title: Expression of follicle-stimulating hormone receptor in vascular anomalies.
abstract: BACKGROUND
  The mechanism for the growth of infantile hemangioma and vascular malformations is unknown. Follicle-stimulating hormone secretion mirrors the life cycle of infantile hemangioma and increases during adolescence, when vascular malformations often progress. The purpose of this study was to determine whether vascular anomalies express the receptor for follicle-stimulating hormone.
  
  
  METHODS
  Human vascular tumors (i.e., infantile hemangioma, congenital hemangioma, kaposiform hemangioendothelioma, and pyogenic granuloma) and vascular malformations (i.e., capillary, lymphatic, venous, and arteriovenous) were subjected to immunofluorescence for follicle-stimulating hormone receptor. Control specimens included normal skin/subcutis, mucosa, liver, spleen, Crohn disease, granulation, pancreatitis, rheumatoid arthritis, and synovitis. Receptor and microvessel density were quantified using imaging software.
  
  
  RESULTS
  Follicle-stimulating hormone receptor was found in the endothelium of all vascular anomalies but was not present in control specimens. Expression was greater in proliferating infantile hemangioma (6.0 percent) compared with other vascular tumors (congenital hemangioma, 0.61 percent; kaposiform hemangioendothelioma, 0.55 percent; pyogenic granuloma, 0.56 percent; p < 0.0001), despite similar microvessel density (p = 0.1). Follicle-stimulating hormone receptor was elevated in arteriovenous malformations (2.65 percent) compared with other types of vascular malformations (capillary, 1.02 percent; lymphatic, 0.38 percent; venous, 0.76 percent; p < 0.0001).
  
  
  CONCLUSIONS
  Vascular anomalies express follicle-stimulating hormone receptor on their endothelium, in contrast to vascular control tissues. Vascular anomalies are the only benign, pathologic tissue known to express this receptor. Because the secretion of follicle-stimulating hormone correlates with the growth pattern of infantile hemangioma and vascular malformations, follicle-stimulating hormone might be involved in the pathogenesis of these lesions.
authors.affiliation: Boston, Mass. From the Departments of Plastic and Oral Surgery, Pathology, Medicine, and Surgery, Vascular Anomalies Center Boston Children's Hospital, Harvard Medical School.
authors.forename: Reid A
authors.initials: RA
authors.lastname: Maclellan
authors.forename: Matthew P
authors.initials: MP
authors.lastname: Vivero
authors.forename: Patricia
authors.initials: P
authors.lastname: Purcell
authors.forename: Harry P
authors.initials: HP
authors.lastname: Kozakewich
authors.forename: Amy D
authors.initials: AD
authors.lastname: DiVasta
authors.forename: John B
authors.initials: JB
authors.lastname: Mulliken
authors.forename: Steven J
authors.initials: SJ
authors.lastname: Fishman
authors.forename: Arin K
authors.initials: AK
authors.lastname: Greene
mesh_terms: D002648:Child; D002675:Child, Preschool; D005260:Female; D017789:Granuloma, Pyogenic / Q000378:metabolism; D006391:Hemangioma / Q000378:metabolism; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D011962:Receptors, FSH / Q000096:biosynthesis*; D054079:Vascular Malformations / Q000378:metabolism*; D019043:Vascular Neoplasms / Q000378:metabolism*
chemical_list: D011962:Receptors, FSH