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

Recurrent pituitary tumors can sometimes pose a diagnostic and therapeutic challenge. We report a case of a 43-year-old man who presented twice, 13 years apart, with pituitary adenoma marked by headaches, visual impairment, and no signs of endocrinologic abnormality. At initial presentation computed tomographic scan documented a pituitary mass eroding the sellar floor, with suprasellar and parasellar extension. The patient underwent transsphenoidal surgery and the tumor was classified as a silent corticotroph adenoma, subtype 2. Thirteen years later, clinical symptoms of a destructive pituitary mass reappeared. This time, the adenoma revealed typical ultrastructural features of an oncocytoma; it had a different immunocytochemical profile from the first tumor. Given these striking morphologic differences, we consider the two adenomas to represent asynchronous, de novo formations. We conclude that the recurrence of a resected pituitary tumor may also represent a metachronous development of two distinct pituitary adenomas.
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PMID:Asynchronous pituitary adenomas with differing morphology. 764 33

A 57-year-old woman was admitted to our hospital with occipital headache and nausea. She had severe hypertension (192/122mmHg), hypokalemia (2.8mEq/l) and fasting hyperglycemia (127 mg/dl). Further examination revealed elevated plasma ACTH (124pg/ml) and cortisol (26.5 mu g/dl) with a lack of diurnal rhythm. Plasma ACTH or cortisol did not increase by injection of corticotropin releasing hormone (CRH). Rapid ACTH test resulted in an exaggerated response of plasma cortisol. Abdominal MRI scan showed a left adrenal tumor. Since the bilateral adrenal venous blood sampling revealed a significant increase of cortisol on the left, left adrenalectomy was performed. Histological examination of the resected adrenal gland revealed marked cortical hyperplasia. Postoperative investigations revealed that despite a small dose of steroid replacement for only 20 days, plasma ACTH level was decreased for a period of 6 months. Both plasma ACTH and cortisol increased by a CRH injection 38 days after surgery. CRH test during bilateral inferior petrosal sinus sampling indicated that this patient had no functioning pituitary tumor. Although the exact mechanism of high plasma ACTH level in this case was unknown, these findings suggest that any substance secreted from primary adrenal nodular hyperplasia adrenal nodular hyperplasia may stimulate pituitary ACTH production. This is a very rare case of Cushing's syndrome due to unilateral primary adrenal nodular hyperplasia with elevated plasma ACTH.
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PMID:[A case of unilateral primary adrenal nodular hyperplasia with elevated plasma adrenocorticotropin (ACTH)]. 785 19

The long-term efficacy and tolerability of CV 205-502, a non-ergot dopamine agonist with D-2 receptor affinity, were studied for up to 36 months in 16 patients with macroprolactinomas. Prolactin values were reduced in all cases, becoming either normalized or suppressed in 12. The pituitary tumor size was reduced in the 13 patients with an obvious tumor and visual function normalized in all six patients with initial defects. Concomitantly we observed improvement in gonadal function, galactorrhea, headache, libido and general well-being. Adverse reactions were experienced by 15 patients during dosage increment and caused one patient to discontinue the medication. Seven patients had persistent adverse effects which prohibited a dosage increase of CV 205-502, sufficient to normalize PRL levels in three. Two patients experienced serious adverse events, causing the discontinuation of treatment in one case. In eight patients treatment with CV 205-502 and bromocriptine could be compared. Three patients responded better to CV 205-502 than to bromocriptine treatment. Only one patient preferred bromocriptine to CV 205-502 for long-term treatment. We conclude that CV 205-502 is an effective and in most cases well-tolerated treatment for patients with macroprolactinomas. CV 205-502 is preferable to bromocriptine as an initial treatment and should also be tried in patients where treatment with bromocriptine has failed.
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PMID:Long-term treatment of macroprolactinomas with CV 205-502. 809 91

