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 61-year-old woman with Addison's disease and malignant lymphoma for several years was admitted to hospital with a 2-month history of fatigue and a 7 kg weight loss. The erythrocyte sedimentation rate was 92 mm h-1 and a temporal biopsy was performed as a part of the clinical investigation. She suddenly suffered a paresis of the right arm, sudden blindness and her blood pressure fell to 100/60 mmHg. Hydrocortisone was given intravenously followed by betamethasone, and an Addison crisis as well as a giant cell arteritis (GCA) was suspected. Activity in the malignant lymphoma was also a possibility. The patient did not improve and died 8 d later. The temporal biopsy indicated GCA. The autopsy showed a pronounced intimal inflammatory reaction of the intracerebral arteries and an infarction in the left posterior hemisphere. A possible link between GCA and other autoimmune diseases is discussed.
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PMID:Addison's disease, malignant lymphoma and death from cerebral giant cell arteritis. 279 51

Primary adrenal insufficiency is characterized by cortisol and aldosterone deficiency; in the secondary form, cortisol alone is decreased. The symptoms are usually nonspecific and include hypotension, weight loss, and fatigue; volume depletion, hyperkalemia, and hyperpigmentation may be present in the primary form but are uncommon in the secondary form. The most common cause of secondary adrenal insufficiency is steroid therapy, which produces adrenal suppression in relation to the dose and duration of use. Sudden withdrawal may precipitate adrenal crisis; therapy must be continued until adrenocortical function recovers. Because cortisol deficiency increases vulnerability to stress, patients with known or suspected adrenal insufficiency require glucocorticoid prophylaxis before any surgical procedure, major or minor. Hydrocortisone, not cortisone acetate, should be used.
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PMID:Preventing adrenal insufficiency during surgery. 737 7

A certain number of HIV-infected patients (about 17% in our series) manifest symptoms of cortisol resistance--weakness, weight loss, hypertension, chronic fatigue and intense mucocutaneous melanosis--symptoms which are also typical of Addison's disease. The diagnosis of cortisol resistance is determined through the increased plasma and urinary cortisol values and limited increases in ACTH values. Compared with patients with primary glucocorticoid resistance, AIDS patients have no symptoms of mineral-corticoid or androgen excess, only of glucocorticoid deficiency at target tissues. Mononuclear leukocytes from these patients show receptor changes which consist of an increased receptor number and decreased receptor affinity for glucocorticoids. They also show defective glucocorticoid-induced inhibition of [3H]thymidine incorporation. Glucocorticoid-resistant AIDS patients have a characteristic persistent increase in interferon-alpha production. The inverse correlation between plasma values of interferon-alpha and the receptor affinity for glucocorticoids clearly suggests that interferon production is regulated by the glucocorticoid receptor: the smaller the glucocorticoid effect on lymphocyte cells is, the greater interferon production is. Owing to the antiviral effect of interferon-alpha, it is possible that glucocorticoid-resistant AIDS patients have greater defences against viral infection than other AIDS patients. As interferon-alpha is melanogenetic, its increased production may also explain the intense skin pigmentation found in patients with the glucocorticoid-resistance syndrome.
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PMID:The syndrome of acquired glucocorticoid resistance in HIV infection. 781 Dec 21

We reported a case of Addison's disease, caused by adrenal tuberculosis. The patient was female, seventy four years old. She complained cough and body weight loss. She complained cough from June, 1989, but her home doctor didn't take care of her symptoms. September 1989, she felt appetite loss, and easy fatigue, so her home doctor suspected her disease as pulmonary tuberculosis, so he introduced our hospital, and she admitted. When she admitted, her chest roentogenogram revealed bIII2. Sputum smear examinations were negative. Laboratory data on admission, we observed slightly eosinophilia, severe iron deficiency anemia, and accenturation of blood sedimentation rate. Immediately after admission, she complained nausea, vomiting, coldness, and powerless. On 25 days after admission, she lost her senses suddenly, and her blood pressure fell 5 days after, she fell in shock state, too. We found out her blood sugar data was 29. After blood examinations, we found out that ACTH was high, cortisole, 17-KS, 17-OHCS were low. So we thought she got acute hypoadrenocorticism. We found her abdominal CT revealed calcification in her right adrenal gland. We diagnosed her disease as Addison's disease caused by adrenal tuberculosis so we began to give prednisolone, 7.5 mg per day. After giving, her state made better. We thought her disease as Addison's disease caused by adrenal tuberculosis, revealed acute hypoadrenocorticism.
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PMID:[A case of Addison's disease caused by adrenal tuberculosis, and revealed acute hypoadrenocorticism]. 826 25

A 66-year-old female presented with anorexia, fatigue, skin pigmentation, weight loss and low grade fever. Imaging studies demonstrated bilateral bulky masses confined to the adrenal glands. Ultrasonography guided needle biopsy of the mass showed findings of diffuse large B-sell lymphoma. Low levels of serum cortisol, urinary 17-OHCS and 17-KS, a high level of ACTH and a non-reactive pattern on the rapid ACTH test led to a diagnosis of Addison's disease. Only a partial regression was achieved by the first chemotherapy. She died due to disease progression, while the next course of chemotherapy had been postponed because of interstitial pneumonitis due to methotrexate.
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PMID:[Bilateral non-Hodgkin's lymphoma of the adrenal glands with adrenal insufficiency]. 891 78

