Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diagnosis of acute mild myocarditis in vaguely defined. Therefore we studied 185 consecutive young men in military service with electrocardiographic changes arousing a suspicion of myocarditis in connection with an acute infectious disease. It was possible to classify 160 patients into seven electrocardiographic groups; definite or probable myocarditis was observed in 104 patients. The electrocardiographic patterns considered characteristic for acute myocarditis were: ST segment elevations followed by T wave inversions; gradually changing T wave inversions not corrected by beta blockade; and ventricular extrasystoles more than 10 per minute triggered by acute infection. Thirty-nine subjects without myocarditis had "functional" T wave abnormalities completely normalised by beta blockade, or stable T wave inversion. The leading symptoms in acute myocarditis were fatigue and chest pains; loud S3 gallop, paradoxical cardiac pulsation, pericardial friction rub, or enlargement of the heart were noted altogether in 50% of the patients. Echocardiography disclosed segmental wall motion abnormalities related to the T wave inversions. Serum creatine kinase MB fraction increased in 70% of the acute myopericarditis patients during the ST segment elevation stage. In the non-myocarditis groups the clinical and pertinent laboratory findings remained normal. Thus, we noted in clinically mild acute infectious myocarditis clear-cut and early signs of myocardial dysfunction, suggesting that the direct and often local viral invasion of the myocardium is the basic pathogenetic mechanism. The present electrocardiographic classification based on serial tracings and beta blockade proved useful in the evaluation of patients suspected of having mild acute myocarditis.
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PMID:Evaluation of mild acute infectious myocarditis. 612 67

Lyme borreliosis is a worldwide, multistage, and multi-system disease caused by borrelia spirochetes, which are transmitted by ixodes ticks. It is focally endemic in temperature climates of the northern hemisphere. Primary erythema migrans occurs at the site of inoculation. Secondary erythema migrans occurs at sites of hematogenous dissemination. Variations in genospecies account for variations in presentation, including borrelial lymphocytoma. Disseminated disease includes constitutional signs and symptoms, intermittent oligoarticular arthritis, meningitis, cranial neuritis, radiculoneuropathy, encephalopathy, atrioventricular block, and myopericarditis. Late persistent disease includes acrodermatitis chronica atrophicans, chronic arthritis, neurological impairment, and fatigue. There can be difficulties with both clinical and laboratory diagnosis. First-line oral therapies for early uncomplicated disease are doxycycline and amoxicillin. First-line intravenous therapy for complicated or resistant disease is ceftriaxone. Prevention includes avoiding tick habitats, dressing sensibly, judicious use of repellants, and early removal of imbedded ticks. Vaccination is indicated only for frequent or prolonged exposure to tick-infested habitat.
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PMID:Lyme borreliosis. 1083 3

In the period 1998-, we registered four sudden and unexpected cardiac deaths in male athletes due to myopericarditis during or after physical exercise. Three of them were professional soccer players and the fourth was engaged in swimming. One aged 29, had symptoms of tiredness, heart enlargement and left ventricular premature beats during training. Three of them, aged 17-18-18, were without symptoms. Three died during training and the fourth died in the hospital after head trauma at training. In the first one, aged 29, forensic autopsy showed chronic myopericarditis, thickening of the left ventricular wall of 15 mm and enlargement of the whole heart. The second one, aged 17, had subacute diffuse myopericarditis, suppurative tonsillitis and narrowed ascending aorta. The third, aged 18, had chronic myopericarditis and cardiac aneurysm of the left ventricle. The fourth, aged 18, had fibrinous pericarditis, thickening of the left ventricle 20 mm, hypoplastic ascending aorta, bilateral bronchopneumonia and cerebral contusion with edema. In Croatia, death rate among athletes, including all its causes, reached 0.15/100,000, in athletes suffering from myopericarditis it was 0.34/100,000, in others who practice exercise recreatively it amounted to 0.57/100,000 (p=0.0068), and in all males who practice exercise it measured 0.75/100,000 (p=0.0014). Physical exercise has to be contraindicated in cases of myopericarditis for at least six months from the onset of the illness.
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PMID:Myopericarditis and sudden cardiac death due to physical exercise in male athletes. 1875 88

Novel influenza A (H1N1) has created a major worldwide health problem within a short time after its emergence. This infection is often self-limited, but sometimes can cause severe and fatal complications. In this study, we present two rare complications of pandemic influenza A, who were referred to Razi University Affiliated Hospital in northern Iran. The first case was a 30-year-old man with severe headache and high fever accompanied with chills, generalized myalgia, and arthralgia. Cerebrospinal fluid analysis was consistent with aseptic meningitis. The second case, a 25-year-old pregnant woman with high fever, chills and severe fatigue and malaise, developed tachypnea, tachycardia, respiratory distress, cyanosis and loss of consciousness a few hours after admission. Echocardiography reported myopericarditis. The patient was transferred to the intensive care unit and mechanical ventilation was begun. The next day, the patient started vaginal bleeding which progressed to spontaneous abortion three days later. Diagnosis of novel influenza A (H1N1) was confirmed using real-time reverse-transcriptase PCR of a pharyngeal swab.
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PMID:Report of two rare complications of pandemic influenza A (H1N1). 2233 53

Myopericarditis remains a prominent infectious inflammatory disorder throughout a patient's lifetime. Moreover, viral pathogens have been proven to be the leading contributors to myopericarditis in the pediatric and adult populations. Despite the current comprehensive knowledge of myocardial injury in viral and post-viral myopericarditis, the cellular and molecular mechanisms of SARS-CoV-2-induced myopericarditis are poorly understood. This report presents a case of coronavirus (COVID-19) fulminant myopericarditis and acute respiratory distress syndrome (ARDS) in a middle-aged male patient: a 51-year-old man with a history of hypertension who arrived to the emergency department with a dry cough, fatigue, dyspnea, and a fever. A real-time reverse transcriptase-polymerase chain reaction (RT-PCR) assay confirmed a diagnosis of COVID-19 infection, resulting in the patient's admission to the airborne isolation unit for clinical observation. When his condition began to deteriorate, the patient was transferred to the cardiac care unit after electrocardiography detected cardiac injury, demonstrating diffuse ST-segment elevation. Laboratory evaluations revealed elevated troponin T and BNP, with an echocardiogram indicating global left ventricular hypokinesia and a reduced ejection fraction. The patient was treated with hydroxychloroquine, azithromycin, dobutamine, remdesivir, and ventilatory support. This specific case highlights the severity and complications that may arise as a direct result of COVID-19 infection.
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PMID:Coronavirus (COVID-19) Fulminant Myopericarditis and Acute Respiratory Distress Syndrome (ARDS) in a Middle-Aged Male Patient. 3260 4