A case of systemic lupus erythematosus (SLE) complicated with hypopituitarism after steroid pulse therapy is reported. A 46-years-old-female with a history of SLE starting in 1975 was admitted to our hospital in February 1991 for lupus nephritis. Steroid pulse therapy, 1000 mg methyl-prednisolone for 3 successive days as one therapy unit, was administered. Proteinuria improved remarkably, however, general fatigue and headache appeared 2 weeks after initiation of therapy. Endocrinological examination revealed hypopituitarism including the levels of TSH, FSH, GH and ACTH. The secretion of FSH and LH gradually improved after replacement therapy of dried thyroid. MRI examination of the brain revealed an empty sella. It is known that pituitary tumor, cerebrovascular accident and autoimmune lymphocytic hypophysitis cause hypopituitarism. In this case, it is unlikely that the pulse therapy may be responsible for the infarction of the anterior pituitary artery furthermore, there has been no articles describing such incidence after steroid pulse therapy. This case may be indicative of a very rare case in which the empty sella might have been exacerbated by the pulse therapy in the causation of hypopituitarism.
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PMID:[Hypopituitarism associated with empty sella after steroid pulse therapy in a patient with SLE]. 814 29

Obstruction of the internal carotid artery by a pituitary tumor is a rare occurrence, particularly in the absence of pituitary apoplexy. A cas of occlusion of the right internal carotid artery caused by a nonhemorrhagic pituitary adenoma is reported. The patient presented with a 3-month history of headaches and a progressive loss of vision in his right eye, leading to sudden complete right-sided blindness on the day of admission. Except for the visual system, the patient's clinical examination revealed nothing remarkable. There was complete restoration of blood flow in the internal carotid artery after emergency transsphenoidal resection of the tumor was performed. The patient's vision also substantially improved shortly after the surgery. Neurodiagnostic correlation, using various imaging studies, is presented. This cas also demonstrates the importance of using magnetic resonance imaging with and without contrast to demonstrate complete occlusion or thrombosis in the affected vessel.
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PMID:Nonhemorrhagic pituitary macroadenoma producing reversible internal carotid artery occlusion: case report. 884 74

In 1992, we reported a lymphocytic adenohypophysitis (LIH) (Neurol Med Chir). We considered this case unusual in that the case was that of a menopausal female and that it was accompanied with diabetes insipidus as classical lymphocytic adenohypohysitis (LAH). Subsequently, Ahmed reported two cases which presented a similar pathological manifestation, except for necrosis, as did our case and named them "necrotizing infundibulo-hypophysitis." Recently we encountered another similar case, which is reported hereunder. A female, 34 years of age, had suffered from headache, polyuria, and amenorrhea. CT scan showed a pituitary mass, and pituitary tumor was surgically removed transcranially at a local hospital. The pathological examination revealed the findings of chronic inflammation and necrosis. One month after the operation, however, she was an in-patient again under the suspicion of meningitis for fever and, when antibiotic therapy at the local hospital resulted in no improvement, she was referred to our hospital. Endocrinological studies showed low FSH, LH, ACTH and plasma cortisol level. Antibodies of serum to RNP, Sm, mitochondria, nucleus, AChR, and DNA were all negative. Because of an intrasellar mass with suprasellar extension on MRI, transsphenoidal operation was conducted four months after the initial operation. The pathological examination revealed the infiltration of lymphocytes, plasma cells, and foamy macrophages, and necrosis. After this operation, the headache was cured and the patient was discharged. Two months subsequent to the second operation, headache recurred and temporal upper quadrantic anopsia was noted. An enlarged tumor was found, but prednisolone worked to cure the pain and the visual field defect was found to have been remedied. The patient's diabetes insipidus is presently persisting, and she still relies on the use of desmopressin acetate and is still in need of cortisol replacement therapy. Including our cases, ten cases of lymphocytic hypophysitis, not related to pregnancy or delivery but with diabetes insipidus, have been reported. Several clinical and anatomical features distinguish these 10 cases from classical LAH. The classical LAH was predominantly related to pregnancy or delivery. However 6 of 10 cases were male in LIH. LAH related to pregnancy or delivery does not accompany diabetes insipidus, but all reported cases of LIH had a diabetes insipidus. Visual field and/or ocular movement disturbance are LAH's chief complaints (15 out of 25 cases) but visual field disturbance seldom occurs in LIH (1 out of 10 cases). Hypopituitarism is more serious in LAH, and 4 cases became fatal from an adrenal crisis. Anatomically, inflammatory change of LIH is located anterior and posterior to the pituitary gland and extends to the pituitary stalk and, at times, hypothalamus. On the other hand, LAH relates to pregnancy or delivery, the inflammatory change localizes to the adenohypophysis. Ahmed emphasized necrosis, while necrosis was not a prominent histological finding in LIH. Necrosis was noted only in 3 of 10 cases. To be stressed, rather, are the inflammatory changes seen on the neurohypophysis and the pituitary stalk, together with the characteristic diabetes insipidus. We believe, in view of the above, that what Ahmed named necrotizing infundibulo-hypophysitis should be named "LIH with diabetes insipidus." Whereas differential diagnosis is necessary between this said new disorder and the conventional LAH, we advocate that the latter, which is related to pregnancy or parturition but is free from neurohypophysitis be identified as "LAH related to pregnancy or delivery." With respect to treatment, steroid therapy is essential. If the symptoms do not improve, a transsphenoidal operation for diagnosis (LIH and LAH) and decompression (the case of LAH with visual or external ocular movement disturbance) is advisable. However, extensive surgery is not recommended, because per
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PMID:[Lymphocytic infundibulo-hypophysitis with diabetes insipidus as a new clinical entity: a case report and review of the literature]. 902 95

