of serious spontaneous bleeding is high with a platelet count this low. Any patient experiencing severe bleeding symptoms is also usually treated. The threshold for treating ITP has decreased since the 1990s, and hematologists recognize that patients rarely spontaneously bleed with platelet counts greater than 10,000—though there are documented exceptions to this observation.Treatments for ITP include:

  • Prednisone and other corticosteroids
  • Intravenous immune globulin
  • Splenectomy
  • Danazol
  • Eltrombopag
  • Rituximab
  • Romiplostim

Thrombopoetin analogues have been tested extensively for the treatment of ITP. These agents had previously shown promise but had been found to stimulate antibodies against endogenous thrombopoietin or lead to thrombosis.

Romiplostim (trade name Nplate, formerly AMG 531) was found to be safe and effective for the treatment of ITP in refractory patients, especially those who relapsed following splenectomy.[11][12][13]

Heparin-induced thrombocytopenia Discontinuation of heparin is critical in a case of HITT. Beyond that, however, clinicians generally treat to avoid a thrombosis, and patients started directly on warfarin after a diagnosis of HITT are at excess risk of venous limb gangrene. For this reason, patients are usually treated with a type of blood thinner called a direct thrombin inhibitor such as lepirudin or argatroban, which are approved by the U.S. Food and Drug Administration (FDA). Other blood thinners sometimes used in this setting that are not FDA-approved for treatment of HITT include bivalirudin and fondaparinux. Platelet transfusions are not a routine component of the treatment of HITT, since thrombosis, not bleeding, is the usual associated problem in this illness.
Congenital amegakaryocytic thrombocytopenia Bone Marrow/Stem Cell Transplant is the only thing that ultimately cures this genetic disease. Frequent platelet transfusions are required to keep the patient from bleeding to death until transplant is done, although this is not always the case.

Veterinary treatment

Thrombocytopenia caused by Feline Leukemia Virus and Feline immunodeficiency virus retroviral infections is treated with Lymphocyte T-Cell Immune Modulator.


Dengue-Aid is a potent herbal supplement in capsules which is taken from pure extracts from the Euphorbia hirta Linn herbs which is commonly known as “Tawa-Tawa” by the local residents in the Philippines.  Tawa-Tawa or Asthma weed  had been popular among dengue fever victims due to its profound properties on increasing low blood platelet count which is one of the symptoms of this serious viral infection. Dengue fever can cause thrombocytopenia by direct infection of bone marrow megakaryocytes as well as immunological shortened platelet survival

Read more about Tawa-Tawa (Euphorbia hirta Linn) Herbal Plant

Learn more on Asthma Weed “Tawa-Tawa” Capsules

Information Taken from :

Soursop or Graviola as Cancer Cure

Are soursop and cancer cure related? What is soursop? Cancer cure studies have shown that this miraculous plant may be helpful in treating cancer. Read on to know all about soursop and cancer cure…

Soursop and Cancer Cure
The soursop, also known as Graviola, is a broadleaf flowering evergreen tree that is native to parts of Mexico, Central America, the Caribbean and the northern portion of South America. Soursop is also native to the sub-Saharan Africa countries that lie within the range of the tropics. Nowadays, Graviola tree is also grown in some parts of south-east Asia. The reason why this plant has managed to garner so much publicity is because it has been claimed that soursop and cancer cure are related. It is only now that the world has come to know of the benefits of soursop. Cancer cure has always been a huge topic of research the world over, and soursop has said to be a breakthrough in this field. Given below are details regarding soursop and cancer cure. .

Although it is yet to be finalized on how and whether soursop and cancer cure are actually related or not, there have been studies conducted to validate this claim. Studies to check for Graviola effect on cancer cells began sometime around the 1970’s. It was the National Cancer Institute that performed the first ever scientific research on the possibility of soursop cancer cure in 1976. The results showed that Graviola’s ‘leaves and stems were found effective in attacking and destroying malignant cells.’ Furthermore, it has been claimed that since that year, Graviola was proven to be a potent killer of cancer cells in over twenty different laboratory tests and studies that were undertaken.

A study that was published in the Journal of Natural Products, following a recent study that was conducted at Catholic University of South Korea, stated that a certain chemical that is found in Graviola can selectively kill colon cancer cells at almost ‘ten thousand times the potency of Adriamycin’. (Adriamycin is the drug that is commonly used as a part of chemotherapy). Another interesting fact regarding the healing power of soursop is that Graviola selectively targeted only the harmful cancer cells, while leaving the healthy cells of the body untouched.

Thus, unlike chemotherapy, which indiscriminately kills all cells (especially the superficial ones, like hair cells) in the affected region, Graviola does not harm the healthy cells. It also spares the person of the side effects of chemotherapy like severe nausea, hair loss, weight loss and deforming skin changes.

Some studies even claim that soursop can target and help in treating nearly twelve different types of cancer, including colon cancer, breast cancer, lung cancer, pancreatic cancer and prostate cancer. It is also claimed that during the course of chemotherapy, Graviola manages to protect the immune system by preventing it from getting harmed due to the effects of chemotherapy.

This was all about soursop and cancer cure. Being a healthy citrus fruit, there are many benefits of soursop. Cancer cures may or may not be one of those benefits but in the end, the fact is that chemotherapy and radiation can only do so much to help in treating cancer and not curing it. Hence, any natural way of, if not curing, at least mitigating the effects or slowing down the progress of cancer are always welcome. However, one needs to be wary of taking in excess of Graviola in the name of alternative cancer treatment. This is because it has been seen that in some people, especially when taken in excess amounts, soursop can lead to neurological damage that closely resembles Parkinson’s disease. Hence, it is always best to consult your oncologist or health care provider before trying out this supposed natural remedy for cancer.

Reference: (excerpt from)
By Dr. Sumaiya Khan
Published: 5/29/2010