title: Excessive paternal transmission in psoriatic arthritis.
abstract: OBJECTIVE
  The differential expression of a disease according to the sex of the disease-transmitting parent has been demonstrated in several autoimmune disorders. The purpose of the present study was to determine whether there are differences in the transmission and expression of psoriatic arthritis (PsA) that are dependent on the sex of the affected parent.
  
  
  METHODS
  All probands (patients with PsA) were identified from among the patients attending the University of Toronto Psoriatic Arthritis Clinic. A self-reported family history of psoriasis or PsA was noted for each proband. Differences in parental and offspring transmission with respect to the proband were evaluated. In addition, the expression of PsA according to the sex of the affected parent was assessed at the time of the proband's presentation to the clinic.
  
  
  RESULTS
  Ninety-five probands had affected parents: 62 (65%) had an affected father, and 33 (35%) had an affected mother. Thus, the proportion of paternal transmission (0.65) was significantly greater than was expected (0.5) (P = 0.001). Twelve of 74 offspring from male probands (16.2%) were affected with psoriasis or PsA, as compared with 9 of 108 offspring from female probands (8.3%) (P = 0.10). Probands whose fathers were affected had a higher frequency of skin lesions prior to arthritis (P = 0.047), an erythrocyte sedimentation rate > 15 mm/hour (P = 0.044), and a lower incidence of rheumatoid factor (P = 0.044). No differences were noted with respect to age at the onset of psoriasis or PsA, the severity of the PsA, or the frequency of HLA antigens.
  
  
  CONCLUSIONS
  There appears to be excessive paternal transmission in PsA. Further clinical confirmation and elucidation of its genetic basis is warranted.
authors.affiliation: University of Toronto, Ontario, Canada.
authors.forename: P
authors.initials: P
authors.lastname: Rahman
authors.forename: D D
authors.initials: DD
authors.lastname: Gladman
authors.forename: C T
authors.initials: CT
authors.lastname: Schentag
authors.forename: A
authors.initials: A
authors.lastname: Petronis
mesh_terms: D000328:Adult; D015535:Arthritis, Psoriatic / Q000097:blood / Q000235:genetics*; D001175:Arthrography; D001799:Blood Sedimentation; D005220:Fathers; D005260:Female; D008040:Genetic Linkage / Q000235:genetics; D020022:Genetic Predisposition to Disease / Q000097:blood / Q000235:genetics*; D018392:Genomic Imprinting; D015395:Histocompatibility Antigens Class I / Q000097:blood; D000949:Histocompatibility Antigens Class II / Q000097:blood; D006801:Humans; D008297:Male; D008875:Middle Aged; D009035:Mothers; D012217:Rheumatoid Factor / Q000097:blood; D012867:Skin / Q000473:pathology
chemical_list: D015395:Histocompatibility Antigens Class I; D000949:Histocompatibility Antigens Class II; D012217:Rheumatoid Factor