The case history of a 54-year-old male suffering from pituitary macroadenoma with suprasellar extension is reported. A TRH-test with 200 micrograms i.v. was followed by severe headache and vomiting after 60', and by development of ophthalmoplegia on the following day. Hyperdens patches on the CT scan showed haemorrhage into the tumor. A chromophobic adenoma with macroscopic and histological signs of haemorrhage was removed via the transsphenoidal route. In the postoperative period the ophthalmoplegia gradually disappeared but central hypoadrenia and hypothyroidism occurred. This is the second case in the literature showing that TRH alone and in a low dose may cause pituitary tumor apoplexy. It is concluded that TRH-testing is a risk for the patient with pituitary apoplexy. If, due to the size of the tumor the patients have to be operated on in any case, and the test is not of essential diagnostic value, the TRH-test should be done only in selected cases. Its use in the postoperative evaluation however is without risk for the patients.
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PMID:Apoplexy of a pituitary macroadenoma as a severe complication of preoperative thyrotropin-releasing hormone (TRH) testing. 928 12

We report the case of a 31-year-old woman with a pituitary adenoma who suffered symptomatic pituitary apoplexy. The patient developed a severe headache 2 min after undergoing a combined anterior pituitary function (CAP) test. Emergent computed tomography revealed a hemorrhagic pituitary tumor with evidence of a small subarachnoid hemorrhage. The headache improved spontaneously within half a day. Transsphenoidal surgery was performed 4 days later. Histologic examination demonstrated that the tumor was an eosinophilic adenoma with areas of diffuse hemorrhage. Although pituitary apoplexy caused by endocrinological testing has been reported in only 28 patients, apoplexy caused by a CAP test has been reported in only 1 patient. All of the previous cases had pituitary macroadenomas, 69% of which were involved in suprasellar extension. Non-functioning adenomas (24%) and prolactinomas (24%) were the most often affected by endocrine stimulation tests. With respect to the stimulants of pituitary adenomas, gonadotropin-releasing hormone (76%), TSH-releasing hormone (69%), and insulin (34%) were primarily responsible for the apoplexy. This case report with the literature review suggests that routine testing on pituitary function should be ordered cautiously given the risk of possible apoplexy.
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PMID:Pituitary apoplexy induced by a combined anterior pituitary test: case report and literature review. 979 Feb 75

A 32-year-old woman presented with severe headache, photophobia, fever, nausea, vomiting, and worsening vision. She had also noted several months of amenorrhea. She was febrile to 38.9 degrees C. Laboratory evaluation revealed a markedly elevated erythrocyte sedimentation rate. Lumbar puncture revealed a cerebrospinal fluid lymphocytic pleocytosis and an elevated protein level. Endocrine studies revealed evidence of panhypopituitarism without diabetes insipidus. A magnetic resonance imaging study showed a 2-cm pituitary mass with optic chiasmal compression. The patient had a trans-sphenoidal resection of the mass. Pathology revealed multinucleated giant cells in necrotic debris, but no evidence of pituitary tumor. Studies looking for evidence of systemic granulomatous disease were negative. The patient was considered to have idiopathic giant-cell granulomatous hypophysitis. After surgery, the patient's vision improved and hormone replacement therapy was initiated. This case illustrates that idiopathic giant-cell granulomatous hypophysitis should be considered in the differential diagnosis of a patient presenting with a pituitary mass, hypopituitarism, and meningitis-like symptoms.
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PMID:Idiopathic giant-cell granulomatous hypophysitis mimicking acute meningitis. 1055 98

