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)

From 1960 through 1972, 236 cases of amyloidosis with histologic proof were found. The amyloidosis was primary (without evidence of preceding or coexisting disease) in 132 cases (group 1) and associated with multiple myeloma in 61 (group 2). Secondary amyloidosis appeared in 19 cases (associated with rheumatoid arthritis or osteomyelitis in two-thirds of them). There were 22 patients with amyloid localized to a single organ (bladder, lung, skin, or larynx in more than half of them). Two patients had familial amyloidosis. In group 1 and group 2, the most common presenting symptoms were fatigue, weight loss, edema, dyspnea, light-headedness or syncope, and paresthesias. Symptoms of the carpal-tunnel syndrome were frequent. The liver was palpable in almost 50% of the series, but splenomegaly was an initial finding in less than 10%. Macroglossia was recorded in 26% of group 2 and in 12% of group 1. Enlargement of submandibular structures was noted in about 10% of cases; and purpura, particularly around the eyes, was a significant feature. Substantial numbers of the patients had carpal-tunnel syndrome, nephrotic syndrome, congestive heart failure, sprue, peripheral neuropathy, or orthostatic hypotension. Approximately 50% of patients had renal insufficiency at the time of diagnosis. Proteinuria was found in more than 90%. A monoclonal protein was found in the serum of 49% of group 1 and in 74% of group 2. Monoclonal proteins were found in the urine of 35% and 81%, respectively. Only 12% of patients in group 1 had no monoclonal protein when both serum and urine were analyzed, and all patients of group 2 had a monoclonal protein in the serum or urine when both were analyzed. Lambda light chains were more common than kappa. None of the patients in group 1 had more than 15% plasma cells in the marrow, whereas more than half of group 2 had more than 15% plasma cells. Roentgenograms showed no evidence of skeletal disease in 94% of group 1, but 50% of group 2 had skeletal abnormalities. Rectal biopsy was positive for amyloid in 84% of cases. Kidney, liver, and carpal-tunnel biopsies were positive in 90% or more. Follow-up of all 193 patients in groups 1 and 2 revealed that 80% of group 1 and 97% of group 2 had died. The median survival was 14.7 months in group 1 and 4 months in group 2. Cardiac failure was the most common cause of death, accounting for 30% of the fatalities. We also reclassified all cases by the method of Isobe and Osserman (105), which is based on clinical patterns: pattern I--principal involvement of tongue, heart, gastrointestinal tract, muscle, nerves, skin, and carpal ligaments; pattern II--principal involvement of liver, spleen, kidneys, and adrenals; and mixed pattern I and II. This analysis failed to reveal predictive value in the clinical pattern classification, and did not discern the survival differences between primary amyloidosis (group 1) and amyloidosis with myeloma (group 2). Consequently, for the present we prefer the classification used in this study.
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PMID:Amyloidosis: review of 236 cases. 115 71

We present a patient with pericardial tamponade due to amyloid heart disease. A 64-yr-old man was admitted to the hospital because of fatigue and the abrupt development of chest pain and dyspnea. Echocardiography showed severe pericardial effusion and total pericardiectomy was necessary. Ten months later laboratory studies revealed proteinuria and high serum creatinine. A rectal biopsy showed amyloid deposition that was also found in the pericardial tissue. Pericardial tamponade is an extremely rare complication of cardiac amyloidosis. To our knowledge, only one previous case of cardiac tamponade due to amyloid heart disease has been reported.
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PMID:Cardiac tamponade as presentation of systemic amyloidosis. 142 40

We recently saw a patient who had aortitis syndrome associated with secondary amyloidosis. To our knowledge, she is the fourth report of this complication occurring in aortitis syndrome. In November 1985, the patient, a 18 year-old woman, was admitted to our hospital because of a high fever, back pain, abdominal pain and general fatigue. On physical examination, bruit was audible on the abdomen, bilateral radial artery was weakly palpable. Angiography showed the stenosis of bilateral carotid artery, subclavian artery, renal artery and superior mesenteric artery. From the above findings, she was diagnosed aortitis syndrome, and treatment was begun with prednisolone. However, she developed recurrently a high fever, chest pain, abdominal pain and exertional dyspnea. Laboratory findings at the active stage revealed the marked elevation of leukocytes, erythrocyte sedimentation rate and C-reactive protein. On her clinical course, the number of circulating thrombocytes was paralleled with the activity of the disease. On June 1988, she developed suddenly a high fever and severe pain of abdomen. Pathological findings of her stomach showed the deposition of amyloid protein A. Laboratory findings depicted the marked increment of thrombocytes, beta-thromboglobulin and platelet factor 4. These results suggest that circulating thrombocytes may play a role in product ion of amyloid protein.
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PMID:[A case of aortitis syndrome complicated with amyloidosis, type AA]. 176 46

