Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

TSH tumors are associated with both hypothyroid and hyperthyroid states. The proposed mechanism of thyrotroph secretion is illustrated in Figure 8. Pituitary enlargement in hypothyroidism is usually due to reactive hyperplasia and correlates with the degree of TSH elevation. Although this often translates to long-standing hypothyroidism and severe symptoms, this is not always the case. Patients may be asymptomatic or present with other endocrine syndromes. Children may have precocious puberty, and adults may have amenorrhea or decreased libido. One important message to remember is that whenever a patient has evidence of a pituitary tumor, a serum T4 and TSH level must be obtained. The dramatic reduction in pituitary size and resolution of endocrine dysfunction with thyroid hormone is gratifying. Thyrotropinomas producing thyrotoxicosis are autonomous tumors. Given their infrequent occurrence, one could question the cost effectiveness of ordering a serum TSH on all new patients with hyperthyroidism. Features that might favor the possibility of there being a tumor include male sex, headaches, visual impairment, and the absence of ophthalmopathy. Unfortunately, these are not reliable clinical features to suggest the presence of this disorder, and the diagnosis requires a serum TSH determination. Fortunately, the newer assays available are able to provide the sensitivity needed. Therapy should be aimed at the pituitary gland, but currently it is less than optimal. Surgery with or without external irradiation offers the best prognosis and, hopefully, will yield better results when cases are identified earlier. Medical therapy to suppress TSH is still in its infancy. More effective agents will hopefully be discovered in the near future.
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PMID:Thyrotropin-secreting pituitary tumors. 331 2

A 34-year-old woman was admitted for the chief complaints of headache and blurred vision. She had bilateral papilledema and slight increase in CSF pressure (175mmH2O) with normal visual acuity and field. Neurological and hormonal examination were normal except for over response of PRL and TSH to TRH test. The sella was enlarged and MRI and metrizamide CT demonstrated intrasellar CSF filling with remodeling of the pituitary gland. The patient was diagnosed as primary empty sella syndrome associated with benign intracranial hypertension. The complaints did not subside for six months. The patient was treated via the transsphenoidal approach. The dura mater of the floor of the sella was elevated by extradural balloon expansion filled with silicone, and subsequently the empty sella was obliterated. Her headache disappeared and amblyopic attack also improved. Obliteration of the empty sella with an extradural silicone balloon via the transsphenoidal approach seemed to have been effective for headache and visual complaints of primary empty sella syndrome which did not respond to medical therapy.
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PMID:[Primary empty sella syndrome treated by transsphenoidal extradural balloon expansion--a case report]. 362 70

Prolactin (PRL) and the placental hormones, estradiol (E2), estriol (E3), progesterone (PG), chorionic gonadotropin (HCG), and placental lactogen (HPL) were serially measured throughout pregnancy and early postpartum in three patients with prolactinomas in whom pregnancy was achieved by one of the three modalities of treatment: bromocriptine administration (patient I), irradiation of the pituitary (patient II), and human gonadotropin administration after excision of the adenoma (patient III). It was found that PRL in patient I reached the high pretreatment levels in the 2nd month of pregnancy and increased to further abnormal concentrations in the last 2 months, but fell at the onset of labor 1 week after an episode of severe headache. The PRL changes in this patient were attributed successively to tumor expansion and apoplexy. In patient II PRL decreased after irradiation, but was not normalized. During pregnancy it remained moderately increased presenting minor fluctuations. The third patient with postoperative GH and TSH pituitary insufficiency had low pretreatment PRL levels which remained practically unchanged throughout pregnancy. The two last patients gave birth to identical twins. The placental hormones were found normal in all three patients but E2 and PG were relatively increased during the last weeks of pregnancy in the twin pregnancies. Amniotic fluid and umbilical cord PRL and E2 concentrations were normal. The patients presented agalactia and suckling did not induce a PRL increase. We conclude that a) serial PRL measurements during pregnancy reflect the changes occurring in the prolactinomas and are essential in monitoring the patients bearing these tumors; b) maternal hyperprolactinemia or failure of PRL to increase during pregnancy do not influence either the secretion of placental hormones or PRL concentration in amniotic fluid and the newborn; and c) hyperprolactinemia during pregnancy is of maternal pituitary origin.
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PMID:Prolactin and placental hormone levels during pregnancy in prolactinomas. 611 69

