Some observations on telescoped urinary sediments.

Case Reports1 August 1945ACUTE LUPUS ERYTHEMATOSUS DISSEMINATUS: A REPORT OF A CASE IN A MALE WITH ASSOCIATED ATYPICAL VERRUCOUS ENDOCARDITIS (LIBMAN-SACKS)S. GILBERT BLOUNT JR., M.D., JOHN T. BARRETTS. GILBERT BLOUNT JR., M.D.Search for more papers by this author, JOHN T. BARRETTSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-23-2-251 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe present concept of the symptom-complex known as acute lupus erythematosus disseminatus has been formulated over the period of the last 100 years.Hebra,1in 1845, first -described lupus erythematosus as a local cutaneous lesion under the name "seborrhea congestiva." Six years later Cazenave2gave the disease its present name. It was not until 1872 that Kaposi3subdivided the disease into "lupus erythematosus discoides" and "lupus erythematosus discretus and aggregatus." He was the first to realize the generalized and systemic manifestations of the latter form with its attending grave prognosis, as three of his 11 cases died while under observation....Bibliography1. HEBRA F: Ztschr. d.k.k. Gesellsch. d. Aerzte zu Wien, 1845, i, 40. Cited by KLEMPERER ET AL.8 Google Scholar2. CAZENAVE A: Ann. d. mal. de la peau. 1851, iii, 297. Cited by KLEMPERER ET AL.8 Google Scholar3. KAPOSI M: Arch. f. Dermat. u. Syph., 1872, iv, 36. Cited by KLEMPERER ET AL.8 CrossrefGoogle Scholar4. OSLER W: On the visceral manifestations of erythema exudativum multiforme, Am. Jr. Med. Sci., 1895, cx, 629. CrossrefGoogle Scholar5. OSLER W: The visceral lesions of the erythema group. (2nd series of cases), Brit. Jr. Dermat., 1900, xii, 227. Google Scholar6. OSLER W: On the visceral manifestations of the erythema group of skin diseases, Am. Jr. Med. Sci., 1904, cxxvii, 1. Google Scholar7. LIBMANSACKS EB: A hitherto undescribed form of valvular and mural endocarditis, Arch. Int. Med., 1924, xxxiii, 701. CrossrefGoogle Scholar8. KLEMPERERPOLLACKBAEHR PADG: Pathology of disseminated lupus erythematosus, Arch. Path., 1941, xxxii, 569. Google Scholar9. LIBMAN E: Some general considerations concerning affections of the heart valves, Med. Clin. N. Am., 1917, i, 573. Google Scholar10. BELOTERATNER GHS: The so-called Libman-Sacks syndrome: Its relation to dermatology, Arch. Dermat. and Syph., 1936, xxxiii, 642. CrossrefGoogle Scholar11. GROSS L: Unpublished data; cited by FRIEDBURG, C., GROSS L., and WALLACH, K.:Nonbacterial thrombotic endocarditis associated with prolonged fever, arthritis, inflammation of serous membranes and widespread vascular lesions, Arch. Int. Med., 1936, lviii, 662. Google Scholar12. O'LEARY discussion of paper by BELOTE and RATNER.11 Google Scholar13. GINZLERFOX AMTT: Disseminated lupus erythematosus : a cutaneous manifestation of a systemic disease (Libman-Sacks), Arch. Int. Med., 1940, lxv, 26. CrossrefGoogle Scholar14. ROSEPILLSBURY EDM: Acute disseminated lupus erythematosus—a systemic disease, Ann. Int. Med., 1939, xii, 951. Google Scholar15. GROSS L: The cardiac lesions in Libman-Sacks disease with consideration of its relationship to acute diffuse lupus erythematosus, Am. Jr. Path., 1940, xvi, 375. Google Scholar16. KAISER I: The specificity of periarterial fibrosis of the spleen in disseminated lupus erythematosus, Bull. Johns Hopkins Hosp., 1942, lxxi, 31. Google Scholar17. FOXROSAHN RPD: The lymph node in disseminated lupus erythematosus, Am. Jr. Path., 1943, xix, 73. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: *Received for publication April 29, 1944. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited bySYSTEMIC LUPUS ERYTHEEMATOSUS WITH MULTIPLE CALCIFIED FIBROUS NODULES OF THE SPLEENSplenic Atrophy in Systemic Lupus ErythematosusAILEEN M. DILLON, M.B., B.Ch., B.A.O., HOWARD B. STEIN, M.D., RODERICK A. ENGLISH, M.D., C.M.Pericardial Effusion, a Manifestation of Systemic Lupus ErythematosusThe heart in systemic lupus erythematosusDisseminated Lupus Erythematosus in the Male 1 August 1945Volume 23, Issue 2Page: 251-267KeywordsEndocarditisLesionsLupus erythematosusMedical staffPathologistsSystemic lupus erythematosus ePublished: 1 December 2008 Issue Published: 1 August 1945 PDF downloadLoading ...

