purpura fulminans/inflammation

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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

What may underlie recurrent purpura fulminans?

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A woman presenting with recurrent purpura fulminans was eventually found to have inflammatory bowel disease. We suggest the inflammatory state resulted in a deficiency of functional protein C.

Development of Bilateral Heterotopic Ossification After Survival of Life Threatening Purpura Fulminans.

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Heterotopic ossification has been reported in patients who have undergone traumatic amputations, burn injuries, and total hip arthroplasty; however, the incidence of heterotopic ossification following purpura fulminans has only been reported in one case with unilateral involvement. Here we present a

Pneumococcal purpura fulminans successfully treated with activated protein C.

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Evidence suggests that sepsis is a systemic inflammatory condition complicated by dysequilibrium in coagulation and fibrinolytic homeostasis, with a shift in the balance towards increased coagulation over fibrinolysis. Protein C is a natural anticoagulant consumed and inactivated during sepsis. We

Fatal group A Streptococcus purpura fulminans in a child receiving TNF-α blocker.

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Inhibition of tumor necrosis factor alpha (TNF-α) is effective in the treatment of many pediatric autoimmune diseases and inflammatory conditions. Commonly available biologic agents blocking TNF-α are infliximab, etanercept, and adalimumab. These agents have changed the management of rheumatic

Protein C anticoagulant pathway and its role in controlling microvascular thrombosis and inflammation.

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OBJECTIVE To review the physiologic and biochemical mechanisms that suggest that protein C and activated protein C (APC) have unique properties that make them good candidates for the treatment of microvascular thrombosis, disseminated intravascular coagulation, and sepsis. METHODS A summary of

Neonatal purpura fulminans due to homozygous protein C or protein S deficiencies.

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Homozygous protein C deficiency or homozygous protein S deficiency are rare genetic diseases with catastrophic and fatal purpura fulminans-like or thrombotic complications occurring during the neonatal period. These diseases can now be successfully treated. Purpura fulminans is at least in part a

Staphylococcal Purpura Fulminans: Report of a Case.

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Purpura fulminans (PF) is associated with several infections and most commonly with meningococcemia. However, there are only a few reports of this entity in association with toxic shock syndrome toxin-1-producing Staphylococcus aureus. We report a 53-year-old man who presented with fever,

Proposed classification and pathologic mechanisms of purpura fulminans and skin necrosis.

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The syndromes of purpuric lesions associated with a thrombotic mechanism are very rare in the general population. Dermal vascular thrombosis, however, can be devastating and associated with significant morbidity and mortality. These syndromes share common features in their clinical course,

Human protein C concentrate in the treatment of purpura fulminans: a retrospective analysis of safety and outcome in 94 pediatric patients.

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BACKGROUND Purpura fulminans (PF) is a devastating complication of uncontrolled systemic inflammation, associated with high incidence of amputations, skin grafts and death. In this study, we aimed to clarify the clinical profile of pediatric patients with PF who improved with protein C (PC)

Successful Corticosteroid Treatment for Purpura Fulminans Associated with Quinolone.

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Purpura fulminans (PF) is a life-threatening syndrome comprising progressive hemorrhagic necrosis due to disseminated intravascular coagulation and dermal vascular thrombosis that leads to purpura and tissue necrosis. Various therapies have been used to arrest the progression of this disease,

Massive soft tissue infections: necrotizing fasciitis and purpura fulminans.

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Necrotizing fasciitis and purpura fulminans are two destructive infections that involve both skin and soft tissue. Necrotizing fasciitis is characterized by widespread necrosis of subcutaneous tissue and the fascia. Historically, group A beta-hemolytic streptococcus has been identified as a major

[Inflammatory myopathy following acute meningoccemia in a properdin-deficient patient: A case report].

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Myalgia is a classical sign in invasive meningococcal diseases (IMD), but severe and persistent myalgia following an IMD have never been reported to date.A 20-year-old man presented with purpura fulminans and meningitis caused by Neisseria meningitidis

[Post-varicella purpura fulminans: potentially fatal].

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Although varicella is usually a benign disease, some of its complications, such as post-varicella purpura fulminans, can be fatal. Its pathophysiological mechanism is caused by the production of antibodies to protein C and protein S in the coagulation cascade. This could have fatal consequences for

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