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During a 3-year period of 16 Black and Indian patients were diagnosed as having hypopituitarism. Their ages ranged from 9 to 58 years; 9 were women. Headaches and visual disturbances constituted the commonest presenting symptoms, and this was related to the fact that tumours accounted for the hypopituitarism in 11 of the 16 patients. The commonest hormonal deficiency was of growth hormone and the commonest combined deficiency was of growth hormone and gonadotrophin. Hyperprolactinaemia was present in 4 patients. The spectrum of hypopituitarism ranged from 1 patient with monohypopituitarism to 2 patients who were deficient in all the hormones tested, the majority of patients, however, being deficient in only some of the hormones.
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PMID:Hypopituitarism. A 3-year study. 722 71

Pituitary adenomas are frequently encountered, benign intracranial tumours. Clinically classified according to their capacity to produce and secrete hormones, pituitary tumours are diagnosed from the clinical manifestations and biochemical findings of specific pituitary hormone overproduction or of impaired pituitary function due to pressure on normal pituitary cells, the pituitary stalk or the hypothalamus. Additionally, the tumour may result in neurological manifestations due to its effect as an intracranial space-occupying lesion. Pituitary adenomas may present acutely with pituitary apoplexy after intrapituitary haemorrhage or infarction. The subsequent hypofunction of the pituitary with concomitant neurological sequelae of an expanding intracranial mass are often associated with excruciating headache, diplopia and visual field defects. Gradually developing neurological deficits or secondary endocrine failure over several years may precede the recognition of non-secretory tumours (30-40% of pituitary adenomas) as well as some of the hormone-producing adenomas, especially when they expand beyond the confines of the sella turcica. Asymptomatic masses occur in the pituitary in 5-27% of unselected autopsy series. About 10-20% of pituitaries imaged as part of a brain study contain lesions 'consistent with a pituitary adenoma', with about half being pituitary adenomas ('incidentalomas'). Many advocate screening such cases for a wide spectrum of pituitary function abnormalities. Clinical judgement should be utilized to determine the extent of the work-up and the frequency of follow-up. Acromegaly, a clinical syndrome caused by excess growth hormone secretion, accounts for one-sixth of resected pituitary tumours. This disorder leads to chronic progressive disability and a shortened life span, with approximately 50% of untreated acromegalic patients experiencing premature death. The prevalence of acromegaly has been estimated to range from 50 to 70 per million, with the age of diagnosis usually between the third and fifth decades. Conditions associated with acromegaly include glucose intolerance, diabetes mellitus, lipid abnormalities, cholelithiasis, goitre, and hyperthyroidism, respiratory complications, hypertension, cardiovascular disease, and calcium metabolism abnormalities. An association between acromegaly and cancer, especially of the colon, is now recognized. Epidemiological series have indicated that cancer of the colon, breast and other types of malignancy are a cause of death with increased frequency in acromegalics compared with expected rates. Hypopituitary symptoms secondary to the mass effect of macroadenomas in acromegalic patients are common. Among premenopausal women, menstrual irregularities and galactorrhoea have been reported in 40-70%, while more than half of the men complain of impotence and decreased libido.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical features and differential diagnosis of pituitary tumours with emphasis on acromegaly. 762 86

1. The effects of fluparoxan, an alpha 2-adrenoceptor antagonist, on the pharmacodynamic changes induced by clonidine were investigated in this placebo-controlled, double-blind, two-period, cross-over study in 16 healthy male volunteers (aged 19 to 44 years). 2. Subjects received either fluparoxan or placebo, twice-daily for 5 1/2 days (11 doses). One hour after the first and last dose of each treatment period, clonidine (200 micrograms) was infused intravenously over 5 min. 3. Indices of clonidine-mediated pharmacodynamic responses (growth hormone secretion, bradycardia, hypotension, xerostomia and sedation) were taken before and after clonidine infusion. Growth hormone secretion was assessed by quantifying serum growth hormone concentrations; sedation was assessed by both visual analogue scales (VAS) and by a visual psychomotor response meter, measuring critical flicker fusion (CFF). 4. The majority of subjects reported minor adverse events such as lethargy, headache and dry mouth following clonidine infusion. All adverse events were likely to be related to clonidine, as they occurred consistently between treatment groups. Fluparoxan has, however, in previous studies been reported to cause headache and light-headedness. 5. Prior to the clonidine infusion, fluparoxan caused small but statistically significant increases in systolic blood pressure (4 mm Hg) and salivary flow (approximately 30%) after both single and repeated doses. A small increase in heart rate (2 beats min-1) was seen after a single dose which was also statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antagonism of the effects of clonidine by the alpha 2-adrenoceptor antagonist, fluparoxan. 766 82