THE PURPOSE of this presentation is to refer to a previously noted structural alteration that has been observed in lupus erythematosus and to emphasize its significance, which has become evident only after cytochemical analysis. In 1932 Gross 1 reported the presence of clumps and packets of hematoxylin staining bodies in the cardiac lesions (fig. 1) of Libman-Sacks disease, later identified with acute lupus erythematosus. He expressed the conclusion that these masses originated in nuclear material and that they were pathognomonic. In 1940, Ginzler and Fox 2 found similar masses in necrotic lymph nodes in this disease (fig. 2). They also described basophilic particles in the glomerular loops of the kidney, which observation was confirmed in 1941 by Klemperer, Pollack and Baehr. 3 In the past two years my associates and I have observed 4 cases of acute lupus erythematosus in which the same hematoxylin-staining masses were found in

Background: Systemic Lupus Erythematosus (SLE) is a complex autoimmune disease with diverse clinical manifestations and relapsing - remitting disease course. Nephritis is a major cause of morbidity and mortality in patients with lupus. Many clinical parameters and laboratory markers can be used to evaluate disease activity and nephritis. Neutrophil to lymphocyte ratio (NLR) and platelet to lymphocyte ratio (PLR) are positively associated with inflammatory disorders. Objectives: To evaluate the correlation between NLR and PLR in peripheral blood and renal involvement in systemic lupus erythematosus. Methods: 63 patients were diagnosed with SLE according to the criteria of the Systemic Lupus International Collaborating Clinics 2012 (SLICC 2012) and were treated at the Internal Medicine Department of Hue University of Medicine and Pharmacy Hospital, Thua Thien Hue province, in central Vietnam, from February 2020 to July 2021. This study included 41 SLE patients with lupus nephritis (LN) and 22 SLE patients without renal involvement. Results: The mean age of the study group was 31.67 ± 12.10. The most common age group was 21-50 years old, accounting for 69.8%. Females accounted for 90.5% and the female-to-male ratio stood at 9.5:1. Clinical and laboratory characteristics: acute cutaneous lupus 50.8%, subacute cutaneous lupus 11.1%, oral ulcers 27%, non - scarring alopecia 47.6%, arthritis 61.9%, pleural or pericardial effusion 30.2%, renal involvement 65.1%, neuropsychiatric damage 4.8%, anemia 81.0%, leukopenia 22.2%, neutropenia 11.1%, lymphopenia 41.3%, thrombocytopenia 15.9%, hemolytic anemia 15.9%, positive ANA antibody 61.9%, positive anti-ds DNA antibody 52.4%. Acute cutaneous lupus and arthritis in SLE patients without the nephritis group were higher than in the LN group (p < 0.05). Anemia, lymphopenia, thrombocytopenia, positive ANA, anti-ds DNA in the LN group were higher than SLE patients without nephritis (p < 0.05). SLE patients with LN had higher levels of NLR than those without nephritis. While PLR had no remarkable difference between these two groups. NLR was positively correlated with CRP, serum creatinine, and 24-hour urinary protein. PLR was positively correlated with the SLEDAI score. The best NLR to predict LN was 4.97 with a sensitivity of 51.2% and a specificity of 95.5% (AUC = 0.742, 95% CI, 0.617 - 0.866, p = 0.002). Conclusion: Most of the clinical manifestations in SLE patients according to SLICC 2012 criteria were lupus nephritis, arthritis, and acute cutaneous lupus. PLR was positively correlated with the SLEDAI score. NLR could predict renal involvement in SLE patients. Keywords: Lupus nephritis, ANA, anti-ds DNA, NLR, PLR.

