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)

A thirty-eight year-old lady with a history of bilateral adrenalectomy for Cushing's disease seven years previously, presented with sudden onset of severe headache, nausea, vomiting and loss of consciousness. She was somnolent and confused. She had neck stiffness, sixth nerve palsy and mydriasis on the left side. Computerized tomography (CT) and magnetic resonance imaging (MRI) studies revealed a non-homogeneous, grade IV D pituitary mass lesion associated with hemorrhage in the chiasmatic, interhemispheric, cerebellopontine, perimesencephalic cisterns and a hematoma within the frontal lobe. Angiography showed only bilateral elevation of horizontal segments of the anterior cerebral arteries. According to this angiographic evidence, it was presumed that the subarachnoid hemorrhage and the intracerebral hematoma were linked to pituitary adenoma apoplexy. ACTH level was 450 pg/ml. The hemorrhagic lesion with suprasellar extension was totally removed by left pterional craniotomy. Histological examination revealed a necrotic, ACTH-secreting pituitary adenoma. Even though apoplexy is a well known complication of pituitary adenomas, to our knowledge subarachnoid hemorrhage and intracerebral hematoma as a result of pituitary apoplexy in the context of Nelson's syndrome has not previously been reported.
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PMID:An unusual presentation of Nelson's syndrome with apoplexy and subarachnoid hemorrhage. 1455 76

Lymphocytic hypophysitis (LYH) is an uncommon autoimmune disease in which the pituitary gland is infiltrated by lymphocytes, plasma cells and macrophages and its function is usually impaired. It has to be suspected in pregnant women and in women with recent delivery presenting with hyperprolactinemia, headache, visual field alterations and changes of one or more pituitary hormone secretions with secondary impairment of related peripheral target glands, especially when associated with other autoimmune endocrine or non-endocrine disorders. It can also occur less frequently in prepubertal or post-menopausal women and in men. Headache, visual field impairment and more rarely diplopia are due to extrasellar pituitary enlargement with optic chiasma compression and/or to invasion of cavernous sinuses. Among the 'isolated' pituitary hormone deficiencies, ACTH deficit is usually the earliest and most frequent hormonal impairment and in rare cases can induce an acute secondary hyposurrenalism as the first sign of the disease, with high mortality in affected patients. Histopathological findings from pituitary biopsy show lymphoplasmacytic infiltrate with lymphoid aggregates surrounding atropic acini of pituitary cells; immunohistochemical analysis shows numerous mast cells randomly distributed and also localized in the vicinity of capillaries, suggesting a possible influence on capillary permeability and angiogenesis, thus favoring the inflammatory and immunological aggression against pituitary cells. Nuclear magnetic resonance imaging shows uniform sellar floor depression and an extrasellar symmetrical pituitary enlargement, usually displacing the optic chiasma, which shows a rapid homogeneous enhancement after gadolinium also involving the adjacent dura (dural tail). Antipituitary antibodies have been detected in several patients with LYH but their role needs to be clarified. Since a possible spontaneous remission can occur, a careful follow-up is required in subclinical patients without important hyposurrenalism or symptomatic extrasellar expansion. Medical (immunosuppressive, replacement and antiprolactinemic) and neurosurgical (decompression) treatments are needed in clinical symptomatic patients.
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PMID:Lymphocytic hypophysitis: a rare or underestimated disease? 1458 81

