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)

A 69-year-old white woman presented with a 3-month history of progressive dyspnea, orthopnea, fatigue and weakness. Clinical, diagnostic imaging and echocardiographic investigations suggested an occult primary cancer with metastasis to the heart. The patient's condition deteriorated gradually, and she died 2 months later. At autopsy, a malignant tumor encasing the heart and a 1-cm solitary tumor nodule in the lower lobe of the left lung were found. Histologic and electron microscopic studies revealed a plasmacytoma predominantly involving the epicardium and a small solitary plasmacytoma located in the left lung. The two tumors were further confirmed by immunohistochemical studies that showed monoclonal IgG expression and kappa light chain restriction.
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PMID:Cardiac plasmacytoma. 1476 85

The objective of this study was to describe the predictive value of dyspnea at rest in the diagnosis of heart failure in older adults. We have conducted a retrospective chart review of older adults hospitalized with heart failure in 11 hospitals in Alabama, US. We defined dyspnea at rest as dyspnea not accompanied by activities, sleep, or lying down. We confirmed diagnosis of heart failure using modified Framingham criteria (based on available variables). We estimated values for sensitivity, specificity, predictive value positive and likelihood ratio positive of dyspnea at rest along with their 95% confidence intervals (95% CI). Patients had a mean (+/-S.D.) age 79 (+/-7.5) years, were 60% female and 18% African-American. The prevalence (pre-test probability) of heart failure was 77%. Dyspnea at rest was reported by 975 (89%) patients. Dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea were, respectively, reported by 279 (26%), 356 (33%) and 230 (21%) patients. The sensitivity, specificity and positive predictive value (post-test probability) of dyspnea at rest were, respectively, 92% (95% CI = 90 - 94%), 19% (95% CI = 14 - 24%) and 79% (95% CI = 77 - 82%). Patients with dyspnea at rest were 13% (likelihood = 1.13; 95% CI = 1.06 - 1.20) more likely to have heart failure than those without. Presence of any three of the symptoms of dyspnea at rest, dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, fatigue and lower extremity edema increased the positive predictive value to 90% (95% CI = 87 - 93%). Dyspnea at rest was the commonest symptom among elderly hospitalized HF patients and had high sensitivity, but low specificity and positive predictive value, which increased in the presence of other symptoms.
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PMID:Diagnosis of heart failure in older adults: predictive value of dyspnea at rest. 1506 16

Bilateral diaphragmatic paralysis (BDP) can occur in the course of motor neuron disease, myopathy, or from mechanical damage or the use of "ice slush" during cardiac surgery. BDP has been observed during and after infections, associated with systemic lupus erythematosus and mediastinal tumors, or may have idiopathic etiology. It is a serious and life-threatening condition. A 62-yr-old man presented with slowly progressive dyspnoea that worsened in the supine position and on bending forward. Chest X-rays, fluoroscopy, lung-function parameters and blood-gas analysis revealed respiratory failure. BDP was confirmed from a phrenic nerve stimulation test and measurement of transdiaphragmatic pressure (Pdi). Since there was no evidence of an obvious etiology, BDP was considered idiopathic. Other muscles were not involved. The pathological basis was probably focal demyelination in segments of the phrenic nerve. Because of increasing diaphragmatic muscle fatigue, the patient was treated with a nasal mask providing bi-level positive airway pressure (BiPAP) ventilation during the night. Clinical suspicion of BDP should always be raised in patients suffering slowly progressive dyspnoea without any obvious cardiac, metabolic or traumatic predisposing factors, and orthopnoea and dyspnoea on bending forward. Electromyographic tests and measurement of Pdi can reveal the correct diagnosis.
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PMID:Spontaneous bilateral diaphragmatic paralysis: a rare cause of respiratory failure. 1547 Nov 85

