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

Schmidt syndrome consists of adrenal insufficiency and Hashimoto's thyroiditis, which are probably caused by an autoimmune process. We encountered a patient who manifested severe generalized fatigue due to Schmidt syndrome recurrently. The endocrinological examination tests on the patient showed that the increase in thyroid stimulating hormone (TSH) and ACTH concentrations were not remarkable, despite hypo-function of the peripheral glands. Subsequent cranial magnetic resonance imaging (MRI) exhibited the existence of a pituitary tumor. The pathological findings on the resected tumor and endocrinological stimulation tests proved that the tumor was a FSH-producing adenoma. Although involvement of the pituitary region in Schmidt syndrome on rare occasions presents as hypophysitis, no pituitary adenoma has previously been reported in association with this syndrome. We present a patient with Schmidt syndrome and an accompanying FSH-producing pituitary adenoma. The coexistence of these disorders suggests that the functioning pituitary tumor might be considered as a pituitary lesion in Schmidt syndrome.
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PMID:A case of Schmidt syndrome accompanied by a pituitary adenoma. 898 Aug 88

A 51-year-old woman was admitted because of general fatigue assumed to be due to climacteric disturbance. Laboratory examinations suggested a diagnosis of hyperparathyroidism based on high serum levels of Ca, intact PTH, and high-sensitivity PTH. No abnormalities were found in the cervix. Chest X-ray films and CT scans showed a mass measuring 4 cm in the right postero-upper mediastinum. The tumor was positive on a parathyroid scintigram, and was diagnosed as a mediastinal parathyroid adenoma with hyperparathyroidism. Operative findings showed a tumor surrounded by the superior vena cava, vagus nerve, azygos vein, and brachiocephalic artery. Careful resection of the hypervascular tumor from surrounding tissues was performed using a thoracoscopic technique alone. The postoperative course was uneventful. Serum values of Ca, intact PTH, and high-sensitivity PTH decreased to within normal ranges. after surgery. Pathohistological study confirmed the diagnosis of parathyroid adenoma including a cyst caused by degeneration of the tumor.
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PMID:[Thoracoscopic resection of mediastinal parathyroid adenoma with cyst and hyperparathyroidism--a case report]. 945 9

Primary hyperparathyroidism, characterized by hypersecretion of parathyroid hormone (PTH) leading to hypercalcemia and relative hypophosphatemia, is quite common in the elderly. Most patients with primary hyperparathyroidism have only mild hypercalcemia and are symptomless. But others experience various other organ diseases. Primary hyperparathyroidism is also associated with cardiovascular abnormalities, including QT interval shortening, heart block, cardiac arrhythmias, hypertension, myocardial hypertrophy, myocardial calcification and, though rarely, with valvular heart disease. We described a case of primary hyperparathyroidism associated with cardiac abnormalities. An 82-year-old male presented with the complaints of chest discomfort, fatigue, general weakness, nausea and vomiting over a period of months and was admitted in July 1996. Physical examination with heart auscultation showed a pansystolic murmur over the right sternal border and apex region, and a blowing diastolic murmur over the left sternal border. Biochemistry profiles revealed elevations of serum calcium (14.3 mg/dl) and chloride/phosphate ratio (> 33). Endocrinological studies showed elevations of serum PTH-C (4.8 ng/ml) and PTH-intact (705 pg/ml) concentrations. Kidney ultrasonography revealed a left renal stone. A spine X-ray revealed spondylosis and a compression fracture of the lumbar-spine with osteoporotic change. Thyroid ultrasonography and Thallium (Tl201)-technetium (Tc99m) subtraction scan showed parathyroid adenoma in the low pole of the right thyroid bed. Parathyroid aspiration cytology revealed few and discrete cells. Echocardiogram revealed moderate to severe aortic valvular calcification as well as stenosis with moderate aortic regurgitation, mitral regurgitation and myocardial calcification. The patient received parathyroidectomy one month later. During his postoperative days, he suffered from muscle twitching with positive Trousseau's sign and Chvostek's sign. The patient received calcium carbonate and vitamin D for hypocalcemia, diltiazem and capoten for his heart problems. A repeated echocardiogram two months after surgery showed no improvement of valvular calcification.
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PMID:Primary hyperparathyroidism with cardiac abnormalities: a case report. 950 84

Benign tumors of the small bowel are rare. They present with many different manifestations depending on the size and location, and also cause a variety of symptoms that are often nonspecific. These include abdominal pain, dyspepsia, nausea, vomiting, and gastrointestinal bleeding that may be melena or hematemesis. Most of the time patients are asymptomatic and the lesions are discovered as an incidental finding. When bleeding occurs, and it may be severe in certain situations, the patient may develop signs of anemia, such as dyspnea, fatigue, and even high-output cardiac failure. The authors present a patient who was evaluated for melena and who was found to have a duodenal polyp that proved to be a Brunner's gland adenoma on pathology.
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PMID:A Brunner's gland adenoma as a cause of anemia. 1047 86

