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

We studied the effect of CV 205-502 in 12 patients with macroprolactinomas and 8 patients with PRL-secreting tumors, who were selected because of previous repeatedly shown intolerance to bromocriptine in even small doses. We also investigated serum insulin-like growth factor-I (IGF-I) levels before and during CV 205-502 therapy. In 12 macroprolactinoma patients followed for 1 yr, 0.075-0.450 mg CV 205-502 lowered PRL levels by 91.2 +/- 5.4%. Only 3 of the patients had transient side-effects of nausea, dizziness, or fatigue. In eight patients with PRL-secreting tumors who were bromocriptine intolerant, CV 205-502 (0.075-0.300 mg daily) lowered PRL levels by 80.2 +/- 6.3%. Four of these patients showed transient side-effects (nausea, fatigue, and/or tachycardia). None of the patients discontinued therapy. There was a close correlation between pretreatment circulating PRL levels and tumor size, expressed in cubic millimeters. The decrease in pituitary tumor size after 52 weeks of CV 205-502 therapy (-74 +/- 6%) was also correlated with the decrease in PRL levels (P less than 0.01). In four patients with hypopituitarism, lowered IGF-I levels did not change during CV 205-502 therapy. However, in seven previously untreated patients with macroprolactinoma and normal CV 205-502 is a potent dopaminergic drug, which effectively controls PRL secretion and induces tumor shrinkage. At the doses used in our study, it causes only mild and transient side-effects in a minority of patients and can also be used to treat hyperprolactinemic patients who have shown intolerance to bromocriptine therapy.
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PMID:The efficacy and tolerability of CV 205-502 (a nonergot dopaminergic drug) in macroprolactinoma patients and in prolactinoma patients intolerant to bromocriptine. 167 85

Lymphocytic adenohypophysitis is considered to be an inflammatory disease of the adenohypophysis that is commonly present with visual disturbance and hypopituitarism. Its etiology remains unclear but it is often related to an autoimmune disorder involving other organs, such as the thyroid, parathyroid, or adrenal glands. We encountered a rare case of lymphocytic adenohypophysitis associated with sarcoidosis of the lung and eye during the follow-up period. A 23-year-old woman was hospitalized in July 1986, with a one-month history of headache and visual disturbances which began three days after her second normal delivery. On admission, she showed slight visual impairment and had a left temporal superior quadrantanopia. Endocrinological evaluation revealed thyroid and adrenal hypofunction, and low response of human growth hormone to the loading test. A skull X-ray showed normal shaped sella with some erosion of the dorsum. CT scan showed a rounded contrast-enhanced intrasellar mass extending into the suprasellar cistern. MRI (SR: 500/30) showed a homogeneous low intensity mass which contained a small high intensity area on the relative T2-weighted image (2000/50). A biopsy was performed via right frontotemporal craniotomy. The consistency of the resected tissue was firmer than that of pituitary adenoma. Histologically, the tissue showed diffuse lymphocytic infiltration with some normal adenohypophysis. Her postoperative course was uneventful and the visual impairment improved two months later after the operation. Six months after the operation, she was readmitted with complaints of general fatigue and breathlessness. Chest X-ray showed diffuse infiltration throughout both lung fields, but there was no bilateral hilar lymphadenopathy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of lymphocytic adenohypophysitis associated with sarcoidosis of the lung and eye]. 218 92

The typical patient with post-traumatic hypopituitarism is a young adult male presenting months to years after an automobile accident, following which he was unconscious for several days. He will probably have sustained a fracture of the base of the skull and on recovery is likely to have permanent visual or other neurological sequelae. Temporary or permanent diabetes insipidus may have occurred. The features of panhypopituitarism such as weight loss, fatigue, faintness, loss of libido, and impotence may have been ascribed to depression or the "postconcussion syndrome" and often inappropriate treatment and rehabilitation advised. The striking feature on review of the literature is that the pathological consequences of head injury to the pituitary and hypothalamus have been well described, while only 47 cases of traumatic hypopituitarism have been reported. The most likely reason for this disparity is that head injury of sufficient severity to cause hypothalamic and pituitary damage commonly led to death. More patients now survive, owing to the availability of intensive care; accordingly, most cases have been reported in the last 15 years. However, several patients are described in whom the initiating head injury was not associated with a skull fracture or followed by coma. We recommend that patients with major head injury (defined by post-traumatic amnesia greater than 24 hours), and in particular those with fractures of the base of the skull or diabetes insipidus should be closely monitored for symptoms and signs of endocrine dysfunction and appropriate dynamic pituitary-function tests performed.
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PMID:Post-traumatic hypopituitarism. Six cases and a review of the literature. 301 25

