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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oral contraceptives are clearly contraindicated in patients with a history of thromboembolic disease, ischemic heart attack, or cerebral stroke. Patients requiring long-term anticoagulant treatment can be treated with gonadotropin-releasing hormone analogs to prevent ovulation, because ruptured follicles can cause massive intraperitoneal bleeding. Patients with essential hypertension and severe liver diseases should also discontinue treatment 4 weeks before major elective surgery. Migraine and diabetes mellitus are regarded as relative contraindications, depending on the individual situation. Long-term diseases, such as Crohn's disease, epilepsy, and sickle cell anemia, also require individualized consultation.
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PMID:Oral contraception in disease states. 225 29

The time-dependent recovery of gonadotropin-releasing hormone (GnRH) responsiveness in desensitized gonadotropes was examined under conditions of altered membrane fluidity and GnRH exposure. Cultured pituitary cells were treated for 3 h with GnRH (10(-9) M; to provoke homologous desensitization) or vehicle alone (controls). When cells were washed and immediately rechallenged for 3 h with GnRH, gonadotrope responsiveness (assessed by luteinizing hormone (LH) release) was significantly lower in GnRH-pretreated cells than controls. If gonadotropes were allowed to recover in medium alone, membrane fluidity agents 2-(2-methoxyethoxy)-ethyl-8-(cis-2-n-octylcyclopropyl)-octanoate (A2C; 10(-4) M) or cis-vaccenic acid (CVA; 0.5 mM) or a low dose of GnRH (10(-10) M) for up to 48 h prior to rechallenging with GnRH, responsiveness in all cases was significantly lower in GnRH-pretreated cells than controls. However, if cells were treated with either A2C or CVA in the presence of GnRH (10(-10) M) during the recovery period, gonadotrope responsiveness to a subsequent challenge with GnRH was partially restored by 24 h; by 48 h no differences in the LH secretory response to GnRH was detected between GnRH-pretreated cells and controls. The possibility that restoration of the GnRH receptor-linked Ca2+ channel is associated with recovery of the desensitized gonadotrope was also examined. Identical protocols to those described above were used except that the functional integrity of the Ca2+ channel was assessed by measuring LH release in response to increasing doses of maitotoxin (MTX; a specific Ca2+ channel activator). Again, GnRH-pretreated cells were significantly less responsive to MTX than controls when allowed to recover for 48 h in medium alone, A2C (10(-4) M) or GnRH (10(-10) M). However, allowing cells to recover for 48 h under a condition of increased membrane fluidity and basal GnRH levels completely restored the MTX-stimulated LH secretory response in GnRH-pretreated gonadotropes. Taken together, these studies suggest that the physical state of the gonadotrope plasma membrane together with the appropriate hormonal milieu provide an important environment for the gonadotrope to recover from desensitization. Additionally, our results suggest that functional recovery of the GnRH-linked Ca2+ channel may play a requisite role in restoring GnRH responsiveness to the desensitized gonadotrope.
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PMID:Restoration of the LH secretory response in desensitized gonadotropes. 284 35

Pituitary apoplexy often occurs spontaneously in adenomas. A few cases have been reported after testing anterior pituitary function by means of intravenous injections of a mixture of gonadotropin-releasing hormone and thyrotropin-releasing hormone, or gonadotropin-releasing hormone alone. In these cases the development of visual field defects has necessitated surgical intervention, which confirmed pituitary apoplexy. We describe a patient with a pituitary macroadenoma. He developed symptoms and signs of pituitary apoplexy immediately after intravenous injection of a mixture of hypothalamic releasing hormones. His visual fields remained normal, and he recovered spontaneously.
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PMID:[Pituitary apoplexy after injection of pituitary-hormone releasing hormones]. 807 63

Pituitary apoplexy is rare and endocrine remission in patients with apopletic secreting pituitary adenomas is even rarer. This study reports on two patients with pituitary macroadenomas (one with Cushing's disease and the other with acromegaly) in whom endocrine remission occurred after apoplexy. The first patient had Cushing's disease and had an ictus of headache and vomiting after which she started a progressive remission of hypercortisolism. A post-apoplexy MRI disclosed persistence of a sellar and supra-sellar mass. She was submitted to transesphenoidal surgery. An hypertensive hemorrhagic cyst was found with no tumor. The second patient had acromegaly. While performing a LHRH-stimulation test he had an ictus of headache, vomiting, no visual loss and appearance of diabetes insipidus. A CT scan disclosed an intrasellar hematoma. Despite the size of the tumor and since there was no visual impairment, this patient was followed up without surgery. Imaging follow-up showed a progressive shrinkage and disappearance of the mass, which was corroborated by endocrine remission. A high rate of recurrence is reported in such patients in the literature. Both patients are being currently followed-up on a long-term basis.
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PMID:[Pituitary apoplexy followed by endocrine remission. Report of two cases]. 975 27