Eleven patients with rheumatoid arthritis that had been refractory to conventional drug therapy were treated with total lymphoid irradiation (TLI). Followup continued for 6 months in 9 patients, 12 months in 6 patients, and 24 months in 3 patients. At 6 and 12 months post-TLI, a significant improvement in clinical disease activity was demonstrated. Side effects noted during TLI included fatigue, nausea, diarrhea, and vomiting. One patient died of cardiorespiratory arrest, 2 patients died of kidney failure secondary to generalized amyloidosis, and 1 patient died of septic shock secondary to a multilocular septic arthritis. One patient experienced 2 episodes of septic arthritis; 2 patients manifested delayed wound healing. Immunologic assessments showed consistent lymphopenia in all patients. T lymphocyte subsets decreased after TLI, and showed a transient increase at 6 months post-TLI. The suppressed mitogen responsiveness, which was noted 2 months after irradiation, was found to increase almost to the pre-TLI levels at 12 months. The observed increase in morbidity and mortality after TLI is evidence that discourages the use of this therapeutic technique, at least in its present form.
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PMID:Total lymphoid irradiation in patients with refractory rheumatoid arthritis. 293 45

Eleven patients with intractable rheumatoid arthritis were treated with fractionated total lymphoid irradiation at a total dose of 20 Gy. Lasting improvement in clinical symptoms was found in four patients during treatment and the remaining patients experienced a similar benefit within 2 months of irradiation. There was marked reduction in exacerbations and the number of joints involved. Morning stiffness, joint swelling and tenderness decreased. Complications included severe fatigue during treatment and acute bacterial arthritis in multiple joints in one patient. Four of the patients have since died, one of renal failure and another of cardiogenic shock following surgery 3 and 24 months after total lymphoid irradiation. Both had generalised amyloidosis. The third patient developed joint empyema and died of toxic cardiac failure. The fourth died 3 months after resection of a Kaposi's sarcoma complicated by wound infection which responded to treatment. Immunologically, total lymphoid irradiation resulted in suppression of the absolute lymphocyte count and a reduction in T-helper cells, while the number of T-suppressor cells remained unchanged. These data provide evidence of T-cell involvement in the pathogenesis of rheumatoid arthritis. Total lymphoid irradiation can induce sustained improvement in clinical disease activity, but severe, possibly fatal, side-effects cannot be ignored.
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PMID:Total lymphoid irradiation of intractable rheumatoid arthritis. 294 4

Restrictive cardiomyopathy is uncommon and in its overt form is associated with heart failure, characterized primarily by abnormalities in diastolic function and preserved or nearly preserved systolic function. It may be associated with amyloidosis, hemochromatosis or endomyocardial fibrosis. We describe five patients with restrictive cardiomyopathy, ages ranging from 35 to 71 (mean 49), three of whom were men. Fatigue, dyspnea on exertion and chest pain were the most frequent symptoms. Only one patient had overt heart failure, and three had normal or near-normal hemodynamics at rest that became greatly abnormal with exercise. Four of the five patients are alive now 9 to 77 (mean 33) months following the onset of symptoms. Despite prior emphasis on specific causes, restrictive cardiomyopathy in this series had no definable cause. Moreover, the presence of a "latent" form of restriction (abnormalities only with exercise) suggests that the incidence of the disease may be higher than previously appreciated.
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PMID:Clinical, hemodynamic and endomyocardial biopsy findings in idiopathic restrictive cardiomyopathy. 396 91

An autopsy case of primary systemic amyloidosis with severe cardiac amyloidosis in a 75-year-old Japanese man is reported. The initial signs were dyspnea and cough, followed by general fatigue and loss of appetite. Heart failure, pleural effusion, and liver cysts were found on physiological examination. Autopsy findings were primary systemic amyloidosis with severe diffuse cardiac amyloidosis and cardiac hypertrophy (585 g). Focal necrosis by infarction was found in the liver and spleen. The cause of amyloidosis was unknown.
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PMID:Primary systemic amyloidosis with severe cardiac amyloidosis. 407 77

