Research progress of tradition Chinese medicine treatment mechanism of systemic lupus erythematosus based on biomarkers / 药学实践杂志

Systemic lupus erythematosus (SLE) is an autoimmune disease with multiple organ involvement. There are still many limitations and individual differences in the treatment based on glucocorticoids and immunosuppressants. In recent years, more and more studies have shown that the combination of traditional Chinese medicine in the treatment of SLE has the advantages of good efficacy, low adverse reactions, and high safety. However, the exact regulatory mechanism and combined traditional Chinese medicine in the treatment of SLE are still unclear. This paper reviews the research on the mechanism of traditional Chinese medicine in the treatment of SLE from metabonomic, immune cells, lymphocyte factors and apoptosis, etc, provides ideas for exploring the mechanism of traditional Chinese medicine in the treatment of SLE with modern methods.

Secondary herpes zoster wound cured by allogeneic platelet-rich plasma: a case report / 中国输血杂志

【Objective】 To investigate the feasibility of allogeneic platelet-rich plasma (PRP) for the treatment of herpes zoster wounds secondary to systemic lupus erythematosus (SLE), especially large ulcer wounds. 【Methods】 The treatment process of a patient with massive herpes zoster wounds in perineum and hip accompanied by extensive soft tissue necrosis secondary to SLE was retrospectively analyzed. The clinical efficacy of allogeneic PRP was explored combined with treatment key points and literature review. 【Results】 The patient′s wound bed was prepared until the wound was fresh, then treated externally with allogeneic PRP 3 times a week. The wound was healed completely after 42 days. 【Conclusion】 In the case of autologous PRP unavailable or unsuitable, allogeneic PRP is a safe alternative, which can effectively promote tissue regeneration, and this patient achieved curative effect in a short period of time.

A Teenage Boy with Systemic Lupus Erythematosus Complicated with Acquired von Willebrand Syndrome: A Rare Case and Challenging in Making Diagnosis

@#In systemic lupus erythematosus (SLE), haematological abnormalities are frequent, although they are an uncommon cause of acquired von Willebrand syndrome (AVWS). AVWS is a rare condition that can cause a bleeding disorder. We presented a case of AVWS in the early diagnosis of SLE. One month before admission, the patient had a history of recurrent epistaxis. He presented to the hospital with symptomatic anaemia and was noted to have severe anaemia with iron deficiency. During hospitalisation, recurrent epistaxis recurred and was found to have prolonged activated partial thromboplastin time (aPTT), presence of lupus anticoagulant (LA), and lower von Willebrand factor (VWF), and factor 8 (VIII) levels. Simultaneously, he was diagnosed with SLE based on Systemic Lupus International Collaborating Clinics (SLICC) criteria. He underwent blood transfusions and was treated with immunosuppressive drugs such as steroids, mycophenolate mofetil, and an anti-fibrinolytic agent; he subsequently stopped bleeding and showed clinical improvement.

Total Glucosides of Paeony Improve Renal Injury in Mice with Systemic Lupus Erythematosus by Regulating TLR9/MyD88/NF-κB Pathway / 中国实验方剂学杂志

