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 17 year-old boy was admitted to the hospital because of thirst, polyuria (5-61/day), delayed sexual development and muscle weakness. He appeared obese, had an eunuchoidal body habitus and was excessively tall. Chromosomal analysis revealed a 47XXY karyotype. Serum cortisol was 1.3 microgram/dl, LH, 10.4 mIU/ml, FSH, 2.0 mIU/ml, and testosterone, 10 ng/dl. Endocrinological dynamic tests indicated diabetes insipidus and hypopituitarism of a hypothalamic type. Brain CT disclosed the existence of a tumor shadow around the calcified pineal body, extending towards the suprasellar region. Replacement therapy with glucocorticoid and DDAVP was started. The patient complained of a headache and plasma AFP and hCG concentrations were 868 ng/ml and 68.6 IU/ml respectively. A hCG- and AFP- producing germ cell tumor was suspected and radiation therapy with 60Co was performed. Plasma AFP and hCG were decreased with significant clinical improvement. Soon after irradiation, he started to complain of a headache and had elevated AFP and hCG levels. Right hemiparesis and unconsciousness suddenly appeared and he died of left thalamic bleeding. This is the first case of Klinefelter's syndrome associated with intracranial germ cell tumor. Plasma testosterone levels fluctuated in parallel with the change in plasma hCG levels. This shows that the Leydig cells in this patient could respond to some extent to tumor-producing hCG.
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PMID:A case of Klinefelter's syndrome associated with hypothalamic-pituitary dysfunction caused by an intracranial germ cell tumor. 244 Jun 66

We report the case of a patient with Klinefelter's syndrome who developed a prolactin (PRL)-secreting tumor. The patient developed headaches, visual alterations and also symptoms of hypogonadism despite appropriate testosterone (T) replacement therapy. The diagnosis of hyperprolactinemia was then suspected. The laboratory findings confirmed the hypothesis, showing high levels of serum PRL. The patient was initially treated with oral bromocriptine, and afterwards with the injectable form. There was a marked decrease in PRL levels and in tumor size. Although some neoplasms, like breast carcinoma and germ cell tumors, are known to occur more frequently in patients with Klinefelter's syndrome, an association with PRL-secreting tumor has not been reported yet. In conclusion, symptoms of hypogonadism in patients with Klinefelter's syndrome receiving appropriate T replacement therapy can suggest the presence of hyperprolactinemia.
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PMID:A prolactin-secreting tumor in a patient with Klinefelter's syndrome: a case report. 886 6

Anabolic-androgenic steroid (AAS) withdrawal is established to be an important, though poorly known medical problem, because of AAS potency to cause physical and psychological dependence. Thus discontinuation of high-dose, long-term anabolic steroid use, apart from endocrine dysfunction (hypogonadotropic hypogonadism), may lead to development of withdrawal symptoms. They include mood disorders (with suicidal depression as the most life-threatening complication), insomnia, anorexia, decreased libido, fatigue, headache, muscle and joint pain, and desire to take more steroids. The withdrawal from anabolic steroids usually requires treatment. Clinical management, as with other drugs of abuse, consists of supportive therapy and pharmacotherapy. The goals of treatment are to restore endocrine (hypothalamic-pituitary-gonadal, HPG) function and to alleviate withdrawal symptoms. The endocrine medications that are targeted specifically to ameliorate HPG function include testosterone esters, human chorionic gonadotropin, synthetic analogues of gonadotropin-releasing hormone and antiestrogens. They are indicated in the presence of persistent clinical symptoms or/and laboratory evidence of HPG dysfunction. Other medications, that are targeted to provide symptomatic relief include antidepressants (especially serotonin selective re-uptake inhibitors), nonsteroidal anti-inflammatory drugs and clonidine. Notwithstanding, it should be remembered that many of the above mentioned drugs have their own potential for abuse or side-effects, so their use must be carefully weighted and optimal treatment strategies for AAS withdrawal must await further clinical research.
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PMID:[Treatment strategies of withdrawal from long-term use of anabolic-androgenic steroids]. 1189 57