We report the case of a 31-year-old woman with a pituitary adenoma who suffered symptomatic pituitary apoplexy. The patient developed a severe headache 2 min after undergoing a combined anterior pituitary function (CAP) test. Emergent computed tomography revealed a hemorrhagic pituitary tumor with evidence of a small subarachnoid hemorrhage. The headache improved spontaneously within half a day. Transsphenoidal surgery was performed 4 days later. Histologic examination demonstrated that the tumor was an eosinophilic adenoma with areas of diffuse hemorrhage. Although pituitary apoplexy caused by endocrinological testing has been reported in only 28 patients, apoplexy caused by a CAP test has been reported in only 1 patient. All of the previous cases had pituitary macroadenomas, 69% of which were involved in suprasellar extension. Non-functioning adenomas (24%) and prolactinomas (24%) were the most often affected by endocrine stimulation tests. With respect to the stimulants of pituitary adenomas, gonadotropin-releasing hormone (76%), TSH-releasing hormone (69%), and insulin (34%) were primarily responsible for the apoplexy. This case report with the literature review suggests that routine testing on pituitary function should be ordered cautiously given the risk of possible apoplexy.
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PMID:Pituitary apoplexy induced by a combined anterior pituitary test: case report and literature review. 979 Feb 75

Pituitary apoplexy has been reported as a very rare complication of combined tests of anterior pituitary function and of TRH or gonadotropin-releasing hormone (GnRH) administration in pituitary tumor. A 34-year-old man with a GH-secreting pituitary macroadenoma and diabetes mellitus received an injection of 400 microg TRH, 100 microg GnRH, and 0.15 U/Kg regular insulin. Twenty minutes later, he complained of a severe headache and vomited. Visual acuity and visual field did not change and his headache was persistent during the next 24 hours of conservative management. Magnetic resonance imaging (MRI) of the sella turcica done the day after the event showed definitive elevation of the optic chiasm and slight enlargement of tumor and focal areas of mixed high signal and low signal intensities in the macroadenoma on noncontrast T1-weighted images. Headache subsided markedly within a day of octreotide therapy. Transsphenoidal removal of the pituitary tumor was performed 9 days after the hormone study. Ischemic necrosis and hemorrhage were confirmed in the acidophilic adenoma with positive immunostaining for GH. Postoperative course was uneventful and his serum insulin-like growth factor-1 (IGF-1) level and blood glucose levels were normalized. Three months after the surgery the dynamic test was repeated without adverse effects. To our knowledge, this is a very rare case of apoplexy of GH-secreting pituitary adenoma after a combined stimulation test of anterior pituitary function.
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PMID:Apoplexy of pituitary macroadenoma after combined test of anterior pituitary function. 1103 77

The menopause marks the end of a woman's reproductive life. During the postmenopausal period, plasma estrogen concentrations decrease dramatically and remain low for the rest of her life, unless she chooses to take hormone replacement therapy. During the past 20 years, we have learned that changes in the central nervous system are associated with and may influence the timing of the menopause in women. Recently, it has become clear that estrogens act on more than just the hypothalamus, pituitary, ovary, and other reproductive organs. In fact, they play roles in a wide variety of nonreproductive functions. With the increasing life span of humans from approximately 50 to 80 years and the relatively fixed age of the menopause, a larger number of women will spend over one third of their lives in the postmenopausal state. It is not surprising that interest has increased in factors that govern the timing of the menopause and the repercussions of the lack of estrogen on multiple aspects of women's health. We have used animal models to better understand the complex interactions between the ovary and the brain that lead to the menopause and the repercussions of the hypoestrogenic state. Our results show that when rats reach middle age, the patterns and synchrony of multiple neurochemical events that are critical to the preovulatory gonadotropin-releasing hormone (GnRH) surge undergo subtle changes. The precision of rhythmic pattern of neurotransmitter dynamics depends on the presence of estradiol. Responsiveness to this hormone decreases in middle-aged rats. The lack of precision in the coordination in the output of neural signals leads to a delay and attenuation of the luteinizing hormone surge, which lead to irregular estrous cyclicity and, ultimately, to the cessation of reproductive cycles. We also have examined the impact of the lack of estrogen on the vulnerability of the brain to injury. Our work establishes that the absence of estradiol increases the extent of cell death after stroke-like injury and that treatment with low physiological levels of estradiol are profoundly neuroprotective. We have begun to explore the cellular and molecular mechanisms that underlie this novel nonreproductive action of estrogens. In summary, our studies show that age-related changes in the ability of estradiol to coordinate the neuroendocrine events that lead to regular preovulatory GnRH surges contribute to the onset of irregular estrous cycles and eventually to acyclicity. Furthermore, we have shown that the lack of estradiol increases the vulnerability of the brain to injury and neurodegeneration.
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PMID:Neuroendocrine modulation and repercussions of female reproductive aging. 1201 46