We studied the dopaminergic control of TSH secretion in a patient with hyperthyroidism due to a TSH-secreting pituitary adenoma. A 34-yr-old previously thyroidectomized woman had mild clinical hyperthyroidism and a diffuse goiter without exophthalmos. She complained of headaches and had bitemporal hemianopsia. Serum T4 and T3 by RIA were elevated, and TSH was 112 microU/ml (normal range, 1.1-7.2). The alpha-subunit to TSH molar ratio was 1.7 (normal, less than 1), as reported in other patients with tumoral TSH hypersecretion. After TRH, a marked increase in TSH occurred. There was no evidence of pituitary deficiency. Skull x-rays and computerized axial tomography revealed an intrasellar tumor with suprasellar extension. Selective transsphenoidal adenomectomy was performed, and a pituitary tumor was removed. The tumor was almost entirely composed of cells reactive with antihuman beta TSH serum by indirect immunofluorescence. A unique feature of this patient was the marked increase in TSH levels after L-dopa administration. To our knowledge, this paradoxical response has never been reported previously in such patients. Using [3H]domperidone as ligand, dopaminergic receptors were demonstrated in the membranes of the adenomatous thyrotroph cells. The reason for the paradoxical response of TSH to dopaminergic agents is not known.
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PMID:Paradoxical response of thyrotropin to L-dopa and presence of dopaminergic receptors in a thyrotropin-secreting pituitary adenoma. 643 Sep 50

The endocrinological actions of quipazine, a direct serotonin receptor agonist, were investigated in both normal subjects (NS) and individuals with neurological disorders, i.e., Huntington's disease (HD), myoclonic epilepsy (ME) and cluster headache (CH). In both normal subjects and neurologic patients inconsistent and variable changes in the secretion of anterior pituitary hormones were observed. In fact, oral administration of 50 mg of quipazine elicited a rise in plasma GH in only 9/23 subjects investigated (3 NS, 2 HD, 1 ME, 3 CH), decreased GH in 4 subjects (1 NS, 2 HD, 1 CH) and left unmodified plasma GH in the remaining 10 subjects. Only 7/23 subjects showed a positive PRL response to quipazine (2 NS, 1 HD, 1 ME, 3 CH), in one subject (CH) PRL was inhibited while the drug was ineffective in the remaining 15 subjects. For gonadotropins, 5/21 subjects (2 NS, 1 HD, 2 CH) had a positive LH response and 3/20 subjects (1 NS, 1 ME, 1 CH) had a positive FSH response. In one subject (HD) there was inhibition of baseline LH levels and no effects were present in the remaining individuals. No changes in basal TSH levels were present in the 6 subjects investigated (4 NS, 2 ME). Quipazine was instead competent to increase plasma cortisol levels in 6/8 normal subjects. Pharmacodynamic, mainly gastrointestinal, effects of the drug were present in about 50% of the subjects but were not or only poorly correlated with the endocrine responses. Collectively, based on the neuropharmacologic profile of the drug, and in contrast to many animal data, these findings do not support a major role for the serotoninergic system on basal anterior pituitary hormone secretion in man, possibly with the exception of the ACTH-cortisol secretion.
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PMID:Neuroendocrine effects of quipazine in man in health state or with neurological disorders. 644 95