Primary adrenal insufficiency (Addison's disease) may initially present with cutaneous hyperpigmentation. Addison's disease, when associated with autoimmune thyroid disease and/or insulin-dependent diabetes mellitus, is referred to as polyglandular autoimmune syndrome type II. We present the case of a patient who initially was diagnosed as having Grave's disease and eventually Addison's disease due to persistent cutaneous hyperpigmentation, fatigue, weight loss, hypotension, hyponatremia, peripheral eosinophilia, and positive results of a synthetic corticotropin stimulation test. Addison's disease, polyglandular autoimmune syndrome type II, and cutaneous hyperpigmentation are reviewed.
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PMID:Cutaneous hyperpigmentation and polyglandular autoimmune syndrome type II. 904 Sep 76

Primary adrenal insufficiency (PAI) is a relatively rare but serious condition that can lead to signs and symptoms ranging from mild generalized weakness and fatigue to fulminant shock and death. We present the case of a previously healthy 31-year-old man who developed PAI while undergoing rehabilitation after a severe traumatic brain injury (TBI). The patient suffered a TBI with comminuted skull fractures, bifrontal confusions, and bilateral epidural hematomas in a jet-ski accident. Acute hospitalization was prolonged by several medical complications, and the patient was admitted for subacute rehabilitation 1 month after his injury with cognitive deficits, persistent agitation, confusion, generalized weakness, and poor endurance for therapy. His weakness, fatigue, and orthostasis did not improve with attempts at gradual remobilization. The patient also had persistent anorexia, nausea, and hyponatremia despite various treatment regimens. Endocrinology workup showed normal anterior pituitary function but an abnormal response to adrenocorticotropic hormone (ACTH) stimulation, leading to the diagnosis of PAI. The patient was treated with prednisone and fludrocortisone, which resulted in improvement in clinical symptoms followed by rapid gains in all functional areas. No previous descriptions of PAI following head injury were found in the medical literature. It is important for physiatrists to be aware of this entity because symptoms of adrenal insufficiency can be similar to those commonly seen with TBI alone. PAI may also be confused with other endocrine disorders more frequently seen after TBI such as the syndrome of inappropriate antidiuretic hormone secretion. Recognition and appropriate management of adrenal insufficiency can lead to significant clinical and functional gains.
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PMID:Primary adrenal insufficiency following traumatic brain injury: a case report and review of the literature. 908 56

Nonneoplastic Lambert-Eaton Myasthenic Syndrome (LEMS) is rare. A 27-year-old man as initially having the diagnosis of Addison's disease was admitted to the hospital because of fatigue, dry-mouthness and proximal limb weakness for 1 year. A diagnosis of LEMS was made from electrophysiological studies. Clinical and laboratory studies revealed no malignancy. We report the first case of Addison's disease associated with non-neoplastic LEMS. It is possible that subclinical LEMS might be present in patients with Addison's disease more frequently than currently believed, since the prominent symptoms of LEMS may be confused with symptoms of Addison's disease.
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PMID:A case of Addison's disease associated with the Lambert-Eaton myasthenic syndrome. 929 81

Primary adrenocortical insufficiency (Addison's disease) is characterised by weakness, tiredness, fatigue, weight loss, hypotension, hyperpigmentation and a craving for salt. Without treatment lethality is 100%; correctly treated, life expectancy is normal. Addison's disease may appear isolated or as part of a polyendocrine syndrome. Because several of the symptoms are unspecific and develop over the course of several years, many patients are not diagnosed before a life-threatening adrenal crisis develops. Autoimmune destruction of the adrenal cortex is the main cause of adrenocortical failure in the industrialised world. This condition is characterised by circulating autoantibodies against the steroidogenic enzyme 21-hydroxylase. These autoantibodies can now easily be quantified. More unusual causes of adrenocortical failure are tuberculosis, bleeding, metastasis and adrenoleukodystrophy. Using three cases we highlight the clinical, diagnostic and therapeutic aspects of adrenocortical failure.
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PMID:[Primary adrenal cortex insufficiency--a diagnostic challenge]. 952 May 81

A 76-year-old Japanese woman had suffered from fatigue, weight loss, and cutaneous hyperpigmentation at the age of 38 years and was diagnosed as having tuberculous Addison's disease. Since then, corticosteroids had been administered effectively as hormonal replacement. At the age of 75 years, the patient presented with a progressive, painless swelling in the left eyelid due to an ill-defined tumor of rubbery consistency in the superotemporal aspect of the orbit. Computed tomography, magnetic resonance imaging, and scintigraphy revealed a wide distribution of tumors, but not in the adrenal gland, which led to the suspicion of systemic malignant lymphoma. Histopathologic examination of the excised orbital tumor was compatible with non-Hodgkin's lymphoma of the B-cell type. We believe this is the first report of Addison's disease presenting with non-Hodgkin's lymphoma. This disease process was characterized by the development of a lymphoid malignancy after long-term corticosteroid therapy to control the adrenal insufficiency, and by the widespread involvement of the lymph nodes and orbit but not the adrenal gland. Corticosteroid-induced abnormal immune state was considered to be the pathogenesis of this unusual complication.
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PMID:A case of non-Hodgkin's lymphoma following long-term corticosteroid therapy for Addison's disease. 982 70


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