Identification of highly active systemic lupus erythematosus by combined type I interferon and neutrophil gene scores vs classical serologic markers.

OBJECTIVES: In SLE, heterogeneous clinical expression and activity may reflect diverse pathogenic and/or effector mechanisms. We investigated SLE heterogeneity by assessing the expression of three gene sets representative of type I IFN (IFN-I), polymorphonuclear neutrophil (PMN) and plasmablast (PB) signatures in a well-characterized, multidisciplinary cohort of SLE patients. We further assessed whether individual gene products could be representative of these three signatures. METHODS: Whole blood, serum and clinical data were obtained from 140 SLE individuals. Gene expression was assessed by NanoString technology, using a panel of 37 probes to compute six IFN-I, one PMN and one PB scores. Protein levels were measured by ELISA. RESULTS: Depending on the score, 45-50% of SLE individuals showed high IFN-I gene expression. All six IFN-I scores were significantly associated with active skin involvement, and two of six were associated with arthritis. IFN-induced Mx1 protein (MX1) level was correlated with IFN-I score (P < 0.0001) and associated with a similar clinical phenotype. In all, 25% of SLE individuals showed high PMN gene expression, associated with SLE fever, serositis, leukopoenia and glucocorticoid use. PB gene expression was highly affected by immunosuppressant agents, with no association with SLE features. Combined IFN-I and PMN gene scores were significantly associated with high disease activity and outperformed anti-dsDNA and anti-C1q autoantibody and complement levels for predicting SLE activity. CONCLUSION: IFN-I and PMN gene scores segregate with distinct SLE clinical features, and their combination may identify high disease activity. MX1 protein level performed similar to IFN-I gene expression.

A rare combination: chylous polyserositis and autoimmune myelofibrosis as a presentation of systemic lupus erythematosus.

Chylous polyserositis and autoimmune myelofibrosis occurring concomitantly inn a case of SLE are a rare phenomenon. We here report a case of a 38-year-old woman who was admitted with a history of cough and shortness of breath for 1½ months along with fever and abdominal distension for 1 month. She also had arthralgias, weight loss and pancytopenia. She was diagnosed as a case of SLE with Chylous polyserositis and autoimmune myelofibrosis. She was started on steroids and immunosuppressive therapy, to which she responded. To summarize, this is the first case report where chylous polyserositis and pancytopenia due to autoimmune myelofibrosis occurred which was responsive to steroids and immunosuppressive therapy.

Anti-neutrophil cytoplasmic antibodies in new-onset systemic lupus erythematosus and lupus nephritis.

This study aims to investigate the role of Antineutrophil cytoplasmic antibodies (ANCA) in patients with new-onset systemic lupus erythematosus (SLE). Sixty SLE patients, 28 of whom had lupus nephritis (LN), and 60 normal controls were enrolled; Serum ANCA was measured by enzyme linked immunosorbent assay (ELISA). The clinical and laboratory parameters of the patients were also recorded. Results show that twenty SLE patients were seropositive for ANCA, which was significantly higher than in normal controls. LN patients had significantly higher positive rate of ANCA than patients without nephritis. Compared with ANCA-negative patients, the ANCA-positive patients had significantly higher incidence of nerves system disorder, myocarditis, renal involvement and serositis. The positive rate of gamma-globulin, anti-dsDNA and anti-Sm antibodies were significantly higher in ANCA-positive patients. Elevated IgG and ESR, decreased serum C3/C4 appeared more often in ANCA-positive patients. In addition, serum ANCA level correlated positively with disease activity. Taken together, ANCA might be used as a potential complementary parameter to differentiate LN from SLE without nephritis. In addition, ANCA may serve as a useful marker of the disease activity of SLE.

Anti-cyclic citrullinated peptide-2 (CCP2) autoantibodies and extra-articular manifestations in Greek patients with rheumatoid arthritis.

