Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum myoglobin was determined by radioimmunoassay in 20 cases of sudden and unexpected death resulting from acute coronary occlusion. There was consistent elevation of myoglobin 2 h after death, with peaking at 3 h. No comparable elevation of serum myoglobin level was noted in patients who had succumbed to pulmonary embolism, ruptured aortic aneurysm, or subarachnoid or intracerebral hemorrhage. Thus, determination of serum myoglobin seems useful in confirming or establishing acute coronary occlusion as the cause of sudden and unexpected death.
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PMID:Determination of serum myoglobin level after death in the diagnosis of sudden coronary artery occlusion. 74 96

Although rare, exertional collapse and sudden death are the most serious potential complications of sickle cell trait. Studies suggest that this condition may occur in susceptible persons when poor physical conditioning, dehydration, heat stress or hypoxic states precipitate sickling of the abnormal erythrocytes. Sickling leads to endothelial damage, which can cause vasoconstriction, disseminated intravascular coagulation and local tissue damage. Cardiac effects include acute ischemia and arrhythmias. Muscle damage results in acute compartment syndromes and release of myoglobin into the circulation. Acute renal failure is possible. Diagnosis is based on a high index of suspicion, and characteristic presentation and laboratory findings, including myoglobinuria, hyperkalemia, hypocalcemia, hyperphosphatemia and elevated creatine kinase levels. The differential diagnosis includes pulmonary embolism, acute cardiac events, anaphylaxis and heat stroke. Management is based on stabilization, rehydration, and the treatment and prevention of complications.
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PMID:Exertional collapse and sudden death associated with sickle cell trait. 904 99

The etiology of dyspnea can often be difficult to rapidly and accurately determine and can delay timely and appropriate therapies. The current literature reveals important diagnostic, prognostic, and therapeutic implications of several currently used biomarkers: sensitive d -dimer, myoglobin, creatine kinase-MB, cardiac troponins, and b-type natriuretic peptide. These biomarkers were found to have a high sensitivity and negative predictive value for rapidly ruling out potential serious etiologies of dyspnea, namely, pulmonary embolism (PE), acute myocardial infarction (AMI), and congestive heart failure (CHF). In the setting of a low to moderate pretest probability of PE, a negative sensitive d -dimer can rule out a PE with 97% accuracy. After 10 hours from the onset of symptoms, normal levels of myoglobin, creatine kinase-MB, and cardiac troponin I can rule out an AMI with greater than 96% accuracy. A b-type natriuretic peptide level less than 80 pg/mL can confidently rule out decompensated CHF with greater than 99% accuracy. However, no literature was found analyzing the use of these biomarkers in combination. A dyspnea biomarker panel could rapidly and accurately assist a clinician to rule out PE, AMI, and CHF. If a PE, AMI, or CHF is determined to be the cause of dyspnea, a biomarker panel could help risk stratify and help determine initial therapies. Subsequent clinical research is needed to corroborate this postulation.
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PMID:Evaluation and management of the acutely dyspneic patient: the role of biomarkers. 1591 17

Creatine kinase-MB (CK-MB), cardiac troponin I (cTnI) and myoglobin (Mb) are biochemical markers of myocardial injury; however, Mb is more abundant in skeletal muscles. The present study involved analysis of these markers in pericardial and cerebrospinal fluids (PCF and CSF) from serial medicolegal autopsy cases (n=295, within 48h) to examine their efficacy in determining the cause of death. Although these markers showed a slight postmortem time-dependent elevation, except for CK-MB in CSF, the distribution depended on the cause of death. Mb levels in PCF and CSF were higher in fatal hyperthermia (heat stroke) and methamphetamine abuse, and CK-MB in both fluids was also higher in the latter. In psychotropic drug intoxication, CK-MB, cTnI and Mb were higher in PCF, but only cTnI was elevated in CSF. In electrocution and cerebrovascular disease, each marker was higher in PCF and also relatively high in CSF. PCF cTnI level was higher in acute pulmonary embolism without significant elevation of any other markers, whereas CSF CK-MB was higher in acute blunt brain injury death and methamphetamine abuse. In most cases of delayed brain injury death, hypothermia (cold exposure) and pneumonia, these markers were low or intermediate in both PCF and CSF; however, sudden cardiac death, asphyxiation and fire fatality cases showed few characteristic findings. These observations suggest that combined analyses of these markers in postmortem PCF and CSF, in addition to blood samples, are helpful for evaluating the severity of myocardial and/or skeletal muscle damage in death processes, in particular for investigating deaths due to hyperthermia, hypothermia, electrocution and intoxication.
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PMID:Combined analyses of creatine kinase MB, cardiac troponin I and myoglobin in pericardial and cerebrospinal fluids to investigate myocardial and skeletal muscle injury in medicolegal autopsy cases. 2168 43

Guillain-Barre syndrome (GBS) is a heterogenous group of peripheral-nerve disorders with similar clinical presentation characterized by acute, self-limited, progressive, bilateral and relatively symmetric ascending flaccid paralysis, which peaks in 2-4 weeks and then subsides. The usual complications, which occur in a patient of GBS are pneumonia, sepsis, pulmonary embolism, respiratory insufficiency and cardiac arrest. The clinical course of GBS complicated by acute rhabdomyolysis is extremely rare. We present the case of GBS with marked elevation in serum creatine kinase, serum myoglobin levels and persistent hyperkalemia as a result of associated acute rhabdomyolysis.
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PMID:Guillain-Barre syndrome complicated by acute fatal rhabdomyolysis. 2487 55