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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Turner's syndrome (TS) is associated with a wide spectrum of clinical features, such as short stature and gonadal dysgenesis. While it is a common chromosomal abnormality, the association of Turner's syndrome and hypopituitarism is an uncommon finding. We describe here a girl with concomitant pituitary insufficiency and gonadal dysgenesis. When she was 7 years old, her mother reported that she suffered from frontal headache, asthenia and delayed growth. Basal laboratory thyroid evaluation suggested hypothyroidism, with no evidence of autoimmune disease association. She began taking L-thyroxine. At age 11 years, short stature and complaints of frontal headache still persisted. She was still prepubertal and her bone age was delayed by 2.2 years. Her karyotype was compatible with 45,X/46,XX (100 cells analyzed by FISH) and a CT scan showed empty sella. At 12 years of age, an anterior pituitary stimulation test with insulin, gonadotropin-releasing hormone (GnRH) and thyrotropin-releasing hormone (TRH) showed gonadotropin, thyrotropin (TSH) and growth hormone (GH) deficiency. Replacement therapy with GH was begun and she grew 12 cm during the first year of treatment. This report illustrates that, despite the high incidence of sinusitis, short stature and primary hypothyroidism in TS, we should consider the presence of hypopituitarism when the patient presents low levels of TSH with negative thyroid antibodies and inappropriately low levels of gonadotropins for patients with gonadal dysgenesis.
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PMID:Association of Turner's syndrome and hypopituitarism: a patient report. 1294 5

We report a Taiwanese boy who presented with apoplexy of a prolactinoma. A 12 9/12 year-old boy presented to our clinic with headache and visual deficit of bitemporal hemianopsia. Skull X-ray showed an enlarged sella. Magnetic resonance imaging (MRI) of the sella turcica showed a 4 x 2.5 x 2.5 cm mass, located at the sella turcica and extending upward to compress the optic chiasm. Preoperative laboratory data showed hyperprolactinemia, hypothyroidism and hypocortisonism. After a stress dose of i.v. hydrocortisone was given, he underwent transsphenoid surgery to remove the tumor. Immunohistochemical stains were positive for PRL in the tumor cells. After surgery, he suffered from neurogenic diabetes insipidus, hypopituitarism and hyperprolactinemia, with serum PRL level of 491 ng/ml. Visual field examination was normal 4 months later. In conclusion, pituitary apoplexy is rare in children but should be considered if a patient suffers from headache, vomiting, and visual deficit. Brain MRI is preferred for diagnosis. Dopaminergic agonists should be given if residual tumor or recurrence of prolactinoma is found after transsphenoidal surgery.
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PMID:Pituitary apoplexy due to prolactinoma in a Taiwanese boy: patient report and review of the literature. 1471 55

The Kirkwood high-dose interferon-alpha2b adjuvant therapy in high-risk-of-recurrence melanoma patients (stage IIb-III) demonstrated a benefit in terms of disease-free survival (DFS) (three trials out of three) and overall survival (OS) (two trials out of three). These important and exclusive results match with a grade 3-4 toxicity in about 75% of patients. This problem is the most limiting of this treatment. The aim of the study was to check these results and the feasibility of this treatment using the original Kirkwood schedule of 52 weeks, with appropriate dose modification, until unacceptable toxicity or progression of disease. From 23rd February 1998 until 29th July 2002, 26 patients were treated (mean age 45 years; range 25-70) with high-dose interferon-alpha2b adjuvant therapy. All patients were evaluated for toxicity, whilst 24 out of 26 (92%) were evaluated for OS and DFS. All patients were in stage IIB/III of the new American Joint Committee on Cancer (AJCC) classification. The sentinel node biopsy was performed in 19 out of 26 (73.1%) patients (clinical N0). At 31st December 2002, 20 out of 26 (77%) were still alive, whilst four (15%) had died and two (8%) were lost to follow-up. Of the patients still alive, 14 (70%) were disease free. The patients lost to follow-up refused to continue therapy for toxicity related treatment: one of them was disease free, whereas one was relapsed. There were 11 observed relapses (44%). The DFS ranged from 2 to 27 months. Among the patients, the maximal DFS is, at the time of writing, 59 months. The DFS mean is 29 months, the median is 19 months. The OS calculation will be performed at the end of 5 years observation. Now our attention is on therapy tolerability. In 18 patients out of 26 (69%) we noted at least one grade 3-4 toxicity, in accordance with literature data. The most common toxicities were haematological, hepatic, fever and asthenia. Overall, only two grade 4 events (one hepatic and one haematological) were reported. Grade 3 toxicity was hepatic in 23% of patients and haematological in 50%. Grade 2 toxicity was hepatic in 19%, haematological in 27% and fever in 50%. Grade 1 toxicities were hepatic, haematological and fever in 15, 15 and 35% of patients, respectively. Asthenia was severe in 54%, mild in 31% and not found in 15%. In 39, 4 and 15%, respectively, we have reported no hepatic, haematological or fever events. Less common toxicities were nausea, diarrhoea, headache, arthralgia, alopecia and one case of hypothyroidism. As a result of these reported toxicities, of 23 patients evaluable with regard to the protocol, 12 underwent dose reductions, six suspended treatment for disease progression, eight delayed treatment for toxicity, two interrupted treatment indefinitely for unacceptable toxicity or refused treatment, two refused to continue, two patients had no delay in treatment and three did not receive any delay or dose reduction. Of three patients still in therapy, just one has so far received a delay in treatment. Overall, only four patients (17%) interrupted therapy for toxicity related events, whereas 83% continued with the expected program: 52 weeks of therapy with appropriate dose modifications.
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PMID:Feasibility of high-dose interferon-alpha2b adjuvant therapy for high-risk resected cutaneous melanoma. 1505 49

