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Coagulopathy as a predictor of outcome in meningococcal sepsis and the systemic inflammatory response syndrome with purpura.

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OBJECTIVE To identify simple, contemporary predictors of both morbidity and mortality in pediatric patients with purpuric sepsis syndrome in order to provide a basis for future study of innovative interventions. METHODS Retrospective study. METHODS An 18-bed multidisciplinary intensive care unit

Central nervous system inflammatory demyelination after rituximab therapy for idiopathic thrombocytopenic purpura.

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A 53-year-old female developed unilateral shoulder girdle pain, entire body paresthesiae and imbalance starting 10 days after completing a course of rituximab for chronic idiopathic thrombocytopenic purpura. Neuroimaging studies showed inflammatory demyelinating lesions of the cervical spinal cord

Sequential occurrence of Graves' disease and immune thrombocytopenic purpura as manifestations of immune reconstitution inflammatory syndrome in an HIV-infected patient.

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Immune reconstitution inflammatory syndrome (IRIS) in HIV-infected patients after initiating antiretroviral therapy usually involves worsening manifestations of overt infectious disease. Here, we describe a sporadic case of a late-diagnosed HIV-positive man who developed Graves' disease as the first

Polymorphisms in inflammatory cytokines and Fcgamma receptors in childhood chronic immune thrombocytopenic purpura: a pilot study.

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Inflammatory cytokines and low-affinity Fcgamma receptor (FcgammaR) polymorphisms were investigated in 37 children with chronic immune thrombocytopenic purpura (cITP) and 218 controls. Genotype analysis included common variants in the regulatory regions of cytokines, TNF, LTA, IL1RN, IL1A, IL1B,

An 'inflammatory' variant of solar purpura: a simulant of leukocytoclastic vasculitis and neutrophilic dermatoses.

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To study the clinical and pathological features of cases of apparent solar purpura, with attention to the recently described phenomenon of inflammatory changes within otherwise typical lesions. We studied 95 cases diagnosed as solar purpura and identified 10 cases (10.5%) in which significant

Mechanism of feedback regulation of neutrophil inflammation in Henoch-Schönlein purpura.

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The aim of this study is to investigate the role of complement-neutrophil feedback regulation of inflammatory response in Henoch-Schönlein purpura (HSP) through constructing an animal model of HSP. Twenty-four SPF grade Japanese large-eared white rabbits were randomly divided into normal group and

Inflammatory bowel disease associated with immune thrombocytopenic purpura in children.

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OBJECTIVE Previous reports suggest an association between inflammatory bowel disease (IBD) and immune thrombocytopenic purpura (ITP) in adults. To date, only five children with both diseases have been described. The aim of the study was to describe the characteristics of children with IBD and

Inflammatory Bowel Disease and Immune Thrombocytopenic Purpura: Combined Immune Dysregulation in an Adolescent.

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Concomitant inflammatory bowel disease (IBD) and immune thrombocytopenic purpura (ITP) is a rare phenomenon. A shared immunologic pathway leading to mucosal inflammation and platelet destruction has been proposed. We report a case of a 14-year-old male who presented with abdominal pain,

Serum uric acid and inflammation in patients with immune thrombocytopenic purpura: preliminary results.

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OBJECTIVE The purpose of this study was to evaluate the uric acid (UA) and C-reactive protein (CRP) levels in patients with immune thrombocytopenic purpura (ITP). METHODS Forty patients with newly diagnosed ITP and 40 healthy individuals were enrolled in the study. The patients were divided into two

Purpura simplex (inflammatory purpura without vasculitis): a clinicopathologic study of 174 cases.

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Purpura simplex manifests clinically as macular purpuric and petechial pigmented, golden, annular, or lichenoid lesions. These subtypes have been termed Schamberg's purpura, lichen aureus, Majocchi's purpura, and Gougerot-Blum purpura. Histologically, there is inflammation and hemorrhage without

Adult purpura fulminans associated with non-steroidal anti-inflammatory drug use.

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Purpura fulminans is an acute illness characterized by rapidly progressive dermal vascular thrombosis, leading to hemorrhagic necrosis of the skin. Here, we describe the case of a healthy woman who developed acute disseminated intravascular coagulation (DIC) with purpura fulminans after

Meningococcal purpura fulminans and severe myocarditis with clinical meningitis but no meningeal inflammation: a case report.

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During fulminant meningococcal septicaemia, meningococci are often observed in the cerebrospinal fluid (CSF) although the patients have frequently no meningeal symptoms. Meningococcal meningitis, by contrast, usually features clinical meningeal signs and biochemical markers of

Correlation between serum inflammatory factors TNF-α, IL-8, IL-10 and Henoch-Schonlein purpura with renal function impairment.

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The changes of tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8), interleukin-10 (IL-10) in the serum of Henoch-Schonlein purpura nephritis (HSPN) patients were analyzed to explore the correlation between the above inflammatory factors and progression of the disease. The present study used the

Changes of inflammatory mediators and oxidative stress indicators in children with Henoch-Schönlein purpura and clinical effects of hemoperfusion in the treatment of severe Henoch-Schönlein purpura with gastrointestinal involvement in children.

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To explore the changes of inflammatory and oxidative stress responses in Henoch-Schönlein purpura (HSP) children, and further analyzed the therapeutic effects and mechanisms of hemoperfusion (HP) on HSP with severe gastrointestinal (GI) involvement.There

Acute inflammatory sensorimotor polyradiculoneuropathy associated with immune thrombocytopenic purpura.

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Although acute inflammatory polyneuropathy (AIP) and immune thrombocytopenic purpura (ITP) are both believed to be immune-mediated disorders, only a few cases have been reported in which these two diseases co-existed. We describe a case of a 67-year-old patient who developed quadriparesis,

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