ObjectiveTo investigate the intervention effect of total glucosides of paeony （TGP） on the renal injury of MRL/lpr mice based on the Toll-like receptor 9 （TLR9）/myeloid differentiation factor 88 （MyD88）/nuclear transcription factor-κB （NF-κB） signaling pathway and explore the immunological mechanism of TGP in preventing and treating systemic lupus erythematosus （SLE）. MethodMRL/lpr female mice of SPF grade were randomly divided into a model group， a dexamethasone group （0.15 g·kg-1）， and high- （0.078 g·kg-1） and low-dose （0.039 g·kg-1） TGP groups， and female C57BL/6J mice were assigned to a blank group， with 7 mice in each group. Mice in each group were treated with corresponding drugs or normal saline by gavage at the same time every day. After 4 weeks， samples were collected. The kidney and spleen were weighed， and the organ index was calculated. Serum creatinine （SCr） and blood urea nitrogen （BUN） levels in each group were detected by biochemical assay. Hematoxylin-eosin （HE） staining was used to observe the histopathological changes in the kidney. The degree of renal fibrosis was evaluated by Masson staining. The serum levels of interleukin （IL）-2， interferon （IFN）-α， IL-4， and anti-nuclear antibody （ANA） were detected by enzyme-linked immunosorbent assay （ELISA）. The mRNA expression of TLR9， MyD88， and NF-κB p65 in renal tissues was detected by real-time quantitative polymerase chain reaction （Real-time PCR）. The protein expression of TLR9 and NF-κB p65 in renal tissues was detected by immunofluorescence. The protein expression of TLR9， MyD88， and NF-κB p65 in renal and spleen tissues was tested by Western blot. ResultCompared with the blank group， the model group showed increased SCr， BUN， spleen index， and kidney index （P<0.05）， deteriorated pathological injury and fibrosis in renal tissues， elevated serum levels of IFN-α， IL-4， and ANA， decreased level of IL-2 （P<0.05）， and up-regulated TLR9， MyD88， and NF-κB p65 mRNA and protein levels in the kidney and spleen （P<0.05）. Compared with the model group， the TGP groups displayed reduced SCr， BUN， spleen index， and kidney index （P<0.05）， relieved pathological damage and fibrosis in renal tissues， decreased serum levels of IFN-α， IL-4， and ANA （P<0.05）， increased level of IL-2， and declining mRNA and protein expression levels of TLR9， MyD88， and NF-κB p65 in the kidney and spleen （P<0.05）. ConclusionTGP may inhibit the expression of downstream inflammatory factors to regulate immunity and resist SLE-induced renal injury by regulating the TLR9/MyD88/NF-κB signaling pathway.

Alopecia areata y vitamina D sérica en pacientes iraquíes: un estudio de casos y controles / Alopecia Areata And Serum Vitamin D in Iraqi Patients: a case-control study

Background: Alopecia areata (AA) is a typical hair issue, which may have obliterating mental and social outcomes and is portrayed by the nearness of nonscarring alopecia. Objective: This examination has targets to assess the serum nutrient D levels , with AA; contrast the outcome and clearly sound control; and confirm relationship between AA types and serum nutrient D levels. Patients Also Methods: the examine might have been led clinched alongside Tikrit educating healing facility throughout those time starting with June 2019 of the limit for January 2020. Irrefutably the quantity of subjects associated with the assessment was ninety individuals isolated in two social events; the patients bundle were forty five the people who whimper of AA while the resulting gathering including a forty five age and sex-made solid volunteers were picked as a benchmark gathering. The degree and movement of the alopecia were noted and the patients were meticulously broke down for signs of various ailments. Research center assessments were led to patients and also to those control population, these included serum vitamin D levels were measured as 25-hydroxyvitamin D {25(OH)D} using a chemiluminescence microparticle immunoassay. Blood models were gotten starting with patients and control subjects after totally taught consent was gotten. Results : An essential complexity may have been found for serum 25-OH Vit D levels between patients other than controls. Vitamin D sufficiency were more common in controls than in patients. Serum Vitamin D was deficient in both cases and controls group; but, the deficiency was significantly more throughout AA group (35. 6%) compared to the handle group (11. 1%). Among the list patients gathering, levels associated with nutrient D were totally higher in guys in contrast with females. Conclusions: AA might be related with nutrient D deficiency as mean degrees of nutrient D of patients were seen as fundamentally lower than typical sound controls.

Establishment and validation of predictive model of pregnancy loss in patients with systemic lupus erythematosus / 上海交通大学学报（医学版）

Objective: To establish and verity predictive model of pregnancy loss in systemic lupus erythematosus (SLE). Methods: A total of 338 SLE pregnant patients admitted to Renji Hospital, Shanghai Jiao Tong University School of Medicine from Sept. 2011 to May 2017 (model development group) and 131 SLE pregnant patients admitted from Jun. 2017 to Jun. 2018 (model validation group) were selected. Multivariable Logistic regression model was used to determine the predictive variables and their coefficients of pregnancy loss in model development group. The predictive model was established, the risk score classification was performed, and model validation group was used for external validation. Results: Multivariate Logistic regression analysis showed that unplanned pregnancy (P=0.032), low complement C3 (P=0.002) and 24 h urinary protein ≥ 1.0 g (P=0.000) were the risk factors of the predictive model of SLE pregnancy loss. When the risk score of the model was 0-3, the risk of SLE pregnancy loss was low, and when the risk score is more than 3, it is high risk, with a sensitivity and specificity of 60.5% and 93.3%, respectively. The model was used in the model validation group for external validation, and the prediction accuracy of SLE pregnancy loss was 90.1%. Conclusion: The predictive model of SLE pregnancy loss can help clinicians efficiently screen the high-risk population of SLE pregnancy loss in order to take relevant measures as soon as possible to obtain better pregnancy outcomes.

