Cricoarytenoid arthritis with rheumatoid arthritis and systemic lupus erythematosus

A 56-year-old woman with rheumatoid arthritis (RA) suddenly developed severe respiratory distress and laryngeal stridor, which required endotracheal intubation. She had had RA for 12 years, which had been controlled well with prednisolone (3 mg/day) at the orthopedic clinic. Laryngoscopy revealed cricoarytenoid arthritis. She was finally diagnosed as having overlap syndrome with RA and systemic lupus erythematosus. She was given high dose corticosteroids that improved her clinical symptoms and laryngoscopic findings. She represents the first patient with overlap syndrome who developed an acute airway obstruction due to cricoarytenoid arthritis.     

Neuropsychiatric syndromes in patients with systemic lupus erythematosus and rheumatoid arthritis

OBJECTIVE: The cause of neurologic (N) and psychiatric (P) syndromes in patients with systemic lupus erythematosus (SLE) is mutifactorial and includes primary immunopathogenic mechanisms, nonspecific sequelae of chronic disease, and concurrent illnesses. We compared the prevalence, diversity, and clinical significance of NP syndromes in patients with SLE and rheumatoid arthritis (RA). METHODS: Fifty-three patients with SLE were matched by age and sex to 53 patients with RA attending ambulatory clinics in a single academic medical center. All fulfilled the American College of Rheumatology (ACR) classification criteria for either SLE or RA. Cumulative NP manifestations were determined using the ACR nomenclature and case definitions for 19 NP syndromes. Depression and anxiety were measured by the Hospital Anxiety and Depression Scales (HADS) and symptoms of cognitive dysfunction were assessed by the Cognitive Symptoms Inventory (CSI). Health related quality of life (HRQOL) was evaluated by the SF-36 and fatigue by a 10 point Likert scale. RESULTS: The patients were well matched with regard to age, sex, disease duration, and years of education. There were no significant differences in self-reported HRQOL, fatigue, anxiety, depression, and cognitive symptoms between the 2 groups. The proportion of patients with cumulative NP events was higher in RA than in SLE patients (47% vs 28%; p = 0.045), and of these the occurrence of multiple NP events in individual patients was comparable in both groups (SLE 53%; RA 48%; p = 0.75). Fifty-five percent and 66% of NP events occurred prior to the diagnosis of SLE and RA, respectively. NP events common to both SLE and RA patients were headaches, mood disorders, acute confusional states, anxiety, cerebrovascular disease, and cognitive dysfunction. Seizures and demyelinating syndrome occurred only in SLE patients, but were rare. Depression scores (HADS) were significantly higher in SLE patients with a history of cumulative NP events compared to RA patients with NP events (p = 0.02). Similarly, symptoms of cognitive dysfunction (CSI) were more common in SLE patients with a history of NP manifestations (p = 0.02). However, there were no significant differences in SF-36 subscale or fatigue scores between SLE and RA patients with cumulative NP events. CONCLUSION: NP syndromes, regardless of etiology, are common in both SLE and RA patients. SLE patients with NP syndromes report more symptoms of depression and cognitive dysfunction compared to RA patients with NP syndromes, but do not report significantly poorer HRQOL. These results emphasize the presence of non-disease-specific causes of NP manifestations in SLE patients, which should be acknowledged in future studies of pathogenesis and treatment.     

Treatment adherence in patients with rheumatoid arthritis and systemic lupus erythematosus

This study assessed self-reported adherence in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) from underserved healthcare settings. We conducted a cross-sectional survey of 102 ethnically diverse patients--70 with RA and 32 with SLE--attending rheumatology clinics at publicly funded hospitals in Houston, Texas; 43% were Hispanic, 32% African-American, and 25% White. Treatment adherence was evaluated using the compliance questionnaire rheumatology (CQR; 0, low adherence and 100, high adherence) and the questionnaire of the Adult AIDS Clinical Trials Group (AACTG). The patients were also asked how often they forgot to take their prescribed medications or discontinued them on their own. Mean patient age was 48.5 years; 75% were female, 32% were African-American, 43% Hispanic, and 25% White. Only one third reported never forgetting to take their medications; 40% reported having stopped their medications on their own because of side effects, and 20% because of lack of efficacy. Mean CQR score was 69.1 +/- 10.5, suggesting moderate adherence overall. Differences were also observed across ethnic groups: 23% of ethnic minority patients had problems taking their medications at specified times compared to 11% of Whites (p = 0.03). Lower education and side effects were associated with lower adherence. No differences were observed between RA and SLE patients. Many patients with RA and SLE report problems with treatment adherence. These appear to be more prevalent in African Americans and Hispanics than Whites; the impact of decreased adherence on outcomes could be significant and should be considered when treating patients with RA and SLE.     

