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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A boy aged 9 years and 8 months was evaluated for headache and an enlarged sella. His neurological status and visual fields were normal. After injection of radiographic contrast agent, computerized axial tomography showed evidence of an intrasellar tumor. The most striking endocrine abnormalities were growth hormone insufficiency after arginine infusion and after insulin-induced hypoglycemia, and excessively elevated prolactin levels ranging between 1220 ng/ml and 1560 ng/ml. A slightly granulated, acidophilic pituitary adenoma was selectively removed by the trans-sphenoidal approach. The function of the anterior pituitary improved post-operatively. Growth hormone secretion after insulin-induced hypoglycemia returned to normal, and the basal serum prolactin levels decreased, but are still three times higher than normal.
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PMID:Prolactin-producing pituitary adenoma in a 9 year old boy. 21 87

Some pituitary hormones secrete hormones while others do not. Nonsecreting tumors can interfere with normal pituitary hormone secretion and produce tumor symptoms and signs like headaches and visual field defects. The most frequent hormone-secreting tumors are prolactinomas. Growth hormone or ACTH or gonadotropin or gonadotropin-alpha and beta chain-producing tumors are less frequent, TSH producing tumors are extremely rare. The most important elements of the diagnostic work-up are clinical signs and symptoms, assessment of pituitary function (measurement of TSH, free T4, LH, FSH, oestradiol/free testosteron, growth hormone, IGF-1, prolactin, ACTH, Cortisol, serum and urine osmolality), CT and/or MRI and, in patients with large tumors, a visual field exam. The treatment of choice of pituitary tumors is often surgery. Alternative therapies are radiation treatment (in nonoperable patients or when hormone levels are persistently elevated after pituitary surgery) and drug treatment (dopamine agonists in hyperprolactinemia, somatostatin analogues in acromegaly). Pituitary hormone deficiencies are treated depending on the specific deficiency with thyroxine, cortisone, oestrogen/gestagen/testosterone gonadotropines or ADH analogues.
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PMID:[Hypophyseal dysfunction and tumors]. 158 68

Growth hormone and prolactin levels and their response to various stimuli were studied in patients with cluster headache. All the endocrine responses evaluated were normal.
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PMID:Endocrinological responses in cluster headache. 641 80

A 28-year-old man was admitted to the Kyushu University Hospital with an episode of severe headache. When driving a car, he suddenly developed severe headache and this was followed by nausea and vomiting. he had been quite well except for slightly decreased libido before this episode. On admission, he showed galactorrhea. The pubic and axillary hairs appeared normal and the development of the external genital organs seemed normal. However, the movement of the sperma was decreased. Ophthalmologic examination was negative. Endocrinological studies revealed hyperprolactinemia of 697 ng/ml, and the serum prolactin level was suppressed by bromocriptine and L-DOPA loading test. The serum testosterone level was 282 ng/dl. Growth hormone and gonadotropin levels were normal. Plain films of the skull and tomograms of the sella showed double floor and slight ballooning. CT scan showed an isodensity mass in and above the sella, and this mass was slightly enhanced with contrast media. The suprasellar extension was better demonstrated by metrizamide cisternography and CT. The diagnosis of prolactinoma was made, and a radical removal of the tumor was done through the transsphenoidal route. During surgery, dark reddish fluid was aspirated in an amount of 1.8 ml. Histologically the tumor was chromophobe adenoma, and immunohistochemical stain revealed prolactin granules in the majority of the tumor cells. Postoperative serum prolactin level decreased to 150 ng/ml and finally returned to normal by administration of 2.5 mg of bromocriptine. The serum testosterone level was slightly elevated. The movement of the sperma showed no improvement. There were no postoperative complications such as hypopituitarism and CSF rhinorrhea. The usefulness of combination therapy of operation and medication with bromocriptine was suggested.
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PMID:[A case of prolactinoma with galactorrhea in man]. 654 Mar 73

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

Migraine and cluster headache are the most common disabling primary headache syndromes and are typically episodic. A reliable method of triggering such headache attacks facilitates the study and treatment of these disorders. There is sufficient clinical and laboratory evidence to suggest that somatostatin withdrawal may be a useful way of triggering headache. We studied 15 subjects, eight migraineurs, four cluster headache sufferers and three healthy controls. Each subject had a standard somatostatin infusion, 250 microg/h for 3.5h. Subjects were followed for 24h post-infusion. Growth hormone was suppressed in each subject demonstrating a biologically active infusion of somatostatin. None of the non-headache sufferers had pain. Seven of eight migraine sufferers had no immediate headache and no delayed headache. One migraineur experienced short lasting headache with no migrainous features. Three of four patients with cluster headache had no significant pain with the infusion, while one had pain after 1h. The results suggest that somatostatin infusion is not a reliable way to produce headache in experimental settings in either migraine or cluster headache. The data do not exclude a role for somatostatinergic mechanisms in primary headache.
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PMID:Somatostatin infusion withdrawal: a study of patients with migraine, cluster headache and healthy volunteers. 1267 Jun 64

Growth hormone is essential for normal linear growth and the attainment of an adult mature height. It also plays an important role in cartilage growth and the attainment of normal bone mass. There is only one rheumatic disorder, namely acromegaly, in which abnormalities of growth hormone production play a major etiologic role. However, there is increasing appreciation that suboptimal growth hormone secretion, leading to a state of adult growth hormone deficiency, may occur in the setting of chronic inflammatory disease, chronic corticosteroid use, and fibromyalgia. Therefore, the evaluation and effective management of growth hormone oversecretion and undersecretion is relevant to practicing rheumatologists.
Curr Pain Headache Rep 2005 Oct
PMID:Growth hormone in musculoskeletal pain states. 1615 62