PRESENTING FEATURES: An 85-year-old black woman presented to the Osler Medical Service complaining of a pruritic, erythematous scaly rash that was on her right thigh and abdomen and that had been worsening over the prior 3 months. She also complained of increasing fatigue, decreased exercise tolerance, and a 5-lbs weight loss. There was no orthopnea, paroxysmal nocturnal dyspnea, fevers, chills, or night sweats. She denied recent travel and exposures to or contact with ill people. Her past medical history was unremarkable. There was no history of eczema, atopy, or dermatologic conditions. Her only medication was a baby aspirin taken daily. On physical examination, she was afebrile, her blood pressure was 110/72 mm Hg, and her pulse was 82 beats per minute with a room air oxygen saturation 98%. She was mildly obese but in no apparent distress. She had 1-cm anterior cervical lymphadenopathy bilaterally and a 1-cm left axillary lymph node. Cardiovascular and chest examination was unremarkable. Her abdomen was soft and nontender, with a faint, erythematous rash that was mildly scaly but nontender in her abdominal skin fold. Her right thigh showed a large erythematous area, approximately 15 x 20 cm, which was scaly with multiple areas of discoloration (Figure 1). There was no palpable mass. She had slight edema in her right leg. Her left thigh was normal. Neurologic examination was nonfocal. Laboratory studies were notable for a white blood cell count of 17,000 cells/microL, with a differential of 46% lymphocytes. The absolute lymphocyte count was 8000 cells/microL. Hematocrit was 28%. Platelet count was normal. A comprehensive metabolic panel was normal. A peripheral blood smear (Figure 2) showed numerous atypical lymphocytes with cerebriform nuclei. Peripheral blood flow cytometry showed the presence of a clonal population of T cells that expressed CD4 and CD5 but showed a loss of CD7. What is the diagnosis?
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PMID:Cases from the Osler Medical Service at Johns Hopkins University. 1550 Dec 9

The guideline entitled 'Heart failure' from the Dutch College of General Practitioners has been revised. The general practitioner makes the diagnosis of heart failure in a patient with the core symptoms (dyspnoea, fatigue, oedema) in combination with paroxysmal nocturnal dyspnoea, orthopnoea, crepitations, elevated central-venous pressure, a third heart sound or ifictus cordis is visible outside the mid-clavicular line. Further investigations include a panel of laboratory investigations, an ECG and possibly echocardiography and radiographic chest investigations. One new recommendation is that on suspicion of heart failure the plasma concentrations of B-type natriuretic peptide (BNP) or N-terminal pro-BNP should be investigated. The step-by-step medication plan has been changed; beta-blockers have been introduced to the plan. In the treatment of acute heart failure, rapidly working sublingual nitrates should be given first and foremost.
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PMID:[Summary of the practice guideline 'Heart failure' (first revision) from the Dutch College of General Practitioners]. 1635 12

Almost one mountain trekker or climber out of two develops several symptoms of high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. Individual susceptibility is the most important determinant for the occurrence of high altitude pulmonary oedema (HAPE). Symptoms associated with HAPE are incapacitating fatigue, chest tightness, dyspnoea at the slightest effort, orthopnoea, and cough with due to haemoptysis in an advanced stage of the disease pink frothy sputum. The hallmark of HAPE is an excessively elevated pulmonary artery pressure (mean pressures of 35 and 55 mm Hg), which precedes the development of pulmonary oedema. Elevated pulmonary capillary pressure and protein- as well as red blood cell-rich oedema fluid without signs of inflammation in its early stage are characteristic findings. Furthermore, decreased fluid clearance from the alveoli may contribute to this non-cardiogenic pulmonary oedema. Immediate descent or supplemental oxygen and nifedipine are recommended until descent is possible. Susceptible individuals can prevent HAPE by slow ascent: an average gain of altitude not exceeding 400 m/day above an altitude of 2500 m. If progressive high altitude acclimatization is not possible, a prophylaxis with nifedipine should be recommended.
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PMID:High altitude-induced pulmonary oedema. 1690 89

Insomnia is highly prevalent in patients with chronic disease including chronic heart failure (CHF) and is a significant contributing factor to fatigue and poor quality of life. The pathophysiology of CHF often leads to fatigue, due to nocturnal symptoms causing sleep disruption, including cough, orthopnea, paroxysmal nocturnal dyspnea, and nocturia. Inadequate cardiac function may lead to hypoxemia or poor perfusion of the cerebrum, skeletal muscle, or visceral body organs, which result in organ dysfunction or failure and may contribute to fatigue. Sleep disturbances negatively affect all dimensions of quality of life and is related to increased risk of comorbidities, including depression. This article reviews insomnia in CHF, cardiac medication side-effects related to sleep disturbances, and treatment options.
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PMID:Insomnia and chronic heart failure. 1875 45