A case of primary amyloidosis associated with intramucosal adenocarcinoma of the stomach, diagnosed by preoperative biopsy, is reported. A 77-year-old man was admitted to our hospital with complaints of vertigo and general fatigue. X-ray and endoscopic examination revealed a IIb-like IIa type protruded lesion on the cardia of the stomach. A biopsy specimen from the protruded lesion disclosed well differentiated tubular adenocarcinoma and amyloid deposition. Partial gastrectomy was performed on August, 18, 1981. Upon histological study, a diagnosis of primary amyloidosis associated with intramucosal well differentiated tubular adenocarcinoma was made. We suggest that the histogenesis of this gastric carcinoma was related to the gastric lesion due to primary amyloidosis. Careful review of the Japanese literature disclosed that ours is the first case report of primary amyloidosis associated with early gastric carcinoma diagnosed by pre-operative gastric biopsy.
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PMID:[Primary amyloidosis associated with early gastric carcinoma(IIb like IIa type) diagnosed by preoperative gastric biopsy--a case report]. 666 17

With advancing age of the population and with echocardiographic means of diagnosis, amyloid disease of the heart is of increasing clinical interest. Advanced age, restrictive myocardiopathy, arrhythmias, and conduction disorders are familiar features of this disease. A 92 year old man with past history of hemiblock followed by complete heart block and transvenous pacemaker was admitted to the hospital because of increasing fatigue and the abrupt development of dyspnea. Examination revealed paradoxic pulse, markedly elevated central venous pressure, and echocardiographically demonstrated large pericardial effusion. Shortly after admission signs of tamponade developed; 1,000 ml of pericardial fluid was removed with prompt relief of dyspnea dna disappearance of paradoxic pulse and return of central venous pressure to normal. However, dyspnea soon recurred and subsequent hemodynamic measurements indicated increased right ventricular and left ventricular filling pressures. Echocardiography revealed no recurrent effusion or ventricular hypokinesis. Left ventricular ejection fraction by radionuclide ventriculogram was 64 percent. Echocardiography revealed ventricular wall thickening, normal chamber size, and glittering, sparkling myocardial echoes. On postmortem examination, there was extensive myocardial amyloidosis. There was no evidence of constrictive pericarditis or recurrent effusion. The unique aspect of this case was the combined presence of restrictive myocardiopathy and pericardial tamponade. To our knowledge, no previous case of tamponade due to amyloid heart disease had been reported.
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PMID:Pericardial tamponade, a new complication of amyloid heart disease. 709 Nov 68

High cardiac output failure/state (HCOF) is regular feature of some illnesses e.g. thiamine deficiency, hyperthyroidism, severe anemia, Paget's disease or arteriovenous fistulae. HCOF in multiple myeloma is reported quite rarely. 31-year-old man was admitted because of fatigue, dyspnea and subfebrilities. Heart rate was 116/min, sinus rythm blood pressure 110/60 mmHg. Chest film showed cardiomegaly with sings of interstitial pulmonary edema, echocardiography mild dilatation of the left ventricle with hyperkinetic wall motion and small pericardial effusion. Hemoglobin was 104 g/l, leukocyte count 13.5 x 10(9)/l with 30% of plasmatic cells. Serum protein electrophoresis demonstrated a monoclonal gammapathy, X ray studies of the skelet multiple osteolytic lesions. Diagnosis of plasmocytic leukemia-form of multiple myeloma was established and chemotherapy (vincristine + adriamycine + dexamethason) was started. Patient cardiac status deteriorated. Cardiac catheterisation demonstrated mean righ atrial pressure of 25 mmHg, mean pulmonary artery pressure of 28 mmHg and pulmonary artery wedge pressure of 24 mmHg. Co was 20.0 l/min (C.I. 11.5 l/min/m2). In continuing of chemotherapy and symptomatic therapy for heart failure patients status gradually improved and complete remission of the myeloma and normalisation of cardiac parameters was achieved. Heart failure in multiple myeloma patients has been attributed to amyloidosis of myocardium, hyperviscosity syndrome, co-existing CAD or anthracycline toxicity. HCOF should be considered in patients with clinical evidence of heart failure and normal left ventricular function.
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PMID:[Hypercirculatory heart failure in a patient with plasmacytic leukemia]. 855 97


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