Clinically unsuspected pituitary adenomas are common among adults on autopsy and MRI survey. Acute pituitary hemorrhage is far more rare. We report a case of a 61-year-old male patient with locally advanced prostate cancer who presented with an acute picture of pituitary apoplexy after his first dose of leuprolide. He developed headache and neck pain within a few hours of treatment followed by nausea, vomiting, ptosis and diplopia. Pituitary apoplexy is a potentially life threatening medical emergency. Although the pathophysiology is poorly defined, various conditions and treatments have been reported to trigger apoplexy. Apoplexy has been reported in response to pituitary stimulation by GnRH or GnRH-agonists. Initial stimulatory effects of gonadotropin releasing hormone (GnRH) analogue may induce apoplexy in patients with asymptomatic gonadotroph adenomas.
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PMID:Pituitary apoplexy after leuprolide. 1683 87

LHRH analogs have become a promising modality in prostate cancer therapy as an alternative to surgical castration, and the use of these agents is generally considered to be safe. Since now, only few cases of an apoplexy of previously undiagnosed pituitary adenoma (usually gonadotropinoma) at the beginning of therapy have been described in the medical literature. We present a case of a 74 year old patient who was diagnosed of prostate cancer at the age of 68. There was no evidence of metastatic disease. Radical prostatectomy was performed and LHRH analog gosereline (Zoladex 3.6 mg s.c.) was administered. During the first day after gosereline injection the patient developed headaches that became more severe over the next 3 days. Then the patient experienced nausea and vomiting, double vision and eyelid ptosis. On the 5th day the patient temporarily lost consciousness and was admitted to hospital. Imaging (computerized tomography, magnetic resonance imaging) revealed the presence of a pituitary tumor and hemorrhage within the gland. There was no evidence of pituitary dysfunction in hormonal studies. Neurosurgical intervention was postponed for 5 days after admission. Pathological mass with signs of recent hemorrhage was removed via transsphenoidal route. The tumor had negative immunohistochemical GH, ACTH and PRL staining. Neurological impairment resolved within 9 months after the operation. As a result the patient required adrenal and thyroid replacement. During 6 years of follow-up there was no evidence of prostate cancer recurrence.
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PMID:Apoplexy of clinically silent pituitary adenoma during prostate cancer treatment with LHRH analog. 1715 26

Pituitary apoplexy occurs as a very rare complication following pituitary function tests. Signs and symptoms are due to the rapid expansion of an infarcted and/or haemorrhagic pituitary adenoma. We report a case of macroadenoma, in which pituitary apoplexy developed 30 minutes after administration of thyrotropin-releasing hormone (TRH) and gonadotropin-releasing hormone (GnRH) injections. Magnetic resonance (MR) imaging had earlier revealed several haemorrhagic zones. After the TRH and GnRH injections, the patient complained of visual defect. MR imaging demonstrated an increase in the size of the pituitary adenoma and several haemorrhagic zones that formed a fluid-fluid level at the centre of the lesion. The pituitary mass was removed using the transsphenoidal approach. On immunostaining, follicle-stimulating and luteinising hormones were strongly positive, while prolactin was weakly positive. Pituitary functions were evaluated by dynamic function tests at six weeks post operation. The patient's pituitary functions and visual acuity were found to be normal.
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PMID:Development of pituitary apoplexy during TRH/GnRH test in a patient with pituitary macroadenoma. 2114 Jan 3


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