In schizophrenia, when treatment using antipsychotics fails, lithium, which is known as an antimanic drug, can also be administered. It is reported that 12~20% of patients taking lithium develop nephrogenic diabetes lactotrophs. Hyperprolactinemia is induced by typical antipsychotics, as they block the dopamine-2 receptors of latotrophs in the pituitary gland. Therefore, atypical antipsychotics for decreasing the side effect, such as hyperprolactinemia, can be used. However, hyperprolactinemia can be induced by risperidone, one of the atypical antipsychotics. Here, a case of drug induced nephrogenic diabetes insipidus and simultaneous hyperprolactinemia, which occurred in a patient with schizophrenia, is reported.
Antipsychotic Agents ; Diabetes Insipidus, Nephrogenic* ; Humans ; Hyperprolactinemia* ; Lactotrophs ; Lithium ; Pituitary Gland ; Risperidone ; Schizophrenia*

This study was performed in order to establish the culture system optimal for the study on pituitary prolactin cells using growth factor and extra cellular matrix components as the culture substrate. The effect of epidermal growth factor (EGF) alone or along with extracellular marix components on GH3 cell growth and PRL expression was assessed using cell count, BrdU-immunocytochemistry and PRL-immunocytochemistry in in vitro cultures on plastic, laminin and Matrigel. EGF decreased the cell growth, BrdU-labeling and increased the PRL-immunoreactive cells regardless of the culture substrate by day 3 of the culture. Matrigel was the best culture substrate to decrease the cell growth and to increase the PRL expression. EGF treatment in the Matrigel culture showed about 80.5% of PRL-immunoreactive cells by day 6 of the culture. These results indicated that Matrigel is the better culture substrate than plastic or laminin to inhibit the overgrowth and to increase the prolactin expression of the GH3 cell and that EGF and Matrigel causes very effective culture environment for the long-term culture of the GH3 cell by synergistic mechanism.
Cell Count ; Epidermal Growth Factor* ; Extracellular Matrix* ; Lactotrophs ; Laminin ; Pituitary Neoplasms* ; Plastics ; Prolactin

BACKGROUNDS: Pituitary hyperplasia can mimic pituitary adenoma. In MRI, enlarged pituitary gland is enhanced homogenously with upward convexity of the superior margin of the gland .The best definition of hyperplasia in the pituitary hyperplasia seems to be a multiplication of one or more cell types. But definition, etiology and clinical courses of this disease are not clear, METHOD: We reviewed clinical symptoms, MRI, and pathologic findindings in 6 patients with pituitary hyperplasia. RESULT: 1. Major clinical symptoms were headache (100%), visual field defect (84%), polyuria/polydipsia (64%), and irregular mensturation (32%). Other symptoms were amenorrhea (16%) and galactorrhea (16%). 2. Three of five cases showed abnormal responses to combined pituitary function test, 3. MRI findings were pituitary hyperplasia (4), macroadenoma (l), and microadenoma (1). 4. In two operated cases, there was no adenoma. One case showed hyperplasia of lactotroph cells, the other was hyperplasia of gonadotroph cells confirmed by the examination of immunocytochemistry. CONCLUSION: Pituitary hyperplasia should be considered in patients with enlarged pituitary gland without focal mass lesion.
Adenoma ; Amenorrhea ; Female ; Galactorrhea ; Gonadotrophs ; Headache ; Humans ; Hyperplasia* ; Immunohistochemistry ; Lactotrophs ; Magnetic Resonance Imaging ; Pituitary Function Tests ; Pituitary Gland ; Pituitary Neoplasms ; Pregnancy ; Visual Fields

Background: Prolactin(PRL) secretion is tonically inhibited by doparnine that originates from the hypothalamic tuberoinfundibular tract and reaches the lactotroph via the hypophyseal portal vessel. Hyperprolactinemia associated with oligomenorrhea-amenorrhea, galactorrhea and/or infertility is mainly due to PRL-secreting pituitary adenoma(PA). The diagnosis of idiopathic hyperprolac- tinemia(IHP) is made, when hyperprolactinemia is sustained and all causes of hyperprolactinemia are excluded without radiological abnormality. It is not known, whether IHP and PA are two distinct entities or two subsequent phases of the same disease. The etiology of both disorders remains unresolved. We investigated that PRL hypersecretion in patients with IHP and PA may be the result of a defect in the central nervous system(CNS)-dopamine release, and that there may be some differences in pathogenesis of both diseases. Methods: We measured 24 hour-urinary dopamine, norepinephrine, epinephrine, and serum and 24 hour-urinary VMA(vanillyl rnandelic acid), HVA(homovanilic acid), DOPAC(3,4-dihydroxy phenylaceticacid), MHPG(3-methoxy 4-hydroxy phenylglycol) in 10 normal controls, 9 patients with IHP, and 17 patients with PA in the early follicular phase. Results: Urinary HVA and DOPAC concentrations, the major metabolites of CNS dopaminergic activity, were signficantly lower in both patients with IHP and PA compared with those in normal controls(p 0.05), whereas they were not different in both disease groups. Dopamine, norepine-phrine, epinephrine, MHPG concentrations were similar to those of the normal controls. Although VMA concentrations of both disease groups were significantly higher than those of normal controls, all of them were within normal range. Conelusion: Although our data are unable to establish the precise biochemical defect responsible for central dopamine deficiency in pathogensis of IHP and PA, we can support the presence of a pathological reduction of brain dopamine activity in IHP and PA.
3,4-Dihydroxyphenylacetic Acid ; Brain ; Diagnosis ; Dopamine ; Epinephrine ; Female ; Follicular Phase ; Galactorrhea ; Humans ; Hyperprolactinemia ; Infertility ; Lactotrophs ; Methoxyhydroxyphenylglycol ; Norepinephrine ; Pregnancy ; Prolactinoma ; Reference Values