Disease relevance of Purpura

• A patient developed disseminated intravascular coagulation with purpura fulminans 1 month after starting Dilantin therapy for a seizure disorder [1].
• It has been established that amelioration of murine immune thrombocytopenia purpura (ITP) by IVIg is dependent on the inhibitory receptor FcgammaRIIB [2].
• Positive results were obtained in 16 of 19 sera of patients with various diseases including 2 of 4 patients with idiopathic thrombocytopenic purpura, 2 of 2 with post-transfusion purpura, 2 of 3 with neonatal purpura, and all 9 polytransfused patients [3].
• Heparin is indicated in patients with purpura fulminans and venous thromboembolism, but there is little evidence that heparin reverses organ dysfunction associated with DIC [4].
• To better understand factors regulating TPO levels, we measured blood levels of TPO in patients with impaired platelet production due to aplastic anemia (AA) and with platelet destructive disorders, including idiopathic thrombocytopenic purpura (ITP), posttransfusion purpura (PTP), drug purpura (DP), and X-linked thrombocytopenia (XLTP) [5].

High impact information on Purpura

• Treatment of homozygous protein C deficiency and neonatal purpura fulminans with a purified protein C concentrate [6].
• Purpura due to ethanol [7].
• Tumor necrosis factor and interleukin-1 in the serum of children with severe infectious purpura [8].
• Purpura due to inhaled quinidine [9].
• Prophylaxis of steroid-induced purpura [10].

Chemical compound and disease context of Purpura

• When posttransfusion purpura serum was studied, antibody binding to the PlA1 antigen on glycoprotein IIIa was readily distinguished from the nonspecific binding of immunoglobulin to a protein of 200,000 mol wt [11].
• Use of protein-C concentrate, heparin, and haemodiafiltration in meningococcus-induced purpura fulminans [12].
• Coumarin prophylaxis for fulminant purpura syndrome due to homozygous protein C deficiency [13].
• Adult Schönlein-Henoch purpura after enalapril [14].
• Adult Schönlein-Henoch purpura after lisinopril [15].

Biological context of Purpura

• In patients with immune thrombocytopenia purpura (ITP), with decreased PLT survival, but intact bone marrow megakaryocytopoiesis, endogenous IL-11 levels were significantly increased (328.0 +/- 92.6 pg/mL, [PLT: 20,900 +/- 3,000/microL], P < .05, n = 25) [16].
• We present 2 children from 2 unrelated Arab families with purpura fulminans who were double heterozygotes for factor V Leiden inherited from their fathers and protein S deficiency inherited from their mothers [17].
• Thus, in individuals with severe disease expression, the risk of purpura fulminans with death or deformity was significantly increased when the platelet count was < 50,000 cells/mm3 (P = .0001) and protein C levels were low (P = .0158) [18].
• Abnormalities of immunoglobulin A1 (IgA1) glycosylation have been described in patients with IgA nephropathy (IgAN), whether primitive or secondary to Henoch-Schönlein purpura [19].
• Posttransfusion purpura: conversion of PLA1-negative platelets to the PLA1-positive phenotype by stored plasma is not due to the presence of soluble PLA1 antigen [20].

Anatomical context of Purpura

• ACTH-secreting medullary carcinoma of the thyroid presenting a severe idiopathic osteoporosis and senile purpura: report of a case and review of the literature [21].
• To investigate the role of human hepatocyte growth factor (hHGF) in vascular lesions associated with endothelial injury, we measured serum hHGF concentrations in subjects with retinal arteriosclerosis, coronary atherosclerosis, or arteriolitis due to Henoch-Schönlein purpura [22].
• 2. Dexamethasone treatment (0.4-4 mg kg-1, daily for 1-6 days) produced time- and dose-dependent damage to the glandular mucosa of the stomach as characterized by extensive, uniform hyperaemia with multiple, focal petechiae and erosions [23].
• A latex assay revealed the CS index (CSI) was significantly low in patients with podocyte disease (group A), including SSNS, focal and segmental glomerulosclerosis (FSGS) and Finnish-type congenital nephrotic syndrome (FCNS), but high in those with Alport syndrome (AS), IgAN, Henoch-Schönlein purpura nephritis (HSPN), and MPGN (group B) [24].
• The episodes of purpura fulminans were controlled by infusions of fresh frozen plasma containing protein C. The requirement of frequent plasma infusions, however, eventually resulted in several complications secondary to hyperproteinemia [25].

Gene context of Purpura

• The metalloprotease ADAMTS-13 cleaves von Willebrand factor (VWF), and is absent or severely reduced in the plasma of patients with thrombotic thrombocytopenia purpura (TTP) [26].
• Postinfectious purpura fulminans caused by an autoantibody directed against protein S [27].
• High plasma MMP-9 is indicative of definite pSS but may paradoxically have a preventive effect on the eruption of purpura and on the development of autoantibody reaction in pSS [28].
• The IL4 -509 T allele and IL13 +2044 A allele carriers less often had purpura than the corresponding non-carriers [29].
• Coumarin necrosis, neonatal purpura fulminans, and protein C deficiency [30].

Analytical, diagnostic and therapeutic context of Purpura

• An effective therapeutic regimen for thrombotic throbocytopenic purpura would include initial therapy with exchange plasmapheresis, aspirin, and dipyridamole and maintenance therapy with antiplatelet agents [31].
• Serologic tests for quinidine- or quinine-dependent antibodies can help elucidate some obscure cases of purpura that may be self-induced [32].
• The clinical course of IgA-nephropathy and Henoch-Schönlein purpura following renal transplantation [33].
• Topical nitroglycerin has been previously described as an adjunctive therapy to increase perfusion to areas of purpura affected in purpura fulminans [34].
• Erythematous macules, nonpalpable and palpable purpura, and flaccid pustules developed in a 59-year-old man with acute lymphocytic leukemia 8 days after reinduction chemotherapy with cytosine arabinoside and daunorubicin [35].

References