The atrophy produced by endocrine disorders is primarily due to alterations in protein and carbohydrate metabolism. Type II muscle fibers are more severely affected than are Type I fibers. Steroid myopathy and the myopathy associated with excess ACTH have a typical pattern of proximal weakness affecting the legs more than the arms. Steroid myopathy is usually not apparent until other signs of glucocorticoid excess are present. Treatments of steroid myopathy are as follows: Lower the dose of steroid, use a nonfluorinated glucocorticoid, and exercise or physical therapy. Adrenal insufficiency produces generalized weakness, muscle cramping, and fatigue in 50 per cent of patients. Some patients also develop hyperkalemic paralysis. The treatment is hormone replacement. Thyrotoxicosis produces myopathy caused by net protein catabolism, accelerated basal metabolic rate and impaired carbohydrate metabolism. Shortening of contraction time may result from accelerated myosin ATPase activity and enhanced calcium uptake by the sarcoplasmic reticulum. Depolarization of the muscle fiber and impaired Na-K activity in muscle may predispose to thyrotoxic periodic paralysis. Neuromuscular presynaptic impairment may account for the worsening of myasthenia gravis by thyrotoxicosis. In hypothyroidism, impaired energy metabolism may limit force generation. Slow contraction and relaxation reflect reduction in myosin ATPase activity and impaired calcium uptake by the sarcoplasmic reticulum. Treatment for thyroid-associated muscle disorders is restoration of a euthyroid state. Muscle weakness associated with hypopituitarism is due to loss of thyroid and adrenal cortical hormones. Children require growth hormone for muscle development. T3 and growth hormone synergize to maintain normal protein synthesis. Primary and secondary hyperparathyroidism and osteomalacia are often associated with proximal weakness and fatigability. The myopathy improves with restoration of normal PTH levels and vitamin D replacement. Hypoparathyroidism and pseudohypothyroidism are associated with tetany. Tetany is worsened by alkalosis and is treated by calcium and magnesium replacement.
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PMID:Endocrine myopathies. 306 2

Pituitary abscess is relatively rare. Only about 80 cases have been reported. Preexisting lesions in pituitary fossa, such as pituitary adenoma, craniopharyngioma and Rathke's cleft cyst, are inclined to be complicated by infection more than the normal pituitary glands are. We reported a case of pituitary abscess caused by infection of Rathke's cleft cyst. A 67-year-old male had general fatigue and loss of appetite 4 months before admission. On admission he was found to have diabetes mellitus, diabetes insipidus, and hypernatremia. These defects were controlled by medication but he gradually became comatose and febrile. CT and MRI revealed an intrasellar lesion with ring enhancement. Lumbar puncture demonstrated an increase of mononuclear cells and protein. Blood chemistry revealed a marked increase of CRP. He was operated on via the transsphenoidal approach, which revealed sphenoid sinusitis and abscess formation in the pituitary gland. Histological examination of the surgical specimen revealed infection of Rathke's cleft cyst but the fluid in the cyst was sterile. By the drainage of the cyst and the use of antibiotics the patient became alert and signs of infection disappeared. He was discharged with a slight hypopituitarism and returned to normal life. Mortality rate of pituitary abscess is decreasing but is still high because of hypopituitarism and severe infection. Accurate diagnosis and operation are necessary. Transsphenoidal surgery is preferable for postoperative drainage of the abscess.
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PMID:[A case of pituitary abscess caused by infection of Rathke's cleft cyst]. 747 22

A fifty-year-old woman was admitted to our hospital because of generalized edema, progressive symptoms of fatigue and weakness of ten years' duration. After an uneventful third delivery, 24 years before admission, she could not lactate and developed oligomenorrhea and then amenorrhea. Laboratory evaluation revealed panhypopituitarism and pituitary cell antibodies were positive. Both CT scans and MR images showed empty sella. This case is postpartum hypopituitarism without a preceding history of excessive bleeding and may be autoimmune hypophysitis.
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PMID:A case of postpartum hypopituitarism associated with empty sella: possible relation to postpartum autoimmune hypophysitis. 792 Aug 96

