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Table 2 Impact of puberty on autoimmune rheumatic disease-related outcomes (listed as per year of publication)

From: A systematic review exploring the bidirectional relationship between puberty and autoimmune rheumatic diseases

First author, year of publication Type of study Country of origin Participants, disease
N (F:M)
Study groups, comparison Ethnic group Disease outcomes measured Results Quality of the study using the Newcastle-Ottawa scale /9
Abdawani et al., 2019 [34] Retrospective cohort Oman
Single Centre
103 JSLE patients
39 (27:12) pre-pubertal onset
Mean age 5.12 ± 1.98 years
29 (24:5) pubertal onset
Mean age 10.8 ± 0.99 years
35 (32:3) post-pubertal onset
Mean age 15.3 ± 1.59 years
JSLE patients stratified based on pubertal status at disease onset Arab Association between clinical manifestations and antibody frequencies in JSLE patients stratified based on pubertal status at disease onset Increased renal disease in pre-pubertal compared to pubertal and post-pubertal groups, respectively (51% vs 23% vs 20%; P = 0.039)
Pre-pubertal onset JSLE had a higher incidence of cutaneous manifestations than the post-pubertal group (74% vs 46%; P = 0.029)
Pre-pubertal onset JSLE had increased frequencies of anti-cardiolipin antibodies (47%), anti-glycoprotein antibodies (42%), ANCA (62%), and low complement levels (97%)
Pre-pubertal group also has the lowest frequency of positive SSA antibodies (18%) and SSB antibodies (5.1%)
Sperotto et al., 2014 [35] Prospective cohort Italy
4 centres
261 (137:124) baseline healthy children
184 pre-pubertal
77 pubertal
Mean age 10.6 (range 8–13) years
3 year-follow-up of pre-pubertal and pubertal children with ANA positivity (n = 32) or chronic musculoskeletal pain (n = 77) at baseline Not stated Musculoskeletal chronic pain assessed by rheumatologic examination, ANA, dsDNA and ENA antibody titres Already positive ANA titres increased in value during puberty (P = 0.002).
ANA positivity has no relationship with chronic non-inflammatory musculoskeletal pain.
After puberty, more females than males were ANA positive (50% vs 28%)
Hoeve et al., 2012 [36] Retrospective cohort The Netherlands
Multi centre
62 (40:22) patients with JIA-associated uveitis
Mean age at diagnosis of uveitis 4.9 ± 1.7 years
Follow-up of patients before, after and during puberty Not stated Influence of puberty on the long-term course of uveitis Similar incidence of cystoid macular oedema and papillitis between pre-puberty and in-puberty, but more boys developed ocular hypotony during puberty compared to pre-puberty (P = 0.026)
More systemic treatment for uveitis was required for girls during puberty compared to pre-puberty (P < 0.001)
JIA-associated uveitis encompasses a biphasic course: a high initial disease activity, followed by a quiet stage and a new wave of activity during early teenage years.
Hui-Yuen et al., 2011 [37] Retrospective cohort USA
Single centre
34 (27:7)
pre-pubertal JSLE
34 (27:7)
pubertal JSLE
Age at diagnosis
Pre-pubertal 8.7 ± 2.6 Post-pubertal 14.8 ± 2.0 years
Pre pubertal (Tanner I-II) patients were matched to pubertal (Tanner III-V) patients African-American, Asian, Caucasian, Hispanic, Other Clinical and lab characteristics, medication use, organ involvement, paediatric intensive care unit (PICU) admissions, disease activity. Early onset JSLE (pre-pubertal):
-required greater number of PICU admissions (18 vs. 5, P = 0.01)
-required higher daily steroid dose (0.6 mg/kg prednisone-equivalent versus 0.2 mg/kg, P < 0.05)
-received cyclophosphamide earlier in their disease course (mean 13.7 versus 19.9 months, P < 0.001)
Descloux et al., 2009 [38] Retrospective cohort France
Single centre
56 (39:17) JSLE patients
Mean age at disease onset
12.6 ± 3.2 years (median 13 years)
JSLE patients with damage were compared with those without damage Caucasian, Afro-Caribbean, Asian, Middle Eastern Damage as measured by SDI or death. The risk of damage (SDI ≥ 1) significantly decreased when age at disease onset increased (89% in pre-pubertal JSLE, 57% in peri-pubertal JSLE and 38% in post-pubertal JSLE) (P = 0.032) 7/9
Costenbader et al., 2007 [39] Prospective cohort UK
NHS (Nurses’ Health Study) and NHSII UK national data base of female nurses
238,308 (238,308:0) women from two national cohorts
121,700 ages 30–55 years
116,608 ages 25–42 years
Nurses who developed SLE were compared to the ones who did not Caucasian (> 97%), African, and Hispanic. Development of SLE. 262 incident cases of SLE were confirmed.
In multivariable models adjusted for reproductive and other risk factors, age less than 10 years at menarche (pooled RR 2.1, 95% confidence interval [95% CI] 1.4–3.2) was associated with development of SLE.
Pluchinotta et al., 2007 [40] Retrospective cohort Italy
Single centre
42 JSLE patients + 11 infantile JSLE cases reported in literature
13 (1.2:1) infantile (age of diagnosis < 2 years old)
11 (1.2:1) pre-pubertal (age of diagnosis 2–10 years)
29 (6.3:1) post-pubertal (age of diagnosis 10–16 years)
Comparison between infancy, prepubertal and post-pubertal JSLE patients Caucasian (92%), Indian,
African American
Prevalence and severity of organ involvement, blood count and auto-antibodies. Infantile JSLE was more severe than childhood SLE with a higher prevalence of cardiovascular (P < 0.05) and pulmonary involvement (P < 0.05), anaemia (P < 0.05) and thrombocytopenia (P < 0.01)
Post-pubertal patients had a higher frequency of musculoskeletal involvement (P < 0.005) and leukopenia.
Silva et al., 2002 [31] Retrospective cohort Brazil
Single centre
23 (23:0) SLE patients
Age range 16.75–22.83 years
No; compared to historical healthy control data on 2578 Brazilian adolescents Not stated Disease duration, cumulative prednisone dose, disease activity measured by SLEDAI Delay in menarche correlated positively with disease duration (P = 0.0085) and cumulative dose of prednisolone prior to menarche (P = 0.0013).
Gonadal function did not correlate with mean SLEDAI score.