Possible role of leptin in hypoandrogenicity in patients with systemic lupus erythematosus and rheumatoid arthritis

BACKGROUND: Hypoandrogenicity is common in obesity and in chronic inflammatory diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Adrenal androgens such as androstenedione (ASD) and dehydroepiandrosterone (DHEA) sulphate are low, which partly depends on the influence of TNF in chronic inflammatory diseases. Leptin is stimulated by TNF and is associated with hypoandrogenicity in non-inflammatory conditions. OBJECTIVE: To study the interrelation between serum levels of leptin and adrenal steroids in SLE and RA. METHODS: In a retrospective study, serum levels of leptin, ASD, DHEA, and 17-hydroxyprogesterone (17OHP) were measured by ELISA, and serum levels of cortisol by radioimmunoassay in 30 patients with RA, 32 with SLE, and 54 healthy control subjects (HS). RESULTS: In SLE and RA but not HS, serum levels of ASD correlated negatively with serum levels of leptin (p<0.01) independently of prior prednisolone treatment in patients with SLE (p = 0.013) and tended to be independent of prednisolone in patients with RA (p = 0.067). In a partial correlation analysis, this interrelation remained significant after controlling for daily prednisolone dose in both patient groups. In both patient groups, serum leptin levels correlated negatively with the molar ratio of serum ASD/serum cortisol and serum ASD/serum 17OHP, and positively with the molar ratio of serum DHEA/serum ASD. CONCLUSIONS: The negative correlation of serum leptin and ASD or, particularly, ASD/17OHP, together with its known anti-androgenic effects indicate that leptin is also involved in hypoandrogenicity in patients with SLE and RA. Leptin may be an important link between chronic inflammation and the hypoandrogenic state.     

Macrophage activation and coronary atherosclerosis in systemic lupus erythematosus and rheumatoid arthritis

Objective

Activation of macrophages may contribute to increased atherosclerosis and coronary artery disease in systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Neopterin, a pteridine derivative, is a novel marker of monocyte and macrophage activation that is associated with atherosclerosis and cardiovascular risk in the general population. We examined the hypothesis that macrophage activation is associated with accelerated atherosclerosis in SLE and RA.

Methods

We compared serum neopterin concentrations, adjusted for age, race, sex, and serum creatinine concentration, in patients with SLE (n = 148) or RA (n = 166) and control subjects (n = 177). In patients with SLE or RA, serum neopterin concentrations were then tested for association (adjusted for age, race, sex, serum creatinine, and medication use) with measures of disease activity or damage, inflammatory markers and mediators, and coronary artery calcium measured by electron beam computed tomography.

Results

Neopterin concentrations were significantly higher in patients with SLE (median 8.0, interquartile range [IQR] 6.5–9.8 nmoles/liter) and RA (median 6.7, IQR 5.3–8.9 nmoles/liter) than controls (median 5.7, IQR 4.8–7.1 nmoles/liter), and were higher in SLE patients than in RA patients (all P < 0.001). In SLE, neopterin was significantly correlated with higher erythrocyte sedimentation rate (ESR; P = 0.001), tumor necrosis factor α (P < 0.001), monocyte chemoattractant protein 1 (P = 0.005), and homocysteine concentrations (P = 0.01), but in RA, it was only associated with ESR (P = 0.01). Neopterin was not associated with coronary calcium in either SLE (P = 0.65) or RA (P = 0.21).

Conclusion

Macrophage activation, reflected by increased serum neopterin concentrations, was increased in both SLE and RA. Neopterin was more robustly associated with atherogenic mediators of inflammation and homocysteine in SLE than in RA, but was not associated with coronary atherosclerosis in either disease.     