Ectopic ACTH syndrome is rarely caused by pheochromocytoma. We report a case of a 28-year-old woman with Cushing's syndrome due to ACTH-producing adrenal pheochromocytoma. She had delivered preterm baby at 32nd week of gestation with 'severe preeclampsia'. After delivery, persistent hypertension accompanied by severe headache led her to being misdiagnosed as Cushing's syndrome due to right adrenal adenoma (normal plasma ACTH level) and cerebral vasculitis of unknown etiology. She was referred to our hospital for surgical treatment. Repeated biochemical studies suggested coexistence of ectopic ACTH syndrome and pheochromocytoma. To reverse her clinical deterioration, right total and left subtotal adrenalectomy was performed with presumptive diagnosis of 1) right adrenal pheochromocytoma causing ectopic ACTH syndrome or 2) coexistence of ACTH-dependent Cushing's syndrome and right adrenal pheochromocytoma. Pathologic examination of right adrenal mass revealed pheochromocytoma which showed strong immunostaining for ACTH. Plasma ACTH and urinary cortisol excretion normalized after surgery, but she succumbed to multiple cerebral infarcts and disseminated intravascular coagulation. Pregnancy and inappropriately low plasma ACTH at initial evaluation might have hampered early diagnosis. To our knowledge, this is the first description of a case with ectopic ACTH syndrome due to pheochromocytoma associated with pregnancy.
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PMID:A case of ACTH-producing pheochromocytoma associated with pregnancy. 1470 46

Primary fibromyalgia syndrome (PFS) is characterized by widespread chronic pain that affects the musculoskeletal system, fatigue, anxiety, sleep disturbance, headache and postural hypotension. The pathophysiology of PFS is unknown. The hypothalamic-pituitary-adrenal (HPA) axis seems to play an important role in PFS. Both hyperactivity and hypoactivity of the HPA axis have been reported in patients with PFS. In this study we assessed the HPA axis by 1 microg ACTH stimulation test and metyrapone test in 22 patients with PFS and in 15 age-, sex-, and body mass index (BMI)- matched controls. Metyrapone (30 mg/kg) was administered orally at 23:00 h and blood was sampled at 08:30 h the following morning for 11-deoxycortisol. ACTH stimulation test was carried out by using 1 microg (iv) ACTH as a bolus injection after an overnight fast, and blood samples were drawn at 0, 30 and 60 min. Peak cortisol level (659.4 +/- 207.2 nmol/l) was lower in the patients with PFS than peak cortisol level (838.7 +/- 129.6 nmol/l) in the control subjects (p < 0.05). Ten patients (45%) with PFS had peak cortisol responses to 1 microg ACTH test lower than the lowest peak cortisol detected in healthy controls. After metyrapone test 11-deoxycortisol level was 123.7 +/- 26 nmol/l in patients with PFS and 184.2 +/- 17.3 nmol/l in the controls (p < 0.05). Ninety five percent of the patients with PFS had lower 11-deoxycortisol level after metyrapone than the lowest 11-deoxycortisol level after metyrapone detected in healthy controls. We also compared the adrenal size of the patients with that of the healthy subjects and we found that the adrenal size between the groups was similar. This study clearly shows that HPA axis is underactivated in PFS, rather than overactivated.
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PMID:Investigation of the hypothalamo-pituitary-adrenal axis (HPA) by 1 microg ACTH test and metyrapone test in patients with primary fibromyalgia syndrome. 1505 42

