Anti-platelet autoantibodies in a pregnant woman with ITP will attack the patient's own platelets and will also cross the placenta and react against fetal platelets. Therefore, ITP is a significant cause of fetal and neonatal immune thrombocytopenia. 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 infants with neonatal alloimmune thrombocytopenia (NAIT).

No lab test can reliably predict if neonatal thrombocytopenia will occur. The risk of neonatal thrombocytopenia is increased with:

- Mothers with a history of splenectomy for ITP

- Mothers who had a previous infant affected with ITP

- Gestational (maternal) platelet count less than 100,000/uL

It is recommended that pregnant women with thrombocytopenia or a previous diagnosis of ITP should be tested for serum antiplatelet antibodies. A woman with symptomatic thrombocytopenia and an identifiable antiplatelet antibody should be started on therapy for their ITP which may include steroids or IVIG. Fetal blood analysis to determine the platelet count is not generally performed as ITP-induced thrombocytopenia in the fetus is generally less severe than NAIT. Platelet transfusions may be performed in newborns, depending on the degree of thrombocytopenia. It is recommended that neonates be followed with serial platelet counts for the first few days after birth.,

Hydroxycarbamide and anagrelide are contraindicated during pregnancy and nursing. Essential thrombocytosis can be linked with a three-fold increase in risk of miscarriage. Throughout pregnancy, close monitoring of the mother and fetus is recommended. Low-dose low molecular weight heparin (e.g. enoxaparin) may be used. For life-threatening complications, the platelet count can be reduced rapidly using platelet apheresis, a procedure that removes platelets from the blood and returns the remainder to the patient.

The incidence of ET is 0.6-2.5/100,000 per year, the median age at onset is 65–70 years and it is more frequent in females than in males. The incidence in children is 0.09/100,000 per year.

There has been no general recommendation for treatment of patients with Giant Platelet Disorders, as there are many different specific classifications to further categorize this disorder which each need differing treatments. Platelet transfusion is the main treatment for people presenting with bleeding symptoms. There have been experiments with DDAVP (1-deamino-8-arginine vasopressin) and splenectomy on people with Giant platelet disorders with mixed results, making this type of treatment contentious.

Many of the further classifications of Giant Platelet Disorder occur as a result of being genetically passed down through families as an autosomal recessive disorder, such as in Bernard-Soulier syndrome and Grey Platelet syndrome. To get this disorder both of the parents have to have it for it to be passed down to the child. It has to be transmitted in an autosomal recessive pattern. There chromosome number is 17.

The incidence of acute TTP in adults is around 1.7–4.5 per million and year. These cases are nearly all due to the autoimmune form of TTP, where autoantibodies inhibit ADAMTS13 activity. The prevalence of USS has not yet been determined but is assumed to constitute less than 5% of all acute TTP cases. The syndrome's inheritance is autosomal recessive, and is more often caused by compound heterozygous than homozygous mutations. The age of onset is variable and can be from neonatal age up to the 5th–6th decade. The risk of relapses differs between affected individuals. Minimization of the burden of disease can be reached by early diagnosis and initiation of prophylaxis if required.

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. Hence one may be considered thrombocytopenic below that range, although the threshold for a diagnosis of ITP is not tied to any specific number.

The incidence of ITP is estimated at 50–100 new cases per million per year, with children accounting for half of that amount. At least 70 percent of childhood cases will end up in remission within six months, even without treatment. 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). 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.

ITP is usually chronic in adults and the probability of durable remission is 20–40 percent. The male to female ratio in the adult group varies from 1:1.2 to 1.7 in most age ranges (childhood cases are roughly equal for both genders) and the median age of adults at the diagnosis is 56–60. The ratio between male and female adult cases tends to widen with age. In the United States, the adult chronic population is thought to be approximately 60,000—with women outnumbering men approximately 2 to 1, which has resulted in ITP being designated an orphan disease.

The mortality rate due to chronic ITP varies but tends to be higher relative to the general population for any age range. In a study conducted in Great Britain, it was noted that ITP causes an approximately 60 percent higher rate of mortality compared to gender- and age-matched subjects without ITP. This increased risk of death with ITP is largely concentrated in the middle-aged and elderly. Ninety-six percent of reported ITP-related deaths were individuals 45 years or older. No significant difference was noted in the rate of survival between males and females.

