BACKGROUND: Type 1 diabetes (T1D) patients are at risk for additional autoimmune diseases (AID). OBJECTIVE: To compare the characteristics of associated autoimmunity among familial (parent-offspring and sib-pair) subgroups and sporadic T1D patients. PATIENTS AND METHODS: Data regarding AID in T1D patients and their nuclear family members were extracted from medical files of 121 multiplex T1D families (58 parent-offspring, 63 sib-pairs) and 226 sporadic controls followed between 1979 and 2008. RESULTS: The prevalence of associated autoimmunity was similar in familial and sporadic cases (33.6 vs. 32.7%). The frequency of additional AID and percentage of patients with two or more coexistent AID were significantly higher among sib-pairs than parent-offspring (p = 0.05 and p = 0.04, respectively). The median time elapsed between diagnosis of T1D and occurrence of additional autoimmunity tended to be shorter in the sib-pairs. Only in familial cases did a positive autoimmune family background predict the development of coexistent autoimmunity (OR = 2.11, CI [1.0, 4.49] p = 0.05). CONCLUSIONS: Among sib-pairs with T1D, the higher prevalence of additional AID, the increased number of diseases per person, and the relatively earlier appearance of associated AID suggest an increased susceptibility for coexistent autoimmunity in this subgroup. Positive family history for autoimmunity in multiplex T1D families increased their risk for co-occurrence of AID.
BACKGROUND:Type 1 diabetes (T1D) patients are at risk for additional autoimmune diseases (AID). OBJECTIVE: To compare the characteristics of associated autoimmunity among familial (parent-offspring and sib-pair) subgroups and sporadic T1D patients. PATIENTS AND METHODS: Data regarding AID in T1D patients and their nuclear family members were extracted from medical files of 121 multiplex T1D families (58 parent-offspring, 63 sib-pairs) and 226 sporadic controls followed between 1979 and 2008. RESULTS: The prevalence of associated autoimmunity was similar in familial and sporadic cases (33.6 vs. 32.7%). The frequency of additional AID and percentage of patients with two or more coexistent AID were significantly higher among sib-pairs than parent-offspring (p = 0.05 and p = 0.04, respectively). The median time elapsed between diagnosis of T1D and occurrence of additional autoimmunity tended to be shorter in the sib-pairs. Only in familial cases did a positive autoimmune family background predict the development of coexistent autoimmunity (OR = 2.11, CI [1.0, 4.49] p = 0.05). CONCLUSIONS: Among sib-pairs with T1D, the higher prevalence of additional AID, the increased number of diseases per person, and the relatively earlier appearance of associated AID suggest an increased susceptibility for coexistent autoimmunity in this subgroup. Positive family history for autoimmunity in multiplex T1D families increased their risk for co-occurrence of AID.
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Authors: Lindsey A Criswell; Kirsten A Pfeiffer; Raymond F Lum; Bonnie Gonzales; Jill Novitzke; Marlena Kern; Kathy L Moser; Ann B Begovich; Victoria E H Carlton; Wentian Li; Annette T Lee; Ward Ortmann; Timothy W Behrens; Peter K Gregersen Journal: Am J Hum Genet Date: 2005-02-17 Impact factor: 11.025
Authors: M R Velaga; V Wilson; C E Jennings; C J Owen; S Herington; P T Donaldson; S G Ball; R A James; R Quinton; P Perros; S H S Pearce Journal: J Clin Endocrinol Metab Date: 2004-11 Impact factor: 5.958
Authors: P Peterson; H Salmi; H Hyöty; A Miettinen; J Ilonen; H Reijonen; M Knip; H K Akerblom; K Krohn Journal: Clin Immunol Immunopathol Date: 1997-01
Authors: Olga Kordonouri; Albrecht Klinghammer; Egbert B Lang; Annette Grüters-Kieslich; Matthias Grabert; Reinhard W Holl Journal: Diabetes Care Date: 2002-08 Impact factor: 19.112
Authors: Deborah Smyth; Jason D Cooper; Joanne E Collins; Joanne M Heward; Jayne A Franklyn; Joanna M M Howson; Adrian Vella; Sarah Nutland; Helen E Rance; Lisa Maier; Bryan J Barratt; Cristian Guja; Constantin Ionescu-Tîrgoviste; David A Savage; David B Dunger; Barry Widmer; David P Strachan; Susan M Ring; Neil Walker; David G Clayton; Rebecca C J Twells; Stephen C L Gough; John A Todd Journal: Diabetes Date: 2004-11 Impact factor: 9.461