A 57-year old patient presented with an 8 week history of headache and diplopia. Left-sided incomplete oculomotor nerve paresis was found, whereas further clinically relevant visual impairment was not seen. Magnetic resonance imaging of the head showed an extensive intra-, para- and suprasellar tumor which in combination with a markedly elevated serum prolactin level was identified as a macroprolactinoma. The symptoms began 7 years ago with a loss of libido and virility. The application of a dopamine agonist lead to a reduction of serum prolactin level to 0.5% of the initial value and a considerable tumor regression within three months. The development of oculomotor nerve paresis is an unusual manifestation of prolactinoma. By contrast, long-term medical history with slowly developing signs and symptoms of hypogonadotropic hypogonadism are often to be found in men. The delayed diagnosis is responsible for the high percentage of macroprolactinomas in male subjects.
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PMID:[57-year-old patient with diplopia and headache]. 1296 89

Intrasellar arachnoid cyst (IAC) is a very rare pathological lesion occurring in 5 of 1000 autopsy cases, and constitutes 9% of all arachnoid cysts. As a space-occupying mass, IAC may cause headaches, visual disturbances, hypopituitarism, precocious puberty, and the "bobble-head doll" syndrome. The pathogenesis of IAC remains controversial. Magnetic resonance imaging (MRI) is the neurodiagnostic tool of choice to evaluate IAC. The authors presented a 38 year-old woman suffering from severe chronic headaches, dysmenorrhea, and visual disturbance. MRI revealed an intrasellar cystic lesion that had compressed the optic chiasma. Preoperative endocrinological assessment revealed hyperprolactinemia and hypogonadotropic hypogonadism. The patient underwent transsphenoidal surgery. The cyst membrane was opened and clear, serous fluid was evacuated. The postoperative course was complicated by CSF leakage, which was corrected by an autologous fat graft placement. Visual field defects improved immediately after surgery but a transient panhypopituitarism and diabetes insipidus occurred. Postoperative MRI revealed no recurrence of the lesion during the four-year follow-up.
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PMID:[Intrasellar arachnoid cyst. A case report and review of the literature]. 1696 58

Increasing evidence of impaired pituitary function in many subjects with primary empty sella (PES) has been reported. We conducted a retrospective analysis of our patients with PES, in order to ascertain presenting symptoms and endocrine status on diagnosis and during follow-up. Magnetic resonance imaging (MRI) of the pituitary leading to the diagnosis of PES was performed in 8 patients (5 F and 3 M, age: 60.1 +/- 3.3 years, M +/- SE; group 1) after the diagnosis of global anterior hypopituitarism (H), and in 20 patients (F, age 56.9 +/- 2.2 years, group 2) for other clinical reasons. Baseline determinations of pituitary and target gland hormones and of IGF-I were performed. GH response to GHRH plus arginine stimulation was also evaluated. Ten age- and BMI-matched subjects (7 F, 3 M, age: 53.0 +/- 4.0 years) with normal pituitary function served as controls (C). In group 1, the presenting symptoms leading to the diagnosis of H were consciousness disturbances, hyponatremia and chronic fatigue. The GH response to stimulation was absent (peak:1.0 +/- 0.3 ng/ml) and IGF-I levels (60.1 +/- 9.3 ng/ml) were significantly lower (p<0.001) than in C and group 2 PES patients. Among group 2 PES patients, the main presenting symptoms were headache and visual alterations. Baseline hormone levels proved normal in 17 subjects, while slight hyperprolactinemia was observed in 2 and hypogonadotropic hypogonadism in one. The GH response to stimulation (12.9 +/- 3.4 ng/ml) and IGF-I levels (141.7 +/- 12.0 ng/ml) were lower (p<0.05) than in C (GH: 33.4 +/- 8.8 ng/ml, IGF-I: 193.1 +/- 20.3 ng/ml). PES is a heterogeneous condition that ranges from hypopituitarism to various degrees of isolated GH deficiency, and which needs careful endocrine assessment, treatment and follow-up.
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PMID:Primary "empty sella" in adults: endocrine findings. 1698 77

