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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two patients who developed bilateral renal cortical necrosis as a consequence of Neisseria meningitidis infections are described: 1 patient had meningococcemia and the other had meningococcal meningitis. Both patients developed a Shwartzman-like reaction, disseminated intravascular coagulation and irreversible renal failure. Renal biopsy showed sclerosis of the majority of glomeruli; some glomeruli showed capillary congestion, thrombosis and an increased number of neutrophils; the intralobular arterioles showed thrombotic occlusions.
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PMID:Bilateral renal cortical necrosis in two patients with Neisseria meningitidis sepsis. 180 40

A 20-year-old woman with a transient diabetes insipidus as a complication to meningococcal meningitis is presented. This condition has only been described once before. Culture of blood and spinal fluid yielded Neisseria meningitidis group B, sensitive to penicillin. The diabetes insipidus arose on day 4 after admission and continued to day 15. Treatment comprised benzylpenicillin, DIC therapy, assisted ventilation, and vasopressin.
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PMID:Meningococcal meningitis and diabetes insipidus. 340 74

A series of patients with meningococcal infections have been studied and divided in two groups: Group I patients with meningococcal sepsis and group II, those with meningococcal meningitis. Patients in group I presented with more severe encephalopathy, shock, DIC and acute systemic complications. Both groups showed a marked hypoaminoacidemia compared with normal controls (other than for the sulfur containing amino acids and phenylalanine). The concentration of aromatic and basic amino acids, the phenylalanine/tyrosine ratio, the transaminase levels and the negative nitrogen balance were higher in group I patients. The ratio of branched chain to aromatic amino acids was lower in group I. All these differences were statistically significant. The close association between the metabolic derangements and clinical manifestations may help in the understanding of several physiopathological aspects of meningococcal infections.
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PMID:Significance of the changes in plasma amino-acid levels in meningococcal infection. 365 98

There are occasional reports in medical literature of peripheral gangrene and subsequent extremity amputation following systemic infection. Although the authors of these case reports speculated that the gangrene was due to septic embolization, pathologic study of the amputated tissue failed to reveal evidence of septic emboli. In reviewing reports of amputation following scarlet fever, varicella, pneumococcemia, and appendicitis, we found cases with clinical, hematologic, and pathologic evidence of disseminated intravascular coagulation (DIC). We describe 2 patients who required extremity amputation following an acute, systemic infection: transmetatarsal and Lisfranc amputation following meningococcal meningitis and bilateral below-knee amputation following pneumococcal meningitis. Both of these patients had clinical, hematologic, and pathologic evidence of DIC. Following amputation, both of these patients had significant problems with skin healing and prosthetic fitting. The presence of an acute systemic bacterial or viral infection, coagulation abnormalities and pathologic tissue indicative of DIC, and skin lesions of the extremities progressing to dry gangrene and ultimately requiring bilateral amputation are the key clinical features of this syndrome. We conclude that DIC is a major pathophysiologic mechanism responsible for peripheral gangrene following systemic infection.
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PMID:Extremity amputation: disseminated intravascular coagulation syndrome. 736 47

Thrombopoietin (TPO), interleukin (IL)-6, and platelets were measured serially in 9 patients with fulminant meningococcal septicemia and consumption coagulopathy. The results were compared with those of patients with meningococcal meningitis and mild meningococcemia (n=10) and with those of healthy control subjects (n=19). TPO levels in control subjects were below the detection limit (<63 pg/mL). In patients with fulminant meningococcal septicemia, the median TPO level on admission was 193 pg/mL (range, 133-401 pg/mL), and the level peaked within 3-7 days (median, 488 pg/mL; range, 239-1334 pg/mL). Platelet counts remained low, despite the elevated TPO levels. In patients with meningitis or meningococcemia, the median TPO level on admission was 112 pg/mL (range, <63-695 pg/mL), and the TPO level was not detectable within 48 h. Platelet counts for these patients remained within normal limits. Maximum IL-6 levels in patients with septicemia were observed on admission (median, 5317 pg/mL; range, 188-651,000 pg/mL) and increased earlier than TPO levels. In patients with fulminant septicemia, TPO level increases significantly whereas the level of circulating platelets does not.
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PMID:Fulminant meningococcal septicemia: dissociation between plasma thrombopoietin levels and platelet counts. 1077 Jul 23

In order to asses the clinical forms of meningococcal disease, we reviewed 201 cases diagnosed as meningococcal disease in the University Hospital of the Fluminense Federal University in Rio de Janeiro, 185 of which met the inclusion criteria. Clinical and laboratorial characterization allowed for grouping of the cases as follows: meningococcal meningitis, 18%; meningitis with septicemia, 62%; and septicemia, 20%. Available epidemiological data did not differentiate clinical forms. The following were significantly greater in meningococcal meningitis: duration of clinical history; frequency of neurological manifestations; positive bacterioscopy; culture and latex test in cerebrospinal fluid. The following were significantly predominant in septicemia: shock; fatal outcome and higher partial thromboplastin time. Septicemia and meningitis with septicemia were differentiated from meningococcal meningitis in the following: duration of clinical history; occurrence of focal neurological signs; disseminated intravascular coagulation; and arthritis. Clinical and laboratory data lead us to admit meningococcal meningitis as a localized form of Meningococcal disease, and meningitis with septicemia and septicemia as variations in severity of the systemic form of the disease.
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PMID:[Meningococcal disease: comparison between clinical forms]. 1765 66

The Gram-negative pathogen Neisseria meningitidis, is one of the leading causes of bacterial meningitis worldwide (1). The host range for this organism is restricted to humans, where it colonizes the mucosal epithelium of the upper airway. It occasionally disseminates causing invasive disease (sepsis, disseminated intravascular coagulation [DIC], meningitis). Epidemic meningococcal meningitis is a major health problem, most notably in sub-Saharan Africa. In 1999, an outbreak of meningococcal disease spread across Guinea-Bissau, a region that is part of what is commonly called the African meningitis belt (2). There were 2,169 reported cases and 404 deaths resulting from meningococcal disease in this outbreak from Jan. 1 to April 5, 1999. Also in 1999, there were reported outbreaks in Sudan (22,000 cases and 1,600 deaths) Rwanda (29 cases and 11 deaths), Angola (253 cases and 147 deaths), Ethiopia (126 cases and 4 deaths) and Senegal (2,709 cases and 372 deaths) (2). According to the World Health Organization (WHO), each year approx 500,000 cases of meningitis and 50,000 deaths are attributable to N. meningitidis worldwide. In the United States, meningococcal disease is less common, although small outbreaks are reported each year (3).
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PMID:Isolation and analysis of radiolabeled meningococcal endotoxin. 2133 60