Case Reports1 April 1956MILIARY TUBERCULOSIS DEVELOPING DURING PROLONGED CORTISONE THERAPY OF SYSTEMIC LUPUS ERYTHEMATOSUSHAROLD M. HILL, M.D., J. D. KIRSHBAUM, M.D., F.A.C.P.HAROLD M. HILL, M.D.Search for more papers by this author, J. D. KIRSHBAUM, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-44-4-781 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptA recently published case, reported by Davidson, Fox and Gold,1described the appearance of miliary tuberculosis in a case of systemic lupus erythematosus during the course of ACTH and cortisone therapy. This paper presents an additional case of miliary tuberculosis developing under the same circumstances, and is of particular interest because of its many similarities to the previously reported one, including the absence of characteristic microscopic lesions of systemic lupus erythematosus at autopsy, in spite of typical clinical findings and the demonstration of L. E. cells. In addition, this case demonstrates several of the hazards of prolonged maintenance of therapeutic...Bibliography1. DavidsonFoxGold AGLJJ: Appearance of miliary tuberculosis following therapy with ACTH and cortisone in a case of acute disseminated lupus erythematosus, Ann. Int. Med. 38: 852-862, 1953. LinkGoogle Scholar2. Harrison TR, Ed.: Principles of internal medicine, 1st Ed., 1950, The Blakiston Co., New York, N. Y., p. 466. Google Scholar3. Dubois EL: The effect of the L. E. cell test on the clinical picture of systemic lupus erythematosus, Ann. Int. Med. 38: 1265-1294, 1953. LinkGoogle Scholar4. JessarLamont-HaversRagan RARWC: Natural history of lupus erythematosus disseminatus, Ann. Int. Med. 38: 717-731, 1953. LinkGoogle Scholar5. SofferBader LJR: Corticotropin and cortisone in acute disseminated lupus erythematosus, J. A. M. A. 149: 1002-1008, 1952. CrossrefMedlineGoogle Scholar6. Slocumb CH: Rheumatic complaints during hypercortisonism and syndromes during withdrawal of cortisone in rheumatic patients, Proc. Staff. Meet., Mayo Clin. 28: 655-657 (Nov. 18) 1953. MedlineGoogle Scholar7. KlempererPollockBaehr PADG: Pathology of disseminated lupus erythematosus, Arch. Path. 32: 569, 1941. Google Scholar8. DuboisCommonsStarrSteinMorrison ELMDPCSR: Corticotropin and cortisone treatment for systemic lupus erythematosus, J. A. M. A. 149: 995-1002, 1952. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Redlands, California*Received for publication January 14, 1955.From the Departments of Medicine and Pathology, Redlands Community Hospital, Redlands, California, and San Bernardino County Hospital, San Bernardino, California. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byTuberculosis-associated hemophagocytic lymphohistiocytosis misdiagnosed as systemic lupus erythematosus: A case reportRole of Infections in the Pathogenesis of Rheumatoid Arthritis: Focus on MycobacteriaDisseminated tuberculosis masquerading as a presentation of systemic lupus erythematosusMycobacteria and autoimmunityCan Lupus Flares be Associated with Tuberculosis Infection?Case 48-1986Steroid therapy of systemic lupus erythematosus based on immunologic considerationsProphylaxis in patients receiving adrenal steroid therapyTuberculosis occurring in association with corticosteroid treatmentPulmonary tuberculosis following treatment with corticosteroidsRHEUMATISM AND ARTHRITIS: REVIEW OF AMERICAN AND ENGLISH LITERATURE OF RECENT YEARS (THIRTEENTH RHEUMATISM REVIEW)*CHARLEY J. SMYTH, M.D., F.A.C.P., ROGER L. BLACK, M.D., FELIX E. DEMARTINI, M.D., IVAN F. DUFF, M.D., F.A.C.P., EPHRAIM P. ENGLEMAN, M.D., F.A.C.P., DONALD C. GRAHAM, M.D., F.R.C.P.(C), MAX M. MONTGOMERY, M.D., F.A.C.P., HOWARD F. POLLEY, M.D., F.A.C.P., EDWARD F. ROSENBERG, M.D., F.A.C.P., CARLOS F. SACASA, M.D., F.A.C.P., OTTO STEINBROCKER, M.D., HANS WAINE, M.D., GEORGE M. WILSON JR., M.D.PLEURITIS IN SYSTEMIC LUPUS ERYTHEMATOSUS: ITS IMPORTANCE AS AN EARLY MANIFESTATION IN DIAGNOSIS*WILLIAM A. WINSLOW, M.D., LESTER N. PLOSS, M.D., BERNARD LOITMAN, M.D.ACTH and Adrenocorticosteroids as Therapeutic Adjuncts in Infectious DiseasesEmergency Aspects of Corticosteroid Therapy 1 April 1956Volume 44, Issue 4Page: 781-790KeywordsAdrenocorticotropic hormoneDuodenal ulcersGastric ulcersHospital medicineLupus erythematosusMiliary tuberculosisNecrosisOral administrationPancreasTuberculosis ePublished: 1 December 2008 Issue Published: 1 April 1956 PDF downloadLoading ...

