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

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

A 39 year-old man was admitted to our hospital because of severe headache with fever continuing over two weeks. Three days after admission he developed aphasia and right hemiparesis, when his CT revealed subarachnoid hemorrhage at the left sylvian fissure. He was diagnosed as suffering from cerebral venous thrombosis because empty delta sign was positive on the enhanced brain CT. Suprasagittal sinus and bilateral transverse sinuses were not detected on the cerebral angiography. He was also diagnosed as having Graves' disease for the first time on the basis of free T3 13.56 pg/ml, free T4 4.65 ng/dl, TSH < 0.01 IU/ml, anti-TSH receptor antibody 4.3 IU/l, and thyroid stimulating antibody 224%. On the examination, homocystine and activities of antithrombin III, protein C, and protein S were normal. Antinculear, anti-DNA, anti-Sm, anticardiolipin beta2GP-I antibodies, and PR3ANCA were negative. Factor VIII activity, however, markedly increased over 300%, which has been known to increase in the cases of hyperthyroidism. He recovered well after the treatment with thiamazole in addition to warfarin followed by intravenous heparin. There are only six cases of cerebral venous thrombosis due to hyperthyroidism with increased factor VIII level. All of those cases were female, and 5 of them were taking oral contraceptives. This is a first Japanese male case.
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PMID:[Case of cerebral venous thrombosis due to graves' disease with increased factor VIII activity]. 1676 94

For twelve years, the subject of this report, a 38-year-old man, presented a clinical condition compatible with the SUNCT (short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing) syndrome. He presented a stabbing and intense daily pain located in the left pre-auricular and temporal regions. Each of these intense pain attacks lasted around one minute and presented a frequency of two to eight times per day. The pain was associated with ipsilateral lacrimation, conjunctival injection and rhinorrhea. MRI revealed a pituitary tumor with little suprasellar extent. The subjects serial assays of prolactin, GH, TSH and ACTH were within normal levels. Following transsphenoidal hypophysectomy, with complete removal of the tumor, the subject no more presented pain. The pathological diagnosis was non-secreting adenoma. Fourteen months after the surgery, he remains symptom-free.
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PMID:SUNCT syndrome associated with pituitary tumor: case report. 1691 28

Twenty chronic post-traumatic headache subjects (16 men and 4 women) were considered, together with age and sex matched normal controls. Pituitary function was challenged by means of luteinising hormone releasing hormone (100 microg, i.v.), thyrotropin (TSH) releasing hormone (200 microg, i.v.) and regular insulin (.1 U/kg, i.v.). The responses of gonadotropins, TSH, somatotropin (STH) and prolactin (PRL) were studied in the group as a whole and in clinical subgroups. No differences were found in the baseline levels of the hormones. No significant changes were observed in the responses of gonadotropins and STH. A decreased response was found for TSH and, in the female series, an enhanced response of PRL was observed. Patients complaining for a decreased libido showed a larger PRL response. The smaller response of TSH exhibits a straight inverse relationship to the clinical severity. The periodicity of PRL secretion studied in male patients with a harmonic analysis according to the Fourier's theorem showed the preservation of the physiological sleep-entrained night surge. The per cent incidence of the harmonics with a period shorter than 24 hours decreases according to the clinical severity, at variance to the finding in normal controls. The only persisting harmonic is the one with a 24 hour period. In the absence of major post-traumatic endocrine syndromes, post-traumatic headache subjects show changes of the neuroendocrine regulation of pituitary secretion. The findings are consistent with the hypothesis of an hyperactivity of serotoninergic neurotransmission.
Headache 1982 Jan
PMID:Neuroendocrine data in chronic post-traumatic headache. 1715 44

We report the case of a 28-year-old woman who presented simultaneously with superior sagittal sinus thrombosis and thyroid crisis, and was subsequently found to have protein C deficiency. February 3, 2003, she admitted complaining of abdominal pain. The diagnosis of appendicitis was made, and she was operated on under lumbar anaesthesia. Day 7, she developed acute headache and distal weakness of the left lower limb. On examination she was alert, with a temperature of 38 degrees C, a sinus tachycardia of 124/min and blood pressure 164/84 mmHg. Neurological examination revealed neck stiffness and left hemiparesis, predominantly in her lower limb. Gadlinium-enhanced brain MRI revealed extensive superior sagittal sinus thrombosis. CT scan demonstrated infarction in the right frontal cortex, and subarachnoid hemorrhage adjacent to the right cerebellar tentorium. The patient was treated with a free radical scavenger edarabon, and glycerin. No anticoagulant therapy was instituted. Over the next 24 hours, her condition worsened. She became comatose, as well as developing a generalized tonic-clonic seizure. Day 12, laboratory examinations revealed an undetectable TSH-level CTSH (thyroid stimulating hormone) <0.005 mcIU/ml), with a level of free thyroxin 7.77 ng/dl (0.9-1.7), free triiodothyronin 29.6 pg/ml (2.3-4.3), and positive anti-TSH receptor antibodies determined subsequently. Coagulation factor VIII activity was 155% (normal range 60-150). Protein C deficiency (antigen 59%, activity 49%) was also present, suggesting a congenital type I heterozygous deficiency. A diagnosis of thyroid crisis on the basis of Graves' disease was made. The patient remained comatose and died on Day 16, with renal failure. The patient had protein C deficiency, a well-established risk factor for cerebral venous thrombosis (CVT). However, additional risk factors are required in most cases to precipitate CVT. In our case, this trigger was most likely thyroid crisis, suggesting that thyrotoxicosis, probably through hypercoagulability, may be a predisposing factor for the development of CVT.
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PMID:[Thyroid crisis and protein C deficiency in a case of superior sagittal sinus thrombosis]. 1737 Jun 53

