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)

102 patients using Trinordiol, a triphasic oral contraceptive (OC) containing ethinyl estradiol and d-norgestrel, were followed for 932 cycles in a study of secondary effects. Follow-up visits were scheduled after 1,3, and 6 months and every 6 months thereafter. 26 patients discontinued use of the pills during the study after using them for a total of 159 cycles. 5 discontinued because of abdominal pain, 1 for breast tenderness, and 1 because of headaches or migraines. 7 discontinued because of metrorrhagia, 4 for weight gain, 3 for amenorrhea, 2 for nausea and vomiting, and 1 each for nervousness, water retention, acne, desire for pregnancy, leaving the country, hypertension, and unknown motivation. the average age of patients was 23.6 years, with a range from 14-48. 76% were aged 15-29 years. 52.9% were nulliparas. 58.8% were Belgian, 21.6% were from Mediterranean Europe, 10.8% were Moroccan, and 7.9% were from black Africa. Only 1 patient, a 37 year old, developed hypertension. 15 patients gained more than 2 kg and 17 lost more than 2 kg. 15.8% complained of spotting during the 1st cycle compared to 3.1% during the 6th cycle, 5.2% during cycle 7-12, and 9.1% during cycle 13-30. Among 35 patients who did not discontinue treatment, 7 complained of amenorrhea and 1 of scanty menstrual bleeding, 14 of pain including 7 cases of pelvic pain, 2 of dysmenorrhea, 3 of breast tenderness, and 2 of headaches, 15 of leukorrhea, 3 of nausea, 2 of dizziness, and 1 each of fatigue, acne, galactorrhea, and cutaneous pruritus. 1 case of myoma at the level of the uterine cornu was identified after 24 cycles of treatment. In all, 61 patients had some complaint, while 41 were totally satisfied. No patient became pregnant during the study.
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PMID:[Clinical study of the secondary effects associated with taking a triphasic anti-ovulatory contraceptive]. 670 4

A large pituitary prolactinoma was found in a mentally deficient 45 year old woman presenting with amenorrhoea, galactorrhoea, headache, anaemia and hypertension, and removed surgically. She was subsequently found to have multiple adrenal aldosterone-producing adenomas, a gastric schwannoma and colonic polyadenomas. All these tumors were also removed surgically. Despite the absence of parathyroid and islet-cell hyperplasia, this case seems to be a variant of multiple endocrine neoplasia (MEN) type I.
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PMID:Pituitary prolactinoma, adrenal aldosterone-producing adenomas, gastric schwannoma and colonic polyadenomas: a possible variant of multiple endocrine neoplasia (MEN) type I. 711 90

A biographic and clinical investigation of 101 patients with hyperprolactinemia and/or galactorrhea is reported. Fifty-one patients were reared without their fathers and 18 with an alcoholic, violent one. These situations were uncommon in the control population, and the differences were statistically significant. There was a high frequency of complaints of obesity, headaches, frigidity, lightheadedness, and fullness of the abdomen, limbs, or face. There was a significant temporal correlation of external events in the natural history with onset or worsening of the symptoms. It is concluded that exposure during childhood to an environment characterized by an absent or alcoholic, violent father conditions some women to develop hyperprolactinemia and/or galactorrhea later in life as a response to specific environmental changes. These conclusions apply similarly to patients with prolactinoma, idiopathic hyperprolactinemia, and euprolactinemic galactorrhea, suggesting a close relationship among the 3 entities.
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PMID:Psychosomatic factors in patients with hyperprolactinemia and/or galactorrhea. 718 68

Two women evaluated for amenorrhea, galactorrhea, and hyperprolactinemia had radiographic changes of the sella turcica (localized erosion on trispiral tomography) suggestive of a pituitary tumor. Both patients experienced spontaneous regression of apparent prolactin-secreting adenomas with a marked decrease in the quantity of galactorrhea and a reduction of serum prolactin concentrations to the normal range. One patient noted a marked improvement of headaches and spontaneous menses resumed in the other patient.
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PMID:Spontaneous regression of prolactin-producing pituitary adenomas. 718 26