Role of long noncoding RNA AC073046.25 in regulation of systemic lupus erythematosus susceptibility gene TET3 expression / 上海交通大学学报（医学版）

Objective: To investigate the regulatory effect of long noncoding RNA (lncRNA) AC073046.25 on the expression of Tet methylcytosine dioxygenase 3 (TET3) in monocytes, and analyze the feasibility of AC073046.25 as a biomarker for the diagnosis of systemic lupus erythematosus (SLE). Methods: The cell specificity and function of AC073046.25 were predicted by epigenetic modification and cytoplasm/nuclear location experiment. In U-937 cells, antisense oligonucleotide (ASO) was used to knock down AC073046.25. The effect of ASO knockdown on TET3 expression was analyzed by quantitative real-time PCR. Monocytes from healthy volunteers (n=32) and SLE patients (n=46) were collected. The correlation between AC073046.25 and TET3 expression was analyzed by Pearson coefficient. Healthy volunteers were included in the healthy control group, and the SLE patients were divided into SLE-inactive group and SLE-active group according to the systemic lupus erythematosus disease activity index (SLEDAI). The differences of AC073046.25 and TET3 expression in healthy control group and different disease activity groups were compared by unpaired bilateral student's t test. Results: The epigenetic modification and cytoplasm/nuclear location experiment showed that AC073046.25 may be involved in the regulation of TET3 expression in monocytes. In U-937 cells, after ASO knocked down AC073046.25, TET3 expression level decreased (both P=0.002 in ASO groups). Correlation analysis showed that AC073046.25 expression was positively correlated with TET3 expression in primary monocytes (r=0.650, P=0.000). Unpaired bilateral student's t test showed that the expression level of AC073046.25 in the SLE-active group was lower than that in the healthy control group (P=0.002) and the SLE-inactive group (P=0.000). Conclusion: In monocytes, AC073046.25 can regulate the expression of TET3, and its expression is significantly decreased in monocytes derived from disease active SLE patients, which implicating that AC073046.25 can be thought as a biomarker for SLE disease activity diagnosis.

Circulating exosomal micrornas as biomarkers of systemic lupus erythematosus

OBJECTIVES: Many studies indicate that microRNAs (miRNAs) could be potential biomarkers for various diseases. The purpose of this study was to investigate the clinical value of serum exosomal miRNAs in systemic lupus erythematosus (SLE). METHODS: Serum exosomes were isolated from 38 patients with SLE and 18 healthy controls (HCs). The expression of miR-21, miR-146a and miR-155 within exosomes was examined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Using receiver operating characteristic (ROC) curves, we evaluated the diagnostic value of exosomal miRNAs. RESULTS: Exosomal miR-21 and miR-155 were upregulated (p<0.01), whereas miR-146a expression (p<0.05) was downregulated in patients with SLE, compared to that in HCs. The expression of miR-21 (p<0.01) and miR-155 (p<0.05) was higher in SLE patients with lupus nephritis (LN) than in those without LN (non-LN). The analysis of ROC curves revealed that the expression of miR-21 and miR-155 showed a potential diagnostic value for LN. Furthermore, miR-21 (R=0.44, p<0.05) and miR-155 (R=0.33, p<0.05) were positively correlated with proteinuria. The expression of miR-21 was negatively associated with anti-SSA/Ro antibodies (R=−0.38, p<0.05), and that of miR-146a was negatively associated with anti-dsDNA antibodies (R=−0.39, p<0.05). CONCLUSIONS: These findings suggested that exosomal miR-21 and miR-155 expression levels may serve as potential biomarkers for the diagnosis of SLE and LN.