The objective of this article is to review clinical outcomes in patients presenting with pituitary apoplexy and compare the results of conservative and surgical management. It took the form of a retrospective review of 30 patients (23M, 7F; age range: 17-86 years) with pituitary apoplexy diagnosed between 1988 and 2004. Presenting features included headache in 27 patients, 'collapse' in three and vomiting in 14. Complete blindness occurred in four patients, monocular blindness in two, decreased visual acuity in 12, visual field loss in 10 and ophthalmoplegia in 15. Only five had no initial visual deficit. CT was the initial mode of imaging in 22 patients: three such scans were initially reported as 'normal' and a further 10 as pituitary tumour only, with no haemorrhage. Ten patients proceeded to early pituitary surgery and 20 were managed conservatively. There was one death 24 days after admission in a patient with multiple co-morbidities. Of the six patients with blindness, three (two conservatively treated) regained partial vision. Of the remaining 19 patients with visual deficits, 10 (two surgically treated) recovered fully and eight (four surgically treated) partly so. At latest follow-up the following pituitary hormone deficiencies were identified: ACTH 19; TSH 20; testosterone 18; ADH (diabetes insipidus) eight. Later recurrence of a pituitary adenoma was observed in seven cases (including six of the 10 surgically treated patients). There was no evidence that those patients managed surgically had a better outcome. Early neurosurgical intervention may not be required in most patients presenting with pituitary apoplexy.
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PMID:Pituitary apoplexy: retrospective review of 30 patients--is surgical intervention always necessary? 1743 89

Concomitant thyroid cancer with pituitary tumor is uncommon. This study reports a case of advanced papillary thyroid carcinoma with pituitary adrenocorticotropic hormone (ACTH)-secreting tumor. A 58-year-old male patient had thyroid cancer in 1991 and presented with headache caused by pituitary tumor with apoplexy in 1993. Due to hypopituitarism, the patient underwent radioactive iodide ((131)I) for detection and treatment of metastatic thyroid cancer after the use of recombinant human thyroid-stimulating hormone (rhTSH) in 2000. During follow-up for thyroid cancer, (201)thallium scan proved to be an effective tool for detecting metastatic thyroid cancer in the patient without pituitary TSH reserve. Pituitary ACTH-secreting tumor was confirmed in 2001 based on the high serum ACTH level and positive immunohistochemical stain for ACTH. The patient had no Cushingoid features. Moreover, serum ACTH levels were 337 and 232 pg/mL with normal serum cortisol and urine-free cortisol. Although the patient underwent three operations and a total of 370 mCi (131)I therapy for recurrent thyroid cancer, the cancer continued to progress. Finally, the patient died of pneumonia with septic shock 12 years after the diagnosis of thyroid cancer.
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PMID:Concurrent papillary thyroid cancer with pituitary ACTH-secreting tumor. 1747 13

Endocrine dysfunction is a rare but known cause of benign intracranial hypertensio (BIH) in adults. Here we describe a rare case of BIH in the pediatric age group associated with autoimmune hyperthyroidism. A 12-year-old girl presented with a 3-month history of headaches. Ophthalmic examination revealed bilateral papilledema. The ocular findings were otherwise normal, with no exophthalmos. Cranial and orbital magnetic resonance imaging was unremarkable. Lumbar CSF opening pressure in recumbent and relaxed position was elevated (31 cm water). Thyroid hormones fT3 and fT4 were elevated while TSH was completely suppressed. As TSH receptor stimulating antibodies (TSHR-Ab) were elevated Graves' disease was diagnosed. Thyroid suppressive therapy with carbimazole was initiated and supplemented by propranolol. As hyperthyroidism improved over two weeks the headaches subsided and the papilledema slowly resolved over the next 2 months. This case illustrates that hyperthyroidism should be considered as a cause of BIH in children.
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PMID:Reversible benign intracranial hypertension in a child with hyperthyroidism. 1918 7

