title: Changes in the epithelium of Rathke cleft cyst associated with inflammation.
abstract: OBJECTIVE
  Rathke cleft cysts (RCCs) are composed of tall, well-differentiated, ciliated columnar epithelia. Their structures are altered by hyperplasia or squamous metaplasia, but their cause remains unknown.
  
  
  METHODS
  The authors studied pathological findings and anterior pituitary function in 20 patients harboring RCCs. They classified RCC epithelium as either single (a single ciliated columnar cell lining or a flattened cuboidal cell lining) or stratified (a stratified ciliated columnar cell lining, basal cell hyperplasia, columnar cell hyperplasia, or squamous metaplasia). Inflammation was classified as acute, subacute, chronic, or end stage. The epithelial cell lining was observed in 13 specimens obtained during surgery (six specimens contained single and seven contained stratified epithelia). Inflammation had penetrated the cyst epithelium or subjacent stroma in 10 patients, and the stage of inflammation correlated well with the type of epithelia group: early stages of inflammation in the single epithelium group and chronic or end-stage inflammation in the stratified epithelia (p = 0.0027). The adenohypophysis was identified in 21 surgical specimens. Postoperatively, growth hormone (p = 0.019), cortisol (p = 0.027), and thyroid-stimulating hormone (p = 0.039) responses significantly worsened as the inflammation progressed. The presence of diabetes insipidus correlated well with advanced stages of neurohypophysitis (p = 0.025).
  
  
  CONCLUSIONS
  Epithelial stratification in the RCC is caused by inflammation that may extend into the adjacent adenohypophysis or neurohypophysis and overwhelm the hypophysis, resulting in panhypopituitarism. Transsphenoidal excision may represent the best choice for treatment, at least for cases of RCC in which there is partial impairment of hypophysial function.
authors.affiliation: Department of Neurosurgery, Hiroshima University School of Medicine, Japan. ml-hns@hiroshima-u.ac.jp
authors.forename: Seiji
authors.initials: S
authors.lastname: Hama
authors.forename: Kazunori
authors.initials: K
authors.lastname: Arita
authors.forename: Takashi
authors.initials: T
authors.lastname: Nishisaka
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Fukuhara
authors.forename: Atsushi
authors.initials: A
authors.lastname: Tominaga
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Sugiyama
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Yoshioka
authors.forename: Kuniki
authors.initials: K
authors.lastname: Eguchi
authors.forename: Masayuki
authors.initials: M
authors.lastname: Sumida
authors.forename: Yuji
authors.initials: Y
authors.lastname: Heike
authors.forename: Kaoru
authors.initials: K
authors.lastname: Kurisu
mesh_terms: D000328:Adult; D000368:Aged; D020863:Central Nervous System Cysts / Q000473:pathology* / Q000503:physiopathology* / Q000601:surgery; D004848:Epithelium / Q000473:pathology* / Q000503:physiopathology* / Q000601:surgery; D005260:Female; D006801:Humans; D007249:Inflammation / Q000473:pathology* / Q000503:physiopathology* / Q000601:surgery; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D010903:Pituitary Gland, Anterior / Q000473:pathology* / Q000503:physiopathology* / Q000601:surgery; D010904:Pituitary Gland, Posterior / Q000473:pathology / Q000503:physiopathology / Q000601:surgery; D010911:Pituitary Neoplasms / Q000473:pathology* / Q000503:physiopathology* / Q000601:surgery; D012189:Retrospective Studies; D012720:Severity of Illness Index