Treatment of asymptomatic congenital dysfibrinogenemia depends in part on the expectations of developing bleeding and/or thrombotic complications as estimated based on the history of family members with the disorder and, where available, determination of the exact mutation causing the disorder plus the propensity of the particular mutation type to develop these complications. In general, individuals with this disorder require regular follow-up and multidiscipline management prior to surgery, pregnancy, and giving childbirth. Women with the disorder appear to have an increased rate of miscarriages and all individuals with fibrinogen activity in clotting tests below 0.5 grams/liter are prone to bleeding and spontaneous abortions. Women with multiple miscarriages and individuals with excessively low fibrinogen activity levels should be considered for prophylaxis therapy with fibrinogen replacement during pregnancy, delivery, and/or surgery.

Individuals experiencing episodic bleeding as a result of congenital dysfibrinogenemia should be treated at a center specialized in treating hemophilia. They should avoid all medications that interfere with normal platelet function. During bleeding episodes, treatment with fibrinogen concentrates or in emergencies or when these concentrates are unavailable, infusions of fresh frozen plasma and/or cryoprecipitate (a fibrinogen-rich plasma fraction) to maintain fibrinogen activity levels >1 gram/liter. Tranexamic acid or fibrinogen concentrates are recommended for prophylactic treatment prior to minor surgery while fibrinogen concentrates are recommended prior to major surgery with fibrinogen concentrates usage seeking to maintain fibrinogen activity levels at >1 gram/liter. Women undergoing vaginal or Cesarean child birth should be treated at a hemophilia center with fibrinogen concentrates to maintain fibrinogen activity levels at 1.5 gram/liter. The latter individuals require careful observation for bleeding during their post-partum periods.

Individuals experiencing episodic thrombosis as a result of congenital dysfibrinogenemia should also be treated at a center specialized in treating hemophilia using antithrombotic agents. They should be instructed on antithrombotic behavioral methods fur use in high risk situations such as long car rides and air flights. Venous thrombosis should be treated with low molecular weight heparin for a period that depends on personal and family history of thrombosis events. Prophylactic treatment prior to minor surgery should avoid fibrinogen supplementation and use prophylactic anticoagulation measures; prior to major surgery, fibrinogen supplementation should be used only if serious bleeding occurs; otherwise, prophylactic anticoagulation measures are recommended.

Harris platelet syndrome (HPS) is the most common inherited giant platelet disorder.

HPS was identified among healthy blood donors in the north-eastern part of the Indian subcontinent, characterized by absent bleeding symptoms, mild to severe thrombocytopenia (platelets rarely <50 X 109/L)with giant platelets (Mean platelet volume 10fL) and normal platelet aggregation studies with absent MYH9 mutation.

In the blood donors with HPS authors found a statistically higher MPV, RDW and a lower platelet count and platelet biomass.

At present the diagnosis of HPS is made by ascertaining the ethnicity of the patient, as well as assessing for conditions causing acquired thrombocytopenias, and after also excluding the known inherited giant platelet disorders(IGPD) and other congenital thrombocytopenias. Unfortunately some patients with IGPD are treated inappropriately with corticosteroids, immunoglobulin infusions and even splenectomy.

It is extremely important to recognize Harris platelet syndrome, as one third the population of certain parts of Indian subcontinent is affected.

In terms of treatment/management, bleeding events can be controlled by platelet transfusion.

Most heterozygotes, with few exceptions, do not have a bleeding diathesis. BSS presents as a bleeding disorder due to the inability of platelets to bind and aggregate at sites of vascular endothelial injury. In the event of an individual with mucosal bleeding tranexamic acid can be given.

The affected individual may need to avoid contact sports and medications such as aspirin, which can increase the possibility of bleeding. A potential complication is the possibility of the individual producing antiplatelet antibodies

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

- Essential (primary)

- Essential thrombocytosis (a form of myeloproliferative disease)

- Other myeloproliferative disorders such as chronic myelogenous leukemia, polycythemia vera, myelofibrosis

- Reactive (secondary)

- Inflammation

- Surgery (which leads to an inflammatory state)

- Hyposplenism (decreased breakdown due to decreased function of the spleen)

- Splenectomy

- Asplenia (absence of normal spleen function)

- Iron deficiency anemia or hemorrhage

Over-medication with drugs that treat thrombocytopenia, such as eltrombopag or romiplostim, may also result in thrombocytosis.