The objective of our study was to establish whether there is an association between rheumatoid arthritis with extra-articular manifestations (exRA) and anti-cyclic citrullinated peptide 2 (anti-CCP2) antibodies in Greeks. A retrospective study of 220 Greek patients with RA, 95 with exRA and 125 without extra-articular manifestations (cRA). Serum anti-CCP2 antibodies and IgM rheumatoid factor (RF) were measured. CCP2(+) were 65.3% of exRA and 58.4% of cRA patients. RF(+) were 69.5% of exRA and 60.0% of cRA patients. Among exRA patients, 37.9% had high serum anti-CCP2 antibody levels (>100 IU/ml) compared to 21.6% cRA patients (p = 0.008). Serositis and pulmonary fibrosis were found to be associated with high levels of anti-CCP2 antibodies (52.9 vs 26.6%, p = 0.02 and 63.6 vs 26.8%, p = 0.008, respectively). Serum RF levels were 265.0 +/- 52.0 IU/ml (mean +/- SEM) in exRA and 205.1 +/- 40.6 (mean +/- SEM) in cRA (NS). High serum RF levels (>268 IU/ml) were more likely to have sicca syndrome. In Greek patients with rheumatoid arthritis (RA), high serum anti-CCP2 antibodies are associated with serositis and pulmonary fibrosis. Therefore, anti-CCP2 antibodies have prognostic significance in patients with RA.

Diagnosis of active tuberculous serositis by antigen-specific interferon-gamma response of cavity fluid cells.

BACKGROUND: To develop a more accurate methodology for diagnosing active tuberculous pleurisy, as well as peritonitis and pericardits of tuberculous origin, we established an antigen-specific interferon gamma (IFN-gamma)-based assay that uses cavity fluid specimens. METHODS: Over a 19-month period, 155 consecutive, nonselected patients with any cavity effusion were evaluated. Study subjects were 28 patients with bacteriologically confirmed active tuberculous serositis and 47 patients with definitive nontuberculous etiology. Culture was performed for 18 h with fluid mononuclear cells in the supernatant of the effusion together with saline or Mycobacterium tuberculosis-specific antigenic peptides, early secretory antigenic target 6 and culture filtrate protein 10. IFN-gamma concentrations in the culture supernatants were measured. RESULTS: In patients with active tuberculous serositis, antigen-specific IFN-gamma responses of cavity fluid samples were significantly higher than those of nontuberculous effusion samples. Area under the receiver operating characteristic (AUROC) curve was significantly greater for cavity fluid IFN-gamma response (AUROC curve, 0.996) than for cavity fluid adenosine deaminase and whole-blood IFN-gamma responses (AUROC curve, 0.882 and 0.719, respectively; P = .037 and P < .001, respectively). Although the AUROC curve was greater for cavity fluid IFN-gamma response than for background cavity fluid IFN-gamma level (AUROC curve, 0.975), the AUROC curves were not statistically significantly different (P = .74). However, multivariate logistic regression analysis revealed that cavity fluid IFN-gamma responses were significantly associated with the diagnosis, even after adjustment for background IFN-gamma level (adjusted odds ratio, 1.21; 95% confidence interval, 1.03-1.42; P < .001). CONCLUSIONS: The cavity fluid IFN-gamma assay could be a method for accurately and promptly diagnosing active tuberculous serositis.

[Rituximab for treatment of patients with systemic autoimmune diseases]. / Utilidad del rituximab en el tratamiento de pacientes con enfermedades sistémicas autoinmunitarias.

BACKGROUND AND OBJECTIVE: To assess the value of rituximab in systemic autoimmune diseases which are refractory to others treatments. PATIENTS AND METHOD: Prospective study on 12 patients -7 with systemic lupus erythematosus (SLE), 4 with Wegener's granulomatosis (WG), and 1 with overlapping connective disease and autoimmune thrombocytopenia-, controlled in a specialized unit of a tertiary hospital. Four weekly doses of rituximab, 2 biweekly doses of cyclophosphamide, and glucocorticoids were administered to all patients, and other immunosuppressants were also administered as considered necessary in each case. RESULTS: Mean follow up after treatment with rituximab was 12.8 moths for SLE patients and 12.3 for WG patients. In SLE patients, proteinuria was reduced below 1 g daily in 5 cases (83%), with a clear parallel improvement in the urinary sediment. Serositis was resolved in both cases. One patient required 3 treatment cycles to obtain an adequate response and another required a second cycle for relapse. Only one patient with WG had a favorable response. The patient treated for autoimmune thrombocytopenia had a favorable response, with no relapses, and creatine-kinase levels also tended to return to normal. There were 2 serious adverse events (terminal renal failure and serious colitis in a patient with SLE, and death of one patient with WG), that were not adjudicated directly to rituximab. Immunoglobulin levels did not change substantially. There were no infusion reactions or associated infections. CONCLUSIONS: Rituximab was useful in patients with SLE refractory to other immunosuppressants. On the contrary, its efficacy in WG was limited. The response of thrombocytopenia was complete and maintained.

