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)

A 22-year-old man developed unconsciousness, severe quadriplegia and muscle atrophy, and had markedly elevated serum creatine kinase levels after using the high-dose steroid and nondepolarizing neuromuscular blocking agents during the course of sepsis and DIC. On neurological examination, he was lethargic. The patient had generalized muscle weakness and wasting, and diminished deep tendon reflexes. He weakly responsed to painful stimuli on the legs. The motor nerve conduction study demonstrated decreased CMAP (compound muscle action potential) amplitudes. Motor and sensory nerve conduction velocities and their distal latencies were normal. Muscle biopsy revealed marked muscle fiber atrophy predominantly in type 2 fibers and numerous basophilic and a few necrotic fibers. Some atrophic fibers had decreased to absent myosin adenosine triphosphatase activity in their center. Accordingly, he was diagnosed as having acute quadriplegic myopathy (AQM), which has been reported mainly in Western countries. The mechanism of muscle fiber degradation in this myopathy is still unknown. On immunohistochemical analysis to our patient, enzyme activities of various proteases such as calpain, cathepsin B, and proteasomes were increased in the sarcoplasm, especially in the atrophic fibers. We suggest that lysosomal cathepsin, nonlysosomal calpain, and ATP-ubiquitin-proteasome proteolytic pathways participate in muscle fiber degradation in AQM.
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PMID:[A case of acute quadriplegic myopathy]. 1108 98

The typical explosive form of malignant hyperthermia caused by following isoflurane anaesthesia is a well-known phenomenon. Nevertheless, since dantrolene is used, its evolution toward a multiple organ failure has been rarely described. We report a case of typical explosive malignant hyperthermia caused by an isoflurane anaesthesia complicated by a cardiovascular failure, a disseminated intravascular coagulation, an acute liver failure and an acute renal failure. Afterwards, muscle weakness of the right calf was the only aftermath.
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PMID:[Anesthetic malignant hyperthermia and multiple organ dysfunction syndrome]. 1153 Jul 54

A peri-parturient fifteen-month-old female Maine Coon cat was presented with extreme weakness and depression, profound hypovolaemia and hypothermia. Severe hyperkalaemia, hyponatraemia and anaemia were detected. Disseminated intravascular coagulation was suspected due to marked prolongation of activated partial thromboplastin time. Uterine torsion was diagnosed at exploratory laparotomy. The cat made a full recovery following ovariohysterectomy and intensive supportive therapy.
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PMID:Successful treatment of uterine torsion in a cat with severe metabolic and haemostatic complications. 1171 4

We report a 58-year-old man with slowly progressive muscle atrophy and weakness in the four extremities, accompanying cerebellar ataxia and sensory impairment of all modalities. He was a product of consanguineous marriage. His neurological manifestations began in childhood. He was admitted to our hospital because of marked abdominal distension and pretibial edema with hypoalbuminemia and hyperlipidemia. Neuroimaging studies showed marked atrophy of the cerebellum and spinal cord. Nerve conduction studies presented with slowing and sural nerve biopsy revealed demyelination with onion-bulbs. Abdominal distension was interpreted to be caused by chronic idiopathic intestinal pseudo-obstruction (CIIP), leading to protein-losing gastroenteropathy and hypalbuminemia caused by the CIIP. He died of DIC by myelodysplasic syndrome and DIC, two years later. Postmortem study demonstrated with severe loss of anterior horn cells and gliosis in the spinal cord. The Clarke's column was also affected. There was symmetrical degeneration in the dorsal column and corticospinal tracts. The cerebellum showed atrophy of molecular layer, prominent loss of Purkinje's cells and sparse granular cell layer, but no obvious change in the dentate nucleus. Neuronal loss in the dorsal root ganglia was remarkable. There were no alternations in the cerebral cortex, striatum, thalamus, subthalamic nucleus, and pontine nucleus, except for mild changes in substantia nigra and inferior olivary nucleus. This case was clinically suspected either of variant of Friedreich's ataxia or an early onset ataxia associated with hypoalbuminemia (EOAHA), although marked autonomic dysfunction was atypical. But the postmortem study, demonstrated with marked neuronal loss in anterior horn cells and cerebellan cortex and rather suggested an independent category of this case.
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PMID:[An autopsy case of atypical Friedreich's ataxia with chronic idiopathic intestinal pseudo-obstruction]. 1180 52

