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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient, 38-year-old man, with hemorrhage into a prolactin-secreting pituitary adenoma, or pituitary apoplexy, is reported. On his admission, clinical examinations revealed typical stigmata indicating that he suffered from an acute attack of pituitary apoplexy probably induced by acute meningitis. He survived the acute attack and recovered spontaneously without an urgent operation. Although there was no suspicious sign and symptom of hypopituitarism, the first study performed immediately after the attack suggested strongly that hypopituitarism might acutely developed during the hemorrhage into the tumor. Moreover, the follow-up studies indicated that TSH, LH and ADH recovered spontaneously from the initial damage following the resorption of hemorrhage for the next 3 months.
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PMID:A case of pituitary apoplexy with spontaneous recovery. 68 74

The levels of tropic and peripheral hormones (ACTH, TSH, STH, T3, T4, hydrocortisone, insulin) have been assessed in 74 patients, aged 16 to 64 years, operated on for posterior cranial fossa tumors. Depending on the basic anesthesia component the patients were divided into 3 groups: patients on halothane anesthesia, patients on anesthesia with azeotropic mixture, patients on neuroleptanalgesia. Three hemodynamic variants in the course of operation and postoperative period have been established: patients with normal blood pressure, heart rate, stroke volume; patients with elevated and high blood pressure; patients with unstable hemodynamics. It has been found that general halothane and azeotropic mixture anesthesia is associated with marked changes in intraoperative endocrine function. Endocrine function is changed on the 3rd and 7th day postoperatively due to surgical brain trauma.
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PMID:[General anesthesia, hormones and hemodynamics during the excision of tumors of the posterior cranial fossa]. 149 78

The basal and GH-releasing hormone-stimulated secretion of GH declines in the elderly. We tested the ability of cytidine 5'-diphosphocholine, a drug used in the treatment of stroke and Parkinson's disease, to alter GH secretion in 11 healthy elderly volunteers, aged 69-84. Each subject received an iv infusion of 2 g of cytidine 5'-diphosphocholine or normal saline. GHRH and TRH were also administered during cytidine 5'-diphosphocholine infusions. The infusion of cytidine 5'-diphosphocholine induced a 4-fold (p less than 0.05) increase in serum GH levels over basal values. A small increase in GH was seen after GHRH administration. However, the addition of GHRH to the cytidine 5'-diphosphocholine infusion resulted in a GH response which was significantly greater than that seen after GHRH alone; the integrated concentration of GH was more than 2-fold greater in the cytidine 5'-diphosphocholine treated group (706.85 +/- 185.1 vs 248.9 +/- 61.4 micrograms.l-1.(120 min)-1; p = 0.01). The PRL and TSH responses to TRH were not significantly affected by cytidine 5'-diphosphocholine infusion, indicating that dopaminergic mechanisms are not involved. These studies demonstrate that cytidine 5'-diphosphocholine can enhance basal and GHRH-stimulated GH release in the elderly, but the mechanism of action of the drug remains unclear.
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PMID:Effects of cytidine 5'-diphosphocholine administration on basal and growth hormone-releasing hormone-induced growth hormone secretion in elderly subjects. 202 9

Sera obtained during the Hajj seasons of 1985, 1986, 1987 and 1988 from 125 heat stroke patients were collected and subjected to chemical analysis which included determination of glucose, lactate, cholesterol, and triglycerides, as well as assay of T3, T4, TSH and cortisol. Hyperglycaemia and lactic acidaemia were found to be the most frequent metabolic abnormalities. The changes in cholesterol did not exhibit a specific pattern. Triglycerides were significantly elevated in only 6% of patients. Cortisol levels were very significantly elevated in precooled patients. Although the mean T3 levels remained within the normal range, the mean concentration on admission was significantly higher than the post-cooling mean. TSH and T4 levels did not show significant changes.
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PMID:Metabolite and hormonal profiles in heat stroke patients at Mecca pilgrimage. 226 43