The outcome of 24 months of cabergoline treatment on prolactin (PRL) normalization, tumor shrinkage, restoration of pituitary function, and semen alterations was prospectively investigated in 41 men with macro- (age 17-70 yr) and 10 with microprolactinoma (age 18-53 yr). Fifty-one age-matched men served as controls for semen analysis. At study entry, of the 41 patients with macroprolactinoma, 17 (41.4%) had visual field defects, 14 (34.1%) had headache, eight (19.5%) had galactorrhea, 22 (53.6%) had hypopituitarism apart from hypogonadism, and 30 (73.2%) had low testosterone levels; of the 10 patients with microprolactinoma, none had visual field defects, galactorrhea, or hypopituitarism apart from hypogonadism, two had headache (20%), and five had low testosterone levels (50%; P = 0.3). After 24 months of therapy, 1) PRL levels normalized in 31 patients with macro- (75.6%) and in eight with microprolactinoma (80%; P = 0.9), and galactorrhea disappeared in all patients; 2) maximal tumor diameter reduced by 73.7 +/- 22.6% in macro- and 72.8 +/- 28.3% in microprolactinomas (P = 0.91), and 15 macro- (30%) and seven microprolactinomas (46.7%; P = 0.37) disappeared; 3) visual field defects disappeared in 15 (75%) patients with macroprolactinoma, and headache disappeared in 15 (83%) patients with macro- and in one with microprolactinoma (50%); 4) GH secretion recovered in 62.5% and ACTH secretion in 60% of patients; 5) testosterone levels normalized in 25 patients with macro- (60.9%) and six with microprolactinoma (60%) after 6 months, and 20 patients required testosterone or gonadotropin replacement (in 14 or six patients, respectively); and 6) sperm volume and count normalized in all patients who normalized testosterone levels, whereas motility normalized in more than 80%. Cabergoline therapy was well tolerated; only 4.5% of patients had side effects at high doses. These data demonstrate that cabergoline treatment is as effective and safe in men as in women with prolactinoma and can be successfully used as primary therapy even in men bearing large macroprolactinomas.
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PMID:Outcome of cabergoline treatment in men with prolactinoma: effects of a 24-month treatment on prolactin levels, tumor mass, recovery of pituitary function, and semen analysis. 1507 Sep 34

Craniopharyngiomas are rare brain tumors of the hypothalamo-pituitary region, developing from embryonic remnants of Rathke's pouch and sac. Their overall incidence is 0.13 per 100,000 person years. Most frequently, they are suprasellar, start growing in childhood and originate neurological and hormonal symptoms. We retrospectively studied patients treated in our institution for craniopharyngioma in the last 10 years, in order to evaluate their clinical, imaging and pathological characteristics. Of the 32 patients analysed, 18 were females and 14 males with ages ranging between 6 and 81 years (early onset group--EOG aged 5-14 years: 7 patients; middle age onset group--MAOG aged 15-49 years: 15 patients; late age onset group--LOG aged > or = 50 years: 10 patients). Visual impairment was the most frequent presenting clinical feature in EOG (71.4%) and MAOG (86.6%), while in the LOG personality and cognitive changes including memory loss predominated (60%). Headaches were very frequent in all groups (EOG 42.8%, MAOG 60%, LOG 40%). Meningitis and seizures were presenting features, each in one patient. Regarding endocrine symptoms and signs, growth failure was present in 57.2% of the EOG. Amenorrhea was present in 5 of 10 female patients of the MAOG. Preoperatively, TSH was deficient in 25%, ACTH in 15.6% and gonadotropin in 25% of the patients. There were no cases of diabetes insipidus. Preoperative CT and MR revealed a calcified mass in 12 (37.5%), a partially cystic mass in 20 (62.5%) and a lesion involving or extending into the third ventricle in 7 (21.9%) patients. Twenty seven (84.4%) patients were treated primarily by surgery. In 4 (12.5%) cases the tumour was considered inoperable and 1 (3.1%) patient refused surgery; all were in the LOG. Surgical approach was transsphenoidal in 2/27 (7.4%) (all of them in the LAOG) and by craniotomy in the others. The tumour removable was considered complete in 10 (37%--EOG 2/7, MAOG 6/15, LOG 2/5) and subtotal in 17 (62.9%) patients. Eight (29.6%) patients were reoperated for recurrent tumour. Postoperative radiotherapy was administered in 12 cases with residual tumor, and 3 inoperable tumors were treated primarily by conventional external radiotherapy. Pathological study revealed the adamantinomatous type in 25 (92.6%) and the papillary type in 2 (7.4%--all men in the MAOG) tumors. The average follow-up was longer in the EOG (82.6 +/- 40.7 months) than in MAOG (57.2 +/- 48.5 months) and in LOG (48 +/- 92 months). Four (12.5%) patients died, 1 during the follow-up period due to a radiation-induced astrocytoma and 3 in the postoperative period because of cerebral hemorrhage and hydrocephalus (1 in the EOG and 2 in the LOG). In summary, we found the clinical presentation to be different in the 3 age groups, with a large number of patients in the MAOG. In this group were the only examples of the papillary form. Better prognosis was associated with a total resection at initial surgery.
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PMID:[Craniopharyngiomas. Clinicopathological aspects in different age groups]. 1552 57