Rituximab‐associated posterior reversible encephalopathy syndrome

Case Reports1 September 1952PERIARTERITIS NODOSA: REPORT OF A CASE TREATED WITH PARA-AMINOBENZOIC ACIDTHOMAS J. MCGURL JR., M.D.THOMAS J. MCGURL JR., M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-37-3-606 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptPeriarteritis nodosa continues to be a disease of unknown etiology with protean manifestations for which there is no known specific therapy. Many causes of this disease have been postulated, including sensitization to serums, drugs, infections, etc. However, no factor common to all cases has been found.1, 2It is characterized by an inflammatory, necrotizing reaction in the walls of small arteries and arterioles, the earliest stage of which consists of a period of hyaline degeneration of the media. This is followed by infiltration of the coats with polymorphonuclears, eosinophils, lymphocytes and plasma cells. Later there is fibroblastic proliferation, with partial...Bibliography1. LogueMullins RBF: Polyarteritis nodosa; report of 11 cases with review of recent literature, Ann. Int. Med. 24: 11-26 (Jan.) 1946. LinkGoogle Scholar2. MillerDaley HGR: Clinical aspects of polyarteritis nodosa, Quart. J. Med. 15: 255-283 (Oct.) 1946. CrossrefMedlineGoogle Scholar3. Rich AR: The role of hypersensitivity in periarteritis nodosa as indicated by seven cases developing during serum sickness and sulfonamide therapy, Bull. Johns Hopkins Hosp. 71: 123, 1942. Google Scholar4. Rich AR: Additional evidence of the role of hypersensitivity in the etiology of periarteritis nodosa, Bull. Johns Hopkins Hosp. 71: 375, 1942. Google Scholar5. RichGregory ARJE: The experimental demonstration that periarteritis nodosa is a manifestation of hypersensitivity, Bull. Johns Hopkins Hosp. 72: 65, 1943. Google Scholar6. KlempererPollackBaehr PADG: Diffuse collagen disease; acute disseminated lupus erythematosus and diffuse scleroderma, J. A. M. A. 119: 331-332 (May 23) 1942. CrossrefGoogle Scholar7. Zarafonetis JD: Therapeutic possibilities of para-aminobenzoic acid, Ann. Int. Med. 30: 1188-1212 (June) 1949. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: New York, N. Y.*Received for publication March 21, 1951.From Medical Service, Veterans Administration Hospital, Providence, R. I.Reviewed in the Veterans Administration and published with the approval of the Chief Medical Director. The statements and conclusions published by the author are the result of his own study and do not necessarily reflect the opinion or policy of the Veterans Administration. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byKrankheiten der GefäßePeriarteriitis nodosaPERIARTERITIS NODOSA WITH PREDOMINANT SYMPTOMS FROM THE SPINAL CORDRHEUMATISM AND ARTHRITIS REVIEW OF AMERICAN AND ENGLISH LITERATURE OF RECENT YEARS (ELEVENTH RHEUMATISM REVIEW)* Part IIWILLIAM D. ROBINSON, M.D., F.A.C.P., JOSEPH J. BUNIM, M.D., F.A.C.P., WILLIAM S. CLARK, M.D., DARRELL C. CRAIN, M.D., F.A.C.P., EPHRAIM P. ENGLEMAN, M.D., F.A.C.P., DONALD C. GRAHAM, M.D., F.R.C.P. (C), MAX