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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty consecutive patients with recurrent Tolosa-Hunt syndrome were studied. One had a parent who suffered from recurrent Tolosa-Hunt syndrome. Thirty-three percent of the patients had also recurrent periods of weeks to months of unilateral periorbital pain without ophthalmoplegia. One patient had cluster headache before the Tolosa-Hunt syndrome started. Some patients had involvement of cranial nerves outside the cavernous sinus region during Tolosa-Hunt syndrome and also between episodes. The same systemic symptoms, i.e. back pain, cold feet, arthralgia, gut problems, varices, vertigo, chronic fatigue, thrombophlebitis, memory deficiency and signs of inflammation in serum, occurred in Tolosa-Hunt syndrome as earlier found in patients with orbital venous vasculitis. Seventy-three percent of the patients had pathologic orbital phlebograms. All patients treated with steroids reacted promptly; four who developed chronic pain syndromes were treated satisfactorily with azathioprine.
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PMID:Recurrent Tolosa-Hunt syndrome. 155 57

We describe the histopathologic changes of skin, muscle, vessels, and fascia in 11 patients with eosinophilia myalgia syndrome, a newly described entity that has been linked to the ingestion of L-tryptophan. This syndrome is defined clinically by severe incapacitating myalgias and a peripheral eosinophilia. Arthralgias, edema of the extremities, morbilliform rashes, skin induration, weakness, fatigue, and respiratory weakness may be present as well. The earliest apparent histologic changes were observed at the septa between subcutaneous fat lobules and in the deep dermis or fascia. The septa and fascia were infiltrated with a sparse mixture of lymphocytes and histiocytes. In the deep fascia, in addition to inflammatory cells, there were distinctive, reactive mesenchymal cells that showed features of both histiocytes and fibrocytes. Minimal tissue eosinophilia was seen despite the extent of blood eosinophilia. Dermal thickening and homogenization of collagen bundles occurred with replacement of fat and adnexa (changes indistinguishable from scleroderma or morphea). Vessel walls in the dermis and fascia showed thickening and endothelial swelling, but no overt vasculitis was noted. Skeletal muscle biopsies showed a perimysial, epimysial, and/or fascial inflammatory infiltrate of lymphocytes and distinctive reactive mesenchymal cells with some eosinophils. Minimal myofiber atrophy, regeneration, or necrosis was seen despite the clinical history of severe myalgias in almost all patients. This syndrome should help gain insight into the mechanisms of fibrosis in environmental-induced, scleroderma-like syndromes and in idiopathic, scleroderma-like disorders as well.
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PMID:Pathologic manifestations of the eosinophilia myalgia syndrome: analysis of 11 cases. 156 45

Many endocrine diseases can cause fatigue. Tiredness is a frequent symptom of primary and secondary hypothyroidism, hyperthyroidism, excessive glucocorticoid or mineralocorticoid production, primary and secondary adrenal insufficiency, primary and secondary hypogonadism and hyperprolactinemia in the male, acromegaly, diabetes mellitus and diabetes insipidus. A great number of medical diseases other than those mentioned in the articles on cardiological and pneumological fatigue can also cause abnormal tiredness (infectious diseases, hematological, renal, hepatic, gastrointestinal and rheumatological disturbances, vasculitis and malignant tumors). The pathogenesis of tiredness caused by endocrine or medical illnesses, i.e. how the sensation of fatigue is produced, is not clear. The fatigue of the various endocrine or other medical diseases is not disease-specific, i.e. its characteristics do not differentiate it from the fatigue of other illnesses.
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PMID:[Endocrine and other medical causes of abnormal fatigability]. 175 71

A 25 year old man was admitted to our hospital on June 1, 1989 because of general fatigue and pleural effusion. He had noticed purpuras and nodules on his bilateral lower legs in July 1988. He was admitted to Nihon University Hospital and was diagnosed as allergic granulomatous angiitis. Methylprednisolone was administered. In March, 1989, a nodular shadow was detected in his lung CT films. From the findings of TBLB a granulomatous lesion was suspected. However, his clinical course was rather stable so he was discharged from the hospital. Two months later, he was suffered from fever and general fatigue. On his chest X ray film pleural effusion was detected in the lower part of his left lung. The nodular shadow was increasing gradually. Laboratory findings on his admission showed leukocytosis, thrombocytosis, elevated CRP and a high titer of RA factor. He was diagnosed as hypersensitivity angiitis in a broad sense based on his biopsy findings of the skin lesion. Furthermore, the diagnosis of an early stage of Wegener's granulomatosis (WG) or limited type of WG was also made from the clinical course of his lung lesion. The combination therapy with cyclophosphamide and methylprednisolone was started. It was so effective that the nodule of his left lung was almost disappeared. It seems that this case is one of the polyangiitis overlap syndrome proposed by Fauci.
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PMID:[A case of polyangiitis overlap syndrome]. 176 47

The case of a young woman with a rare syndrome of acute encephalopathy followed by deafness and retinopathy developing over 1 year is reported. Unlike previously described similar cases, she had considerable systemic symptoms and signs including polyarthralgia-arthritis, diffuse myalgia, malar rash, livedo reticularis, night sweats, and fatigue suggestive of systemic lupus erythematosus. However, results of most immunological investigations were repeatedly normal, including antinuclear antibodies. Anticardiolipin antibodies were elevated on one occasion. Cyclophosphamide has been the most effective treatment for exacerbations of the disease, which have continued to occur over 6 years. This microangiopathic syndrome more likely relates to an immunologically mediated vasculitis of small blood vessels than to a thromboembolic etiology.
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PMID:Microangiopathy with retinopathy, encephalopathy, and deafness (RED-M) and systemic features. 178 49