Moyamoya disease is a rare cerebrovascular disorder which, according to a few literature reports, can coexist with hypothalamic-pituitary dysfunction. We report a 16 year-old boy referred to our Department because of short stature and headaches. He additionally, at admission, presented discrete facial dysmorphy, bruxism, luxation of temporomandibular joint and cryptorchidism. The height was 146 cm (-4.3 SDS); the sexual development was P2G2A1 and the bone age 11.5 years. The intellectual development was normal. No focal neurological deficits were observed. Based on baseline and stimulated hormonal values, isolated growth hormone deficiency was diagnosed. Malformation of the cerebral vessel was suspected on magnetic resonance imaging and upon angiocomputed tomography and panangiography, a picture suggesting moyamoya disease was obtained. Growth hormone has been administered with daily injections at the dose of 0.025 mg/kg/24h, and the first year height velocity was 12 cm/yr. No adverse events resulting from the treatment have been noted so far. This case indicates that GH deficiency may be associated with moyamoya disease, possibly resulting from chronic cerebrovascular insufficiency.
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PMID:Growth hormone deficiency associated with moyamoya disease in a 16 year-old boy. 1698 94

Growth hormone replacement therapy has been used regularly in adult Growth hormone deficiency since the availability of recombinant GH in the 1980's. GH replacement improves quality of life, bone turnover markers, cardiovascular risk markers and adverse body composition. Originally, GH doses in replacement regimes were determined by weight and surface area and dose increases based on body composition outcomes analogous to pediatric practice. These regimens led to significant side effects related to excess GH, arthralgias, headaches and peripheral edema and IGF-I levels above the upper limit of the reference range. Newer treatment regimes therefore account for known factors affecting serum GH and IGF-I levels, i.e. age, gender, estrogen replacement and pre-treatment IGF-I levels. Monitoring is now via clinical symptomatology combined with serum total IGF-I levels, potentially this avoids excessive GH exposure and allows monitoring of compliance and dose titration. There is a lack of data relating IGF-I to biological endpoints, but analysis suggests that dose titration of IGF-I to the upper half of the age and gender related reference range is acceptable. The use of reliable IGF-I assays and extensive age and gender related reference ranges is necessary and centralized monitoring is preferable. Free IGF-I and bioavailable IGF-I measurements are available but their use in the monitoring of GH replacement remains to be determined.
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PMID:IGF-I measurements in the monitoring of GH therapy. 1741 Apr 71

Thyrotropin (thyroid-stimulating hormone (TSH))-producing pituitary adenomas have been known to be quite variable in clinical features covering from typical functioning TSH-producing adenomas (FTSHomas) associated with hyperthyroidism to clinically silent TSH cell adenomas (STAs) that are apparently unassociated with hyperthyroidism. It is important to distinguish STAs from other types of clinically non-functioning adenomas for adequate postoperative managements. However, because of rareness of TSH-producing adenomas, their histopathological features linking to the clinical manifestations have not been well characterized. Herein, we investigated clinical and histopathological findings to characterize 29 TSH-producing adenomas including 20 FTSHomas and nine STAs. Clinical symptoms of the patients with STAs included headache, visual defect, vertigo, and nausea. All STAs and 19 FTSHomas were macroadenoma. The average tumor size of STAs was significantly larger than that of FTSHomas (P < 0.05). The invasiveness was detected in 33% STAs and in 20% FTSHomas. Both STAs and FTSHomas showed a variety of morphological features and immunohistochemical profiles. Chromophobic polygonal or short-spindled tumor cells usually proliferated in a diffuse pattern, while they exhibited globoid or whorl-like appearance with intertwined cytoplasmic processes in both subgroups. Stromal fibrosis and calcification were often noted. Their nuclei were somehow pleomorphic. Ultrastructural features of all four STAs examined were similar to those of normal thyrotrophs. Thus, STAs and FTSHomas were indistinguishable by histology alone. Immunohistochemically, the number of TSH-positive cells in individual FTSHomas was highly various. Six tumors showed only a few TSH-positive cells (1-5%), and three were negative for TSH by conventional method without antigen retrieval. After proteinase K treatment, these tumors turned out TSH positive. As defined, STAs were TSH positive in more than 20% of tumor cells and three of them in more than 50%. Growth hormone- and/or prolactin-positive cells were detected in 55% STAs and 63% FTSHomas. Both pituitary-specific transcription factor 1 and GATA-binding protein 2 were expressed in all STAs and 20 FTSHomas. Membranous somatostatin receptor (SSTR)-2A immunoreactivity was found in 89% STAs and 94% FTSHomas, whereas SSTR5 was positive in 78% of both STAs and FTSHomas. MIB-1 labeling index was related to tumor invasiveness and tumor size (P < 0.05, P = 0.09, respectively). Thus, although both STAs and FTSHomas showed unique histopathological features distinct from other type adenomas, these two subgroups were indistinguishable by histopathology. Immunohistochemistry for TSH by use of antigen retrieval, transcription factors, and SSTRs may be useful to confirm STAs and to determine the postoperative therapy among various kinds of clinically non-functioning adenomas.
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PMID:Clinicopathological characterization of TSH-producing adenomas: special reference to TSH-immunoreactive but clinically non-functioning adenomas. 1977 99


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