M. MONTGOMERY, M.D., F.A.C.P., BERNARD M. NORCROSS, M.D., F.A.C.P., CHARLES RAGAN, M.D., F.A.C.P., MARIAN W. ROPES, M.D., F.A.C.P., EDWARD F. ROSENBERG, M.D., F.A.C.P., CHARLEY J. SMYTH, M.D., F.A.C.P.PERIARTERITIS NODOSA: REPORT OF A CASE WITH BRAIN INVOLVEMENT*ZACHARY SAGAL, M.D., F.A.C.P.THE CLINICAL MANIFESTATIONS OF ESSENTIAL POLYANGIITIS (PERIARTERITIS NODOSA), WITH EMPHASIS ON THE HEPATIC MANIFESTATIONS*FRED H. MOWREY, F.A.C.P., EDWARD A. LUNDBERG, M.D. 1 September 1952Volume 37, Issue 3Page: 606-611KeywordsAlbuminsEosinophilsRed blood cellsSigns and symptomsSulfonamideTemperatureThoraxUrineVaccinesWhite blood cells ePublished: 1 December 2008 Issue Published: 1 September 1952 PDF downloadLoading ...

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BackgroundCardiovascular disease is common in patients with systemic lupus erythematosis (SLE) and lupus nephritis (LN). Up to 80% of children with SLE develop kidney disease, which is also associated with increased risk for cardiovascular disease and death compared to those without renal involvement. Hepcidin is an iron-regulatory protein which may contribute to atherosclerosis and is elevated in autoimmune disease. Pulse wave velocity (PWV) is a validated indicator of arterial stiffness, an early marker of cardiovascular risk, and is increased in children with SLE versus healthy controls. Our objective was to quantify hepcidin and PWV in children with SLE and investigate if those with biopsy-proven LN have higher hepcidin levels and higher PWV compared to those without kidney disease.MethodsCross-sectional analysis with hepcidin was measured via ELISA assay in 16 children aged 10–21 years with SLE recruited from a single center. Subjects were classified as having LN if histologic evidence of the disease was documented on a clinical renal biopsy. Serum hepcidin was quantified using a validated competitive enzyme-linked immunoassay. Carotid-femoral PWV was measured using applanation tonometry. Wilcoxon rank sum testing was used to compare median levels of hepcidin, PWV, and other continuous variables by nephritis status.ResultsThe cohort (n = 16) was 93.8% female and 68.8% African-American with mean (SD) 16 (3.6) years. 37.5% (n = 6) had LN. Overall median (IQR) hepcidin was 34.4 (18.9, 91.9) ng/ml, and PWV 4.4 (4, 4.6) meters/second. Although significance was limited by small sample size, both hepcidin and PWV were higher in the subjects with LN. Median (IQR) hepcidin in subjects with LN was 71.5 (26.4, 116.4) ng/ml compared to 27.9 (18.7, 59.7) ng/ml in those with SLE(p = 0.19). Similarly, median (IQR) PWV in those with LN was 4.4 (4.4, 4.9) meters/second compared to 3 (3.75, 4.55) meters/second in those with without kidney involvement (p = 0.10).ConclusionPWV and serum hepcidin were higher in subjects with LN compared to those with SLE alone, suggesting that elevated hepcidin levels may be associated with morbid CV changes in children with LN. This association, along with identification of additional predictors of arterial stiffness in patients with LN, warrants further investigation.