Effect and Mechanism of Active Fraction of Polyrhachis vicina in Treatment of Systemic Lupus Erythematosus(SLE) / 中国实验方剂学杂志

Objective: To observe the effect of an active fraction of Polyrhachis vicina (AFPV) on systemic lupus erythematosus (SLE) and its possible mechanism based on animal and cell models. Method: Totally 60 SD rats were randomly divided into normal control group, model group, prednisone acetate group (5 mg·kg-1), and high, medium and low-dose AFPV groups (400, 200, 100 mg·kg-1). SLE model was replicated with bovine serum albumin-Freund's complete (incomplete) adjuvant. Arthus reaction was observed to study the effect of AFPV on the diameter of back skin redness in rats with SLE. The expressions of anti-double-stranded DNA (dsDNA) antibody, complements 3 (C3), complement 4 (C4), immunoglobulin M (IgM), interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-31 (IL-31) and interleukin-33 (IL-33) in serum were detected by enzyme-linked immunosorbent assay. CD4+T cells were isolated from the spleens of MRL/lpr and C57BL/6J mice at the age of 16 to 18 weeks by immunomagnetic beads method. The expressions of miR-200a and miR-155 and the levels of zinc-finger-enhancer binding protein 1(ZEB1) and suppressor of cytokine signaling1(SOCS1) in CD4+T cells were observed to explore the effect of AFPV on SLE and its possible mechanism. Result: Compared with the normal group, the diameter of back skin swelling in the model group was significantly increased (PPPPPPP+T cells of MRL/lpr lupus mice. Compared with the model group, the expression of microRNA-200a increased significantly, the expression of microRNA-155 decreased significantly (PPConclusion: AFPV has therapeutic effect on rats with SLE, its mechanism may be related to the regulation of miR-200a/ZEB1 and miR-155/SOCS1.

Risk factors for cytomegalovirus disease in systemic lupus erythematosus (SLE): a systematic review

Abstract Background: Cytomegalovirus (CMV) is an opportunistic pathogen causing reactivation and disease in Systemic Lupus Erythematosus (SLE) patients. This study aims to systematically review the literature for risk factors associated with CMV disease in SLE patients, in order to identify those more susceptible to CMV infection during their treatment. Methods: A systematic review was conducted on 4 different search engines and via hand search until May 2017. Studies were included after quality assessment via the Standard Quality Assessment Criteria for Evaluating Primary Research Papers from a Variety of Fields (HTA KMET). Results: Two studies on CMV disease were included. Elevated CMV viral load, higher steroid doses, use of immunosuppressants and disease duration were the most commonly associated risk factors for CMV disease. Conclusion: High CMV viral loads, longer SLE disease duration and higher steroid doses were associated with CMV disease. Further studies studying the risk of treatment drugs and role of interventions in the development of CMV infection are needed.

Glomerulopatía colapsante en lupus eritematoso sistémico con respuesta positiva a tratamiento con mofetil micofenolato / Collapsing Glomerulopathy in systemic lupus erythematosus with positive response to the treatment with mycophenolate mofetil

La glomerulonefritis colapsante es una enfermedad poco frecuente que puede estar asociada a distintas causas, una de ellas son las enfermedades autoinmunes y dentro de estas el lupus eritematoso sistémico (LES). De manera frecuente se presenta con un cuadro de severas alteraciones renales que tienden a progresar la enfermedad renal terminal, con escasa respuesta a los tratamientos. Se presenta un caso de glomerulonefritis colapsante asociado a lupus eritematoso sistémico que tuvo una respuesta completa al tratamiento de inducción con la combinación de glucocorticoides, antimaláricos y mofetil micofenolato iniciado precozmente por el diagnóstico temprano realizado por biopsia renal(AU)

Collapsing glomerulonefritis is a slightly frequent disease that can be associated to different causes. Autoimmune diseases are part of those, and inside these, the systemic lupus erythematosus (SLE). It frequently appears with manifestations of severe renal alterations that tend to develop the renal terminal disease, with scanty response to the treatments. It is presented a case of collapsing glomerulonefritis associated to systemic lupus erythematosus that had a complete response to the treatment of induction with the combination of glucocorticoids, antimalarials and mycophenolate mofetil used prematurely after the early diagnosis performed by renal biopsy(AU)

Células dendríticas e interferones en el lupus eritematoso sistémico / Dendritic cells and interferons in systemic lupus erythematosus