Functional outcome after stroke in patients with rheumatoid arthritis and systemic lupus erythematosus

OBJECTIVE: To compare outcomes following stroke rehabilitation among patients with rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE) versus patients with neither RA nor SLE (non-RA/SLE). METHODS: We conducted a retrospective analysis using a national database of patients with stroke admitted to inpatient rehabilitation between 1994 and 2001. Primary outcomes were discharge disposition and functional status, rated by the Functional Independence Measure (FIM) Instrument, at discharge and at followup. The independent variable was RA or SLE. Covariates were age, sex, race/ethnicity, admission FIM ratings, additional comorbidities (none, 1-3, and >3), type of stroke, and length of stay. RESULTS: We studied 47,853 patients with stroke, 368 with RA, and 119 with SLE. Discharge dispositions were similar for patients with RA and non-RA/SLE (81% discharged home). At discharge, the average FIM rating for patients with RA was 85.8, compared with 87.8 for non-RA/SLE patients. At followup, the average FIM rating for patients with RA was 95.9, compared with 99.6 for non-RA/SLE patients. RA was associated with lower FIM ratings at discharge and followup in multivariate analyses. SLE was associated with younger age (17.5 years). However, patients with SLE had similar discharge dispositions and FIM ratings to non-RA/SLE patients. CONCLUSION: RA was associated with lower functional status ratings at discharge and followup. Outpatient therapy for patients with RA may reduce long-term assistance. Patients with SLE were younger, but had similar functional outcomes to patients without RA/SLE, suggesting early morbidity from stroke among patients with SLE.     

The role of stress and trauma in rheumatoid arthritis and systemic lupus erythematosus

Only one study, albeit inconclusive, has specifically addressed the etiologic role of physical trauma in RA. The weight of evidence from a variety of studies strongly suggests a role for psychologic stress in inducing, exacerbating, and effecting the ultimate outcome in RA. Well designed controlled trials aimed specifically at deciding these issues are urgently needed. This also applies to SLE, where the role of physical trauma has never been investigated, and disease exacerbation induced by emotional stress has been strongly suggested, but not yet verified in a scientifically acceptable fashion. Stress can depress immune responsiveness, but the end result of this (eg, increased susceptibility to infection, increased disease activity) is not known. It is uncertain how much or what kind of stress is required to depress responsiveness, or even how differing degrees of stress can be quantitated or reproduced. Even though eight million Americans have RA and SLE, we still know very little about the influences of stress and trauma on these disorders.     

Cortisol catabolism by lymphocytes of patients with systemic lupus erythematosus and rheumatoid arthritis

We have shown that low cortisol catabolism by lymphocytes correlates with a high sensitivity of the cells to the steroid. In the present study, we aimed to assess whether high resistance to corticosteroid treatment correlates with a high rate of cortisol catabolism by lymphocytes. Since patients with systemic lupus erythematosus (SLE) usually require high doses of corticosteroids, while patients with rheumatoid arthritis (RA) respond to relatively low doses of steroids, we compared the capability of lymphocytes of patients with SLE and RA to catabolize cortisol. The rate of cortisol catabolism obtained with the RA group was not significantly different from that obtained with the control group. The catabolism of cortisol by lymphocytes of the SLE group was significantly higher than both the control group (p less than 0.05) and the RA group (p less than 0.01). A significant correlation was demonstrated between the SLE disease activity index and rates of cortisol catabolism attained by lymphocytes of SLE patients (p less than 0.001).     

Thyroid disorders and autoantibodies in systemic lupus erythematosus and rheumatoid arthritis patients