The study of circadian rhythms of hormones in PAD reveals impairments in the hypothalamo-pituitary-adrenal axis, GH, PRL, TSH and melatonin secretion. Twenty-four hour cortisol curves show increased number of secretory episodes, increased duration of each episode, increased amount of total cortisol secretion for each episode and of cortisol secretion per minute. Moreover, secretory bursts appear in the late afternoon-evening, when in normal subjects secretion is blunted. In some cases the acrophase is phase-advanced by 1-4 h. GH nocturnal peak is often blunted. PRL nocturnal secretion may also be low, especially in bipolar patients, or the acrophase is 6-8 h phase-advanced. Melatonin nocturnal peak may be blunted and abnormal diurnal peaks are sometimes observed. TSH secretion is normal in bipolar patients; in unipolars, the nocturnal peak, the mean 24-h secretion and the ratio sleep/wakefulness are reduced. The acrophase may be advanced.
Cephalalgia 1983 Aug
PMID:Circadian rhythms of hormones in primary affective disorders. 661 93

Neurohumoral correlations of sleep are considered from three aspects: 1. Metabolism and cerebral blood circulation (CBF, EEG, endocranial pressure, cerebral temperature); 2. Neuromediators and neuropeptides (5-HT, hypnogen neuropeptides); 3. The influence of the sleeping-waking cycle on adeno-hypophyseal secretion rhythms (GH, PRL, LH, TSH). Variations of these parameters can play an important role in the onset of night crises of migraine and cluster headache.
Cephalalgia 1983 Aug
PMID:Pituitary secretions and wake-sleep cycle. 661 8

In 18 men with Horton's headaches the levels of the following hormones were determined in the serum: TSH, T3 and T4. The determinations were performed during disease relapse and before starting treatment. The control group included 18 blood donors. In the control group the mean TSH level was 3.97 +/- 0.88 microunits/ml, T4 level was 109.06 +/- 26.88 nmol/l, and T3 1.48 +/- 0.14 nmol/l. In the group of patients the mean values were: 2.58 +/- 2.09 microunits/ml, 97.62 +/- 21.81 nmol/l, 1.07 +/- 0.21 nmol/l respectively. The analysis of the results showed statistically significant differences in the concentrations of T3 between the compared groups. In the light of these results the authors believe that there is not sufficient support of the hypothesis on a hypothalamic pathogenesis of the disease. The causes of reduced T3 concentration in these patients are discussed.
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PMID:[Thyrotropic and thyroid hormone (T3 and T4) content in Horton' s headache patients]. 734

Anti-thyroid hormone autoantibodies are occasionally found in Hashimoto's disease. They can interfere with thyroid hormone assays. The authors report the case of a 35-year-old hypothyroid (TSH between 29 and 46 microIU/ml) female patient with Hashimoto's disease and surprisingly high free and total levels of plasma T4 and T3 assayed with different solid phase radio-immunologic kits. Two immunoenzymologic assay kits gave a T4 level close to the one expected. The presence of circulating anti-T4, T3 and reverse T3 autoantibodies was demonstrated by precipitating the corresponding tracers with the patient's serum in the presence of polyethylene glycol without heterologous antibodies. The replacement treatment of 150 micrograms l-thyroxine allowed normalization of TSH at 3.4 microIU/ml, but the patient remained tired and anxious, with headaches and tachycardia. After discontinuing treatment for one month a series of four plasma exchanges was carried out in six days. After the first exchange the binding percentages were already much lower and went even lower after the other exchanges. After the fourth one, the free T4 and T3 levels were closer to the expected levels:7.3 pmol/l (N:10-30 pmol/l) and 4.3 pmol/l (N:3-9 pmol/l). Treatment by prednisone made it possible to maintain the percentages of binding to the three tracers for two weeks at the levels reached after the fourth plasma exchange. Two months after discontinuing corticosteroid treatment they returned to the initial levels and were again interfering with the free T4 and T3 assays. This finding suggests that usefulness of the thyroid hormone immuno-enzymologic assay, which apparently is not affected by the anti-thyroid hormone autoantibody interference.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduction of anti-thyroid hormone autoantibodies through plasma exchange and corticosteroid therapy. 775 92

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


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