A 72-year-old man was admitted to the emergency ward in our hospital on July 20, 2001, because of consciousness disturbance, fever, generalized skin eruption, and severe general weakness beginning 7 days previously. Physical examination on admission revealed marked systemic cyanosis, erythema, and purpura. Laboratory findings indicated disseminated intravascular coagulation (DIC) and multiorgan failure (platelet count, 0.9 x 10(4)/micro l; fibrin degradation product, 110 micro g/ml; C-reactive protein, 22.6 mg/dl). Soluble interleukin 2-receptor (sIL-2R) was markedly increased to 14 710 U/ml. Blood gas analysis demonstrated severe metabolic acidosis. He was diagnosed with multiorgan failure due to DIC. Administration of heparin and sodium bicarbonate was started immediately, but respiratory failure was exacerbated and systemic spasm caused by encephalitis was noted. Although he was supported by an artificial ventilator, deterioration of metabolic acidosis occurred, and the blood pressure decreased to less than 60 mm Hg. He died 5.5 h after admission. The serological test showed no positive antibody titers against Orientia tsutsugamushi, Rickettsia japonica, or Rickettsia typhi. However, a specific DNA band derived from R. japonica was detected by the polymerase chain reaction (PCR) method using a primer from a blood clot. Therefore, he was definitively diagnosed as having Japanese spotted fever. The PCR method may be markedly useful for establishing a definitive diagnosis of Japanese spotted fever during the critical stage.
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PMID:Fulminant Japanese spotted fever definitively diagnosed by the polymerase chain reaction method. 1237 93

Rhabdomyolysis is a severe clinical symptom of variable etiology. Acquired factors of exogenous origin such as traumata and endogenous metabolic disturbances have to be separated from hereditary disease as causative mechanism. Most frequently, exertional stress during hyperthermia, traumatic damage or ethanol abuse are observed. Almost independent of the diverse initial events, the pathogenesis follows a common final pathway with intracellular calcium accumulation and ATP depletion. Clinical symptoms vary. Seldom, the classical triad of muscle pain, weakness, and dark urine is observed. Recurrent episodes should raise suspicion of an inherited disorder. Severe complications are hypovolemia, electrolyte disorders with hyperkalemia and hypocalcemia resulting in life threatening arrhythmias, a compartment syndrome, disseminated intravascular coagulation and acute renal failure, which is frequently oligo-anuric. In combination with often severe underlying disease, renal failure causes death in 1/5 of the patients. The diagnosis is made with the determination of serum creatine kinase and the myoglobin levels in plasma and urine. Therapeutic options are to correct the hypovolemia with sufficient fluid supply, the prevention of oliguria using loop diuretics, alkalinization of the urine, normalization of serum electrolytes with reduction of hyperkaemia, and decompression of compartment syndromes. An underlying disease should be evaluated to initiate specific therapeutical and preventative steps. Avoiding pre-disposing factors by identifying the mechanisms of disease will reduce the occurrence of rhabdomyolysis with its still high mortality.
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PMID:[Rhabdomyolysis]. 1295 32

A 61-year-old man was admitted to our hospital because of edematous erythema on his upper eyelids and dry cough. No subjective nor objective findings suggestive of skeletal muscle involvement, such as muscle weakness and elevated levels of aldolase and creatine phosphokinase were noted. Chest high-resolution computed tomography revealed a ground glass opacity and consolidation of his lower lung. Skin biopsy findings were compatible with dermatomyositis. Therefore, he was diagnosed as amyopathic dermatomyositis (ADM) with acute interstitial pneumonia and treatment with steroid pulse therapy was started. Since histological evaluation showed diffuse alveolar damage during the initial treatment, the treatment was changed into the combination therapy of prednisolone and cyclosporine. However, his acute interstitial pneumonia did not respond to this treatment and passed away by aggravation of a breathing state and concurrence of disseminated intravascular coagulation. Japanese patients with ADM have been shown to be more frequently associated with intractable acute interstitial pneumonia than Caucasian patients, suggesting that the racial difference influences the occurrence of acute interstitial pneumonia in ADM. Since autoantibodies specific for ADM have not been detected, we performed immunoprecipitation analysis using 35S methionine-labeled K562 cells to identify them. His sera immunoprecipitated a polypeptide of 140 kDa. The 140 kDa polypeptide might be one of autoantibodies specific for ADM with acute interstitial pneumonia, although future analysis using a larger number of patients with ADM will be required to confirm this result.
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PMID:[A case of amyopathic dermatomyositis with acute interstitial pneumonia (DAD pattern)]. 1516 31