About seven to ten percent of all brain tumours are neoplasias of the pituitary gland. Pituitary gland tumours can cause different clinical symptoms often making it difficult to come to the correct diagnosis. They can lead to severe complications such as hypopituitarism with secondary hypogonadism, hypothyroidism, and adrenocortical insufficiency, compression of the optic tract or obstructive hydrocephalus. We report on two patients with hormone-secreting pituitary tumours that were unknown prior to pregnancy. The first woman suffered from a growth hormone-producing pituitary adenoma, causing persistent headaches after birth. The second woman showed a significant loss of vision and visual field defects in the 32nd week of gestation, caused by a prolactin-producing pituitary tumour.
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PMID:[Primary diagnosis of hormone-secreting pituitary adenoma during pregnancy and after birth -- a rare occurrence]. 1532 57

Craniopharyngioma is one of the leading causes of hypothalamic-pituitary dysfunction in childhood, caused either by the tumor itself or the consequences of treatment. Tumor management in terms of recurrence rate, quality of life and complications is still controversial. Sixty-six patients with craniopharyngioma at pediatric age were reviewed for symptoms, signs, types of treatment, recurrence rates, complications, and endocrinological outcome. The majority of symptoms was related to the neurological system. Complaints only affecting the endocrinological system were seen in 6% of patients. The most frequent complaints were headache and vomiting (74.2%). The main endocrinological complaints were polyuria and polydipsia (15%), and lassitude (10.6%). Although short stature was a symptom in 9.1% of patients, it was a finding in 39.7% of patients. Plain skull X-rays raised the suspicion of intracranial tumor in more than 90% of children with craniopharyngioma. Recurrence rates were independent of the extent of tumor removal (total or subtotal). The frequency of endocrine dysfunction increased significantly after treatment. The most frequent hypothalamic-pituitary dysfunction was growth hormone deficiency (100%) and gonadotropin deficiency (80%). Hypothyroidism was diagnosed in 74% of patients. The frequency of hypothalamic-pituitary dysfunction was not affected by the extent of tumor removal. Radiotherapy did not increase the frequency of endocrine dysfunctions further. In conclusion, growth follow-up in childhood seems to be an important indicator of craniopharyngioma in early diagnosis. Radiotherapy and extent of tumor removal - either total or subtotal - did not influence endocrine outcome.
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PMID:Endocrinological outcome of different treatment options in children with craniopharyngioma: a retrospective analysis of 66 cases. 1536

A 21-year-old woman complaining of 8-month amenorrhea associated to weight gain, galactorrhea and frequent headaches, presented for clinical evaluation; her laboratory tests were: TSH: 1192 mUI/ml (0.27-4.2); TT4: 1.0 microg/dl (4.4-11.4 l); TT3: 0.41 ng/ml (0.7-2.1); prolactin: 69.2 ng/ml (3-20) and a diagnosis of myxedema associated to galactorrhea was made. A hypothalamic-pituitary magnetic resonance imaging (MRI) showed a suprasellar and intrasellar mass lesion of 1.9 x 1.4 x 1.9 cm, determining compression and deviation of the optic chiasm. Due to the possibility of hyperplasia of the TSH-producing cells, treatment of hypothyroidism was initiated with levothyroxine. Two months later, upon normalization of thyroid hormones and TSH levels, a second MRI showed an anatomically normal pituitary gland. Regression of the pituitary mass after treatment with levothyroxine confirmed the hypothesis of pituitary hyperplasia secondary to primary hypothyroidism. Our findings support the importance of determining thyroid function tests during the investigation of pituitary masses and thus avoiding an unnecessary surgery.
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PMID:[Primary hypothyroidism mimicking pituitary macroadenoma]. 1564 Sep 8

We report the case of an 11-year-old girl with primary autoimmune hypothyroidism causing secondary pituitary enlargement. She presented with headaches and a pituitary mass on MRI thought to be due to a pituitary macroadenoma. Resolution of the pituitary mass and symptoms occurred with thyroxine therapy. It is mandatory to rule out primary hypothyroidism as a cause of pituitary enlargement before surgery is considered.
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PMID:Primary hypothyroidism in a child mimicking a pituitary macroadenoma. 1566 25