Resumen El lupus eritematoso sistémico (LES) es un trastorno autoinmune con base genética, caracterizado por la aparición de autoanticuerpos, formación y depósito de complejos inmunes circulantes e inflamación crónica en varios órganos. La etiología es multifactorial y, en individuos genéticamente predispuestos, factores medioambientales y componentes hormonales juegan un rol clave en el sistema inmune de esta enfermedad. Cerca de 25 loci genéticos han sido identificados, indicando la importancia en esta enfermedad; sin embargo, la tasa de concordancia para el LES es de tan solo el 25% entre gemelos monocigotos (1,2). Un ejemplo de ello son las deficiencias de los componentes iniciales en la vía clásica del complemento sérico como el C1q, C2 o C4, que si bien es infrecuente, confieren susceptibilidad genética para el LES en una tasa del 30% en caso de deficiencia del C4 y de más del 90% para una deficiencia del C1q (3). Por otro lado, se demostró que el C1q inhibe a las células dendríticas plasmocitoides (CDP) en la secreción de interferón alfa (IFN-a), proporcionando así un nuevo enlace entre la deficiencia del complemento y la activación de la vía del IFN (4). Por ello, el IFN-a es considerado como un actor central en la patogénesis del LES, encontrándose concentraciones séricas altas en los brotes de esta enfermedad (5). En consecuencia, estos IFN ejercen efectos claves en la fisiopatología del LES, lo que sugiere que esta citoquina no solo posee un efecto a nivel del sistema inmune innato, sino también en las respuestas inmunes adaptativas. Teniendo en cuenta estos hechos, se puede anticipar que las CDP, fuente principal de secreción de IFN, están involucradas en dicha enfermedad autoinmune. En esta revisión nos centraremos en la participación de las CDP y del IFN en el LES (6,7).

Abstract Systemic Lupus Erythematosus (SLE) is an autoimmune disorder with a genetic basis, and is characterised by the appearance of autoantibodies, the formation and deposition of circulating immune complexes, and chronic inflammation in various organs. It is of multifactorial origin, and in genetically predisposed individuals, environmental factors and hormonal components play a key role in the immune system of the disease. About 25 genetic loci have been identified, indicating the importance in this pathology. However, the concordance rate for SLE is only 25% among monozygotic twins. An example of this is the deficiencies of the initial components in the classical serum complement pathway such as C1q, C2 or C4, which, although rare, confer genetic susceptibility for SLE at a rate of 30% in the case of C4 deficiency, and more than 90% for C1q deficiency. It was also demonstrated that C1q inhibits plasmacytoid dendritic cells (pDCs) in the secretion of interferon-alpha (IFN-a), thus providing a new link between complement deficiency and activation of the IFN pathway. Therefore, IFN-a is considered to have a central role in the pathogenesis of SLE, with high serum concentrations being found in outbreaks of this disease. These IFN exert prominent immunoregulatory effects, suggesting that this cytokine is key, not only in the innate immune system, but also in adaptive immune responses. Taking these facts into account, it can be anticipated that pDCs, the main source of IFN secretion, are involved in this autoimmune disease. In this review, we will focus on the participation of pDCs and IFNs in SLE.

Identification of the Polymorphisms of rs7708392 in TNIP1 Gene and the Association with Systemic Lupus Erythematosus / 现代检验医学杂志

Objective To identify the single nucleotide polymorphism (SNP) of the gene of TNIP1 using high resolution melting (HRM) analysis with unlabeled probe,and funther analyse the association with systemic lupus erythematosuscsle.Methods 297 patients that fulfilled the American College of Rheumatology criteria for SLE and 351 ethnically matched healthy controls were recruited from Shenzhen Hospital of Peking University.The association of TNIP1 SNP rs7708392 (G/C) was determined by high resolution melting (HRM) analysis with unlabeled probe in SLE patients and healthy controls.Results HRMA with unlabeled probe successfully distinguished all genotypes.Genotype frequencies of GG,GC and CC among SLE patients were 36.0％,51.5％ and 12.5％,respectively,while the frequencies among healthy control were 32.5％,46.7％ and 20.8％.Statistically significant differences were observed in both genotype frequencies for rs7708392 in the SLE patients as compared with the controls.Minor allele (C) of rs7708392 (P=0.031,OR 0.78,95％ CI 0.63～0.98) was found to be protective against SLE.The association of SNP rs7708392 with the diagnostic criteria of SLE was also examined.Minor allele (C) exerts protective effect on the incidence of arthritis (P=0.013,OR=0.65,95 ％ CI=0.47 ～ 0.92) and abnormalities of antinuclear antibody (P =0.022,OR =0.68,95 ％ CI =0.49 ～ 0.95).TNIP1 SNPs were irrelevant to other diagnostic criteria of SLE.Conclusion Polymorphisms of rs7708392 in TNIP1 gene were associated with disease risk,as well as arthritis and autoantibody production,of systemic lupus erythematosus in Chinese population.

