Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Purpura fulminans is the cutaneous manifestation of acute activation of the clotting mechanism resulting in massive hemorrhage due to an intravascular consumption coagulopathy. Peripheral necrotizing purpura is a warning signal, and early recognition of the clinical situation and heparin therapy may be lifesaving. Clinical manifestations and histologic features of this condition, along with its pathogenesis, treatment, and differential diagnosis are discussed.
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PMID:Purpura fulminans. 65 39

Purpura fulminans is a rare disease characterized by cutaneous ecchymosis, hypotension and fever associated with disseminated intravascular coagulation. It usually follows a preparatory infectious illness. A case in a 55 year old woman challenges the concept that this disease is limited to childhood. A review of 100 case reports is presented in which the often quoted high mortality of 90 per cent is found to be no longer tenable.
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PMID:Purpura fulminans. 78 14

Purpura Fulminans and DIC were the main clinical manifestations of the antiphospholipid syndrome observed in a 62-year-old man. The patient was well until 44 years of age when he began to suffer from recurrent thrombophlebitis, without other symptoms suggestive of immune disease. At the time of hospital admission the pt. appeared acutely ill, showing high fever, severe anemia, massive urinary blood loss, multiple purpuric patches evolving to hemorrhagic bullae and gangrene rapidly spreading over about 30% of the total body area. No signs of neurological involvement or of visceral thrombotic occlusions were present. Clotting tests were consistent with a diagnosis of DIC, further confirmed by skin biopsy showing the presence of thrombi in dermal arterioles. The autoantibody research was positive as follows: Waaler-Rose 1:40, Anti-DNA 1:80; ANF 1:640, aCA IgG 100 GPL. LA was diagnosed according to standard criteria: prolonged KCT and RVVT not corrected by a mixture of normal plasma and abnormal TTI. Plasma exchange in association with heparin and prednisone was effective in arresting the progression of the skin lesion; nevertheless the patient died ten days after hospital admission for sepsi and acute renal failure.
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PMID:Purpura fulminans as clinical manifestation of atypical SLE with antiphospholipid antibodies: a case report. 180 49

Purpura fulminans is a rare disease characterized by purpura ecchymosis, hypotension, and fever associated with disseminated intravascular coagulation. It often begins as a benign infectious process and subsequently progresses to a severe, catastrophic outcome. It is recognized to originate from congenital or acquired protein C deficiency. We present an unusual case of an adult with Xanthomonas maltophilia sepsis that subsequently developed into purpura fulminans with involvement of the four extremities. We discuss the importance of the protein C system in coagulation homeostasis and its relationship to purpura fulminans.
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PMID:Purpura fulminans secondary to Xanthomonas maltophilia sepsis in an adult with aplastic anemia. 191 97

Purpura fulminans (PF) is a cutaneous manifestation of a dramatic and deadly syndrome of systemic disseminated intravascular coagulation (DIC). It is characterized by microvascular thrombosis in the dermis followed by perivascular haemorrhage. Since two other related syndromes involve the protein C (PC) system, we undertook a serial study to investigate the levels of PC and protein S (PS) in two patients with acquired PF. Laboratory findings were consistent with DIC, and both patients were treated with blood replacement and heparin therapy. The levels of PC activity were very low during the initial 24-36 h after onset and gradually increased until returning to normal levels. The total and 'free' PS were also abnormal during the initial onset of PF. The total and free PS increased to normal after 4-6 d. Although the pathogenesis is not fully understood, the infection and sepsis appears to consume PC and PS selectively during the PF and DIC phase. Acquired PF appears to selectively involve the PC system in a similar fashion to two other syndromes of PF-like lesions.
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PMID:Protein C and protein S levels in two patients with acquired purpura fulminans. 214 90

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 cutaneous manifestation of the syndrome of systemic DIC. It is characterized by microvascular thrombosis in the dermis followed by perivascular hemorrhage, necrosis, and minimal inflammation. Laboratory findings are consistent with DIC. Although the pathogenesis is not fully understood, the DIC in purpura fulminans appears to involve the skin selectively. The development of purpura fulminans from homozygous protein C or protein S deficiencies can be separated into the two distinct phases. The first phase is the time period when the initial reversible lesions develop and grow. This reversible progression can be halted and reversed with the administration of protein C or protein S. The second phase is the irreversible stage in which the lesion continues to develop into a necrotic lesion, whether or not treated with protein C. This irreversible lesion will ultimately develop into a large full-thickness necrotic injury of the skin. It is very similar to the lesions seen in idiopathic purpura fulminans, warfarin-induced skin necrosis, and acute infectious purpura fulminans. Unfortunately, our current understanding of the mechanism or mechanisms of the induction and propagation of the purpura fulminans-like lesions in homozygous protein C or protein S deficiencies is minimal, since it has never been studied. We can only speculate on the mechanism based on laboratory data and comparison with the little that is known about the other similar types of lesions.
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PMID:Neonatal purpura fulminans due to homozygous protein C or protein S deficiencies. 214 4

Purpura fulminans is a rare disease that typically begins as a benign infectious process and subsequently progresses to severe sepsis, hypotension, purpura ecchymosis, and disseminated intravascular coagulation. We present an unusual case of an adult who was seen initially with pneumococcal sepsis that subsequently developed into purpura fulminans with major extremity involvement. A multidisciplinary approach is needed in the treatment of this often catastrophic disease.
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PMID:Purpura fulminans. 229 60

Purpura fulminans is an uncommon catastrophic syndrome that occurs in children, typically one to four weeks after a seemingly benign infectious process. The child usually presents with a high fever, purpuric ecchymosis, hypotension, disseminated intravascular coagulation, and gangrene of the extremities. We have recently treated six children, whose mean age was 22 months; three were male and three were female. Five of the six had a change of mental status upon initial examination. Their mean temperature was 104 degrees F. All six children had purpuric involvement of their extremities; three had involvement of their hands, two had involvement of their faces, and two had involvement of their trunks. All had absent palpable pulses and sluggish capillary refill in the involved hands and feet. Two patients died shortly after admission as a result of severe end-stage sepsis. The platelet counts in these two patients, and the white blood cell counts were markedly depressed. The mean platelet count of the survivors was 370,000 and the mean white blood cell count was 25,000. Lumbar punctures were positive for bacterial meningitis in five patients and viral meningitis in one patient. All patients were treated with intravenous heparin. Of the four survivors, two lost significant tissue and required multiple plastic reconstructive procedures, and two improved on heparin alone with no tissue loss. In addition to systemic support and intravenous antibiotics, the mainstay of treatment is one of immediate heparinization and a continuous heparin drip. Heparin prevents subsequent small vessel thrombosis and limits tissue loss due to ongoing purpura. Conservative management of the purpuric lesions is the treatment of choice until final demarcation occurs.
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PMID:The surgical implications of purpura fulminans. 234 Feb 49

Purpura fulminans is a catastrophic febrile illness, characterized by confluent ecchymosis skin lesions, low blood pressure an disseminated intravascular coagulation. The case of 32 year old female ratify that it is not only a pediatric condition. We emphasize the importance of an early diagnosis and the adequacy of the treatment. The possible etiology is discussed.
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PMID:[Purpura fulminans. Presentation of a clinical case]. 269 17

Purpura fulminans is a rare disease of childhood, manifested by massive hemorrhage into the skin, widespread thrombosis of venules and arterioles and a hematologic picture of disseminated intravascular coagulation. An unusual case in a 68-year-old man is presented and the mode of therapy discussed.
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PMID:Purpura fulminans in an adult. 379 38


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