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)

Seven children (aged 8--17 years) presented with a high fever, headache, confusion, conjunctival hyperaemia, a scarlatiniform rash, subcutaneous oedema, vomiting, watery diarrhoea, oliguria, and a propensity to acute renal failure, hepatic abnormalities, disseminated intravascular coagulation, and severe prolonged shock. One patient died, one had gangrene of the toes, and all have had fine desquamation of affected skin and peeling of palms and soles during convalescence. Five patients were studied prospectively. Staphylococcus aureus related to phage-group I was isolated from mucosal (nasopharyngeal, vaginal, tracheal), or sequestered (empyema, abscess) sites, but not from blood. This organism produces an exotoxin which causes a positive Nikolsky sign in the newborn mouse and which is biochemically, pathologically, and immunologically distinct from phage-group-II stapphylococcal exfoliatin.
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PMID:Toxic-shock syndrome associated with phage-group-I Staphylococci. 8 81

The case of a two-month -old female infant, who after a severe diarrhoea treated with prolonged intravenous infusion in peripheral veins alternated with total parenteral feeding, developed a Candida albicans septicemia (accompanied by disseminated intravascular coagulation syndrome) is reported. The course of her disease was also complicated by multiple foci of osteoarthritis in both knees, in the left hip and in several long-bones. Radiographically the foci of Candida osteitis appeared as fine erosion of the cortex and minute round areas of osteolysis in the spongiosa, surrounded by a rim of perifocal sclerosis. During the acute stage of Candida sepsis a transitory cellular immunodeficiency was present. Treatment of Candida infection by 5-fluorocytosine was followed by complete recovery.
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PMID:Disseminated arthritis and osteitis by Candida albicans in a two month old infant receiving parenteral nutrition. 40 39

The first recognised outbreak of Marburg virus disease in Africa, and the first since the original epidemic in West Germany and Yugoslavia in 1967, occurred in South Africa in February 1975. The primary case was in a young Australian man , who was admitted to the Johannesburg Hospital after having toured Rhodesia. Two secondary cases occurred, one being in the first patient's travelling companion, and the other in a nurse. Features of the illness included high fever, myalgia, vomiting and diarrhoea, hepatitis, a characteristic maculopapular rash, leucopenia, thrombocytopenia, and a bleeding tendency. The first patient died on the seventh day from haemorrhage resulting from a combination of disseminated intravascular coagulation and hepatic failure. The other two patients were given vigorous supportive treatment and prophylactic heparin and recovered after an acute phase lasting about seven days. During this period on developed pancreatitis, the serum amylase remaining raised until the 32nd day after the onset of the illness. The other developed unilateral uveitis after having been asymptomatic for two months. This persisted for several weeks and Marburg virus was cultured from the anterior chamber of the eye.
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PMID:Outbreake of Marburg virus disease in Johannesburg. 81 15

A patient with chronic active hepatitis developed vomiting, dyspnoea, tachycardia, diarrhoea and diffuse pains. For several years she had been treated with azathioprine and for a few weeks before admission with phenformin for mild diabetes. Laboratory examination revealed acute disseminated intravascular coagulation and lactacidaemia. Despite intensive treatment the patient died a few hours after admission, the post-mortem examination revealing diffuse pulmonary haemorrhages. The present case report and those published in the literature suggest that phenformin should not be given to diabetics who also have renal or hepatic disease. In any case, if phenformin is given, it should be stopped if hepatic, renal, infectious or thrombotic complications occur. In these cases and those of sudden unexplained deterioration in diabetics, hospitalisation is essential and lactic acid levels should be determined and coagulation tests performed.
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PMID:[Lactacidaemia and disseminated intravascular coagulation associated with phenformin medication (author's transl)]. 114 86

Gangrene of the extremities complicating diarrhoea and severe hypernatraemic dehydration occurred in 6 infants. This is a rare complication of gastroenteritis, and its association with hypernatraemia does not seem to have previously been emphasized. The increased blood viscosity resulting from serum hyperosmolarity may have been responsible for the gangrene, and studies in our patients suggested that disseminated intravascular coagulation was present. In addition to fluid and electrolyte replacement, the infants were treated with heparin with some recovery of the affected extremities.
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PMID:Peripheral gangrene in hypernatraemic dehydration of infancy. 120 Jun 77

