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Journal of Neurosurgical Sciences 1999 March;43(1):25-36

Copyright © 1999 EDIZIONI MINERVA MEDICA

language: English

Pituitary apoplexy. Clinical course, endocrine evaluations and treatment analysis

Casulari Roxo da Motta L. A., Andrade de Mello P., Moreira de Lacerda C., Pereira NEto A., Dominigues Casulari da Motta L., Farage Filho M.

Neurosurgery Unit, Hospital de Base do Distrito Federal (UNC-HBDF), Brasilia, Brasil


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Background. ­The pur­pose ­was to ana­lyze clin­i­cal man­i­fes­ta­tions, hor­mo­nal chang­es, diag­no­sis dif­fi­cul­ties ­and treat­ment of pitui­tary apo­plexy (PA).
Experi­men­tal ­design. A ret­ro­spec­tive ­study of clin­i­cal ­records ­from ­patients ­with pitui­tary aden­o­mas admit­ted ­from Jan­u­ary 1980 to ­June 1996; ­the pur­pose ­was to iden­ti­fy ­the ­patients ­with clin­i­cal evi­dence com­pat­ible ­with PA. Set­ting. Neu­ro­sur­gery ­unit of an insti­tu­tion­al hos­pi­tal. ­Patients. Six­teen (12.8%) of 125 ­patients ­with pitui­tary aden­o­mas ­were ana­lyzed ­because ­they ­had pitui­tary apo­plexy. Inter­ven­tions. Sur­gi­cal treat­ment by ­the trans-­sphe­noid­al or trans­cra­ni­al ­route or ­both ­routes; dex­a­meth­a­sone (­DXM) treat­ment ­with 16 mg/­day i.v. Meas­ures. Hor­mone ­assays ­were per­formed ­either by radio­im­mu­noas­say or by chem­i­cal lumi­nes­cence.
­Results.­Tumors ­were non­func­tion­ing in ­nine ­patients ­and func­tion­ing in sev­en. ­TSH ­and pro­lac­tin ­basal ser­um lev­els ­were ­impaired in 55.5% ­and 10%, respec­tive­ly; ­after exog­e­nous ­TRH 80% of ­the ­patients ­did ­not ­show stim­u­la­tion of ­TSH ­and pro­lac­tin secre­tions. LH ­and ­FSH lev­els ­were ­low in 63.6% ­and 54.6% of ­the ­patients, respec­tive­ly; gon­a­dot­ro­phin-releas­ing hor­mone (­GnRH) test­ing ­was abnor­mal in 75% of ­the ­patients eval­u­at­ed. Cor­ti­sol lev­els ­were ­low in 50% of ­the ­patients. ­After insu­lin-­induced hypo­gly­ce­mia, cor­ti­sol ­and GH ­failed to ­rise in 25% ­and 40% of cas­es, respec­tive­ly. ­Ten ­patients ­were sub­mit­ted to sur­gi­cal treat­ment, ­but ­none dur­ing PA. ­The aver­age ­time ­from ­the ­onset of apo­plec­tic symp­toms ­and sur­gery ­was 70±50 ­days. ­Only ­one ­patient ­died ­two ­months ­after sur­gery. ­Five ­patients ­were treat­ed ­with dex­a­meth­a­sone (­DXM) dur­ing ­the apo­plec­tic symp­toms: ­three ­patients ­died; ­one ­patient ­had ­good qual­ity of ­life; ­the oth­er ­patient ­was treat­ed initial­ly ­with ­DXM ­with improve­ment of ­vision, ­but ­after sur­gery he devel­oped pan­hy­po­pit­uir­ar­ism. ­Two oth­er ­patients ­did ­not ­receive spe­cif­ic treat­ment ­for PA.
Con­clu­sions. PA is ­not a ­rare pitui­tary aden­o­ma com­pli­ca­tion ­and ­its prog­no­sis ­may be ­poor; base­line hor­mone lev­els ­showed a ­wide ­range of abnor­mal­ities of pitui­tary func­tion; sur­gi­cal treat­ment ­was ­required in ­the major­ity of ­patients ­and ­the prog­no­sis ­was rel­a­tive­ly ­good; on ­the con­trary, ­the treat­ment ­with ­DXM ­only ­had ­high lev­els of mor­tal­ity.

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