Severe polyserositis induced by the 13-valent pneumococcal conjugate vaccine: a case report.

BACKGROUND: The United States Advisory Committee on Immunization Practices recommends administration of the 13-valent pneumococcal conjugate vaccine in series with the 23-valent pneumococcal polysaccharide vaccine for prevention of pneumonia in the elderly. Reports of autoimmune or auto-inflammatory diseases as a result of pneumococcal vaccination, especially pneumococcal conjugate vaccine, are extremely rare. CASE PRESENTATION: We present a case of severe serositis in a 75-year-old Caucasian woman complicated by pericardial and pleural effusions in the setting of recent 13-valent pneumococcal conjugate vaccine vaccination and no other obvious etiology. Our patient required steroid treatment, thoracentesis, chest tube, and pericardial window and subsequently recovered to her baseline. CONCLUSIONS: To the best of our knowledge, no such reaction to the 13-valent pneumococcal conjugate vaccine has previously been documented. Although the benefits of vaccination outweigh the risks, knowledge of this potential side effect can help clinicians in diagnosis and treatment of similar patients.

Anti-SmD1 antibodies are associated with renal disorder, seizures, and pulmonary arterial hypertension in Chinese patients with active SLE.

Detection of autoantibodies in systemic lupus erythematosus (SLE) plays an important role in timely diagnosis and earlier treatment of SLE. In this study, we used a SmD1 polypeptide-based ELISA to determine anti-SmD1 antibody in 269 SLE, including100 naïve (had not been treated with steroids or immunosuppressants at study inception) SLE patients and 169 non-naive SLE patients; 233 controls with other rheumatic diseases (RDC) (70 RA, 40 AS, 73SSc, and 50 SS), and 110 healthy controls (HC) group. The positive rate of anti-SmD1 among all SLE patients was 60.97%, higher than that in the RDC group (13.30%, P = 0.000) or the HC group (9.09%, P = 0.000). The positive rate of anti-SmD1 in non-naive SLE patients was higher than that for anti-dsDNA antibodies (44.97%, P = 0.03). Positivity for anti-SmD1 only was found in 14.00% of naive SLE patients and 16.00% of non-naive SLE patients. In naive SLE patients, the serum concentration of anti-SmD1 was lower after treatment than before treatment (P = 0.039). Active SLE patients positive for anti-SmD1 were more likely to have malar rash, rash, nonscarring alopecia, PAH and hypocomplementemia. High positivity for anti-SmD1 only in patients with SLE indicated the importance and necessity of detection of anti-SmD1 in patients with SLE.

Serositis with autoimmune endocrinopathy: clinical and immunogenetic features.

Twenty patients with autoimmune endocrinopathies experienced 45 episodes of pleural and/or pericardial serositis. Seventeen of these patients were women and 15 had clinical or serologic evidence of 2 or more endocrinopathies. Idiopathic primary hypoadrenalism (10 cases), Graves' disease (8 cases), Hashimoto's disease (4 cases), atrophic thyroiditis with hypothyroidism (3 cases), idiopathic primary hypogonadism (3 cases), transient thyroiditides (2 cases), and type I diabetes mellitus (1 case) were diagnosed at a mean age of 24 years. Serositis recurred after asymptomatic intervals of months to years even in patients treated for endocrine dysfunction. Fourteen of 16 Caucasians had circulating immune complexes, including all 9 patients with a C4AQ0 (C4A null) phenotype and including all 12 patients with HLA antigens B8 and DR3, antigens associated with systemic lupus and with autoimmune endocrinopathies. Serositides associated with autoimmune endocrinopathies can occur with chest pain, fever, and exudative effusions in young Caucasian women with the HLA B8 DR3 C4AQ0 phenotype. These serositides may have a common pathophysiologic mechanism.

Systemic lupus erythematosus presenting as chronic serositis with no demonstrable antinuclear antibodies.