Sleep-disturbed breathing, which includes apneas, hypopneas, and oxygen desaturations, occurs in asymptomatic individuals and increases with age. Obstructive apnea is the most frequent type of respiratory disturbance documented by polysomonography, the gold standard test for assessing sleep-disturbed breathing. Many of the prevalence studies done to date have had one or more methodological weaknesses, including selection biases, varying definitions of obstructive sleep apnea, failure to distinguish types of apneas, failure to control for confounding variables, and small sample size. Although there is consensus on the definitions of sleep-disturbed breathing, the appropriate number of apneas and hypopneas for diagnosing clinically significant obstructive sleep apnea is uncertain. While the cutoff of five or more apneas and hypopneas per hour is historically considered abnormal, the origins of this number are vague, and the longevity of those who have this value on polysomnography is not necessarily reduced. This is particularly true among those without symptoms of obstructive sleep apnea syndrome, which include excessive daytime sleepiness, snoring, nocturnal awakenings, and morning headaches. Investigators should be careful to distinguish symptomatic study subjects from asymptomatic subjects, and to exclude central apneas in calculating their estimates. In addition, various studies have used different definitions of sleep apnea syndrome, making comparisons of point estimates difficult. It would be more appropriate for researchers to estimate morbidity and mortality indices with confidence intervals, using several different cutoff points. Subject selection in all studies should follow a two-stage sampling procedure. All subjects with symptoms compatible with obstructive sleep apnea syndrome and a subsample of asymptomatic individuals should be studied with all-night polysomnography. If portable monitoring is used, the validity and reproducibility of this diagnostic method should be assessed. Subjects with significant comorbidity should be excluded from prevalence studies. Factors that clearly increase the risk of sleep-disturbed breathing and obstructive sleep apnea and its related symptoms include age, structural abnormalities of the upper airway, sedatives and alcohol, and probably family history. Although endocrine changes such as growth hormone, thyroid hormone, and progesterone deficiency also have been suggested as risk factors for exacerbating obstructive sleep apnea syndrome, there is minimal epidemiologic evidence to support this. Case-control studies are recommended to assess the relation of endocrine factors to obstructive sleep apnea syndrome in a rigorous fashion. A limited number of mortality studies have suggested decreased survival in persons with the obstructive sleep apnea syndrome, possibly primarily due to vascular-related disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Epidemiology of obstructive sleep apnea. 771 77

We report 13 cases of benign intracranial hypertension (IH) in children with growth hormone (GH) deficiency treated with GH in the United States. The group consisted of eight boys and five girls, 3 to 16 years of age (median, 9 years). The interval from starting GH therapy to diagnosis of IH was 2 weeks or less in six patients, between 2 and 12 weeks in four, 8 months in one, 5 years in one, and unknown in one. Seven patients were not known to have previously described IH risk factors; the other six had at least one factor each. All patients but one had headache, nausea, vomiting, and visual changes. All had papilledema, and cerebrospinal fluid pressures were elevated (> 250 mm H2O) in all nine patients tested. The GH dosage range was 0.17 to 0.35 mg per kilogram body weight per week (median, 0.30 mg/kg per week) for the 11 patients with dosage data. After discontinuation of GH and treatment with lumbar punctures and/or medications, signs and symptoms resolved in eight children; in two of these children signs and symptoms reappeared when GH therapy was restarted. In four patients signs and symptoms resolved while GH therapy was continued; one child was treated with a ventriculoperitoneal shunt because of an arachnoid cyst, after which GH was restarted without subsequent IH. In the 12 patients with idiopathic GH deficiency the course of IH was benign, with complete resolution of all signs and symptoms. Because doses and scheduling of GH administration have changed since the introduction of recombinant GH, higher doses and increased frequency of administration may be contributing to the development of IH in some patients. We suggest beginning therapy at the lowest recommended dose, with gradual titration to higher doses, and the performance of routine funduscopic examinations during initiation of GH therapy and whenever signs or symptoms of IH develop.
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PMID:Benign intracranial hypertension in children with growth hormone deficiency treated with growth hormone. 777 16

It has long been known, that irregular, heavy snoring and daytime sleepiness are common features of acromegaly. Only recently has the high incidence (30-60%) and clinical relevance of the sleep apnoea underlying these symptoms been recognized. Both diseases have a group of common symptoms and prognostic features: Increased cardiovascular and respiratory mortality, elevated incidence of hypertension, daytime sleepiness, decreased vitality, headaches and depression. These are very prominent in sleep apnoea and often reversible under treatment. In acromegaly their etiology has been widely unexplained and they commonly persist even when human growth hormone (hGH) levels remain normal after operative treatment. We report on 2 patients presenting with excessive daytime sleepiness and severe obstructive sleep apnoea caused by acromegaly. Both had macroglossia and hypertrophy of hypopharyngeal tissues regressive after surgical therapy. The average hGH-levels were 20 and 31 ng/ml before and 3 and 1.7 ng/ml several months after operation respectively. Apnoea indices and minimal oxygen saturations (SO2) were 59/h and 55/h, and 60% and 58% initially and improved postoperatively to 40/h and 50/h, and 72% and 70%. Polysomnographic parameters were normalized by NCPAP-therapy pre- and postoperatively and daytime sleepiness improved dramatically. In one patient the NCPAP-pressure could be decreased postoperatively. Since patients with sleep apnoea have an increased perioperative risk of hypoxia and because transsphenoidal operation and postoperative nasal tamponade were performed, both patients were tracheostomized perioperatively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sleep apnoea in acromegaly--prevalence, pathogenesis and therapy. Report on two cases. 783 Dec 13

