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PubMed1969

Pituitary hormones.

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Chorionic Gonadotropin↗
PubMed2002

Adrenocorticotrope deficiency with clinical evidence for late onset in combined pituitary hormone deficiency caused by a homozygous 301-302delAG mutation of the PROP1 gene.

Combined pituitary hormone deficiency (CPHD) can be caused by mutation of the pituitary transcription factors POU1F1 or PROP1. More recently mutations in the HESX1, the LHX3 and LHX4 transcription factor genes have also been described as a cause in patients with CPHD. In most patients the disorder is characterized by an impaired production of GH, TSH, PRL and gonadotropins. In some cases of CPHD adrenocorticotropin deficiency is also present. We report the progressive CPHD and its molecular etiology in a woman with CPHD presenting with first symptoms of ACTH/cortisol deficiency at the age of 48 years. The 49 year old patient's initial symptoms were growth retardation at the age of 2 years and symptoms of hypothyroidism at the age of 5 years. The patient never entered puberty spontaneously. No familial history of delayed puberty, growth retardation or other symptoms of CPHD were present. At the age of 48 years the patient presented with the first symptoms of hypocortisolism such as recurring hypoglycaemias and hyponatriaemia with coma. Cortisol, ACTH, TSH, fT3, fT4 and GH as well as LH, FSH and PRL were measured in basal conditions. GH, cortisol and ACTH were also measured in response to an Insulin Tolerance Test. Molecular analysis was performed by PCR amplification and sequencing of exon 1-3 of the PROP1 gene. The patient had insufficiencies of TSH, LH, FSH and GH. PRL was normal. Serum cortisol was low and basal ACTH was normal. However, there were no responses of cortisol, ACTH and GH to hypoglycaemia. Magnetic resonance imaging showed a hypoplastic anterior pituitary lobe. Direct sequencing revealed a homozygous 2 base-pair deletion 301-302delAG in exon 2 of the PROP1 gene. This case suggests that in patients with CPHD ACTH producing cells may be involved at a rather late age.

Adrenocorticotropic Hormone↗
PubMed2003

Sporadic heterozygous frameshift mutation of HESX1 causing pituitary and optic nerve hypoplasia and combined pituitary hormone deficiency in a Japanese patient.

HESX1/Hesx1 is a member of the paired-like class of homeobox genes and is essential for pituitary and forebrain development. Mice with a targeted homozygous deletion of the Hesx1 show severe central nervous system defects, absence of optic vesicles, and a very small anterior pituitary gland. This phenotype is similar to the abnormalities observed in the human disorder called septo-optic dysplasia, a syndromic form of congenital hypopituitarism. To date, four missense mutations in the human HESX1 have been described in individuals with phenotypes ranging from severe septo-optic dysplasia, relatively mild combined pituitary hormone deficiency (CPHD), to isolated GH deficiency. Here we report a Japanese patient with CPHD (GH, TSH, LH, FSH, and ACTH deficiency) due to a novel sporadic HESX1 mutation. Brain magnetic resonance imaging examination revealed hypoplastic anterior pituitary, ectopic posterior lobe, and left optic nerve hypoplasia. Molecular analysis identified the insertion of a heterozygous mutation (306/307ins AG) in the exon 2 of the HESX1. This mutation changes a reading frame and introduces a premature stop codon soon after the mutation site. Therefore, this mutation would be predicted to generate a protein lacking the carboxyl-terminal homebox domain (DNA-binding domain) and cause the disease. Family analysis demonstrated that neither of the patient's parents harbored this mutation, indicating that the mutation had arisen de novo. In conclusion, a de novo heterozygous frameshift mutation in exon 2 of the HESX1 causes severe CPHD with optic nerve hypoplasia in a human.

Asian People↗
PubMed1997

Effects of acute and subchronic cadmium administration on pituitary hormone secretion in rat.