Approximately 5 percent of patients with systemic lupus erythematosus by clinical and pathologic criteria have no demonstrable antinuclear antibodies. This figure is likely to be an underestimate, as it does not include the antinuclear antibody-negative patients with limited manifestations in whom the diagnosis of systemic lupus erythematosus is missed. A 23-year-old woman is described who had a history of perplexing bilateral pleural effusions with development of peritoneal effusion after 18 months and positive antinuclear antibody results after 22 months. Tissue pathologic features, initially interpreted as nonspecific, on review revealed striking lymphocytic periarteritis with endothelial swelling and leukocytoclastic vasculitis often seen in systemic lupus. A selective defect in the suppression of T cell effector function, such as direct cell-mediated cytotoxicity, with intact suppressor systems for B cell effector function, such as antibody production, can be postulated in this patient. This would explain the active cellular tissue pathology with the lack of prominent antinuclear antibody production.

Syndrome and pancreatic disease, subcutaneous fat necrosis and polyserositis. Case report and review of literature.

Immunologic evaluation of a patient with pancreatitis, subcutaneous fat necrosis, pleuritis, pericarditis and synovitis is presented. The previously recognized syndrome of pancreatic disease, subcutaneous fat necrosis and arthritis is reviewed. Based on analysis of all the cases described in the English language literature it is suggested that this syndrome be expanded to include polyserositis rather than arthritis alone. Although experimental and clinical evidence tends to implicate physiocochemical tissue injury by pancreatic lipase as the primary pathogenic mechanism in this syndrome, studies in our patient suggest the possible contribution of immune-mediated injury. Supporting data include eosinophilia, biopsy demonstration of vasculitis antedating the subcutaneous fat necrosis, immunofluorescent identification of immunoglobulin G (IgG) and C3 in the pleura, and reduced levels of total hemolytic complement in the serum, and pleural and pericardial effusions.

Anti-neutrophil cytoplasmic antibodies in 566 European patients with systemic lupus erythematosus: prevalence, clinical associations and correlation with other autoantibodies. European Concerted Action on the Immunogenetics of SLE.

OBJECTIVES: To evaluate, in a cohort of 566 patients with systemic lupus erythematosus (SLE) drawn from 11 European centres: (i) the prevalence of ANCAs and their subspecificities in a large series of European SLE patients; (ii) the possible associations of ANCA with the most common clinical manifestations of the disease; and (iii) whether ANCAs correlate with some of the autoantibodies commonly found in SLE. METHODS: ANCA detection was performed by indirect immunofluorescence (IIF), and by ELISA for lactoferrin (LF), myeloperoxydase (MPO), proteinase3 (PR3) and lysozyme (LZ) subspecificities. RESULTS: The prevalence of ANCA was 16.4% (IIF). The prevalence of LF was 14.3%, LZ 4.6%, MPO 9.3%, and PR3 1.7%. Our results show that ANCA is associated with certain clinical manifestations of SLE. In particular, positive correlations were found between IIF ANCA and serositis (p = 0.026), livedo reticularis (p = 0.01), venous thrombosis (p = 0.03) and arthritis (p = 0.04), while anti-LF antibodies were associated with serositis (p = 0.05) and livedo reticularis (p < 10(-3). Nevertheless, multivariate analysis demonstrated that other autoantibodies, such as aCL and SSA/Ro, are more closely correlated than ANCA with some of the aforementioned clinical features. CONCLUSION: Our results demonstrate that ANCA are detectable in SLE sera and that some of them are associated with particular clinical manifestations. Whether ANCA plays a direct pathogenetic role in the vascular damage of SLE or only represents an epiphenomenon or a marker of disease activity remains to be elucidated.

Mycoplasma hyorhinis infection of pigs selectively bred for high and low immune response.

Pigs have been selected for high (H) or low (L) combined antibody and cell-mediated immune response to test the high immune response phenotype as a candidate for an indirect approach to improving health and productivity in livestock. Mycoplasma hyorhinis infection was induced in H and L pigs of the 4th generation of selection to test the hypothesis that immune response lines differ in response to infection. The major disease sign, arthritis, was more severe in the H pigs both clinically and at necropsy. M. hyorhinis was isolated at higher colony counts from synovial fluids of the H pigs. In contrast, pleuritis and peritonitis were less severe in pigs of the H than those of the L line. Pericarditis, although less in H than L pigs, did not differ significantly by line. Synovial fluid antibody to M. hyorhinis did not differ by line but H pigs produced serum antibody earlier and to a higher titre than did L pigs. Selection for H or L immune response therefore alters response to M. hyorhinis, however there is no indication of a consistent line-related health advantage.