A woman affected by Cushing's disease underwent bilateral adrenalectomy followed by radiotherapy of the hypothalamic-pituitary area when she was 18 years old. Thereafter, she used hydrocortisone acetate replacement therapy (35.5 mg divided into two daily doses). At the age of 26 years, the patient exhibited the clinical signs of the Nelson's syndrome, i.e. skin and gingival hyperpigmentation accompanied by amenorrhea, and elevated ACTH plasma levels (2,850 pg/ml, normal range 15-80 pg/ml). The magnetic resonance imaging (MRI) analysis of the sellar region evidenced a pituitary macroadenoma, measuring 14 x 13 mm. The patient was initially treated with cyproheptadine hydrochloride (12 mg/day) for 18 months. There was a partial improvement of the symptoms, with a reduction of the ACTH plasma levels to 112 pg/ml, but without any modification of the tumor mass. Due to sleepiness and weight gain, the cyproheptadine treatment was interrupted and substituted by a cabergoline (0.5 mg twice a week) therapy. Soon after cabergoline was applied an improvement of the clinical symptoms and signs was observed such as a regression of the tumor mass and the normalization of the ACTH plasma titers (38 pg/ml). Later, cabergoline was substituted by bromocriptine (7.5 mg/day) and the plasma levels of ACTH increased again (247 pg/ml), and headache and cutaneous hyperpigmentation were recorded. When cabergoline was reintroduced there was a clinical improvement and normalization of ACTH plasma levels (64 pg/ml). The MRI analysis of the sella region demonstrated a complete remission of the pituitary adenoma. The results obtained show for the first time that a long-term treatment with cabergoline also brings about a complete remission of Nelson's syndrome in the presence of a pituitary macroadenoma.
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PMID:Nelson's syndrome: complete remission with cabergoline but not with bromocriptine or cyproheptadine treatment. 1555 61

