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1.  Association of Discoid Lupus with other Clinical Manifestations among Patients with Systemic Lupus Erythematosus 
Background
Cutaneous discoid lupus (DLE) among SLE patients may be associated with less severe disease, with low frequency of nephritis and end-stage renal disease (ESRD).
Objective
To investigate associations between confirmed DLE and other SLE manifestations, adjusting for confounders.
Methods
We identified patients with rheumatologist confirmation, according to ACR SLE classification criteria 1997, >2 visits, >3 months of follow-up, and documented year of SLE diagnosis. DLE was confirmed by dermatologist, supported by histopathology and images. SLE manifestations, medications and serologies were collected. Multivariable-adjusted logistic regression analyses tested for associations between DLE and each of the ACR SLE criteria, and ESRD.
Results
A total of 1,043 SLE patients, (117 with DLE and 926 without DLE), were included in the study. After multivariable adjustment, DLE in SLE was significantly associated with photosensitivity (OR 1.63), leukopenia (OR 1.55) and anti-Smith antibodies (OR 2.41). DLE was significantly associated with reduced risks of arthritis (OR 0.49) and pleuritis (OR 0.56). We found no significant associations between DLE and nephritis or ESRD.
Limitations
Cross-sectional data collection with risk of data not captured from visits outside system.
Conclusions
In our SLE cohort, DLE was confirmed by a dermatologist and we adjusted for possible confounding by medication use, in particular hydroxychloroquine. We found increased risks of photosensitivity, leukopenia and anti-Smith antibodies and decreased risks of pleuritis and arthritis in SLE patients with DLE. DLE was not related to anti-dsDNA antibodies, lupus nephritis, or ESRD. These findings have implications for prognosis among SLE patients.
doi:10.1016/j.jaad.2013.02.010
PMCID: PMC3686921  PMID: 23541758
Systemic lupus erythematosus; discoid lupus erythematosus; cutaneous lupus erythematosus; prognosis; epidemiology
2.  Evidence for Mycobacteria in Sarcoidosis 
Despite its recognition as a distinct granulomatous disease for over a century, the etiology of sarcoidosis remains to be defined. Since the early 1900s, infectious agents have been suspected in causing sarcoidosis. For much of this time, mycobacteria were considered a likely culprit, yet until recently, the supporting evidence has been tenuous at best. In this review, we evaluate the reported association between mycobacteria and sarcoidosis. Historically, mycobacterial infection has been investigated using histologic stains, cultures of lesional tissue or blood, and identification of bacterial nucleic acids or bacterial antigens. More recently, advances in biochemical, molecular, and immunological methods have produced a more rigorous analysis of the antigenic drivers of sarcoidosis. The result of these efforts indicates that mycobacterial products likely play a role in at least a subset of sarcoidosis cases. This information, coupled with a better understanding of genetic susceptibility to this complex disease, has therapeutic implications.
doi:10.1165/rcmb.2010-0433TR
PMCID: PMC3361363  PMID: 21659662
sarcoidosis; mycobacteria; granulomas; microorganisms; peptides; immune response
3.  Dendritic Cells in the Pathogenesis of Sarcoidosis 
Sarcoidosis is a noncaseating granulomatous disease, likely of autoimmune etiology, that causes inflammation and tissue damage in multiple organs, most commonly the lung, but also skin, and lymph nodes. Reduced dendritic cell (DC) function in sarcoidosis peripheral blood compared with peripheral blood from control subjects suggests that blunted end organ cellular immunity may contribute to sarcoidosis pathogenesis. Successful treatment of sarcoidosis with tumor necrosis factor (TNF) inhibitors, which modulate DC maturation and migration, has also been reported. Together, these observations suggest that DCs may be important mediators of sarcoidosis immunology. This review focuses on the phenotype and function of DCs in the lung, skin, blood, and lymph node of patients with sarcoidosis. We conclude that DCs in end organs are phenotypically and functionally immature (anergic), while DCs in the lymph node are mature and polarize pathogenic Th1 T cells. The success of TNF inhibitors is thus likely secondary to inhibition of DC-mediated Th1 polarization in the lymph node.
doi:10.1165/rcmb.2009-0033TR
PMCID: PMC2809219  PMID: 19372243
sarcoidosis; granuloma; dendritic cell; macrophage; inflammation
4.  Mixed Connective Tissue Disease 
Western Journal of Medicine  1980;132(4):288-293.
A study was done that involved 46 patients with high-titer serum antibody to ribonucleoprotein (RNP). Common cutaneous manifestations included swollen hands or sclerodactyly (50 percent), cutaneous lupus erythematosus (48 percent), periungual telangiectasia (46 percent), alopecia (46 percent), dyspigmentation (28 percent), photosensitivity (28 percent) and vasculitis (22 percent). Frequent systemic characteristics included Raynaud phenomenon (93 percent), arthritis or arthralgia (91 percent), adenopathy (43 percent), vascular headaches (35 percent), serositis (35 percent), hoarseness (28 percent), myositis (26 percent), sicca syndrome (24 percent), renal disease (17 percent) and central nervous system disease (9 percent). Associated laboratory findings included antinuclear antibodies (100 percent), epidermal nuclear lgG deposition (91 percent), hypergammaglobulinemia (78 percent), esophageal dysmotility (61 percent), abnormal pulmonary function (59 percent), rheumatoid factor (57 percent), lupus erythematosus cells (37 percent), positive lupus band test (34 percent), hypocomplementemia (28 percent) and elevated anti-nDNA (21 percent).
It appears that patients with high-titer anti-RNP (without appreciable amounts of “anti-Sm”) have a high prevalence of Raynaud phenomenon and a low prevalence of progressive renal insufficiency and severe central nervous system disease.
PMCID: PMC1272064  PMID: 7385833

Results 1-4 (4)