A cerebrovascular thromboembolic event may precede the identification of cancer, and be the first clinical evidence of an underlying malignancy. The malignancy can cause either nonbacterial thrombotic endocarditis or hypercoagulable state, both of which may have clinical manifestions such as thrombotic or embolic occlusion of multiple major cerebral vessels. We present three cases with unusual cerebrovascular events. The first case is a 62-year-old woman who was admitted due to acute left limbs weakness and consciousness disturbance. Brain computed tomographic (CT) scan showed right middle cerebral artery (MCA) and posterior cerebral artery (PCA) infarctions with uncal herniation. The second case is a 44-year-old woman who was hospitalized due to acute bilateral limb weakness and consciousness disturbance. Bilateral MCA, left PCA, anterior cerebral artery (ACA) infarctions and deep vein thrombosis in the left leg were diagnosed. The third case is a 63-year-old man who developed sudden onset of right hemiplegia and consciousness disturbance. Brain CT scan showed bilateral MCA and left ACA infarction. The results of a series of examinations including biochemistry, lipid profile, carotid duplex, and transthoracic and transesophageal echocardiography were unremarkable. All patients had positive disseminated intravascular coagulation (DIC) tests with elevated D-dimers and fibrinogen degradation products (FDP). Further systemic evaluation for malignancy revealed ovarian cancer in the first patient, endometrial carcinoma in the second patient, and adenocarcinoma of lung in the third patient. They all died of the underlying malignancy. Because the hemostatic system can be altered by malignancy, intravascular coagulation abnormalities of these malignancy-related strokes may be disclosed by laboratory assays of hemostasis.
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PMID:Cerebrovascular complications in patients with malignancy: report of three cases and review of the literature. 1531

Rhabdomyolysis ranges from an asymptomatic illness with elevation in the creatine kinase level to a life-threatening condition associated with extreme elevations in creatine kinase, electrolyte imbalances, acute renal failure and disseminated intravascular coagulation. Muscular trauma is the most common cause of rhabdomyolysis. Less common causes include muscle enzyme deficiencies, electrolyte abnormalities, infectious causes, drugs, toxins and endocrinopathies. Weakness, myalgia and tea-colored urine are the main clinical manifestations. The most sensitive laboratory finding of muscle injury is an elevated plasma creatine kinase level. The management of patients with rhabdomyolysis includes early vigorous hydration.
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PMID:Bench-to-bedside review: Rhabdomyolysis -- an overview for clinicians. 1577 72

Necrotizing fasciitis (NF) is a rapidly progressive life-threatening infection located in the deep fascia, with secondary necrosis of the subcutaneous tissues. Staphylococcus aureus as a single etiologic agent is rare. The pathogenicity of S. aureus infections is related to various bacterial surface components and extracellular proteins. A 56-year-old man developed fever, hypotension, impaired renal and hepatic functions, disseminated intravascular coagulation, and rapidly progressive NF affecting the 4 extremities due to methicillin-susceptible S. aureus (MSSA). The initial presenting symptoms were general weakness and muscular pain over bilateral thighs and left shoulder, and gradual onset of weakness of the limbs. On the third hospital day, multiple red-purplish discoloration spread across the right lower leg and left forearm. Fasciotomy and debridement was performed on the fifth hospital day, and the diagnosis of NF was confirmed. MSSA was the only pathogen isolated from 4 sets of blood cultures taken on admission and cultures of tissues collected during surgical debridement. The disease progressed rapidly over the 4 extremities despite appropriate antibiotic treatment. He recovered after multiple extensive surgical interventions and 8 weeks of intensive medical care. Early diagnosis, intensive surgical intervention, antibiotic treatment and intensive medical care are crucial for a successful outcome in patients with septic shock and extensive NF caused by S. aureus.
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PMID:Rapidly progressive necrotizing fasciitis caused by Staphylococcus aureus. 1621 Nov 46


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