Case report: distinctive immune abnormalities in a patient with procainamide-induced lupus and serositis.

To gain insight into the immunopathogenesis of drug-induced autoimmune disorders, lymphocyte and immunoglobulin distributions and cytokine levels were monitored in the peripheral blood and pleural fluid of a patient with procainamide-induced lupus and pleural effusion. Approximately 80% of the B cells in both compartments were CD5+ compared to 10% to 25% in normal adults. CD4/CD8 ratio and percentage CD4 were normal in peripheral blood. Serum levels of IgG (particularly IgG2), IL-6, and soluble IL-2R were slightly elevated, and those of IgA were significantly elevated compared to normal controls. Analysis of the pleural effusion revealed an increased CD4/CD8 ratio because of an increased percentage of CD4+CD29+ helper memory T cells, lack of expression of the resting B-cell marker CD21, immune complex deposition and complement consumption, increased relative levels of ANA, abnormally high levels of IL-6 and soluble IL-2R, and detectable levels of IL-1b, IFN-g and TNF-a. These observations provide evidence for the involvement of CD5+ B cells and differential helper T-cell activity in procainamide-induced lupus and for an association between local lymphocyte activation and organ pathology.

Serositis: comparative analysis of histological findings and pathogenetic mechanisms in nonbacterial serosal inflammation.

Peritonitis is the established term for infective inflammation of the peritoneum, while serositis generally refers to nonorganismal inflammation in any serous cavity, including the peritoneum. In continuous ambulatory peritoneal dialysis (CAPD) literature, however, culture-negative peritoneal inflammation is referred to as "sterile" or "chemical" peritonitis. These terms not only imply unwarranted etiologic assumptions, but may also deflect attention from the existence of medical conditions to which the peritoneum is subject. This is evident in CAPD literature where there is little recognition that the peritoneum, as a member of the serosa and a secretor of lamellar bodies, is prey to a wide range of disorders. Thus before, during, and after CAPD, the membrane is liable to fall victim to disease states unconnected with the process of dialysis. Significant peritoneal pathology occurs as part of a pan-serositis, which may be metabolic (uremia, cholesterolosis), autoimmune (systemic lupus erythematosus, rheumatoid disease, acute rheumatism, endocrinopathies), genetic (recurrent hereditary polyserositis), allergic (eosinophilic serositis), and granulomatous in nature. This paper presents a comparative analysis of histopathological presentation and pathogenetic mechanisms involved in all forms of peritoneal serositis. It incorporates recent advances in molecular biology of the membrane into a holistic reappraisal of peritoneal pathology, revealing hitherto unrecognized homologies in peritoneal reaction to diverse disorders.

[Polyserositic syndromes and/or sectorial dysventilation with platelet activation induced by immunoallergic etiopathogenesis]. / Sindromi polisierositiche e/o disventilatorie settoriali con attivazione piastrinica da etiopatogenesi immunoallergica.

The author from a study of 5 dysventilatorial syndromes (bronchiolitis-PNX, pneumomediastinal aerial cystis of lung) and 5 polysierositic syndromes pleuritis and peritonitis) evices that all these syndromes show in the anamnesis or in present a viral infection from influenzal virus or rubeola. In addition to that, the Authors shows the presence of a food allergy asserted by RAST and/or Skin Prick Tests or FBST (Food Bronchostimulation test) and the introduction of a food allergen during the viral infection, and a great platelet's activation. The Author, besides, shows the association normal VES and normal neutrophil cells in the dysventilatorial syndrome and high VES, and high neutrophil cells in the polysierositic syndromes; in all cases the negativity of culture exams. Starting from these points she worked out a new etiopathogenetic theory: the viral localization on the Peyer's plates cause the expression on the epithelial surface of the gut's cells of SELF HLA II type recognition. The food allergens' introduction causes a great reaction of II, III, IV, VI type which involves the bronchus, alveolus, and the serous epithelium by PAF activation, in all cases and in the polisierositic syndrome a neutrophil activation as well. The author advices to prize the importance of cortisone therapy and of exclusion of food allergen by diet, besides advices the antibiotic therapy for covering only.