Two patients with tuberculosis complicated with disseminated intravascular coagulation are presented. The first patient had spleenic and mesenteric lymph nodes tuberculosis (accompanied by gastrointestinal symptoms (diarrhoea) lasting for several years) in which DIC was terminal fatal complication. Coagulation disorder was characterized by a decrease of fibrinogen concentration in blood, thrombocytopenia and other disorders as well as haemorrhagic syndrome. The second patient had miliary tuberculosis presented by X-ray changes on the lungs, granuloma in the liver and positive cultures in the sputum. Both laboratory and clinical signs of DIC manifested in the beginning of the disease. Heparin treatment was successful: haemorrhages stopped already 24 hours later, while an increase of fibrinogen concentration and number of platelets in blood proceeded at slower rate. As the patient had overcome the critical period, treatment of the primary disease was successful and led to complete recovery.
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PMID:[Disseminated intravascular coagulation during a course of miliary tuberculosis]. 122 26

Twenty cases of children with Sclerema observed at a Pediatric Service during five years are presented. Their clinical and laboratory traits are integrated in a dermatosis appearing after various and usually serious complications. In the children observed the most frequent finding was represented by sepsis, some of them with disseminated intravascular coagulation syndrome, diarrhoea with dehydration. The therapy applied, fundamentally was based on parenteral solutions, antibiotics and corticoids, was directed by those diseases and not by the presence of sclerema, which however appeared influenced by the supply of the latterly mentioned medicaments. Microscopic disturbances are discussed too, and a reference is made to the incriminabea pathogenic mechanisms.
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PMID:[Sclerema (clinical review apropos of 20 cases)]. 124 Oct 81

A case of life-threatening adverse effects following intravenous administration of a non-ionic contrast medium is reported. The patient, a 68-year-old diabetic hypertensive male with dyspnoea and cough had an abnormal chest radiograph, revealing congestive heart failure and an enlarged right hilum. Computed tomography (CT) of the chest was performed using 100 cm3 of intravenous iopamidol. Within half an hour the patient developed abdominal cramping, vomiting, and diarrhoea, followed by hypotension, tachycardia, fever to 40 degrees C, and delirium. His course was complicated by disseminated intravascular coagulation, rhabdomyolysis, renal failure, respiratory arrest, and atrial fibrillation. There was no evidence of infection, neoplastic disease, or myocardial infarction. Over the next month the patient slowly recovered. One other case report implicates a contrast agent with a similar syndrome. The features of this case fulfil the criteria for a probable adverse drug reaction of a type and severity rarely encountered.
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PMID:Case report: multisystem failure following intravenous iopamidol. 139 88

A 39 year old woman presented with a short history of bloody diarrhoea. She subsequently developed microangiopathic haemolysis, platelet consumption, and renal impairment. Initial investigations suggested underlying Crohn's disease of the terminal ileum complicated by sepsis and disseminated intravascular coagulation. However, after resection of a perforated caecum and terminal ileum, the diagnosis of thrombotic thrombocytopenic purpura was made. There was weak serological evidence of yersinia infection, this may have caused the early localisation of the lesions to the terminal ileum. This is believed to be the first report of thrombotic thrombocytopenic purpura affecting the small bowel alone at presentation.
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PMID:Thrombotic thrombocytopenic purpura mimicking acute small bowel Crohn's disease. 162 73

Acute infections with group A beta-hemolytic streptococcus normally take a favourable course under therapy with penicillin. Only in a few cases has a completely different manifestation been described with multisystem failure similar to toxic shock syndrome induced by Staphylococcus aureus. We report on 4 patients (1990/91) who showed this manifestation in spite of immediate antibiotic therapy. In 3 patients the suspected portal of entry was the skin, in 1 patient it was unknown. Group A streptococci were grown from blood cultures from all 4 patients. Without an underlying immune deficiency all 4 patients (age 22, 24, 38 and 51) went into septic shock with high fever, hepatic and renal impairment, diarrhea, DIC and cerebral confusion. 2 patients died within a few days after developing acute respiratory distress syndrome and cerebral edema. All strains isolated from the patients were penicillin-sensitive, group A streptococci. 3 of them were M-type 1, which are known to be more invasive. The bacteremia by itself is not sufficient to explain all complications and the high mortality rate. It is probable that streptococcal toxins, such as pyrogenic exotoxin A, streptolysin O, or a new unknown one, play a decisive role.
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PMID:[Toxic shock syndrome in infection due to Streptococcus pyogenes]. 173 21


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