A case of systemic lupus erythematosus (SLE) complicated with hypopituitarism after steroid pulse therapy is reported. A 46-years-old-female with a history of SLE starting in 1975 was admitted to our hospital in February 1991 for lupus nephritis. Steroid pulse therapy, 1000 mg methyl-prednisolone for 3 successive days as one therapy unit, was administered. Proteinuria improved remarkably, however, general fatigue and headache appeared 2 weeks after initiation of therapy. Endocrinological examination revealed hypopituitarism including the levels of TSH, FSH, GH and ACTH. The secretion of FSH and LH gradually improved after replacement therapy of dried thyroid. MRI examination of the brain revealed an empty sella. It is known that pituitary tumor, cerebrovascular accident and autoimmune lymphocytic hypophysitis cause hypopituitarism. In this case, it is unlikely that the pulse therapy may be responsible for the infarction of the anterior pituitary artery furthermore, there has been no articles describing such incidence after steroid pulse therapy. This case may be indicative of a very rare case in which the empty sella might have been exacerbated by the pulse therapy in the causation of hypopituitarism.
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PMID:[Hypopituitarism associated with empty sella after steroid pulse therapy in a patient with SLE]. 814 29

A 33 year-old Japanese woman complained of generalized fatigue, recurrent infections and gradual weight loss 1 year after her first delivery. During delivery, no excessive bleeding or change in blood pressure was noted. On endocrinologic examination 2 years after delivery, she was found to have severe adrenal insufficiency and hypothyroidism. Pituitary function tests revealed impaired responses of ACTH, PRL and gonadotropins, and normal response of GH. TSH response to TRH was delayed but not exaggerated. Cranial magnetic resonance imaging showed an empty sella. The adrenal glands were responsive to extrinsic ACTH, and adequately accumulated 123I-aldosterol. Antipituitary and antithyroid autoantibodies were detected in her serum. She was diagnosed with partial hypopituitarism associated with empty sella syndrome. Approximately 2 months after administration of cortisone acetate 25 mg/ day her general condition was noticeably improved, with normalization of thyroid function and improvement of gonadotropin responses to GnRH. This case suggests that a physiologic dose of glucocorticoid is necessary to maintain not only thyroid function but also some of the remaining pituitary functions in patients with empty sella syndrome manifesting hypopituitarism.
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PMID:Reversible hypothyroidism in empty sella syndrome: a case report. 979 Feb 74

We present here a case of prominent hypercalcemia accompanied by hypothalamic tumor and Graves' disease. A 24-year-old man with hypothalamic tumor showed hypopituitarism, central diabetes inspidus (DI) and hyperthyroidism. Nausea, loss of thirst and appetite, and general fatigue were found with the unveiling of hypercalcemia and hypernatremia. Parathyroid hormone (PTH) and 1alpha-dihydroxyvitamin D levels were suppressed with a normal range of PTH-related protein values. One-desamino-(8-D-arginine)-vasopressin (DDAVP) and half-saline administration normalized hypernatremia, while hypercalcemia was still sustained. Administration of cortisone acetate and thiamazole reduced the elevated serum Ca level. In the present case, concurrent hyperthyroidism was assumed to accelerate skeletal mobilization of calcium into the circulation. Hypocortisolism and central DI was also considered to contribute, to some extent, to the hypercalcemia through renal handling of Ca.
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PMID:Hypercalcemia accompanied by hypothalamic hypopituitarism, central diabetes inspidus and hyperthyroidism. 1041 54

We report a case of a seventy-year-old woman with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and adrenal insufficiency induced by Rathke's cleft cyst. She experienced nausea, vomiting, diarrhea, and headache and disturbance of consciousness induced by hyponatremia at a serum sodium level of 100 mEq/l. In spite of severe hyponatremia, urinary sodium excretion was not suppressed and serum osmolality (270 mOsm/kg) was lower than urine osmolality (304 mOsm/kg), and arginine vasopressin (AVP) remained within normal range. SIADH was diagnosed because she was free from other diseases known to cause hyponatremia such as dehydration, cardiac dysfunction, liver dysfunction, renal dysfunction, hypothyroidism, and adrenal insufficiency. Cranial computed tomographic (CT) scan and cranial magnetic resonance (MR) imaging showed a cystic lesion of approximately 2 cm in diameter in the pituitary gland. These images suggested that the cystic lesion was a Rathke's cleft cyst, which was the cause of SIADH. Water restriction therapy normalized her serum sodium concentration and improved her symptoms. After one year, she suffered from general fatigue, appetite loss, fever, and body weight loss (5 kg/2 months). She had neither hypotension nor hypoglycemia, but her serum sodium level was low and serum cortisol, ACTH, and urine free cortisol were very low. Therefore, secondary adrenal insufficiency was suspected and diagnosed by stimulation tests. After start of hydrocortisone replacement therapy (10 mg/day), her symptoms disappeared. In conclusion, Rathke's cleft cyst should be kept in mind as a potential cause in a patient with SIADH, hypopituitarism, and/or adrenal insufficiency.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and adrenal insufficiency induced by rathke's cleft cyst: a case report. 1107 19


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