We report a successfully treated case of invasive TSH-secreting pituitary adenoma associated with an unruptured internal carotid artery aneurysm by two-stage operation and gamma-knife radiosurgery. A 64-year-old woman was admitted to our department with a 3-year history of general fatigue and 1-year history of anxiety, palpitation and hyperhydrosis. Endocrinological examination revealed hyperthyroidism with elevated TSH, GH and somatomedin C. Magnetic resonance images demonstrated a tumor in the sella turcica which extended into the left cavernous sinus, furthermore, indicated aneurysm-like flow void at the ventral part of the left internal carotid artery. The aneurysm was confirmed by conventional angiography. Neck clipping of the aneurysm was performed through pterional approach as the first operation. One month later, at the second operation, the pituitary adenoma except for cavernous sinus portion was resected via the transsphenoidal approach. Immunohistological examination revealed positive for TSH and GH. Gamma-knife radiosurgery with a central dose of 33.3 Gy and peripheral dose of 17 Gy was carried out for residual tumor at the cavernous sinus under both MRI and CT guidance. Posttreatment course was uneventful with normalization of thyroid function at 16 months after gamma-knife. Two-stage operation and gamma-knife radiosurgery is effective for TSH-secreting adenoma extending into the cavernous sinus associated with an unruptured aneurysm.
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PMID:[A case of TSH-secreting pituitary adenoma associated with an unruptured aneurysm: successful treatment by two-stage operation and gamma-knife]. 1055 92

To evaluate the features of primary hyperparathyroidism (HPT) with normal serum intact parathyroid hormone (iPTH) levels, we studied 271 consecutive patients undergoing surgery for primary HPT. In 20 patients, serum iPTH levels were within the normal range (10-65 ng/l). In their records, the most common clinical features were fatigue (n=13), polyuria (n=6), renal stone (n=5), and hypertension (n=5). Mean serum calcium and phosphorus were 2.78 and 0.85 mmol/l, respectively: 14 had serum phosphorus within the normal range. Mean serum iPTH was 48.5 ng/l, and was <45 ng/l in nine patients. Cervical ultrasound demonstrated a parathyroid adenoma in nine, and was normal in four. Tc sestamibi parathyroid scintigraphy always demonstrated an adenoma (9/9). In eight patients, normal iPTH values delayed diagnosis. Physicians should be aware of the possibility of HPT in patients with hypercalcaemia, even when serum phosphorus and iPTH levels are within the normal limits. Particularly, HPT cannot be excluded when serum iPTH levels are below the upper part of the normal range. In such cases, cervical imaging, which has the same sensitivity as in other HPT, should be undertaken. These explorations are useful, because many patients are symptomatic and can take advantage of surgery.
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PMID:Primary hyperparathyroidism with normal serum intact parathyroid hormone levels. 1087 86

Parathyroid surgery to correct primary hyperparathyroidism is successful in 80 to 97 per cent of initial explorations. Failures are often linked to inability to locate ectopic parathyroid glands. Although ectopic parathyroid glands are relatively common (15%) multiple ectopic glands are rarely reported. We describe a case of multiple ectopic parathyroid glands and the intraoperative approach to their localization and review the anatomy and embryology of ectopic parathyroid glands. A 39-year-old woman presented with fatigue, lethargy, and depression. On biochemical evaluation she was noted to be hypercalcemic and hyperparathyroid. Preoperative parathyroid localization failed to identify abnormal parathyroid glands. At exploration three of four parathyroid glands, including an adenoma, were located in ectopic positions by a meticulous and systematic dissection. A careful exploration coupled with a thorough knowledge of parathyroid anatomy and embryology will produce successful surgical correction of primary hyperparathyroidism in greater than 95 per cent of patients even in the few patients with multiple ectopic parathyroid glands.
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PMID:Multiple ectopic parathyroid glands. 1109 12