Brucellosis which is a endemic in Turkey, is a systemic infection which can affect any organ or system in the body. Since signs and symptoms of brucellosis resemble many other diseases, misdiagnosis and related increase in morbidity rate, are common. In this report, a case of brucellosis complicated with endocarditis, pyelonephritis, sacroileitis and thyroiditis, was presented. The case was a 32-years-old female patient in whom the diagnosis of brucellosis was delayed by 12 months since it was not taken into consideration during the clinical follow-up of the patient in various clinical centers. The patient was admitted to our center with the complaints of fever, headache, back pain, night sweats, fatigue, loss of appetite, weight loss, dysuria and polyuria. The patient had a history of consumption of raw milk and dairy products. Positive Brucella tube agglutination test (1/1280) and isolation of Brucella spp. in blood cultures led to the diagnosis of brucellosis. Sacroileitis was diagnosed upon pain on right hip joint movements, pain and restriction at the same joint in FABER test. The detection of vegetation during echocardiography, cardiac murmur during physical examination and the determination of increased ESR and CRP levels led to the diagnosis of endocarditis. Abdominal ultrasonography and urinalysis results (hematuria, proteinuria and pyuria) revealed pyelonephritis and increased free T3 and T4, decreased TSH and positive anti-thyroid autoantibodies (anti-TG, anti-TPO) revealed thyroiditis. Treatment was started with combination of rifampisin (1 x 600 mg/day) and doxycycline (2 x 100 mg/day). After the diagnosis of endocarditis, trimethoprim-sulfamethoxazole (3 x 960 mg/day) and streptomycin (1 x 1 g/day) were added to the treatment. Valve replacement surgery was planned, however, the patient didn't accept surgical intervention and antimicrobial treatment continued with streptomycin for 21 days and other antibiotics for six months. The patient exhibited significant improvement after the medical treatment. Although sacroileitis is a frequent complication of brucellosis, endocarditis, thyroiditis and pyelonephritis are among the rare complications. In cases of brucellosis with multiorgan involvement including endocarditis, successful results may be achieved by aggressive antimicrobial treatment. In endemic areas, brucellosis should always be taken into consideration in patients with fever of unknown origin and multisystem involvement.
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PMID:[A case of brucellosis complicated with endocarditis, pyelonephritis, sacroileitis and thyroiditis]. 1933 91

Yusho PCB poisoning occurred in 1968, when the human environment had been polluted with PCBs and related compounds. The causal rice oil was contaminated with large amounts of PCBs and PCDFs by accidental leakage at the rice oil producing Kanemi Company on February 7-15, 1968. Much less concentrations of PCBs were identified in the rice oil produced and shipped from the Company before and after the critical days. Concentration trend of PCBs and TEQ in human body were examined for 40 years from 1968 to present. Concentrations in the blood of heavily exposed Yusho patients and normal Japanese were PCBs : 80 and 1.5 microg/g-fat, and TEQ : 60 and 0.1 ng/g-fat, respectively, in 1969, and decreased to PCBs : 1 and 0.2 microg/g-fat, and TEQ : 0.5 and 0.02 ng/g-fat, respectively, in 2007. PCBs and PCDFs have been persistently retained in human body for 40 years. Serious cases of Yusho and Yucheng having very high PCB, PCDF concentrations in blood have suffered from severe chloracne, pigmentation, eye discharge and others at the first stage and recovered very slowly with a lapse of several years. However, their hormone mediated signs and symptoms, such as high triglyceride and thyroxin levels in serum, disorder of immunoglobulin, goiter, decrease of sperm mobility, disorder of teeth and joints conditions, decrease of IQ score in children, headache and numbness, etc, are persisting for more than 30 years. The residents in East Slovakia who have been exposed to PCBs wasted from a PCB factory and have about 3 times higher blood PCB concentrations than the controls, have suffered from disorder of FT4 and T3 levels in serum, disorder of thyroid grand and thymus, dental defects in enamel developmental, hearing impairment at low frequency tone, tendency to diabetes and others. Residents in the Great Lakes area, USA, whose blood PCB levels are estimated to be higher than other places, have shown disorder of thyroid, T4, TSH levels, endometriosis, joint disorder, and low IQ score in children. The levels of PCBs and PCDFs in the blood of Yusho patients and Controls are compared to the normal levels of estradiol, testosterone and thyroxin. In the blood of Yusho patients, concentrations of single congeners of PCB118, PCB153, PCB156 and PentaCDF are high enough to disturb the hormonal effects. Blood PCB concentrations in normal Japanese are higher than the FT3 and FT4 levels, indicating hormonal disturbance will be easily produced. PCBs are metabolized to produce HO-PCBs, which bind to TTR and retain in blood medium. Blood HO-PCB concentrations in Yusho patients and normal persons are higher than the FT3, FT4 levels in serum. Therefore, the hormonal effects of thyroxin will be disturbed in Yusho and normal persons. As HO-PCB will be easily transferred to fetus through placenta, fetus development will be possible to be disturbed. In Yusho and other cases, PCBs and TEQ (PentaCDF, PCB118 etc) were ingested together and the strong enzyme inducers of PentaCDF and others have metabolized PCBs to HO-PCBs, which have retained in the blood. Complex reactions of PCDFs, PCBs and HO-PCBs have disturbed the hormonal effects and the induced symptoms and diseases would have been caused.
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PMID:[Toxic effects of PCB/PCDF to human observed in Yusho and other poisonings]. 1958 43


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