Pituitary tumors cause symptoms by secreting hormones (prolactin, PRL, responsible for amenorrhea-galactorrhea in women and decreased libido in men; growth hormone, GH, responsible for acromegaly; adrenocorticotropic hormone, ACTH, responsible for Cushing's syndrome; thyroid-stimulating hormone, TSH, responsible for hyperthyroidism), depressing the secretion of hormones (hypopituitarism), or by mass-related effects (headaches, visual field abnormalities...). All patients with pituitary tumors should be evaluated for gonadal, thyroid and adrenal function as well as PRL and GH secretion. Specific stimulation and suppression tests for pituitary hormones are performed in selected situations for detecting the type of hypersecretion or the response to treatment. Imaging procedures (mainly magnetic resonance imaging, MRI, nowadays) determine the presence, size and extent of the lesion. The classification of pituitary tumors is based on the staining properties of the cell cytoplasm viewed by light microscopy and immunocytochemistry revealing the secretory pattern of the adenoma. Treatment of pituitary adenomas consists of surgery (performed in more than 99% of cases via a transphenoidal route) and radiotherapy, generally fractionated or, in selected cases, using stereotactic techniques such as gamma-knife. The availability of medical treatment (dopamine, DA, agonists, somatostatin analogs, GH-receptor antagonists...) has profoundly modified the indications of radiotherapy, drugs being now generally used as a second-line treatment, after surgery (or even as first-line treatment). Based on the results of the different treatment modalities for each type of pituitary adenoma, recommendations will be proposed. They may be summarized as follows. For treatment of GH-secreting adenomas, trans-sphenoidal surgery is the first-line therapy except when the macroadenoma is giant or if surgery is contra-indicated; postoperative radiation therapy (fractionated, or by gamma-knife) is performed for partially resected tumors or when GH levels remain elevated (eventually after a trial of somatostatin analog). Somatostatin analogs, now available in slow release form, are proposed when surgery is contra-indicated, or has failed to normalize GH levels, or in waiting for the delayed effects of radiation therapy. If the probability of surgical cure is low (e.g. in patients with very large and/or invasive tumors), then somatostatin analogs may be reasonable primary therapeutic modality provided that the tumor does not threaten vision or neurological function. Pegvisomant, the new GH-receptor antagonist, is indicated in case of resistance to somatostatin analogs. Patients with PRL-secreting microadenomas may be treated either with trans-sphenoidal surgery or medically with DA agonists. In patients with macroadenomas, even in the presence of chiasmatic syndrome, DA agonists are now proposed as primary treatment. Indeed, effects on visual disturbances are often very rapid (within a few hours or days) and tumoral shrinkage is usually very significant. For patients with ACTH-secreting adenomas, primary therapy is generally trans-sphenoidal surgery by a skilled surgeon, whether or not a microadenoma is visible on MRI. Radiotherapy is reserved for patients who are subtotally resected or remain hyper-secretory after surgery. In waiting for the effects of radiotherapy, adrenal steroidogenesis inhibitors (mitotane, ketoconazole) may be indicated. If drugs are not available or not tolerated, bilateral adrenalectomy may be proposed. For patients with clinically non functioning adenomas (generally gonadotropin-secreting adenomas on immunocytochemistry), trans-sphenoidal surgery with or without postoperative radiation therapy is performed for almost all patients whether or not they have visual consequences of their tumor. Selected patients with small, incidentally discovered microadenomas may be carefully followed without immediate therapy.
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PMID:Diagnosis and treatment of pituitary adenomas. 1576 32

Acupuncture treatment uses ultrafine needles which are inserted into specified points on the skin (acupoints). Acupuncture can help alleviate pain and inflammation, possibly through the increased release of pituitary beta-endorphins and ACTH. Hypnosis can also help alleviate pain syndromes, and may have centrally mediated immunomodulatory effects. The use of these 2 treatments simultaneously may potentially assist and augment the effects of each another. Two case reports where both treatments are used together are presented: One showing how hypnosis can help in the treatment of painful acupoints, the other how the response to acupuncture may be augmented by hypnosis in the treatment of headache. Controlled trials of this combined treatment are warranted.
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PMID:Integration of hypnosis with acupuncture: possible benefits and case examples. 1591 51

Pituitary adenomas, almost invariably adenomas, account for 10% to 15% of all intracranial neoplasms and are incidentally detected in up to 27% of non selected autopsies. They are morphologically classified as microadenomas (diameter < 1 cm) or macroadenomas, which can be enclosed, invasive and/or expansive. Functionally, they are classified as secreting adenomas (PRL, GH, ACTH, TSH, LH, and FSH, and those co-secreting two or more hormones), and clinically non secreting or "non functioning" tumors. Diagnosis is based on the hypersecretion phenotype (acromegaly, Cushing, etc), and on mass effect of macroadenomas leading to neurological disturbances, mainly visual complaints and headache. Pituitary tumorigenesis mechanisms include those of primary hypothalamic versus pituitary origin, the latter is supported by evidence of pituitary adenoma monoclonality, as well as the absence of hyperplastic tissue surrounding the surgically removed tumor, and the relative independence of tumor hypothalamic control. Nevertheless, a permissive role of the hypothalamus on tumor progression is also postulated. Several molecular mechanisms involved in pituitary tumorigenesis have been unraveled including oncogenes, tumor suppressor genes and growth factors involved in neoplastic development, and will be described in this review.
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PMID:[Pituitary tumorigenesis]. 1644 45


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