A 28-year-old woman with bilateral headaches and vomiting was found to have normal prolactin levels despite an eight-year history of intermittent galactorrhea and amenorrhea and the current finding of a pituitary microadenoma. The microadenoma contained hemosiderin. It is concluded that pituitary apoplexy is not confined to large tumors that have outgrown their blood supply, but can occur in microadenomas with regression of a positive endocrinopathy.
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PMID:Apoplexy in a prolactin microadenoma leading to remission of galactorrhea and amenorrhea. 719 10

During the last four years 12 Prolactin (PRL) secreting adenomas whose first clinical manifestation appeared before the age of 15 years have been studied. The first signs were a decreased growth rate and arrest of pubertal development in 4 girls and 2 boys in whom the adenoma occurred before or during puberty. In the other six cases (5 girls and 1 boy) the first signs were secondary amenorrhea and galactorrhea in girls and in the boy gynecomastia followed by galactorrhea. Symptoms of the tumour (headaches, and visual disturbances) were almost invariable (11/12) and led to the diagnosis in two cases. Plasma PRL levels were always elevated (80 to more than 5,000 ng/ml) and did not rise in response to TRH. 11 out of 12 were large tumours and pituitary tomography showed that tumour was circumscribed in five cases and invasive in the other seven. The prognosis is related to the short term outcome. The condition may be cured by surgery only (25% cases only) or by surgery and bromocriptine.
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PMID:[Prolactin adenomas in children (author's transl)]. 739 49

A clinicopathological study of 56 pediatric patients with non-ACTH-secreting pituitary adenomas removed by a transsphenoidal neurosurgical approach was undertaken to better define the clinical presentation, to assess demographic factors, to determine the immunohistochemical staining characteristics of the tumors, and to evaluate the outcome of transsphenoidal surgical treatment and other adjuvant therapies. A separate analysis of prolactinoma patients was performed. All tumors were confirmed histologically and immunophenotyped for pituitary hormones. Forty-one patients had tumors that stained for PRL alone, eight patients had tumors that stained for PRL and GH, six patients had plurihormonal adenomas, and one patient had a tumor that stained for glycoprotein hormones. No tumors contained GH alone. Macroadenomas exceeded microadenomas (1.4:1). There were no male patients with microadenomas of any type. Females outnumbered males (3.3:1). Patients presented most frequently with headache, menstrual dysfunction (in females), galactorrhea, and hypopituitarism. All but one of the patients with hypopituitarism at presentation had macroadenomas. Tumor staining characteristics did not always correlate well with clinical status, especially with regard to GH-containing tumors. Pediatric pituitary tumors did not appear to be more invasive or more aggressive than adult pituitary tumors, contrary to some previous reports. The patients with microadenomas had a 70% operative cure rate and a 65% long term cure rate; the recurrence rate for microadenoma patients was 25%. Macroadenoma patients had a 33% operative cure rate, a 55% long term cure rate, and a recurrence rate of 33%. Thus, microadenoma and macroadenoma patients had similar long term cure rates, but macroadenoma patients required more aggressive adjuvant therapy (second surgery, radiation, or bromocriptine) and had higher rates of hypopituitarism (52% of macroadenoma patients vs. 0% of microadenoma patients required long term hormone replacement).
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PMID:Pituitary adenomas in childhood and adolescence. 752 27