Prolactin hypersecretion from a pituitary adenoma usually results in a serum prolactin level less than 1,000 ng/ml. During therapy with a dopamine agonist, prolactin levels usually normalize and the tumors shrink substantially. In the past few years, we have seen three men who presented with serum prolactin levels greater than 10,000 ng/ml. All presented with large tumors, visual field deficits, and hypogonadotropic hypogonadism. All other pituitary hormones were normal. In all three patients, significant tumor shrinkage was achieved with improvement or resolution of headaches and visual field deficits. None of our patients has been able to achieve a normal prolactin or testosterone. A literature review identified 32 patients with prolactin levels of more than 10,000 ng/ml. Twenty-six (81%) were males. Most had large tumors, headaches and visual field defects. Even with the addition of surgery and/or radiation therapy to medical therapy, normalization of serum prolactin occurred in only six patients (19%) and only one man achieved a normal testosterone. We conclude that in patients with massive prolactin hypersecretion, therapy with a dopamine agonist will lead to tumor shrinkage and improvement of mass effects, but usually does not normalize prolactin or testosterone. Rather than waiting for maximal prolactin reduction, we would recommend early institution of testosterone replacement therapy.
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PMID:Clinical presentation and response to therapy in patients with massive prolactin hypersecretion. 1730 59

Hyperostosis frontalis interna (HFI) has been reported in older women, but reports in men are rare. We present a novel case of migraine headache in a gentleman with Klinefelter's syndrome and HFI, along with a discussion of possible pathophysiologic mechanisms underlying both the headache and the HFI.
J Headache Pain 2007 Dec
PMID:Headache in a patient with Klinefelter's syndrome and hyperostosis frontalis interna. 1807 29

Sarcoidosis is a chronic disease of unknown aetiology. Neurosarcoidosis is registered in 5% of patients with sarcoidosis. Clinical manifestations of sarcoidosis are numerous and diverse. Manifestation of Neurosarcoidosis includes partial- and grand-mal seizures, low-grade fever, headache, increased intracranial pressure, visual disturbances, diabetes insipidus, amenorrhea- galacterorrhea syndrome and pituitary failure, hypogonadotropic hypogonadism, hyperprolactinemia, unilateral and bilateral facial palsy, infiltration of meninges (aseptic meningitis) and nerve roots, leptominingitis, pachymeningitis with cranial neuropathies, pseudotumor, mild cognitive disorder, psychosis, delirium, dementia, disorientation, amnesia, progressive visual deterioration and proptosis, axonal polyneuropathies, mononeuropathies, chronic polyradiculoneuritis, peripheral neuropathy, cranial nerve abnormalities, radiculopathies, peripheral neuropathy, mononeuritis multiplex, progressive numbness and deep sensation disturbance in bilateral lower extremities, hemiplegia, hyperreflexia with pathological reflexes and hypesthesia, upward gaze palsy, spinal cord compression, dysarthria, dysphagia, weakness, episodes of blurred vision, diplopia, intracerebral hemorrhage, neuro-ophthalmic manifestations, intranuclear ophthalmoplegia, dysorientation, vasculitis presenting with strokes, intracranial hypothalamic lesion, paresthesis, hemiparesis, myelopathy in the cervico-thoracic region, lumbar pain, sensory level and inability of lateral gaze (Tab. 2, Ref. 60).
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PMID:Clinical manifestations of neurosarcoidosis. 1982 43

We report two cases with primary autoimmune hypothyroidism and an ectopic thyroid gland causing pituitary enlargement mimicking pituitary macroadenoma. One of the cases presented with complaints of headache and short stature and the other case with a complaint of menorrhagia. In both cases, the pituitary mass and symptoms resolved with levothyroxine replacement. Normal menses resumed. However, pituitary dynamic tests revealed persistent growth hormone and gonadotropin deficiency in one case and growth hormone deficiency in the other. To our knowledge, this is the first report in an adolescent of hypogonadotropic hypogonadism, growth hormone deficiency, and menorrhagia associated with pituitary hyperplasia secondary to primary hypothyroidism. The recognition of the association between reversible pituitary hyperplasia and primary hypothyroidism might eliminate unnecessary surgery.
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PMID:Pituitary hyperplasia mimicking pituitary macroadenoma in two adolescent patients with long-standing primary hypothyroidism: case reports and review of literature. 2019 2


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