Pituitary apoplexy is characterized by a wide spectrum of clinical features. A quite rare case of painless thyroiditis, hypopituitarism and central diabetes insipidus (DI) followed by pituitary apoplexy was presented. A 61-year-old woman was admitted to our hospital in May, 1986 because of marked general malaise, polydipsia and weight loss which became progressively worse. Four months earlier she had experienced episodes of abrupt onset of severe headache associated with nausea and blurring vision. Physical examinations revealed a fine tremor, dry skin and nervousness. The thyroid gland was not palpable. Visual fields were intact. Her blood pressure was 105/64 mmHg with variable tachycardia. The routine laboratory studies were normal or negative except for hypoalbuminemia, hypocholesterolemia and hypernatremia. Erythrocyte sedimentation rate was 12 mm/hr. An impairment in corticotropin secretion was suspected from the low plasma cortisol and the low urinary excretion of 17-OHCS and the sufficient response to ACTH. Basal levels of GH and gonadotropin were also low, and responses to the stimulation tests (Insulin-stress, L-DOPA, and LH-RH) were all blunted. Brain computed tomographic scan and magnetic resonance imaging demonstrated a suprasellar mass that, after infusion, developed peripheral ring-like enhancement and large hyperintense pituitary mass, respectively. A diagnosis of pituitary apoplexy with anterior pituitary failure was made. However, the initial levels of thyroid hormones showed elevated as follows: Free T3 7.6 pg/ml, Free T4 3.3 ng/dl and T3-resin uptake 41.1%. TSH responses to TRH were all suppressed. TSH receptor antibody (TBII) was negative. Both antithyroglobulin and antimicrosomal antibodies were repeatedly positive. A thyroid scan with 99mTc revealed no uptake in the thyroid area. These findings led us to the diagnosis of "painless autoimmune thyroiditis". She had become hypothyroid without any medication. At that time radioactive 99mTc and 123I uptakes increased significantly. When hydrocortisone was substituted, daily urine output abruptly increased to about 10 liters with low osmolality, and the presence of DI was suspected. This diagnosis was confirmed by water deprivation and hypertonic saline infusion tests and subsequent pitressin test. She is currently quite well on L-thyroxine, hydrocortisone and desmopressin (1988). This association with pituitary apoplexy must be a rare occurrence, as a literature search has failed to find a similar case. The pathogenetic trigger of "painless thyroiditis" in this case may be responsible for some immunological change due to secondary adrenal insufficiency after pituitary apoplexy.
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PMID:[An unusual association of transient resolving thyrotoxicosis due to painless thyroiditis, hypopituitarism and central diabetes insipidus associated with spontaneous pituitary apoplexy]. 230 57

Serum thyroid hormones were measured in 62 cases of acute cerebrovascular apoplexy. Compared with the control group, T3, FT3 were markedly lowered and rT3, T4 and TSH were significantly increased with lowered T3/rT3 ratio. The patients were divided into two groups, according to whether there was hemorrhage in their CSF. Changes of serum thyroid hormones in cerebral haemorrhage were more remarkable than those observed in cerebral thrombosis. 16 cases with increased T4, FT4 were diagnosed as euthyroid hyperthyroxinemia. It was found that the amount of thyroid hormone changes appeared to be in proportion to the severity of acute cerebrovascular apoplexy. The determination of serum thyroid hormones would be useful in evaluating the severity of the strokes and in studying the thyroid function in acute cerebrovascular apoplexy.
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PMID:[Changes in serum thyroid hormones in acute cerebrovascular apoplexy and their clinical significance]. 239 Aug 78

The pituitary-thyroid axis of 12 patients, exposed to transsphenoidal pituitary microsurgery because of nonfunctioning adenomas (6), prolactinomas (3) and craniopharyngioma (1), or to major pituitary injury (1 apoplexy, 1 accidental injury), was controlled more than 6 months following the incidents. The patients did not receive thyroid replacement therapy and were evaluated by measurement of the serum concentration of thyroxine (T4), 3,5,3'-triiodothyronine (T3), 3,3',5'-triiodothyronine (rT3), T3-resin uptake test and thyrotropin (TSH, IRMA method) before and after 200 micrograms thyrotropin releasing hormone (TRH) iv. The examination also included measurement of prolactin (PRL) and cortisol (C) in serum. Apart from 1 patient with pituitary apoplexy all had normal basal TSH levels and 9 showed a significant TSH response to TRH. Compared to 40 normal control subjects the 12 patients had significantly decreased levels of T4, T3 and rT3 (expressed in free indices), while the TSH levels showed no change. Five of the patients, studied before and following surgery, had all decreased and subnormal FT4I (free T4 index) after surgery, but unchanged FT3I and TSH. The levels of FT4I were positively correlated to both those of FT3I and FrT3I, but not to TSH. The TSH and thyroid hormone values showed no relationship to the levels of PRL or C of the patients exposed to surgery. It is concluded that the risk of hypothyroidism in patients exposed to pituitary microsurgery is not appearing from the TSH response to TRH, but from the thyroid hormone levels.
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PMID:The pituitary-thyroid axis in patients with pituitary disorders. 250 20