To determine the patterns of thyroid dysfunction and autoantibodies associated with SLE and RA patients, twenty patients with SLE and another group of twenty with RA were studied. The results were compared with those of twenty apparently healthy age- and sex- matched controls. All patients were subjected to complete history taking, thorough clinical examination and joint examination. All patients and controls were subjected to the following investigations: T3, T4, TSH, antithyroglobulin antibodies (ATGAb) and thyroid peroxidase antibodies (TPOAb). Also, complete blood picture, ESR, RF, ANA, CRP and LE cells were done. This study revealed that thyroid disorders were significantly increased in SLE patients (50%) when compared to RA (15%) (P<0.05). In SLE group, 20% had euthyroid sick syndrome, 20% had hypothyroidism (10% subclinical and 10% biochemical), and 10% had hyperthyroidism (5% subclinical and 5% biochemical). However, in RA, 10% had hypothyroidism (subclinical) and 5% had subclinical hyperthyroidism. TPOAb was found in 15% of SLE and 5% of RA patients and 10% of controls, but the titres were higher in SLE and RA patients. Also, ATGAb was found in 5% of SLE, 30% of RA patients and 10% of controls, but the titres were higher in SLE and RA patients. It is concluded that thyroid abnormalities are more implicated with euthyroid sick syndrome and hypothyroidism (subclinical and overt) than hyperthyroidism in SLE patients. SLE and RA were associated with antithyroid antibodies (TPOAb in SLE and ATGAb in RA). Performance of thyroid function tests in patients with SLE, in particular and RA as a part of the biochemical and immunological profiles, may help in early detection of associated thyroid disorders.     

Antibody-mediated lymphocytotoxicity in rheumatoid arthritis and systemic lupus erythematosus

Lymphocyte-dependent antibody cytotoxicity (LDAC) was studied using peripheral blood and in some instances synovial fluid cells from patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). No difference from normal controls was observed with peripheral blood lymphocytes from either RA or SLE. Marked decrement in LDAC effector cell activity was present particularly with RA synovial fluid cells. Sera from patients with RA or SLE as well as RA synovial fluids markedly inhibited LDAC.     

Lymphokine production in rheumatoid arthritis and systemic lupus erythematosus

The production of interferon (IFN) by peripheral blood lymphocytes from patients with rheumatoid arthritis (RA) and of IFN and interleukin 2 (IL-2) in systemic lupus erythematosus (SLE) was compared with that of healthy controls. Patients with SLE showed a significant reduction in IL-2 production compared to controls if the PBL were irradiated before mitogen stimulation. No patient with RA or SLE studied had impaired IFN production regardless of disease activity and the IFN produced was always IFN-gamma in type. We conclude that there is an abnormality in IL-2 production in SLE but there is no abnormality in IFN-gamma production in either RA or SLE.     

Thyroid disease in systemic lupus erythematosus and rheumatoid arthritis

SIR, We determined the degree of overlap between autoimmunethyroid disease and two non-organ-specific autoimmune diseases,systemic lupus erythematosus (SLE) and rheumatoid arthritis(RA). Both SLE and RA are commonly encountered in our out-patientpractice and were chosen because of their clinical relevance. Sixty-nine SLE and 64 RA patients fulfilling the American RheumatismAssociation criteria for SLE [1] and RA [2] were selected forthis study. Patients from both groups were found     

Infections in systemic lupus erythematosus and rheumatoid arthritis.

Patients with systemic lupus erythematosus have a higher infection rate than the general population. It is estimated that at least 50% of them will suffer a severe infectious episode during the course of the disease. Improvements in the control of the disease are discussed in this article.     

The coexistence of rheumatoid arthritis and systemic lupus erythematosus

Summary A 29-year-old white female with longstanding classical rheumatoid arthritis (RA) developed clinical and serological manifestations of systemic lupus erythematosus (SLE) with prominent signs of diffuse proliferative lupus nephritis. She fulfilled the ARA criteria for the classification of SLE as well as the ARA criteria for classical RA. The concomitant presence of these two affections in the same patient is rare and the discriminating features suggest that this coexistence may be coincidental. With respect to treatment, our patient had good relief of symptoms by a combined administration of methylprednisolone pulses and cyclophosphamide.     

Frequency of neoplasia in systemic lupus erythematosus and rheumatoid arthritis

A patient population admitted to the hospital for either SLE or RA was surveyed for the subsequent development of neoplasms. The frequency of neoplasm in SLE patients appeared to be exaggerated, whereas the frequency of subsequent neoplasm in rheumatoid patients was unexpectedly low. A paucity of nephritis in the SLE group was noted. Further reports are encouraged so that the magnitude of the risk of malignancy developing with immunosuppressive therapy can be more precisely ascertained.