In this open sequential study we evaluated the long-term effectiveness and tolerability of the i.m. administration of slow release lanreotide 30 mg (SRL) in 18 acromegalics (7 M/11 F, age 50.9+/-12.7 yr). Baseline mean GH and IGF-1 levels were 15.8+/-6.6 ng/ml and 702+/-74 ng/ml, respectively. Four hours, 1, 7, and 14 days after SRL, mean GH levels were 8.9+/-5.9 (p < 0.005), 11.4+/-6.9 (p < 0.05), 9.1+/-4.5 (p < 0.05), and 9.1+/-4.1 ng/ml (p < 0.05), respectively; and the IGF-1 values at 1, 7, and 14 days were 624+/-77 (p < 0.05), 555+/-83 (p < 0.001), and 467+/-58 ng/ml (p < 0.0001), respectively. Four hours after SRL administration GH was < 2.5 ng/ml in 11 patients and decreased 85% of the basal value, without normalizing, in another case. In the following 2 weeks, 7 and 2 patients maintained GH < 2.5 ng/ ml or < 50% of baseline; 3 and 2 of them attained IGF-1 values in the normal range or < 50% of basal levels. A patient developed acute pancreatitis after the injection of the drug and therefore stopped the treatment. Another patient did not continue SRL, and she was turned on octreotide, s.c. administered (OCT), because only the latter treatment ameliorated significantly the headache. In 16/18 patients the treatment was continued until the 24th month. SRL was administered every 14 days until the 24th month in 3 cases, whereas in 13 patients the dose schedule was increased every 10 days since the 7th month because they did not normalize serum GH and IGF-1 levels. In these 16 patients baseline GH and IGF-1 levels were 10.0+/-2.5 ng/ml and 671+/-75 ng/ml, respectively. At the 1st, 3rd, and 6th month of treatment mean GH levels fell to 5.4+/-1.4 (p < 0.05), 5.3+/-1.8 (p < 0.05), and 5.0+/-1.6 (p < 0.05) ng/ml, respectively; and IGF-1 declined to 511+/-87 (p < 0.005), 565+/-85 (p < 0.05), and 525+/-94 (p < 0.01) ng/ml, respectively. Throughout the first semester GH was < 2.5 ng/ml in 5 patients and decreased > 50% in another three. IGF-1 levels normalized in 3/5. Throughout the following 18 months of treatment, mean GH (3.4+/-1.0 ng/ml) and IGF-1 (413+/-75 ng/ml) values decreased significantly in comparison with both the baseline concentrations (GH p < 0.01, IGF-1 p < 0.001) and the levels measured during the 1st semester of treatment (GH p < 0.05, IGF-1 p < 0.001). GH remained < 2.5 ng/ml in 11 patients, and in 8/11 cases IGF-1 fell in the normal range. Serum GH and IGF-1 levels decreased by more than 50% of baseline levels in 2 other cases. At MRI, pituitary adenoma was no longer evident in one patient previously treated with OCT and significantly decreased in another patient previously treated with surgery plus radiotherapy, as well as in a patient previously untreated. During treatment the percentage of patients complaining of headache and fatigue decreased significantly (chi2, p < 0.05 and p < 0.0005, respectively). Overall, the headache (p < 0.005), arthralgia (p < 0.05), and paresthesia (p < 0.01) ameliorated significantly. Ultrasound scan showed gallbladder sludge or sand-like stones in 5/11 patients. This study, which is one of the longest surveys on a relatively large series of acromegalics treated with SRL, confirms the long-term effectiveness of this drug for the treatment of patients with active acromegaly. SRL decreases significantly GH and IGF-1 in most cases and induces the shrinkage of the pituitary tumor in some patients previously either untreated or both treated for acromegaly. SRL improves significantly clinical symptoms and it is well tolerated.
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PMID:Results of a two-year treatment with slow release lanreotide in acromegaly. 1089 51


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