Although thyroid antibodies and thyroid diseases are not included in the classification criteria for SLE, it is reasonable to explore the prevalence of thyroid disease in patients with SLE [9]. Thyroid dysfunction is more common in Juvenile SLE (JSLE) than in the general population. No statistics are available in Egypt about thyroid illnesses in (JSLE) [10]. Therefore, this study was conducted to detect the occurrence of thyroid dysfunction in Juvenile SLE patients for early detection and treatment to prevent morbidity.
This study included 50 patients, six of them were males (12%), and 44 were females (88%), with a (female-to-male ratio = 7:1), which ensures the importance of hormonal factors in the clinical expression of the disease.
This agrees with the study of Abd-Elnabi et al. [9] on the prevalence of JSLE in Egyptian children, which was performed on 40 patients with JSLE. This revealed a female to male ratio (7: 1). In addition, it is similar to the study carried out by El-Gamasy and El-Naghy [11] about the incidence, prevalence of JSLE and sex distribution. It shows that the prevalence was higher for girls. The total number of SLE patients was 80, 70 were females (87.50%), and ten were males (F: M ratio 7:1). This may be attributed to the different numbers of studied cases or may be due to differences in ethnic factors and genetic backgrounds.
In this study, age ranged from 7 to 15 years old with a median of 12 years, while the age of diagnosis ranged from 2 to 13.5 years with a median of 9 years. This is nearly similar to the study of Abd-Elnabi et al. [9] on the prevalence of JSLE in Egyptian children, where the mean age was 13.4 ± 2.54 years.
In this study, there were 32 patients (64%) with thyroid dysfunctions, 19 patients (38%) with euthyroid sick syndrome (normal TSH, low FT4, and normal or low FT3), ten patients (20%) with hypothyroidism (high TSH with low FT4, and normal or low T3), three patients (6%) with subclinical hypothyroidism (high TSH with normal FT4, and FT3), and none of the patients had hyperthyroidism.
Even if they do not have the clinical disease, SLE patients have a high frequency of biochemical abnormalities of thyroid function that are discovered accidentally while performing a thyroid profile [14].
In this study, anti-thyroglobulin antibodies (anti-TG) were normal in (100%) of patients in the studied group, and thyroid peroxidase antibodies (anti-TPO) were normal in 98% of patients and elevated in 2% of patients.
This study is against many of the studies, which found a high level of anti-TG, such as Abd-Elnabi et al. [9], where anti-TG was detected in eight patients (20%). Moreover, anti-TG has been found with greater frequency in SLE than in the general population, even in SLE patients who did not have clinical thyroid disease [15]. In addition, this agrees with the study of Assal et al. [16], which involved 30 juvenile SLE patients and found that anti-TG was detected in 6%.
Polyclonal activation of B-cells is responsible for autoantibody production. The use of glucocorticoid may blunt the immune response leading to a decrease in the appearance of these antibodies. The effect of immunosuppressive therapy on the production of anti-thyroid antibodies has not yet been elucidated. It could reduce the production of antibodies, which might explain the lack of anti-thyroid antibody production in SLE patients [17].
Another finding in the present study is that the mean SLEDAI was quite low, which suggests better observing thyroid autoantibody behavior in patients with mainly high disease activity. Anti-thyroid antibodies in SLE patients may have a fluctuating pattern over time. Some patients who tested positive at a certain point in their disease may test negative during follow-up visits [18].
This study showed a significant negative correlation between disease duration and serum T4, anti-TG, and anti-TPO levels of patients, while non-significant correlations between disease duration, TSH, and FT3. This was close to the study of Abd-Elnabi et al. [9], who found a significant negative correlation between disease duration and serum TSH, and anti-TG levels of patients, while non-significant correlations between disease duration, FT4, and FT3.
In this study, there was no significant correlation between anti-TG, TPO, TSH, FT3, and FT4, and disease activity, which was measured by the SLEDAI score. This agrees with the study of Posselt et al. [19], who found that disease activity and cumulative damage were unrelated to Hashimoto thyroiditis or autoantibodies.
Moreover, it agrees with the results of Franco et al. [20], to determine the prevalence and impact of autoimmune thyroid disease (AITD) and thyroid autoimmunity in patients with SLE who indicated that autoimmune thyroid disease in SLE is frequent and no correlation with severity of the disease.
In this study, regarding manifestations of SLE at the time of diagnosis, the most frequent manifestations were malar rash in 68% of patients, followed by arthritis in 66%, then photosensitivity in 62%, while 52% of patients had nephritis and the least had neurological manifestations, and none of them had the discoid rash.
This agrees with the study of Jebali et al. [12] that was conducted on clinical and renal histological data, treatment modalities, and outcomes of 43 Tunisian children with biopsy-proven lupus nephritis. They reported that musculoskeletal (86%) and mucocutaneous (67%) involvement were the most common presentation, while neurological disorder was the least frequent manifestation. Moreover, it is similar to the study of Ayman Abdel Aziz et al. [13], who studied thyroid dysfunction and thyroid autoantibodies in Egyptian patients with SLE. They found that the most common characteristics of SLE features were malar flush (90.0%), photosensitivity (80.0%), fever (70.0%), arthritis (50.0%), and serositis (30.0%).
Thus, we would recommend the intermittent biochemical screening of thyroid function and thyroid antibodies as part of the clinical profile in SLE patients, particularly if they are known to have thyroid antibodies, to identify clinical/subclinical thyroid disease [21]. Additionally, attention should be paid to screening for connective tissue diseases when diagnosing hypothyroidism.