Other causes include the following

- Kawasaki disease

- Soft tissue sarcoma

- Osteosarcoma

- Dermatitis (rarely)

- Inflammatory bowel disease

- Rheumatoid arthritis

- Nephritis

- Nephrotic syndrome

- Bacterial diseases, including pneumonia, sepsis, meningitis, urinary tract infections, and septic arthritis.

The vast majority of causes of thrombocytosis are acquired disorders, but in a few cases, they may be congenital, such as thrombocytosis due to congenital asplenia.

The prevalence of vWD is about one in 100 individuals. However, the majority of these people do not have symptoms. The prevalence of clinically significant cases is one per 10,000. Because most forms are rather mild, they are detected more often in women, whose bleeding tendency shows during menstruation. It may be more severe or apparent in people with blood type O.

Thrombocytopenia affects a few percent of newborns, and its prevalence in neonatal intensive care units (NICU) is high. Normally, it is mild and resolves without consequences. Most cases affect preterm birth infants and result from placental insufficiency and/or fetal hypoxia. Other causes, such as alloimmunity, genetics, autoimmunity, and infection, are less frequent.

Thrombocytopenia that starts after the first 72 hours since birth is often the result of underlying sepsis or necrotizing enterocolitis (NEC). In the case of infection, PCR tests may be useful for rapid pathogen identification and detection of antibiotic resistance genes. Possible pathogens include viruses (e.g. Cytomegalovirus (CMV), rubella virus, HIV), bacteria (e.g. "Staphylococcus sp.", "Enterococcus sp.", "Streptococcus agalactiae" (GBS), "Listeria monocytogenes", "Escherichia coli", "Haemophilus influenzae", "Klebsiella pneumoniae", "Pseudomonas aeruginosa", "Yersinia enterocolitica"), fungi (e.g. "Candida sp."), and "Toxoplasma gondii". The severity of thrombocytopenia may be correlated with pathogen type; some research indicates that the most severe cases are related to fungal or gram-negative bacterial infection. The pathogen may be transmitted during or before birth, by breast feeding, or during transfusion. Interleukin-11 is being investigated as a drug for managing thrombocytopenia, especially in cases of sepsis or necrotizing enterocolitis (NEC).

Abnormally high rates of platelet destruction may be due to immune or non-immune conditions, including:

- Immune thrombocytopenic purpura

- Thrombotic thrombocytopenic purpura

- Hemolytic-uremic syndrome

- Disseminated intravascular coagulation

- Paroxysmal nocturnal hemoglobinuria

- Antiphospholipid syndrome

- Systemic lupus erythematosus

- Post-transfusion purpura

- Neonatal alloimmune thrombocytopenia

- Hypersplenism

- Dengue fever

- Gaucher's disease

- Zika virus

Therapy involves both preventive measures and treatment of specific bleeding episodes.

- Dental hygiene lessens gingival bleeding

- Avoidance of antiplatelet agents such as aspirin and other anti-inflammatory drugs (NSAIDs) such as ibuprofen and naproxen, and anticoagulants

- Iron or folate supplementation may be necessary if excessive or prolonged bleeding has caused anemia

- Hepatitis B vaccine

- Antifibrinolytic drugs such as tranexamic acid or ε-aminocaproic acid (Amicar)

- Desmopressin (DDAVP) does not normalize the bleeding time in Glanzmann's thrombasthenia but anecdotally improves hemostasis

- Hormonal contraceptives to control excessive menstrual bleeding

- Topical agents such as gelfoam, fibrin sealants, polyethylene glycol polymers, custom dental splints

- Platelet transfusions (only if bleeding is severe; risk of platelet alloimmunization)

- Recombinant factor VIIa, AryoSeven or NovoSeven FDA approved this drug for the treatment of the disease on July 2014.

- Hematopoietic stem cell transplantation (HSCT) for severe recurrent hemorrhages

Glanzmann's thrombasthenia can be inherited in an autosomal recessive manner or acquired as an autoimmune disorder.

The bleeding tendency in Glanzmann's thrombasthenia is variable, some individuals having minimal bruising, while others have frequent, severe, potentially fatal hemorrhages. Moreover, platelet αβ levels correlate poorly with hemorrhagic severity, as virtually undetectable αβ levels can correlate with negligible bleeding symptoms, and 10%–15% levels can correlate with severe hemorrhage. Unidentified factors other than the platelet defect itself may have important roles.

