[1][2] ITP often results in an increased risk of bleeding from mucosal surfaces (such as the nose or gums) or the skin (causing purpura and bruises).

However, since the diagnosis relies on excluding other potential causes of a low platelet count, additional investigations, such as a bone marrow biopsy, may be necessary in certain cases.

[4] A platelet count below 10,000 per μL can lead to the spontaneous formation of hematomas (blood masses) in the mouth or on other mucous membranes.

In cases where platelet counts drop to extremely low levels (<5,000 per μL), serious and potentially fatal complications may arise.

A person with ITP with an extremely low platelet count is susceptible to internal bleeding resulting from blunt abdominal trauma, such as in a motor vehicle crash.

[7] The coating of platelets with IgG renders them susceptible to opsonization and phagocytosis by splenic macrophages, as well by Kupffer cells in the liver.

Then, secondary causes (around 5–10 percent of suspected ITP cases) should be excluded including medications (quinine or heparin), viral infection (HIV or HCV), malignancy (leukemia), autoimmune conditions (systemic lupus erythematosus or antiphospholipid syndrome), onyalai, and others.

[4][12] All patients with presumed ITP should be tested for HIV and hepatitis C virus, as platelet counts may be corrected by treating the underlying disease.

In approximately 2.7 to 5 percent of cases, autoimmune hemolytic anemia and ITP coexist, a condition referred to as Evans syndrome.

An analysis for anti-platelet antibodies is a matter of clinician's preference, as there is disagreement on whether the 80 percent specificity of this test is sufficient to be clinically useful.

Current guidelines recommend treatment for adults with significant bleeding or counts below 30/nL, with very low certainty of evidence.

The dose and mode of administration is determined by platelet count and whether there is active bleeding: in urgent situations, infusions of dexamethasone or methylprednisolone may be used, while oral prednisone or prednisolone may suffice in less severe cases.

[20] Another option, suitable for Rh-positive patients with functional spleens is intravenous administration of Rho(D) immune globulin [Human; Anti-D].

In chronic refractory cases, where immune pathogenesis has been confirmed,[23] the off-label use of the vinca alkaloid[24][25][26] and chemotherapy agent vincristine may be attempted.

Intravenous immunoglobulin (IVIg) may be infused in some cases in order to decrease the rate at which macrophages consume antibody-tagged platelets.

[31] Two such products are currently available: Thrombopoietin receptor agonists exhibited the greatest success so far in treating patients with refractory ITP.

[37] Side effects of thrombopoietin receptor agonists include headache, joint or muscle pain, dizziness, nausea or vomiting, and an increased risk of blood clots.

The procedure is potentially risky in ITP cases due to the increased possibility of significant bleeding during surgery.

[44] In adults, particularly those living in areas with a high prevalence of Helicobacter pylori (which normally inhabits the stomach wall and has been associated with peptic ulcers), identification and treatment of this infection has been shown to improve platelet counts in a third of patients.

In a fifth, the platelet count normalized completely; this response rate is similar to that found in treatment with rituximab, which is more expensive and less safe.

[40] A normal platelet count is considered to be in the range of 150,000–450,000 per microlitre (μL) of blood for most healthy individuals.

[55][56][57] Moreover, a third of the remaining chronic cases will usually remit during follow-up observation, and another third will end up with only mild thrombocytopenia (defined as a platelet count above 50,000).

[55] A number of immune related genes and polymorphisms have been identified as influencing predisposition to ITP, with FCGR3a-V158 allele and KIRDS2/DL2 increasing susceptibility and KIR2DS5 shown to be protective.

[61] The mortality rate due to chronic ITP varies but tends to be higher relative to the general population for any age range.

These include obstetrical causes such as pre-eclampsia, HELLP syndrome (hemolysis, elevated liver enzymes and low platelets), or thrombotic microangiopathies that may occur during pregnancy.

Approximately 10% of newborns affected by ITP will have platelet counts <50,000/uL and 1% to 2% will have a risk of intracerebral hemorrhage, comparable to that of infants with neonatal alloimmune thrombocytopenia (NAIT).

[67][69] The first report of a successful therapy for ITP was in 1916, when a young Polish medical student, Paul Kaznelson, described a female patient's response to a splenectomy.