Background: Rheumatoid arthritis is an immunological disorder with etiology not fully understood. Genetics factors can contribute to development and severity of rheumatoid arthritis (RA) and can be targets of study to personalized medicine. Genes related to immune system as MHC locus has been associated to RA since plays a role in inflammation observed in the disease. Among these, the Class II Major Histocompatibility Complex Transactivator (CIITA) has been highlighted once that plays a role in the activation of the immune system by stimulating MHC II transcription. The polymorphism rs3087456 of CIITA is located at position -168 A/G has attracted attention since it can change your transcriptional level and plays a role in RA inflammation. Some studies in different populations had found controversial results and the relation between this polymorphism and RA in Brazilian population yet is unclear. Thus, our study aims to determine the potential association of rs3087456 CIITA polymorphism in development and severity of RA.
Case report: a 62-year-old previously healthy woman presented to the Rheumatology department complaining of dyspnea, alopecia and polyarthralgia initiated in the preceding twelve months. The patient was already under treatment for heart failure prescribed by a cardiologist, without significant symptomatic improvement. Clinical history revealed unintentional weight loss of 48 percent of habitual body weight in the preceding year, recurrent fever without evident infection, and previous full alopecia. Physical examination showed crackles in both lung bases, painful hepatomegaly and notable lower limbs edema, with the laboratorial findings of anemia, leucopenia, lymphopenia, elevated erythrocyte sedimentation rate, renal dysfunction (creatinine levels of 1.36 mg/dL, with clearance of 31 ml/min/1.73m2; previous creatinine of 0.77 mg/dL) and positive antinuclear antibody (ANA; nuclear homogeneous pattern at a titer superior to 1:640). As her echocardiogram showed ejection fraction of 45 percent (while being pharmacologically treated for heart failure), with diffuse hypokinesia of both ventricles, the diagnosis of systemic lupus erythematosus with myocarditis was established, with the prescription of prednisone 0.5 mg/kg/day (higher doses were avoided at first, because of the advanced age and uncontrolled systemic arterial hypertension at that time). Two weeks later, the patient returned for clinical reassessment, without peripheral edema or dyspnea, and with normal breath sounds and abdominal examination. New laboratory findings demonstrated reduced complement levels, as well as high titers of double-strand anti-DNA and anti-Ro antibodies, when corticoid dose was then increased to 1mg/kg/day. Once 24-h proteinuria fulfilled criterion for nephritis (792 mg; renal biopsy showing class IV lupus nephritis), treatment with monthly intravenous cyclophosphamide for six months was initiated. After a five-dose course of cyclophosphamide, the general clinical status dramatically improved, along with normalization of the cardiac ejection fraction (from 45 percent to 74 percent) and reduction in 24-h proteinuria (which was shown to be 406 mg).
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Case report: Male, 16 years of age, otherwise healthy, presented with migratory arthritis, anasarca and oral ulcers. Approximately 30 days after the onset of such symptoms, the subject experienced choreic movements, dysarthria and mental confusion. The patient denied recent history of seizures, fever or cutaneous lesions. Upon admission, he was alert, feverless, displaying equal and fotorreactive pupils, affective lability, generalized choreic movements (picture 1), appendicular hypotonia, normal deep tendon reflexes, bilateral flexor plantar reflexes and no meningeal signs. Tongue ulcerations on the inferior portion of the tongue were also observed. Left elbow and right metacarpophalangeal joint arthritis were also present. Lab workup revealed positive ANA 1/1280 (homogeneous nuclear and chromosomal metaphase plate pattern), positive Anti-DNA, leukopenia (3000), lymphopenia (1032) and hypocomplementemia. ESR was 28, 61.3 CRP, positive rheumatoid factor, negative P-ANCA and C-ANCA, negative ASO, hepatitis-related serology, VDRL and HIV. Skull CT scan and cerebrospinal fluid showed no abnormalities. The patient was given a diagnosis of SLE with movement disorder (chorea). He was given 1 g methylprednisolone daily for three days, and then started on prednisone 1mg/Kg, hydroxychloroquine 400mg and azathioprine 50 mg daily, achieving full symptom remission.
Case Report: A 62-year-old female patient on CDLE treatment for face and scalp in the last 5 years. Interrupted the use of hydroxychloroquine (HCQ) 2 months ago. In the last month, constitutional symptoms appeared with worsening of cutaneous lesions, in the form of deep and painful ulcers, on the face and scalp with secondary infection (Klebsiella and Pseudomona). Hb 10g/dl; PT, platelets, leukocytes, kidney and hepatic functions tests were normal; ESR: 140mm/hr; ANA, anti-SM, anti-native DNA and anti-Ro unreacted; Anticardiolipin IgG: 9U GPL and IgM: 40U MPL; lupus anticoagulant was present; anti-Beta-2-Glycoprotein I: 22 and 6.1 U/mL, IgG and IgM respectively. Wide antibiotic therapy, warfarin, treatment of skin ulcers with alginate, silver and calcium, reintroduction of HCQ, plus prednisone at a low dose were instituted. During hospitalization, the patient presented thrombosis of the axillary and left basal veins, requiring full anticoagulation. aPLs remained positive in moderate to high titers, confirming the presence of APS. The patient received Rituximab, 1g EV, reinfused 15 days later. In the evolution, it was observed a regression of cutaneous ulcers, elevation of hemogobin levels and normalization of inflammatory activity tests. 2ff7e9595c
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