Serum Vascular Endothelial Growth Factor (VEGF) as a Biomarker for Disease Activity in Lupus Nephritis

Background: Previous studies have shown that serum VEGF levels were elevated in patients with active systemic lupus erythematosus (SLE), especially in those with lupus nephritis (LN). In this case control study, we aimed to compare serum levels of VEGF in SLE patients between LN, non-LN and healthy participants to determine the association between serum VEGF levels and the activity and histological classes of lupus nephritis. Methods: Blood samples were obtained from 92 SLE patients (46 LN and 46 non-LN) and 26 controls. Data were collected from medical records. Serum VEGF assays were performed by specific, enzyme-linked immunosorbent assay kits (ELISA). Laboratory investigations included urinalysis, urine protein–creatinine ratio, serum creatinine, albumin and VEGF levels. Blood pressure, renal biopsy result and treatment were recorded. LN activity was evaluated using the renal subscale of the British Isles Lupus Assessment Group (rBILAG, 2004). The rBILAG measures blood pressure (diastolic and systolic), urine protein, serum creatinine, calculated glomerular filtration rate (GFR), presence of active urinary sediments and histological evidence of active nephritis. Results: Serum VEGF was elevated in SLE patients with LN compared with the non-LN group and healthy controls. The levels found were significantly higher in the sera of patients with active nephritis compared to those with quiescent nephritis (P = 0.024). The study did not find a statistically significant relationship between serum VEGF levels and histological classes of LN. Conclusion: There was no significant difference of serum VEGF level between LN and non-LN SLE groups and between the non-LN group and healthy controls. However, there were increased levels of serum VEGF in the LN group, especially in patients with active nephritis as compared to quiescent nephritis group. This reflects the role of VEGF in the pathogenesis of lupus nephritis, however the clinical potential of this biomarker needs further study.

Complement and membrane-bound complement regulatory proteins as biomarkers and therapeutic targets for autoimmune inflammatory disorders, RA and SLE.

Complement system is a major effecter system of the innate immunity that bridges with adaptive immunity. The system consists of about 40 humoral and cell surface proteins that include zymogens, receptors and regulators. The zymogens get activated in a cascade fashion by antigen-antibody complex, antigen alone or by polymannans, respectively, by the classical, alternative and mannose binding lectin (MBL) pathways. The ongoing research on complement regulators and complement receptors suggest key role of these proteins in the initiation, regulation and effecter mechanisms of the innate and adaptive immunity. Although, the complement system provides the first line of defence against the invading pathogens, its aberrant uncontrolled activation causes extensive self tissue injury. A large number of humoral and cell surface complement regulatory protein keep the system well-regulated in healthy individuals. Complement profiling had brought important information on the pathophysiology of several infectious and chronic inflammatory disorders. In view of the diversity of the clinical disorders involving abnormal complement activity or regulation, which include both acute and chronic diseases that affect a wide range of organs, diverse yet specifically tailored therapeutic approaches may be needed to shift complement back into balance. This brief review discusses on the complement system, its functions and its importance as biomarkers and therapeutic targets for autoimmune diseases with focus on SLE and RA.

Mannose binding lectin (MBL) 2 gene polymorphism & its association with clinical manifestations in systemic lupus erythematosus (SLE) patients from western India.