The effect of a homologous bacterin given to sows prefarrowing on the development of Glässer's disease in postweaning pigs after i.v. challenge with Haemophilus parasuis serotype 5.

UNLABELLED: The trial was carried out to evaluate the impact of maternal antibodies on the development of Glässer's disease after i.v. exposure of weaned pigs with a homologous serovar of Haemophilus parasuis (HPS). Two groups of weaned pigs were formed. Group one VI (n = 10): born to vaccinated sows, weaners i.v. challenged one week postweaning and euthanatized 14 days postweaning. Group two NVI (n = 10 wearners): born to non vaccinated sows, i.v. challenged one week postweaning euthanatized 14 days postweaning. One week postweaning all weaners were i.v. inoculated with HPS serovar 5. The following parameters were evaluated: clinical signs (depression, centralnervous signs, fever, lameness), macroscopic lung, pleura, peritoneum, liver and joint changes, and mortality. All trial sows were HPS seronegative prior to vaccination. The HPS vaccinated sows were proven seropositive on day 3 p.p. (values > 0.24), the non vaccinated ones were tested seronegative (values < 0.23). The progeny of sows vaccinated prefarrowing with two doses of HPS serovar 5 bacterin were partially protected against HPS caused clinical and pathological signs. The majority of clinical signs as fever, depression, recumbency, lack of response to verbal stimuli and lameness showed significant (P < 0.05) milder clinical symptoms in VI than in NVI animals. Respiratory signs (P = .169) and involvement of the central nervous system as ataxia, muscular tremor, incoordination of hind legs and convulsions (P = 1) showed no significant differences between the groups. Except lesions of pericard (VI vs. NVI, P = .14) and pleura (VI vs. NVI, P = .14) there were significant (P < 0.05) macroscopic differences at necropsy in lung, liver, joints and cerebrospinal fluid between the offspring of vaccinated sows and the ones of non vaccinated dams. No HPS were isolated from the nasal mucosa of the pigs prior to inoculation. HPS serovar 5 was recovered at necropsy from the nasal mucosa of all pigs in both groups. One pig from group VI presented in all examined organs the presence of HPS serovar 5. The remaining animals in group VI revealed in lung, pericard, pleura, liver, joints and cerebrospinal fluid no presence of HPS. The rate of isolation between VI and NVI groups revealed a significant (P < 0.05) difference. All the survived piglets of group NVI showed positive ELISA titres against HPS serovar 5 (values > .24). The piglets that died or were euthanatized before the end of the study have not been subjected to ELISA serological testing. One piglet died in group VI before the end of the study. Non of the remaining animals in group VI showed seroconversion to HPS serovar 5. IMPLICATIONS: Vaccination of sows did not influence the colonisation of nasal mucosa, but progeny of sows vaccinated prefarrowing with two doses of HPS serovar 5 bacterin were partially protected against HPS caused diseases.

Utility of T-cell interferon-γ release assays for diagnosing tuberculous serositis: a prospective study in Beijing, China.

BACKGROUND: Diagnosis of tuberculous serositis remains a challenge. The aim of this study was to evaluate the diagnostic efficiency of T-SPOT.TB on serous effusion mononuclear cells (SEMC) for diagnosing tuberculous serositis in a high TB burden area. METHODS: The present prospective study enrolled patients with suspected tuberculous serositis in a tertiary referral hospital in Beijing, China, to investigate the diagnostic sensitivity, specificity, predictive value (PV), and likelihood ratio(LR) of these tests. Clinical assessment, T-SPOT.TB on SEMC, and T-SPOT.TB on PBMC were performed. Test results were compared with the final confirmed diagnosis. RESULTS: Of the 187 participants, 74 (39.6%) were microbiologically or clinically diagnosed as tuberculous serositis and 93(49.7%) were ruled out. The remaining 20 (10.7%) patients were clinically indeterminate and excluded from the final analysis. Compared to that on PBMC, T-SPOT.TB on SEMC showed higher sensitivity (91.9%vs73.0%, P = 0.002), specificity (87.1%vs.73.1%, P = 0.017), PPV (85.0%vs.68.4%, P = 0.013), NPV (93.1%vs.77.3%, P = 0.003), LR+ (7.12vs.2.72) and LR- (0.09vs.0.37), respectively. The frequencies of spot forming cells (SFCs) for T-SPOT.TB on SEMC were 636 per million SEMC (IQR, 143-3443) in patients with tuberculous serositis, which were 4.6-fold (IQR, 1.3-14.3) higher than those of PBMC. By ROC curve analysis, a cut-off value of 56 SFCs per million SEMC for T-SPOT.TB on SEMC showed a sensitivity of 90.5% and specificity of 89.2% for the diagnosis of tuberculous serositis. CONCLUSIONS: T-SPOT.TB on SEMC could be an accurate diagnostic method for tuberculous serositis in TB endemic settings. And 56 SFCs per million SEMC might be the optimal cut-off value to diagnose tuberculous serositis.