Inflammation is important in the development of systemic lupus erythematosus (SLE). Systemic inflammation response index (SIRI) and systemic immune-inflammation index (SII) are novel clinical markers of inflammation with prognostic value in different diseases. However, the value of SIRI and SII as inflammation predictors in SLE remains unclear. This study explores the SIRI and SII as potential biomarkers for SLE. Data from 280 individuals, including newly diagnosed SLE patients and healthy controls, were collected and divided into three groups: SLE without lupus nephritis (NLN) group (n=93), lupus nephritis (LN) group (n=96) and healthy control group (n=91). Differences in SIRI and SII among the three groups were compared. Logistic regression and Pearson linear analysis were used to analyze the predictive value and correlation of SIRI and SII with SLE and systemic lupus erythematosus disease activity index 2000 (SLEDAI-2K). Receiver operating characteristic (ROC) curves evaluated SIRI and SII in predicting SLE, SLE disease activity, and LN. The SIRI and SII values were significantly higher in the LN group compared to the NLN group (p<0.01). SII had the largest area under the ROC curve for predicting LN (AUC: 0.6775, 95%CI: 0.6020 - 0.7531). Logistic regression analysis showed SIRI and SII as independent risk factors for LN. Pearson linear analysis indicated SIRI and SII were positively correlated with SLEDAI-2K (rSIRI=0.25, rSII=0.24, p<0.05). SIRI and SII are biomarkers of disease activity and renal involvement in SLE patients that can be used to evaluate and predict for SLE occurrence, disease activity, and lupus nephritis occurrence assessment.

Objective To investigate the ratios of CD4+ CD25+ regulatory cells (Tregs) and NK/NKT cells in peripheral blood of patients of lupus nephritis and to explore their contribution on the pathogenesis of lupus nephritis. Methods Patients of systemic lupus erythematosus (SLE) with no renal involvement, lupus nephritis and healthy controls were studied.Flow cytometry was utilized to quantify the percentage of CD4+ CD25+ Tregs, CD3+ CD57+ NKT cells, CD3-CD57+ NK, CD3+ CD56+ NKT cells, CD3-CD56+ NK cells and CD3-CD20+ B cells in peripheral blood.Renal biopsy was performed for patients with lupus nephritis.Urine protein and antinuclear antibody were also detected. Results The mean percentage of CD4+ CD25+ Tregs in the peripheral blood of patients with lupus nephritis was significantly lower than the control group (t=1.99, P=0.03), while CD3+ CD57+ NKT from lupus nephritis was significantly higher compared with control (t=1.98, P=0.02). However, levels of CD3-CD57+ NKT cells, CD3+ CD56+ NKT cells, CD3-CD56+ NKT cells and CD3-CD20+ B cells did not show a significant change. Conclusions CD4+ CD25+ Tregs may play an crucial role to prevent the occurrence and progression of lupus nephritis, while CD3+ CD57+ NKT cells in the peripheral blood from patients with lupus nephritis may exert an important effect on kidney damage. Key words: Lupus nephritis; Flow cytometery; CD4+ CD25+ regulatory T cells; NKT cells; NK cells

