Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immune thrombocytopenic purpura is rarely seen in Hodgkin disease and the presence of platelet-associated antibody has not been previously reported in these patients. A patient with Hodgkin disease is described who developed a destructive thrombocytopenia demonstrated by shortened platelet survival. In conjunction with his thrombocytopenia, he had marked elevation of platelet-associated immunoglobulin G levels (nanograms IgG per 10(9) platelets: 15,187 prior to splenectomy and 71,130 and 81,900 after surgery). Mean values (+/-SD) of control subjects averaged 1,975 + 381 and four patients with Hodgkin disease and normal platelet counts had levels ranging from 1,581 to 4,011. We suggest that this patient had immune-mediated thrombocytopenia; whether the increase in platelet-associated immunoglobulin G was due to antiplatelet antibody or to adsorbed or phagocytosed immune complexes cannot be demonstrated by these studies. The platelet-associated immunoglobulin G test may be useful in evaluating these patients.
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PMID:Immune thrombocytopenic purpura in Hodgkin disease. 57 64

Immune thrombocytopenic purpura (ITP) has been observed infrequently in untreated Hodgkin's disease. A patient with an ITP associated with an inapparent Hodgkin's disease, who presented a life threatening CNS haemorrhage as first clinical manifestation, is described.
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PMID:Thrombocytopenic purpura as first manifestation of an inapparent Hodgkin's disease. 375 77

Immune thrombocytopenic purpura (ITP) can be classified as primary (known also as idiopathic thrombocytopenic purpura) or as secondary to an underlying condition such as a malignant or nonmalignant disorder. Commonly occurring conditions associated with secondary ITP include lymphoproliferative disorders (chronic lymphocytic leukemia [CLL], Hodgkin's disease and non-Hodgkin's lymphomas), autoimmune collagen vascular diseases (systemic lupus erythematosus [SLE], thyroid disease, antiphospholipid syndrome [APS]), and chronic infections (human immunodeficiency virus [HIV], Helicobacter pylori, hepatitis C virus [HCV]). The mechanism of platelet destruction in thrombocytopenias associated with lymphoproliferative disorders and collagen vascular diseases is identical to the autoimmune mechanism seen in primary ITP. Drug-induced thrombocytopenias are uncommon and generally resolve quickly upon drug discontinuation, but are often attributed to other causes. Platelet destruction in infection-associated ITP occurs via various mechanisms including accelerated platelet clearance due to immune complex disease as seen in HIV infection or cross-reactivity of anti-platelet glycoprotein antibodies and viral antigens in HIV, HCV, and H pylori infections (antigenic mimicry). In patients with HCV-related cirrhotic liver disease, splenic sequestration secondary to portal hypertension and decreased production of thrombopoietin may further contribute to development of thrombocytopenia. The current treatment paradigm for secondary ITP varies according to the underlying condition. Standard treatments for primary ITP (corticosteroids, IVIG, anti-D, splenectomy) are often successful in secondary ITP. In cases of ITP with H pylori and HCV infection, treatment should focus on the underlying disorder.
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PMID:Other immune thrombocytopenias. 1809 69

Immune thrombocytopenic purpura (ITP), a condition of low platelets, can occur from primary causes, often referred to as idiopathic thrombocytopenic purpura, or secondary to an underlying disease, such as an autoimmune disorder or an infection. Secondary ITP can also occur with lymphoproliferative malignancies, such as chronic lymphocytic leukemia (CLL), Hodgkin's disease (HD), and non-Hodgkin's lymphomas (NHL). ITP associated with lymphoproliferative disorders has the same mechanism of platelet destruction as in idiopathic or primary ITP. The current treatment paradigm for secondary ITP varies according to the underlying condition. Standard treatments for primary ITP, which include corticosteroids, intravenous immunoglobulin (IVIg), anti-D, and splenectomy, are often successful in secondary ITP. However, in most situations with secondary ITP, treatment should focus on resolving the underlying disorder before treating the shortage of platelets, and, in the circumstances of ITP developing in patients with lymphoproliferative disorders, responses are frequently linked to remission of the primary malignancy.
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PMID:Recognizing and treating secondary immune thrombocytopenic purpura associated with lymphoproliferative disorders. 1924 32

Immune thrombocytopenic purpura (ITP) has been associated with several hematologic malignancies such as Hodgkin and non-Hodgkin lymphomas and chronic lymphocytic leukemia, but it is rare in children with acute lymphoblastic leukemia (ALL). Here, we report a 7-year-old girl with chronic ITP during early intensive phase of chemotherapy for ALL. She underwent splenectomy because thrombocytopenia had persisted even after treatment with intravenous immunoglobulin (IVIG), steroids, vincristine, rituximab, and anti-D antibody. After splenectomy, her platelet count had recovered, and maintenance therapy could be resumed with a support of IVIG. To our knowledge, this is the first child case of chronic ITP during chemotherapy for ALL and splenectomy was effective in this patient.
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PMID:Refractory chronic immune thrombocytopenic purpura in a child with acute lymphoblastic leukemia. 1981 66