Pituitary adenomas are frequently encountered, benign intracranial tumours. Clinically classified according to their capacity to produce and secrete hormones, pituitary tumours are diagnosed from the clinical manifestations and biochemical findings of specific pituitary hormone overproduction or of impaired pituitary function due to pressure on normal pituitary cells, the pituitary stalk or the hypothalamus. Additionally, the tumour may result in neurological manifestations due to its effect as an intracranial space-occupying lesion. Pituitary adenomas may present acutely with pituitary apoplexy after intrapituitary haemorrhage or infarction. The subsequent hypofunction of the pituitary with concomitant neurological sequelae of an expanding intracranial mass are often associated with excruciating headache, diplopia and visual field defects. Gradually developing neurological deficits or secondary endocrine failure over several years may precede the recognition of non-secretory tumours (30-40% of pituitary adenomas) as well as some of the hormone-producing adenomas, especially when they expand beyond the confines of the sella turcica. Asymptomatic masses occur in the pituitary in 5-27% of unselected autopsy series. About 10-20% of pituitaries imaged as part of a brain study contain lesions 'consistent with a pituitary adenoma', with about half being pituitary adenomas ('incidentalomas'). Many advocate screening such cases for a wide spectrum of pituitary function abnormalities. Clinical judgement should be utilized to determine the extent of the work-up and the frequency of follow-up. Acromegaly, a clinical syndrome caused by excess growth hormone secretion, accounts for one-sixth of resected pituitary tumours. This disorder leads to chronic progressive disability and a shortened life span, with approximately 50% of untreated acromegalic patients experiencing premature death. The prevalence of acromegaly has been estimated to range from 50 to 70 per million, with the age of diagnosis usually between the third and fifth decades. Conditions associated with acromegaly include glucose intolerance, diabetes mellitus, lipid abnormalities, cholelithiasis, goitre, and hyperthyroidism, respiratory complications, hypertension, cardiovascular disease, and calcium metabolism abnormalities. An association between acromegaly and cancer, especially of the colon, is now recognized. Epidemiological series have indicated that cancer of the colon, breast and other types of malignancy are a cause of death with increased frequency in acromegalics compared with expected rates. Hypopituitary symptoms secondary to the mass effect of macroadenomas in acromegalic patients are common. Among premenopausal women, menstrual irregularities and galactorrhoea have been reported in 40-70%, while more than half of the men complain of impotence and decreased libido.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical features and differential diagnosis of pituitary tumours with emphasis on acromegaly. 762 86

We report the first case of pseudotumoral lymphocytic hypophysitis successfully treated by corticosteroids without surgery. A 27-year-old woman had been monitored for chronic headache 13 months after giving birth, associated with amenorrhea and galactorrhea. Cranial magnetic resonance imaging revealed a markedly enlarged pituitary gland with a suprasellar extension; the only biochemical abnormality was a mild hyperprolactinemia. Because of a putative diagnosis of prolactinoma, bromocriptine was prescribed at a dose of 5 mg daily, soon followed by the transitory appearance of menstruation. Two years later, panhypopituitarism was present and was revealed by acute adrenal insufficiency. Magnetic resonance imaging revealed that the pituitary mass was the same as previously described, but hormonal investigation showed evidence of complete hypopituitarism and no hyperprolactinemia. Nuclear antibodies were negative as well as other autoantibodies. Human leukocyte antigen serological Class II typing was DR3/DR4. Lymphocytic hypophysitis was then suspected; in the absence of visual complication and because this patient refused surgery, corticosteroids were attempted at a daily dose of 60 mg of prednisone for 3 months, progressively decreased for the next 6 months. Under this treatment, a gradual recovery of all pituitary hormones was observed and magnetic resonance imaging showed a reduction of two-thirds in pituitary mass. Five months after the end of corticoid treatment, our patient relapsed with panhypopituitarism and an increase of pituitary volume. She underwent steroid treatment, and a biopsy was performed and confirmed the diagnosis of autoimmune hypophysitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pseudotumoral lymphocytic hypophysitis successfully treated by corticosteroid alone: first case report. 780 Jan 42

Although intrasellar tuberculomas have been reported in post-mortem examinations, they are exceptionally rare in clinical practice. Five patients with biopsy proven intrasellar tuberculoma with suprasellar extension are described. In four cases the clinical and radiological diagnosis was that of a pituitary adenoma. One patient, however, presented similar to a subarachnoid haemorrhage, but the CSF analysis was suggestive of tuberculous meningitis. All these patients presented either with intermittent headache or a sudden severe headache suggestive of an ictus. Hypopituitarism was diagnosed on clinical grounds in two patients and one patient had an associated galactorrhoea-amenorrhoea syndrome. Only one patient had a bitemporal field cut. In all other patients ophthalmological examination was normal. The CT scan showed a hyperdense sellar mass with suprasellar extension brightly enhancing with contrast in all cases. An angiogram in four patients did not reveal any vascular lesion. Laboratory investigation showed some degree of hypopituitarism in all cases. Transsphenoidal surgery was performed in four patients and operative findings were typical, and unlike those of a pituitary adenoma. All patients responded well to antituberculous treatment and at the end of 12 months were clinically and radiologically normal.
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PMID:Intrasellar tuberculoma. 791 89


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