Fifteen women with claudication and increased serum thyrotrophin (TSH) were treated with L-thyroxine (25-75 micrograms). These women were selected from a group of 80 consecutive women presenting with claudication, rest pain or gangrene. One year after their TSH was normal, their progress, serum lipids and lipoproteins were compared with the 58 women with normal levels of serum TSH; the remainder were already receiving thyroxine. Non-invasive assessment showed that three of the 15 (20%) women treated with thyroxine had progression of arterial disease, two in the legs and one in the legs and coronary arteries; two women showed improvement of ankle/brachial pressure indices. There was no accelerated angina, myocardial infarction, stroke or death in this group. Fifty-six of the 58 patients with normal levels of TSH were alive at follow-up and there was progression of distal disease in 24 (43%), coronary artery disease in 6 (11%), increasing carotid stenosis in four and two complained of transient ischaemic attacks. In this group, disease progression affected 32/56 (57%) of the women and this is significantly greater than in the thyroxine treated group chi 2 (P less than 0.05). Treatment with L-thyroxine caused a significant increase in HDL-cholesterol from 1.29 +/- 0.34 to 1.45 +/- 0.49 mmol/L (P less than 0.05) and a significant decrease in cholesterol from 8.0 +/- 1.3 to 7.2 +/- 1.1 mmol/L (P less than 0.01) and apolipoprotein B from 1.23 +/- 0.20 to 1.04 +/- 0.16 g/l (P less than 0.001). Significant changes in apolipoprotein B were observed after 3 months of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Can thyroxine halt the progression of peripheral arterial disease? 271 58

Enalapril, an orally-active, long-acting, nonsulphydryl angiotensin-converting enzyme (ACE) inhibitor, is extensively hydrolysed in vivo to enalaprilat, its bioactive form. Bioactivation probably occurs in the liver. Metabolism beyond activation to enalaprilat is not observed in man. Administration with food does not affect the bioavailability of enalapril; excretion of enalapril and enalaprilat is primarily renal. Peak serum enalaprilat concentrations are reached 4 hours post-dose, and the profile is polyphasic with a prolonged terminal half-life (greater than 30 hours) due to the binding of enalaprilat to ACE. Steady-state is achieved by the fourth daily dose, with no evidence of accumulation. The effective accumulation half-life following multiple dosing is 11 hours. Higher serum concentrations and delayed urinary excretion occur in patients with severe renal insufficiency. Enalapril reduces blood pressure in hypertensive patients by decreasing systemic vascular resistance. The blood pressure reduction is not accompanied by an increase in heart rate. Furthermore, cardiac output is slightly increased and cardiovascular reflexes are not impaired. Once- and twice-daily dosage regimens reduce blood pressure to a similar extent. Enalapril increases renal blood flow and decreases renal vascular resistance. Enalapril also augments the glomerular filtration rate in patients with a glomerular filtration rate less than 80 ml/min. Enalapril reduces left ventricular mass, and does not affect cardiac function or myocardial perfusion during exercise. There is no rebound hypertension after enalapril therapy is stopped. Enalapril does not produce hypokalaemia, hyperglycaemia, hyperuricaemia or hypercholesterolaemia. When combined with hydrochlorothiazide, enalapril attenuates the undesirable diuretic-induced metabolic changes. Therapeutic doses of enalapril do not affect serum prolactin and plasma cortisol in healthy volunteers or T3, rT3, T4 and TSH in hypertensive patients. Enalapril has natriuretic and uricosuric properties. The antihypertensive effect of enalapril is potentiated by hydrochlorothiazide, timolol and methyldopa, but unaffected by indomethacin and sulindac. No interactions occur between enalapril and frusemide, hydrochlorothiazide, digoxin and warfarin. The bioavailability of enalapril is slightly reduced when propranolol is coadministered, but this does not appear to be of any clinical significance. Enalapril increases cardiac output and stroke volume and decreases pulmonary capillary wedge pressure in patients with congestive heart failure refractory to conventional treatment with digitalis and diuretics.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Enalapril: a review of human pharmacology. 299 84

The effect of TRH (200 micrograms) on blood pressure, pulse rate, TSH and GH release was investigated in 10 acromegalics, four patients with non-GH secreting pituitary tumours, and seven normal controls. TRH produced a rapid-onset, short-lived pressor response in the acromegalic group (delta mean blood pressure 33 mmHg) compared to the two control groups (P less than 0.001). There was no response to the same volume of saline. The pressor response in the acromegalic group was not different in those who did or did not release GH. The pressor response to TRH was linearly related over the range 50-200 micrograms. Measurement of plasma noradrenaline and plasma renin activity during TRH testing in six acromegalics indicated that the pressor effect was neither mediated by adrenergic mechanisms, nor the renin-angiotensin system. Echocardiographic monitoring in five of these six patients showed that there was a significant increase in directly measured end systolic, end diastolic dimensions and heart rate (all P less than 0.02), and calculated stroke volume (P less than 0.001) and cardiac output (P less than 0.01) without changes in systemic vascular resistance. These data suggest that increase in preload, probably via venoconstriction, is the most likely factor producing the pressor response to TRH in acromegalics.
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PMID:Cardiovascular and hormonal responses to thyrotrophin releasing hormone in acromegalics. 311 46


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