ObjectiveAssess healthcare costs associated with systemic lupus erythematosus (SLE) flares among patients with and without lupus nephritis (LN).MethodsThis retrospective cohort study used medical and pharmacy claims data from the United States-based Optum Clinformatics database to identify adults with SLE between 1 January 2016, and 31 December 2018. Index was the date of a patient’s earliest SLE diagnosis claim during the identification period. Patients were categorized based on ICD-9/-10 diagnosis codes into one of two cohorts: SLE with LN (LN) and SLE without LN (non-LN). Baseline characteristics were assessed in the 12 months preceding index (baseline period). The presence, severity, and healthcare costs (in 2019 US dollars) of flares were determined in the 12 months following index (follow-up period).ResultsOverall, 11,663 patients with SLE were included (LN, n = 2916; non-LN, n = 8747). During the baseline period, a greater proportion of patients in the LN cohort versus non-LN cohort had a Charlson Comorbidity Index score ≥4 (72.5% vs 13.7%) and inpatient stays (41.0% vs 17.0%). A total of 12,190 flares were identified during the follow-up period (LN, 3494; non-LN, 8696). A greater proportion of flares experienced by patients with LN versus those without LN were moderate (61.2% vs 53.6%) and severe (10.6% vs 5.4%). The mean (standard deviation [SD]) number of moderate and severe flares per patient was greater among the LN cohort than the non-LN cohort (moderate: LN, 1.8 [1.2] and non-LN, 1.4 [1.2]; severe: LN, 0.2 [0.6] and non-LN, 0.1 [0.3]). The mean (SD) total healthcare costs associated with SLE flares of any severity were greater for patients with LN (LN, $5842 [9604]; non-LN, $2600 [4249]). The mean (SD) cost per flare increased with severity (mild: LN, $2753 [4640] and non-LN, $1606 [2710]; moderate: LN, $4561 [7156] and non-LN, $2587 [3720]; severe: LN, $29,148 [27,273] and non-LN, $14,829 [19,533]).ConclusionsPatients with SLE with LN have greater healthcare costs than those without LN. Flares among patients with LN were more frequent, severe, and costly than among patients without LN. This highlights the need for treatments that prevent or reduce flares among patients with SLE, both with and without LN.

Background:Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that affects multiple organs, including the kidneys, leading to lupus nephritis (LN) in 40-75% of patients. Lupus nephritis (LN) is a...

PurposeIn patients with systemic lupus erythematosus (SLE), renal involvement is associated with high morbidity, and renal flare is a major contributing factor to poor long-term prognosis. Lupus nephritis (LN) still...

There are various types of cutaneous lupus erythematosus (CLE), either with or without the association of systemic lupus erythematosus (SLE). In some of the subtypes of cutaneous lupus, histopathology reveals neutrophil infiltration in the lesional skin; however, the significance of neutrophils in CLE is not yet fully elucidated. Recent studies have shown that neutrophil extracellular traps (NETs) formation by activated neutrophils is observed in several types of CLE, including lupus panniculitis, subacute lupus erythematosus, and acute lupus erythematosus, although the number of reports is small. Excessive NETosis, due to either increased NETs formation or defective clearance of NETs, may play a role in the induction of autoimmunity and autoantibody production in SLE, as well as endothelial damage, thrombus formation, and vascular damage in the lesional skin. CLE is an excessive interferon-driven autoimmune disease. Plasmacytoid dendritic cells are located in lupus erythematosus skin and contribute to the etiology of skin lesions as a main producing cell of type I interferon. Neutrophils, monocytes, and keratinocytes also produce type I interferon via several triggers. Neutrophils play an important role in the innate immune response in SLE. In this review, several types of CLE with neutrophil infiltration, as well as the role of neutrophils are discussed.

Incidence of the anti-nuclear factor in human sera.