The objective of this study was to compare newly diagnosed heart failure (HF) patients (n = 64) with chronic HF patients (n = 148) who had been hospitalized on their presenting symptoms and treatment delay times, whom the 2 groups notified and when, the advice they were given by those notified, and the actions they initiated before their hospitalization. Participants in the 2 groups similarly reported shortness of breath on exertion, orthopnea, weakness, edema, and cough. A greater percent of participants in the group with an HF history reported having fatigue compared to the group with no HF history (chi2 = 4.32, P < .05). Both groups were similar in the time they spent with symptoms before hospital admission (median of 7 days), the time until they notified family members after symptom onset (6 hours to 1.5 days), and the time until they notified their physicians after symptom onset (1.5 to 3 days). The 2 groups varied significantly on the following findings: physicians advised participants with an HF history to call 911 significantly more often than they told the participants with no HF history to call 911 (chi2 = 4.33, P < .05), physicians told those with no HF history to come to the office (chi2 = 5.04, P < .05) or wait for an upcoming appointment (chi2 = 4.78, P < .05) more often than they made those recommendations to the group with an HF history, and participants with an HF history were significantly more likely to call 911 than the participants with no HF history do (chi2 = 4.18, P < .05). The clinical implication is that individuals with either new or worsening HF need to recognize a constellation of possible HF symptoms. Those with chronic HF need to also be aware that increasing fatigue may be an important symptom of worsening HF for them. Both groups of HF patients should report their symptoms promptly to their healthcare providers for early intervention.
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PMID:Heart failure patients' time, symptoms, and actions before a hospital admission. 1895 14

Open surgical repair of iliac arteriovenous fistulas is associated with significant morbidity and mortality, making endovascular repair an attractive alternative. This report describes a 39-year-old man who was admitted with two-pillow orthopnea, edema, and fatigue. He had sustained a gunshot wound to the pelvis 13 years previously. Six years after the gunshot wound, he was diagnosed with cardiomegaly and high-output congestive heart failure. A magnetic resonance angiography documented a large pelvic arteriovenous fistula. A diagnostic contrast angiogram confirmed a high-flow fistula between the left distal main internal iliac artery and left common iliac vein. A Gore TAG thoracic endoprosthesis (W. L. Gore and Assoc, Flagstaff, Ariz) was used to repair this large, high-flow internal iliac artery-common iliac vein arteriovenous fistula.
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PMID:Repair of a high-flow iliac arteriovenous fistula using a thoracic endograft. 1914 17

Cardiac tamponade as an initial manifestation of undifferentiated connective tissue diseases (UCTD) is extremely rare, with only one case reported in literature thus far. We describe here, a case of a middle-aged man who presented with symptoms of fatigue, exertional dyspnea and orthopnea. His physical exam was significant for anasarca, elevated JVP and pulsus paradoxus. Chest X-ray showed pleural effusions and cardiomegaly, electrocardiogram revealed electrical alternans and a transthoracic echocardiogram demonstrated massive pericardial effusion with hemodynamic compromise. There was clear evidence of tamponade on right heart catheterization. All common causes of pericardial effusion were assiduously excluded before working up the patient for connective tissue disorders, which revealed a high antinuclear antibody titer (1:160), grossly elevated SSA, SSB antibodies and increased C-reactive protein levels (13.04 mg/dl). Patient had no signs or symptoms suggestive of systemic sclerosis (xerophthalmia or xerostomia) and did not meet criteria for any other known connective tissue diseases. He was therefore diagnosed with UCTD, and successfully treated with colchicine after emergency pericardiocentesis. This case presents UCTD as a rare cause of cardiac tamponade and large pericardial effusions and suggests that colchicine can be used to treat UCTD-associated effusions. These patients once diagnosed, are at risk of developing known connective tissue diseases within 5 years of disease onset and should be followed up in clinic periodically.
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PMID:An unusual case of undifferentiated connective tissue disease presenting as cardiac tamponade. 2001 65


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