Prolactin and autoimmunity: hyperprolactinemia correlates with serositis and anemia in SLE patients.

Evidence points to an association of prolactin to autoimmune diseases. We examined the correlation between hyperprolactinemia and disease manifestations and activity in a large patient cohort. Age- and sex-adjusted prolactin concentration was assessed in 256 serum samples from lupus patients utilizing the LIASON prolactin automated immunoassay method (DiaSorin S.p.A, Saluggia, Italy). Disease activity was defined as present if European Consensus Lupus Activity Measurement (ECLAM) > 2 or Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) > 4. Lupus manifestations were grouped by organ involvement, laboratory data, and prescribed medications. Hyperprolactinemia was presented in 46/256 (18%) of the cohort. Hyperprolactinemic patients had significantly more serositis (40% vs. 32.4%, p = 0.03) specifically, pleuritis (33% vs. 17%, p = 0.02), pericarditis (30% vs. 12%, p = 0.002), and peritonitis (15% vs. 0.8%, p = 0.003). Hyperprolactinemic subjects exhibited significantly more anemia (42% vs. 26%, p = 0.02) and marginally more proteinuria (65.5% vs. 46%, p = 0.06). Elevated levels of prolactin were not significantly associated with other clinical manifestations, serology, or therapy. Disease activity scores were not associated with hyperprolactinemia. Hyperprolactinemia in lupus patients is associated with all types of serositis and anemia but not with other clinical, serological therapeutic measures or with disease activity. These results suggest that dopamine agonists may be an optional therapy for lupus patients with hyperprolactinemia.

Seasonal variation in the activity of systemic lupus erythematosus.

OBJECTIVE: To determine whether there is any seasonal variation in the activity of systemic lupus erythematosus (SLE) overall and by individual organs. METHODS: The study group comprised 2102 patients with SLE who were followed in a prospective longitudinal cohort study. In this cohort, 92.3% of the patients were women. The mean ± SD age of the patients was 47.9 ± 13.9 years, 56.3% were white, 37.1% were African American, and 3.1% were Asian. Global disease activity was recorded by the Safety of Estrogens in Lupus Erythematosus National Assessment - Systemic Lupus Erythematosus Disease Activity Index (SELENA-SLEDAI) and the physician's global assessment. Activity of each organ was also recorded using SLEDAI terms and a visual analog scale (VAS; 0 to 3). RESULTS: There was significant seasonal variation in photosensitive rash (p < 0.0001), which was more frequent in the spring and summer months (p < 0.0001). There was significantly more arthritis activity in spring and summer, as measured by both SELENA-SLEDAI (p = 0.0057) and the joint VAS (p = 0.0047). A decrease in renal activity was found in the summer months compared to the rest of the year (p = 0.0397). Serositis recorded by VAS had higher activity from August to October (p = 0.0392). Anti-dsDNA levels were significantly higher during October and November (p < 0.0001). There was significant seasonal variation in antiphospholipid antibody levels (p < 0.0001) and lupus anticoagulant (p = 0.0003). We found a significant variation in activity through the year in global disease activity as measured by SELENA-SLEDAI (p = 0.048). CONCLUSION: In the Hopkins Lupus Cohort, skin and joint activity is increased during the spring and summer, but other organs have different patterns. These seasonal variations likely reflect environmental factors that influence disease activity, including ultraviolet light and infections.