Cadmium administration is known to be followed by deleterious effects on the endocrine system although its action mechanism is not well understood. The purpose of this study was to determine, in vivo, the effects of acute and/or subchronic cadmium chloride administration (6 mg/kg or 4 mg/kg/day during 14 days) on prolactin, luteinizing hormone (LH), follicle stimulating hormone (FSH), growth hormone (GH) and thyroid stimulating hormone (TSH) secretion in adult male rats. Six h after a single injection of CdCl2, a diminution of plasma levels of prolactin (4.52 +/- 0.53 vs. 16.2 +/- 2.7 ng/mL, p < 0.01), GH (3.39 +/- 0.41 vs. 6.71 +/- 1.30, ng/mL, p < 0.01), TSH (2.76 +/- 0.64 vs. 7.65 +/- 1.15 ng/mL, p < 0.01) and LH (4.1 +/- 1.3 vs. 5.18 +/- 0.28, p < 0.05) was observed, where as plasma FSH levels did not change. On the other hand, subchronic cadmium chloride administration for 14 days, increased plasma levels of GH (13.39 +/- 2.74 vs. 6.71 +/- 1.3 ng/mL, p < 0.05), TSH (27.8 +/- 4.42 vs. 6.65 +/- 1.15 ng/mL, p < 0.001), LH (11.1 +/- 1.3 vs. 5.18 +/- 0.28 ng/mL, p < 0.001) and FSH (53.16 +/- 3.66 vs. 12.51 +/- 1.45, p < 0.001), whereas plasma prolactin levels decreased (6.86 +/- 1.38 vs. 16.2 +/- 2.7 ng/mL, p < 0.01). In animals subchronically treated with CdCl2, body weight gain was lower than in control rats (p < 0.001). The present findings suggest that acute and subchronic cadmium administration modify pituitary hormone secretion differentially and specifically.

Animals↗
PubMed1977

Changes in pituitary hormones serum levels in bromocryptine-treated parkinsonian patients.

In the course of a clinical trial with 2alpha-bromoergocryptin in Parkinson's disease, the serum levels of several pituitary hormones have been studied in the assumption that the drug active on nigro-striatal dopaminergic system might also interfere with hypothalamus-protuberantial neurotransmission, and have effects on the function of the pituitary. No changes in serum levels of FSH, LH, STH and TSH were detected for every dose of the drug employed. Only prolactin serum levels diminished since the beginning of the treatment, the decrease being significant (p less than 0.05 and p less than 0.01). This effect on prolactin does not change in the dose range considered. Clinical improvement was observed for doses of drugs above 15 mg/day, whereas the effect on prolactin secretion occurred with the dose of 7.5 mg/day.

Aged↗
PubMed1977

Effects of chronic stress on pituitary hormone release induced by combined hemi-extirpation of the thyroid, adrenal and ovary in rats.

Morphologic and hormonal changes, induced by combined ablation of a thyroid lobe, one adrenal and one ovary, were studied over a 15-day period in rats, some of whom were subjected to 8 h of daily immobilization. The compensatory hypertrophy (CH) of the contralateral glands in non-stressed animals was associated with a significant increase in the plasma levels of LH (from the 1st to the 10th day), prolactin (PRL, from the 3rd to the 6th day), FSH (on the 3rd day) and corticosterone (from the 6th to the 15th day), whereas GH titers were not altered. Immobilization for 1, 3, 6, 10 or 15 days inhibited the b.w. gain, induced involution of the thymus, enhanced compensatory enlargement of the adrenal, and blocked the CH of the ovary and, to a lesser degree, of the thyroid. This chronic stressor produced a marked rise in plasma corticosterone, antagonized the surge of PRL, FSH and LH, and decreased the plasma levels of GH. On the basis of these morphological and hormonal variations, it appears that severe chronic stress in hemi-thyroidectomized-adrenalectomized-ovariectomized animals further increases the ACTH response but antagonizes the increased secretion of the other pituitary hormones.

Adrenal Glands↗