Background & objectives: systemic lupus erythematosus (SLE) is a prototypical autoimmune disease characterized by production of autoantibodies. Mannose binding lectin (MBL) is an important element of the innate defense system. the present study was undertaken to determine whether variant alleles in MBL2 gene were associated with disease severity in SLE patients. Methods: The MBL alleles [-550, -221, +4, Codon 52, Codon 54 and Codon 57] were studied by PCR- RFLP (restriction fragment length polymorphism) method in 100 SLE patients fulfilling ACR (American College of Rheumatology) criteria along with 100 healthy controls. SLE disease activity was evaluated using SLE Disease Activity Index (SLEDAI) score. Results: Homozygosity for MBL variant allele (O/O) was observed in 24 per cent of the SLE patients compared to 16 per cent of the normal controls, while no difference was found for heterozygosity (A/O) (37 vs 35%). A significant difference was reported in incidence of double heterozygosity for mutant allele B and D (B/D) among SLE patients as against control group (p = 0.015). MBL genotypes did not show any association with renal involvement. Interpretation & conclusions: In this study from western India, MBL gene polymorphism showed an influence as a possible risk factor for susceptibility to SLE, but had no direct effect on disease characteristics. Further studies need to be done on a larger number of SLE patients in different regions of the country.

Salmonella Paratyphi B bacteremia in Systemic Lupus Erythematosus with an unusual presentation- a case report.

Background- Systemic Lupus Erythematosus (SLE) is an inflammatory and multisystem autoimmune disorder. Patients of SLE are at increased risk of infections owing to underlying immunological derangements and to the use of therapeutic regimens like immunosuppressive agents. Among the bacterial infections presenting as bacteremia in these patients, non typhoidal and typhoidal salmonellosis are commonly encountered. We report a rare case of Salmonella Paratyphi B bacteremia in a patient with juvenile onset SLE on treatment with corticosteroids.

Late onset systemic lupus erythematosus with severe hypercalcaemia / Lupus eritematoso sistémico de inicio tardío con hipercalcemia severa

We report a case of a 76-year old female presenting with symptomatic severe hypercalcaemia, and subsequently diagnosed with late onset SLE due to the presence of anaemia, leucopenia, antibodies of antinuclear (ANA), anti-dsDNA, and also kidney impairment. Serum levels of FGF23 and intact-parathyroid hormone (iPTH) were low in this patient. Serum calcium, FGF23 and iPTH levels responded to steroids, which occurred simultaneously with disease activity. On follow-up, the faster increase in FGF23 than in parathyroid hormone suggested that FGF23 might be involved in the pathogenesis of hypercalcaemia in SLE.

Se reporta el caso de una mujer de 76 años de edad que se presentó con hipercalcemia sintomática severa, y a la que posteriormente le fuera diagnosticada LES de inicio tardío con presencia de anemia, leucopenia, anticuerpos antinucleares (ANA), anti-dsDNA, e insuficiencia del riñón. Los niveles séricos del factor de crecimiento fibroblástico 23 (FGF23) y la hormona paratiroidea intacta (iPTH) fueron bajos en este paciente. Los niveles de calcio séricos, FGF23 e iPTH respondieron a los esteroides, que ocurrieron simultáneamente con la actividad de la enfermedad. En el seguimiento, el hecho de que el factor FGF23 aumentara más rápidamente que la hormona paratiroidea, sugiere que el FGF23 podría estar involucrado en la patogénesis de la hipercalcemia en LES.

A Case of Q Fever that may Mimic Systemic Lupus Erythematosus

Q fever is a zoonosis caused by a Coxiella burnetii. Q fever is clinically variable, presenting as asymptomatic infection, pneumonia, hepatitis and endocarditis. Treatment of acute Q fever with doxycycline is usually successful. Autoantibodies, such as anti-mitochondrial antibodies, smooth muscle antibodies (SMA), anti-cardiolipin and lupus anticoagulant, often rise in acute Q fever infection. Some cases may occasionally meet the criteria for autoimmune disease like systemic lupus erythematosus. We report a first case of Q fever that may mimic systemic lupus erythematosus in Korea.

A Case of Q Fever that may Mimic Systemic Lupus Erythematosus

Q fever is a zoonosis caused by a Coxiella burnetii. Q fever is clinically variable, presenting as asymptomatic infection, pneumonia, hepatitis and endocarditis. Treatment of acute Q fever with doxycycline is usually successful. Autoantibodies, such as anti-mitochondrial antibodies, smooth muscle antibodies (SMA), anti-cardiolipin and lupus anticoagulant, often rise in acute Q fever infection. Some cases may occasionally meet the criteria for autoimmune disease like systemic lupus erythematosus. We report a first case of Q fever that may mimic systemic lupus erythematosus in Korea.