We review the clinical, hormonal and imaging features of 24 consecutive patients with symptomatic Rathke's cleft cysts (RCCs), and assess the long-term effectiveness and complications of transsphenoidal cyst removal. Out of 250 consecutive patients, 24 (10%) underwent endonasal transsphenoidal surgery for RCC; 19 (79%) were women. Symptoms at presentation included headaches (83%), hyperprolactinemia (38%), central hypothyroidism (21%), galactorrhea (13%), diabetes insipidus (13%), IGF-1 deficiency (13%), central adrenal insufficiency (8%) and visual loss (8%). In total, 37% of women had irregular menses and 60% of men sexual dysfunction and hypogonadism. Two girls presented with precocious puberty. Cyst size varied from 7 to 25 mm. Fifteen (60%) had a suprasellar component. Initial and 3-month post-operative imaging revealed complete cyst resection in 23 of 24 patients. Headaches resolved in 65% of subjects and visual loss resolved in both patients who presented with this symptom. Of those presenting with endocrinopathy, 56% had improvement of at least one anterior pituitary axis; two subjects (8%), both with suprasellar RCC, developed a new hormone deficiency post-operatively and two sujects young girls, (8%) had RCC recurrence, one at 36 months after surgery, requiring a second operation, and the other had a small asymptomatic recurrence 6 months after surgery. In conclusion, RCC accounts for 10 % of surgically treated sellar and suprasellar masses. Headache, hyperprolactinemia, menstrual irregularities and sexual dysfunction are common presenting symptoms. Simple cyst removal via a transsphenoidal approach offers a safe and effective treatment. Cyst recurrence may be more common in children.
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PMID:Symptomatic Rathke's cleft cysts: a report of 24 cases. 1576 42

A 67-year-old man first noticed loss of pubic and axillary hair in 1992 and then a visual field defect in 2001. He experienced loss of consciousness attributed to hyponatremia in April 2002. Magnetic resonance imaging showed a giant intrasellar cystic mass, 40 mm in diameter, that had compressed the optic chiasm. The patient complained of chronic headache, and neurological examination revealed bitemporal hemianopsia. Preoperative endocrinological examination indicated adrenal insufficiency, and hypothyroidism due to hypothalamic dysfunction. The patient underwent endonasal transsphenoidal surgery. The cyst membrane was opened and serous fluid was drained. Histological examination identified the excised cyst membrane as arachnoid membrane. The patient's headaches resolved postoperatively, but the bitemporal hemianopsia and endocrinological function were unchanged. This arachnoid cyst associated with hypothalamic dysfunction might have been caused by an inflammatory episode in the suprasellar region.
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PMID:Giant intrasellar arachnoid cyst manifesting as adrenal insufficiency due to hypothalamic dysfunction--case report--. 1578 10

Hyperprolactinemia is commonly found in both female and male patients with abnormal sexual and/or reproductive function or with galactorrhea. If serum prolactin levels are above 200 microg/L, a prolactin-secreting pituitary adenoma (prolactinoma) is the underlying cause, but if levels are lower, differential diagnoses include the intake of various drugs, compression of the pituitary stalk by other pathology, hypothyroidism, renal failure, cirrhosis, chest wall lesions, or idiopathic hyperprolactinemia. When a pituitary tumor is present, patients often have pressure symptoms in addition to endocrine dysfunction, such as headaches, visual field defects, or cranial nerve deficits. The large majority of patients with prolactinomas, both micro- and macroprolactinomas, can be successfully treated with dopaminergic drugs as first-line treatment, with normalization of prolactin secretion and gonadal function, and with significant tumor shrinkage in a high percentage of cases. Surgical resection of the prolactinoma is the option for patients who may refuse or do not respond to long-term pharmacological therapy. Radiotherapy and/or estrogens are also reasonable choices if surgery fails. In patients with asymptomatic microprolactinoma no treatment needs to be given and a regular follow-up with serial prolactin measurements and pituitary imaging should be organized. Currently, the most commonly used dopamine agonists are bromocriptine, pergolide, quinagolide and cabergoline. When comparing the plasma half-life, efficacy and tolerability of these drugs, cabergoline seems to have the most favorable profile, followed by quinagolide. Ifprolactin levels are well controlled with dopamine agonist therapy, gradual tapering of the dose to the lowest effective amount is recommended, and in a number of cases medication can be stopped after several years. Evidence to date suggests that cabergoline and quinagolide appear to have a good safety profile for women who wish to conceive, but hard evidence proving that dopamine agonists do not provoke congenital malformations when taken during early pregnancy is currently only available for bromocriptine. Once pregnant, dopamine agonist therapy should be immediately stopped, unless growth of a macroprolactinoma is likely or pressure symptoms occur. At our institution patients with symptomatic prolactinomas, both micro- and macroadenomas, are treated with cabergoline as the first-line aproach. In the small group of patients who do not respond to this treatment, or who refuse long-term therapy, surgery is offered. Radiotherapy is given if both pharmacologic therapy and surgery fail.
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PMID:Hyperprolactinemia: pathophysiology and management. 1587 52


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