In patients with systemic lupus erythematosus (SLE) and concomitant Coombs positive autoimmune haemolytic anaemia (AIHA) anticardiolipin antibodies (aCL) are found more frequently and at higher titres than in SLE patients without AIHA. In order to assess if aCL elevation is primarily associated with the underlying SLE, or with AIHA itself, we examined AIHA patients with and without underlying SLE for the presence of aCL. aCL (IgG and IgM) were determined by ELISA in 74 SLE patients without AIHA, 22 SLE patients with AIHA, 50 patients with idiopathic AIHA (warm-reactive autoantibodies), 52 patients with idiopathic AIHA (cold-reactive autoantibodies) and 50 healthy controls. The mean IgG and IgM aCL titres in SLE patients without AIHA (IgG 37.0 U/ml, IgM 8.9 U/ml) were significantly elevated compared with the values in healthy controls (IgG 9.1 U/ml, IgM 3.2 U/ml; P < 0.005). The mean aCL levels in SLE patients with AIHA (IgG 53.2 U/ml, IgM 28.2 U/ml) were higher than in SLE patients without AIHA (P = 0.09 for IgG, P < 0.005 for IgM). Interestingly, the mean aCL levels of patients with idiopathic AIHA (warm-reactive autoantibody type: IgG 29.2 U/ml, IgM 19.3 U/ml; cold-reactive autoantibody type: IgG 27.4 U/ml, IgM 18.9 U/ml) were also significantly elevated compared with healthy controls P < 0.001). As aCL are elevated not only in SLE (with and without concomitant AIHA) but also in idiopathic AIHA it can be speculated that aCL are involved in the pathomechanism of autoantibody-induced erythrocyte destruction per se irrespective of an underlying SLE.

Pupillary test data of 103 normal and 119 diabetic subjects (47 IDDM, 72 NIDDM) were evaluated by factor analysis. From a total of nine pupillary parameters three factors were extracted in the analysis. Factor 1 represents maximal pupillary area, contraction velocity at 1 s, dilation velocity at 6 s and minimal pupillary area--static and simple dynamic parameters; factor 2 amplitude of pupillary unrest, area under the detrended curve of pupillary unrest and period of pupillary unrest--parameters of pupillary unrest; factor 3 fusion frequency of pupillary response following flicker stimuli and latency time of pupillary light reflex--second order dynamic parameters. Factor analysis was then applied to investigate diabetic patients with a high percentage of autonomic neuropathic participants (about 39% had pupillary and about 35% had cardiorespiratory function disorders), which revealed the same three factors as those identified in normal subjects. Furthermore, an age-related database of parameters of pupillary unrest is given. It demonstrates that normal subjects and diabetic patients did not differ in the period of pupillary unrest (normal vs diabetic (mean +/- SEM): 1550 +/- 29 vs 1536 +/- 27 ms; 2p > 0.5). The difference in amplitude (47.8 +/- 2.8 vs 41.0 +/- 2.6% percentile; 2p = 0.071) and area under the detrended curve of pupillary unrest (47.9 +/- 2.8 vs 40.8 +/- 2.6% percentile, 2p = 0.062) seems to show a trend but was not significant. In conclusion, factor analysis revealed three different pupillary test factors.(ABSTRACT TRUNCATED AT 250 WORDS)

Background Musculoskeletal stiffness in polymyalgia rheumatica (PMR) follows a circadian rhythm. In rheumatoid arthritis (RA) patients, a timed release tablet of prednisone taken at 10pm led to a significant decrease in morning stiffness which was correlated with decreased night time plasma IL-6 [1]. However, the effects of timed release glucocorticoids on morning stiffness and the circadian profile of IL-6 in PMR have not been investigated. Previous studies of cytokines in PMR only collected blood samples at one time point mainly in the morning, without specifying the exact timing [2]. Objectives To determine whether IL-6 follows a circadian rhythm in patients with newly diagnosed untreated PMR, and to compare the effects of morning and night time glucocorticoids on overnight IL-6 and morning stiffness. Methods 10 patients with newly diagnosed PMR were randomised to two treatment groups with either night time modified-release prednisone 7mg (Lodotra) or morning immediate-release prednisolone 7mg. Hourly blood samples over 24-hours were taken before (Night A) and after 2 weeks treatment (Night B) to measure plasma IL-6. Patients were then treated with morning prednisolone 15mg and after 2 weeks a single measurement of IL-6 was performed at 9am (Day C). Duration of morning stiffness was recorded on each occasion. IL-6 assays were performed in Germany using the MILLIPLEX MAP kit. Results IL-6 showed a marked circadian variation in PMR, with a rise during the early hours of the morning which was partially suppressed by 7mg morning prednisolone and almost completely suppressed by 7mg night time prednisone (Figure 1a and 1b). Night time prednisone reduced morning stiffness by 90% compared to 42% with the morning prednisolone (p=0.044, t-test, figure 1c). Conclusions PMR, like RA, has a marked circadian variation in plasma IL-6. Both IL-6 and symptoms of morning stiffness are suppressed more by night time low dose glucocorticoids. This observation raises the possibility that PMR may be controlled by lower doses of glucocorticoids given at night compared to current conventional morning treatment. References Buttgereit, F., et al., Efficacy of modified-release versus standard prednisone to reduce duration of morning stiffness of the joints in RA (CAPRA-1): a double-blind, randomised controlled trial. Lancet, 2008. 371(9608): p. 205-214. Spies, C.M., et al., More Night Than Day - Circadian Rhythms in Polymyalgia Rheumatica and Ankylosing Spondylitis. Journal of Rheumatology, 2010. 37(5): p. 894-899. Disclosure of Interest None Declared

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