Anterior pituitary tumors account for nearly 18% of all intracranial tumors. Pituitary adenomas that cause hypersecretion of growth hormone lead to acromegaly in adults. Patients with acromegaly may present unique problems for the anesthetist because of the overgrowth of airway soft tissues; a difficult mask ventilation and challenging intubation can be expected. A careful preoperative assessment of the patient's airway is essential, and an awake oral or fiberoptic bronchoscopy may be necessary. Postoperatively, these patients are at risk for developing airway problems and diabetes insipidus; therefore, they warrant careful observation. A 42-year-old, 75-kg, ASA physical status III, white male presented 8 months after suffering a head injury in which he was knocked unconscious for approximately 3 minutes. He began experiencing severe headaches, visual changes, and a marked increase in the size of his hands and feet. Four months before admission, he underwent bilateral carpal tunnel repairs. The patient was diagnosed with acromegaly after an extensive endocrine and neurosurgical evaluation. This is a case report of a patient with acromegaly who underwent an elective transsphenoidal hypophysectomy.
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PMID:Acromegaly and transsphenoidal hypophysectomy: a case report. 808 20

Nine cases of symptomatic Rathke's cleft cyst are reported. Their most frequent signs and symptoms included headache, chiasmal syndrome and hypopituitarism, while one of the cases developed a sudden onset of headache and vomiting following diabetes insipidus. Endocrinological findings showed a decreased ACTH, gonadotropin and growth hormone more frequently while there were 2 cases of hyperprolactinemia and 1 case of diabetes insipidus. In a neuroradiological examination, a plain skull X-ray showed 5 cases of ballooning of the sella turcica, and a CT scan demonstrated a low to high density of the cyst and 2 cases of marginal enhancement of the cyst. MRI mostly demonstrated a well delineated mass at the sella extending mostly into the suprasellar region and a low to high intensity of the cyst in the T1-weighted image. Two cases were marginally enhanced after gadolinium DTPA administration. The pathological examination, done on 6 cases, showed either single or multiple layers of the epithelium which were mostly ciliated. The epithelium was positive in PAS and Alcian blue in all cases and a histochemical examination showed 3 cases to be positive in EMA and 2 cases positive in CEA. A resection of the cyst wall and an opening of the cyst is thus recommended in symptomatic cases. Therefore, the transsphenoidal approach should be the choice of treatment in an intra- and suprasellar extension of the cysts with sellar enlargement.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Symptomatic Rathke's cleft cyst: a clinicopathologic study of 9 cases]. 816 47

The cause of cluster headache remains to be determined. The involvement of peripheral neurovascular structures can explain the pain and autonomic signs of a cluster attack, but not its rhythmicity. The central theory of cluster headache attributes the cyclic recurrence to involvement of the hypothalamus. To evaluate hypothalamic dysfunction a number of hormone studies have been carried out on cluster headache patients. Alterations in plasma melatonin, cortisol, testosterone, gonadotrophins, prolactin, growth hormone and thyrotropin have been documented, some only in the cluster period but others in the remission phase of the illness. We believe that the hormonal abnormalities in cluster headache support disorders of hypothalamic function.
Cephalalgia 1993 Oct
PMID:A review of hormonal findings in cluster headache. Evidence for hypothalamic involvement. 824 22

We evaluated the effect of l-deprenyl, a drug that increases the availability of endogenous dopamine, on the plasma levels of prolactin and growth hormone in 10 female patients with migraine and in 10 control subjects matched for age and menstrual phase. The patients showed a significant decrease in prolactin levels at 30, 60 and 120 min after the oral administration of 5 mg of l-deprenyl when compared with the values obtained in controls (p < 0.001). The effects of l-deprenyl on growth hormone plasma levels were not significantly different between patients and controls. These data suggest that l-deprenyl inhibits prolactin release in migraine patients, but not in control subjects. This differential sensitivity could be explained by dopamine receptor supersensitivity in migraine patients.
Cephalalgia 1993 Dec
PMID:l-deprenyl test in migraine: neuroendocrinological aspects. 831 54


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