A series of four patients with pulmonary infiltrates, pleural effusions, hypoxemia, peripheral eosinophilia, and symptoms of dyspnea, fatigue, and weakness is reported. Lung tissue obtained in three patients revealed interstitial pneumonitis, small-to-medium-vessel mixed-cell vasculitis, and alveolar exudate of histiocytes and eosinophils. All patients reported ingestion of L-tryptophan-containing products at a time when an association between L-tryptophan and the eosinophilia-myalgia syndrome was established. This clinical pattern of pulmonary involvement may be part of the continuum of the eosinophilia-myalgia syndrome. The pathophysiology of this syndrome and the relationship with the ingestion of L-tryptophan-containing products have not yet been identified.
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PMID:Acute eosinophilic pulmonary disease associated with the ingestion of L-tryptophan-containing products. 198 92

Intraocular inflammations as chief manifestation of a T. pallidum infection associated with stage II syphilis are rarely documented in the recent literature. We report on a 35 year old patient with bilateral choroiditis, retinal vasculitis and papillitis persisting retrospectively since he had received some medication for syphilis 8 years previously. This patient was at high risk for other sexually transmitted diseases, however, he did not show HIV-seroconversion. General symptoms like uneasiness, fatigue, depressions and intermittent weight loss were mentioned. Reduction of visual acuity with topical corticosteroid therapy led to another medical work-up, and a systemic therapy with Ceftriaxone for 14 days resulted in better vision, better perimetric results and less inflammatory cell in the vitreous but evident optic atrophy.
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PMID:[Disseminated choroiditis, papillitis and vasculitis retinae as main findings in lues II-III]. 202 73

Eight patients who became ill while taking tryptophan had myalgia, fatigue, rash, fever, edema, alopecia, arthralgias, diminished joint motion, skin tightening, muscle cramping, and distal paresthesias. Three had shortness of breath, and one had pulmonary hypertension. Laboratory abnormalities included peripheral eosinophilia, leukocytosis, thrombocytosis, raised erythrocyte sedimentation rate, and elevated serum levels of aldolase, lactate dehydrogenase, and liver enzymes. Of 4 chest radiographs, 3 were abnormal. Of 5 skin and muscle biopsies, 4 showed sclerosis or mixed inflammatory cell infiltration of the dermis, subcutis, and fascia. Eosinophils were often present, but vasculitis was absent. Muscle inflammation was minimal. We conclude that the "eosinophilia-myalgia syndrome" is related to the ingestion of tryptophan and that abnormalities in the secretion of lymphokines may be important in its pathogenesis.
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PMID:Tryptophan-induced eosinophilia-myalgia syndrome. 221 1

Four patients fulfilling the case definition for eosinophilia-myalgia syndrome are described, including one whose disease began in 1986. Each displayed a variety of symptoms: one suffered principally from myalgia and recovered spontaneously on discontinuation of L-tryptophan therapy; one exhibited progressive sclerodermiform skin changes, neuropathy, and myopathy; a third had prominent neuromuscular disease and sclerodermiform skin changes; and the fourth experienced profound weight loss, an axonal polyneuropathy, and perivascular lymphoid infiltrates simulating a lymphoma. Evidence of T-cell activation was present in peripheral blood and affected tissues during the clinically active progressive phase of disease. Among other manifestations pleural effusion, cutaneous vasculitis, joint contractures, and bloody diarrhea were observed. A history of L-tryptophan ingestion should be sought in patients with myalgia, fatigue, or the above outlined symptoms.
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PMID:Eosinophilia-myalgia syndrome associated with L-tryptophan ingestion. Analysis of four patients and implications for differential diagnosis and pathogenesis. 217 45

We report a case of malignant histiocytosis which began with the skin lesions of panniculitis. A 32-year-old woman presented with recurrent erythematous plaques, subcutaneous nodules, and ulcers on the trunk and the extremities and intermittent fever for 7 months. The cutaneous lesions consisted of erythematous and brownish irregular-shaped patches and tender cutaneous nodules 0.5-1.0 cm in diameter. Central necrosis and shallow ulcers were seen in the lesions. The patient also suffered from general fatigue, arthralgia, and weight loss. She was anemic and thrombocytopenic and had progressive impairment of liver function with coagulation defect. Histopathological study of skin lesions showed lobular panniculitis without vasculitis in the subcutaneous fat tissue. In the panniculitis lesion, moderate mixed cell infiltration consisting of lymphocytes and histiocytes was observed. Bone marrow aspiration revealed an increase in the number of histiocytes, mostly immature with active phagocytosis of erythroid cells, myeloid cells, and platelets. She was diagnosed as having malignant histiocytosis and treated with cyclophosphamide, vincristine, and prednisolone which she responded well; her fever subsided and the lesions healed with hyperpigmentation. In this patient, benign histiocytes with hemophagocytosis without immature forms were found in the skin lesions. According to our knowledge, this is the first Thai report of malignant histiocytosis with clinical features of panniculitis.
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PMID:Malignant histiocytosis with panniculitis--a case report. 222 45


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