A 44-year-old woman presented to her GP with excessive tiredness. She had positive thyroid microsomal and thyroglobulin autoantibodies and was found to have an elevated serum thyroid-stimulating hormone (TSH) concentration of 8.37 (normal = 0.15-3.5)mU/L and a low normal total thyroxine (T4) of 86 (reference range 60-145)nmol/L. She was rendered symptom free on a dose of 150 microg of thyroxine per day. However, her TSH failed to return to normal, and following a further increase in her thyroxine dose she was referred to the endocrine clinic for further assessment. Her TSH at this stage was 14mU/L, free T4 (fT4) 28 (normal = 10-27)pmol/L and free T3 (fF3) 10 (normal = 4.3-7.6)pmol/L. She denied any problems with adherence to her medication. Her serum prolactin was elevated at 861 (normal = 60-390)mU/L. A pituitary tumour was suspected and an MRI scan showed a macroadenoma of the right lobe of the pituitary, extending into the suprasellar cistern. The tumour was resected trans-sphenoidally. Electron microscopy showed a dual population of neoplastic cells compatible with a thyrotroph cell and prolactin-secreting adenoma. Immunocytochemistry and cell culture studies confirmed the secretion of TSH, prolactin and alpha-subunit. Postoperative combined anterior pituitary function tests did not demonstrate any deficiency of anterior pituitary hormones. A repeat MRI scan showed no significant residual tumour; however, her serum TSH and prolactin levels remained high and she was given a course of pituitary irradiation. This case illustrates the difficulty of diagnosing a TSHoma when it coexists with autoimmune hypothyroidism. We believe the combination of pathologies reported here is unique.
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PMID:Autoimmune hypothyroidism coexisting with a pituitary adenoma secreting thyroid-stimulating hormone, prolactin and alpha-subunit. 1158 39

A middle-aged woman presented with a history of constipation, easy fatigue, depressive mood, lassitude, polydipsia, and polyuria. The patient posed a challenging diagnostic dilemma due to the presence of persistent severe hypercalcemia and relative lack of clinically manifested symptoms. Clinical, biochemical, and genetic examinations confirmed the diagnosis of familial hypocalciuric hypercalcemia as a result of C562Y calcium-sensing receptor mutation, and a coexisting parathyroid adenoma. After adenectomy, the patient's clinical situation improved markedly, and a modest equilibrium hypercalcemia persisted. This case presents an unusual combination of two relatively common endocrine disorders.
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PMID:Parathyroid adenoma in a subject with familial hypocalciuric hypercalcemia: coincidence or causality? 1188 54

About 3% of our hypertensive patients have high blood pressure induced by corticosteroids. Muscle weakness, tiredness, polyuria and polydipsia may indicate hypokalaemia. Hypokalaemic hypertension in the presence of a low plasma renin activity is the typical finding of corticosteroid hypertension. The most frequent cause of corticosteroid hypertension is primary aldosteronism (Conn's syndrome) due to an adrenal adenoma or bilateral hyperplasia of the adrenal glands. The plasma concentration of aldosterone and the ratio between plasma aldosterone and renin concentrations are high, and the kaliuresis exceeds 30 mmol/24 h in the presence of hypokalaemia. Adrenal carcinomas are rare and very malignant. The localization of an adrenal tumour is made by computer tomography (CT-scan) or nuclear magnetic resonance imaging and by measurement of the aldosterone/cortisol concentrations in the adrenal venous blood. Adenomas are removed under laparoscopy, and adrenal hyperplasias are treated with spironolactone (50-400 mg daily) or amiloride (5-30 mg daily). In rare cases (<1%), excessive stimulation of the mineralocorticoid receptor is due to cortisol (apparent mineralocorticoid excess, Cushing's disease, liquorice, or hereditary deficiency of 11beta-hydroxysteroid dehydrogenase) or to a chimeric gene coding for 11beta-hydroxylase (CYP11B1/CYP11B2). In these rare cases, the synthesis of aldosterone is under the control of the adrenocorticotrophic hormone, so treatment with glucocorticoids (dexamethasone 0.25-1.0 mg daily) is therefore possible (glucocorticoid-remediable aldosteronism). Excessive deoxycorticosterone (DOC) causes the same symptoms and signs as hyperaldosteronism. Excessive DOC is found in patients with adrenal tumours that secrete DOC, in those with hereditary or acquired disorders with dysfunctioning glucocorticoid receptors, or in those with congenital hyperplasia of the adrenal glands (deficiency of 17alpha-hydroxylase or 11beta-hydroxylase). Liddle's syndrome is a constitutive hyperactivity of the transepithelial transport of sodium, which under normal conditions is controlled by the mineralocorticoid receptor. Plasma renin and aldosterone concentrations are suppressed and the plasma potassium concentration may be normal. In contrast, plasma aldosterone and renin concentrations are increased in patients with hypokalaemic hypertension which represents secondary aldosteronism. The increased aldosterone is the consequence of stimulated renin activity due to renal or renovascular or other disorders, antihypertensive drugs or other medications. In conclusion, a work-up for corticosteroid-induced hypertension is indicated in patients with hypokalaemic hypertension and in those with severe hypertension even in the absence of hypokalaemia, and in hypertensive patients with a family history of cardiovascular diseases.
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PMID:Investigating mineralocorticoid hypertension. 1292 4


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