Effect of systemic lupus erythematosus on thyroid function Gao Jianxin, Department of Immunology, Baotou Central Hospital
Gao Jianxin, Department of Rheumatology and Immunology, Baotou Central Hospital (014040)
Systemic lupus erythematosus (SLE) is an autoimmune disease involving multiple systems and organs, and its effect on the endocrine system has been less studied. In this paper, we summarize and analyze the thyroid dysfunction manifestations in 11 cases of SLE patients from 2001 to 2003, in order to deepen the understanding of the disease and better diagnose and treat SLE.
1. Data and methods
1.1 General data: From January 2001 to March 2003, serum thyroxine levels were examined in 11 patients with SLE admitted to our department. 11 cases included one male, 30 years old, whose parents had a history of consanguineous marriage and whose sister died at the age of 11 due to leukemia and who had lupus nephritis. The remaining 10 cases were female. 11 patients were aged 13-53 years, mean 33.7 years, and all cases met the ACR 1997 SLE classification criteria. 2 cases with low T3, T4 and TSH and multiple plasma cavities were given thyroxine supplementation in addition to conventional treatment. One case was combined with autoimmune hepatitis and jaundice for half a month, one case was combined with acute anterior wall infarction, two cases developed lupus encephalopathy, in addition to intrathecal methotrexate and dexamethasone, naloxone was also used to treat lupus encephalopathy with certain effect. one case was combined with thrombocytopenic purpura; one case was hospitalized with aggravation in late pregnancy, and after a female live baby was delivered by cesarean section, the patient died several days later due to failure to resuscitate. A 33-year-old female patient with recurrent hyperthermia lasting 1-2 weeks, accompanied by seronegative spondyloarthropathy, was transferred to a hospital in Beijing and designated as lupus nephritis (type V) by renal puncture biopsy, and was given cyclophosphamide, hormone shock and anti-tuberculosis drugs, combined with traditional Chinese medicine, and her condition was stabilized and is now working normally without recurrence.
1.2 METHODS: Fasting venous blood was taken in the morning, and the serum was separated and sent to the Department of Nuclear Medicine for determination of T3, T4, FT3, FT4, TSH, etc. by radioimmunoassay.
2. RESULTS: Among 11 patients with SLE, 3 had normal thyroid function, 3 had hypothyroidism, 4 had low T3 syndrome, and 1 had subclinical hypothyroidism.
3. Conclusion: Although the number of cases mentioned in this paper is small, it suggests that the combination of SLE with abnormal thyroid function is higher than that of the normal population.
The effect of SLE on thyroid function deserves in-depth study. In particular, the male patient mentioned in this paper is at increased risk of autoimmune disease due to his parents’ consanguineous marriage. In patients with SLE combined with multiplasmic fluid (pericardial, thoracic and abdominal fluid), thyroid function should be paid special attention and treated accordingly; in patients with SLE combined with autoimmune hepatitis, attention should be paid to hepatoprotective therapy and thyroid function should be checked, as it has been reported that severe hepatitis itself can have an effect on thyroid function; in patients with SLE combined with subclinical hypothyroidism and low T3 syndrome, thyroid function will normalize with the control of SLE. The thyroid function is normalized with the control of SLE. Intrathecal MTX and dexamethasone with naloxone are effective in patients with lupus encephalopathy.
The mechanism of thyroid dysfunction in patients with SLE is still unclear, but it may be due to the fact that they share the same genetic and immunological pathogenesis and both contain the histocompatibility antigens HLA-B8 and HLA-DRW3, both of which promote the synthesis of autoantibodies [1]. In SLE, the imbalance of immune balance in the body, low function of T suppressor cells (TS), hyperfunction of T helper cells (TH) and B cells, and decreased TS/TH ratio result in the production of a large number of autoantibodies, which cause hypothyroidism or inhibit TSH formation by damaging thyroid follicular cells and reducing thyroid hormone synthesis [2]. It is also believed that the presence of auto IgG-like antibodies to the antigenic substances of their own cell nuclei in SLE patients, the immune complexes formed by the combination of these antibodies and the corresponding antigens in the walls of small blood vessels in the skin, glomeruli, joints, brain and other organs, activates the complement causing cellular damage, and the release of antigenic substances from the damaged cells stimulates the body to produce more autoantibodies, resulting in the formation of more immune complexes, causing In recent years, immunological studies have also concluded that the following factors are predisposed to SLE: ① Individuals with defects in complement C1q and/or C4 genes Significantly reduced ability to clear immune complexes and increased levels of immune complexes in the body. ② In the human body, apoptosis is constantly occurring and apoptotic granules are formed, due to impaired clearance of apoptotic granules in individuals with DNAase gene defects; individuals with serum amyloid-like protein (SAP) gene defects have impaired envelopment of apoptotic granules and reduced rate of clearance of apoptotic granules. individuals with Fas (CD95)/FasL (CD95 ligand) gene defects activate induced The mechanism of auto-reactive lymphocyte apoptosis is impaired in individuals with Fas (CD95)/FasL (CD95 ligand) gene defects and predispose to autoimmune diseases [3].
REFERENCES
1. Zhang Pei-Lian, Li Xue-Ping, Mao Chang-Chi et al. Thyroid function test results and clinical analysis in patients with systemic lupus erythematosus. Chinese Journal of Rheumatology, 1999.3:248-249.
2. Jiang T R. Endocrine system manifestations in systemic lupus erythematosus. Journal of Continuing Medical Education, 2000, 23:52-54.
3. Yu YL. Autoimmune diseases. In Chen Weifeng, ed. Medical Immunology. Beijing: People’s Health Publishing House, 2005. 201-207.