Table 2 Impact of puberty on autoimmune rheumatic disease-related outcomes (listed as per year of publication)
First author, year of publication | Type of study | Country of origin | Participants, disease N (F:M) Age | 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%) | 7/9 |
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%) | 5/9 |
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. | 6/9 |
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) | 6/9 |
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. | 9/9 |
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. | 6/9 |
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. | 6/9 |