Secondary TTP is diagnosed when the patient's history mentions one of the known features associated with TTP. It comprises about 40% of all cases of TTP. Predisposing factors are:

- Cancer

- Bone marrow transplantation

- Pregnancy

- Medication use:

- Antiviral drugs (acyclovir)

- Certain chemotherapy medications such as gemcitabine and mitomycin C

- Quinine

- Oxymorphone

- Quetiapine

- Bevacizumab

- Sunitinib

- Platelet aggregation inhibitors (ticlopidine, clopidogrel, and prasugrel)

- Immunosuppressants (ciclosporin, mitomycin, tacrolimus/FK506, interferon-α)

- Hormone altering drugs (estrogens, contraceptives, hormone replacement therapy)

- HIV-1 infection

The mechanism of secondary TTP is poorly understood, as ADAMTS13 activity is generally not as depressed as in idiopathic TTP, and inhibitors cannot be detected. Probable etiology may involve, at least in some cases, endothelial damage, although the formation of thrombi resulting in vessel occlusion may not be essential in the pathogenesis of secondary TTP. These factors may also be considered a form of secondary aHUS; patients presenting with these features are, therefore, potential candidates for anticomplement therapy.

aHUS can be inherited or acquired, and does not appear to vary by race, gender, or geographic area. As expected with an ultra-rare disease, data on the prevalence of aHUS are extremely limited. A pediatric prevalence of 3.3 cases per million population is documented in one publication of a European hemolytic uremic syndrome (HUS) registry involving 167 pediatric patients.

The vWF gene is located on the short arm "p" of chromosome 12 (12p13.2). It has 52 exons spanning 178kbp. Types 1 and 2 are inherited as autosomal dominant traits and type 3 is inherited as autosomal recessive. Occasionally, type 2 also inherits recessively. vWD occurs in approximately 1% of the population and affects men and women equally.

Recent studies have found that the life expectancy of males with XLT is not significantly affected. Individuals with XLT typically experience milder symptoms than those with other "WAS"-related disorders. For this reason, the long term prognosis for individuals with XLT is generally positive as long as symptoms are managed appropriately. Enhanced treatment methods in the past two decades have significantly improved the prognosis as well.

Bernard–Soulier syndrome (BSS), also called hemorrhagiparous thrombocytic dystrophy, is a rare autosomal recessive coagulopathy (bleeding disorder) that causes a deficiency of "glycoprotein Ib" (GpIb), the receptor for von Willebrand factor. The incidence of BSS is estimated to be less than 1 case per million persons, based on cases reported from Europe, North America, and Japan. BSS is a giant platelet disorder, meaning that it is characterized by abnormally large platelets.

Gray platelet syndrome (GPS), or platelet alpha-granule deficiency, is a rare congenital autosomal recessive bleeding disorder caused by a reduction or absence of alpha-granules in blood platelets, and the release of proteins normally contained in these granules into the marrow, causing myelofibrosis.

GPS is primarily inherited in an autosomal recessive manner, and the gene that is mutated in GPS has recently been mapped to chromosome 3p and identified as "NBEAL2". "NBEAL2" encodes a protein containing a BEACH domain that is predicted to be involved in vesicular trafficking. It is expressed in platelets and megakaryocytes and is required for the development of platelet alpha-granules. "NBEAL2" expression is also required for the development of thrombocytes in zebrafish.

GPS is characterized by "thrombocytopenia, and abnormally large agranular platelets in peripheral blood smears." The defect in GPS is the failure of megakaryocytes to package secretory proteins into alpha-granules. Patients with the GPS are affected by mild to moderate bleeding tendencies. Usually these are not major bleeds but there has been some life threatening cases. Also Women will tend to have heavy, irregular periods. Myelofibrosis is a condition that usually comes with the Gray Platelet syndrome.

X-linked thrombocytopenia is inherited on the X chromosome. Females that are carriers will have a 50% chance of passing the "WAS" gene mutation on to their male offspring. Female offspring also have a 50% chance of receiving the mutated gene from their mothers and are considered carriers in that event. Males with X-linked thrombocytopenia will not pass the condition to their sons since they pass their Y chromosome on to any male offspring. However, any daughters males with this condition have will be carriers.