Idiopathic thrombocytopenic purpura medical therapy: Difference between revisions
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===Steroids/IVIgG=== | ===Steroids/IVIgG=== | ||
[[Platelet count]] below 20,000 is an indication for treatment; the patients with 20,000–50,000 platelets/μL are considered on a case by case basis, and there is generally no need to treat the patients with above 50,000 platelets/μL.<ref name="pmid15941913"/> Hospitalization is recommended in the cases of significant internal or mucocutaneous bleeding. The treatment begins with intravenous steroids (methylprednisolone or prednisone), [[intravenous immunoglobulin]] (IVIg) or their combination and sometimes platelet infusions in order to raise the count quickly. After the platelet count stabilized and in the less severe cases oral prednisone (1–2 mg/kg) is used. Most cases respond during the first week of treatment (RR ~70%). After several weeks of prednisone therapy, the dose is gradually reduced. However, 60–90% of patients relapse after the dose decreased below 0.25 mg/kg and stopped. | [[Platelet count]] below 20,000 is an indication for treatment; the patients with 20,000–50,000 platelets/μL are considered on a case by case basis, and there is generally no need to treat the patients with above 50,000 platelets/μL.<ref name="pmid15941913"/> Hospitalization is recommended in the cases of significant internal or mucocutaneous bleeding. The treatment begins with intravenous steroids (methylprednisolone or prednisone), [[intravenous immunoglobulin]] (IVIg) or their combination and sometimes platelet infusions in order to raise the count quickly. After the platelet count stabilized and in the less severe cases oral prednisone (1–2 mg/kg) is used. Most cases respond during the first week of treatment (RR ~70%). After several weeks of prednisone therapy, the dose is gradually reduced. However, 60–90% of patients relapse after the dose decreased below 0.25 mg/kg and stopped. Pulsed high-dose dexamethasone shows (in untreated patients) a high RR of ~90% with a long-term RR of ~80% when several cycles of treatment are given. However long term high dose steroids have a myriad of toxicities and should be avoided if possible. | ||
The ITP in [[AIDS]] has a [[thrombocytopenia]] that is multifactorial involving both TPO and platelet problems. Mechanisms may involve [[portal hypertension]] that leads to [[splenomegaly]] causing platelet sequestration. [[Hepatits C]] (HCV) causes decreased TPO production leading to decreased platelet production. Steroids may be helpful but, with their taper, the count usually decreases again. Intravenous [[immunoglobulin]]'s effect is transient. For ITP-HIV the primary treatment should be directed at HIV suppression with HAART. HIV patients whose platelet count fails to increase to > 50,000 with HAART can be treated with steroids. | The ITP in [[AIDS]] has a [[thrombocytopenia]] that is multifactorial involving both TPO and platelet problems. Mechanisms may involve [[portal hypertension]] that leads to [[splenomegaly]] causing platelet sequestration. [[Hepatits C]] (HCV) causes decreased TPO production leading to decreased platelet production. Steroids may be helpful but, with their taper, the count usually decreases again. Intravenous [[immunoglobulin]]'s effect is transient. For ITP-HIV the primary treatment should be directed at HIV suppression with HAART. HIV patients whose platelet count fails to increase to > 50,000 with HAART can be treated with steroids. | ||
Revision as of 15:23, 21 September 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Mechanism-based Approach to Treatment; 1) Inhibit phagocyte-mediated clearance of antibody-coated platelets; Steroids; Splenectomy; Anti-D; IV-IgG 2) Decreased autoantibody production; Rituximab; Steroids; Azathioprine & other immunosuppressants (eg cytoxan, cyclosporine, etc) 3) Impair T & B cell interactions.; Steroids; Rituximab 4) Enhance platelet production.; Thrombopoietic agents; IL-11.
Medical Therapy
Observation
Most children with ITP will recover even without specific treatment. Among adults ITP is typically a chronic disease. It is insidious in onset and, in some patients, refractory to treatment. 90% of childhood ITP cases are an acute, self-limited disease, developing several weeks after a viral illness, lasting for 4-6 weeks, then spontaneously remitting. The bleeding risk is low and treatment is reserved only for the most severely affected patients. Because spontaneous recovery is expected in children wit ITP some pediatric hematologists recommend supportive care only, no drugs. In less than 20% of children thrombocytopenia may persist for >6-12 months and even many of these kids can experience a spontaneous remission.
Steroids/IVIgG
Platelet count below 20,000 is an indication for treatment; the patients with 20,000–50,000 platelets/μL are considered on a case by case basis, and there is generally no need to treat the patients with above 50,000 platelets/μL.[1] Hospitalization is recommended in the cases of significant internal or mucocutaneous bleeding. The treatment begins with intravenous steroids (methylprednisolone or prednisone), intravenous immunoglobulin (IVIg) or their combination and sometimes platelet infusions in order to raise the count quickly. After the platelet count stabilized and in the less severe cases oral prednisone (1–2 mg/kg) is used. Most cases respond during the first week of treatment (RR ~70%). After several weeks of prednisone therapy, the dose is gradually reduced. However, 60–90% of patients relapse after the dose decreased below 0.25 mg/kg and stopped. Pulsed high-dose dexamethasone shows (in untreated patients) a high RR of ~90% with a long-term RR of ~80% when several cycles of treatment are given. However long term high dose steroids have a myriad of toxicities and should be avoided if possible.
The ITP in AIDS has a thrombocytopenia that is multifactorial involving both TPO and platelet problems. Mechanisms may involve portal hypertension that leads to splenomegaly causing platelet sequestration. Hepatits C (HCV) causes decreased TPO production leading to decreased platelet production. Steroids may be helpful but, with their taper, the count usually decreases again. Intravenous immunoglobulin's effect is transient. For ITP-HIV the primary treatment should be directed at HIV suppression with HAART. HIV patients whose platelet count fails to increase to > 50,000 with HAART can be treated with steroids.
Pregnant patients with ITP and platelet counts < 30,000 can be treated with intravenous immunoglobulin (IV-IgG) or steroids at the lowest dose possible to avoid hypertension, eclampsia and adrenal suppression of the fetus. ~10-30% of pregnant females with ITP have an infant with platelets <50,000, however, intracranial hemorrhage is rare. For these females administer prednisone during the last month of pregnancy to decrease the likelihood of thrombocytopenia in the fetus. Mothers with ITP who have previously given birth to infants without thrombocytopenia tend not to be thrombocytopenic. The maternal platelet count doesn't correlate with fetal and females with a prior history of ITP with ITP in remission (eg after splenectomy) may still deliver severely thrombocytopenic infants. This likely occurs because asplenic patients in clinical remission may not necessarily be in immunologic remission and circulating platelet-reactive IgG may still be present in their plasma.