Sir, We report on four Caucasian womenwith SLE presenting splenic microcalcifications (Table 1). Considering our consecutive patients with SLE admitted between 2000 and 2006, the prevalence is 5.7%. At the time of the detection of multiple splenic calcifications, mean SLE duration was 16.75 ± 3.91 years. Patients had malar rash, proliferative glomerulonephritis and non-erosive polyarthritis. According to the Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI 2K), SLE was moderately active in Cases 2 and 4, being inactive in the other two subjects. Serological markers comprised positive anti-nuclear antibodies, anti-dsDNA antibodies and reduced C3 and C4 levels. Anti-phopholipid antibodies (aPL) were positive in two subjects, in one associated with lupus anticoagulant (LAC) (Case 2). None had thrombocytosis. All the patients were on low-dose steroid treatment; in two of them associated with lowdose aspirin. Splenic microcalcifications were incidentally found during a routine chest X-ray (Figure 1 shows multiple calcific nodular shadows as documented in Case 4) or an ultrasound scan of the abdomen. The manifestation was asymptomatic. Previous ultrasound exams showed normal splenic parenchyma. Specific causes of splenic calcifications were ruled out. The mean follow-up of the four subjects, once splenic microcalcifications were documented, was 4.5 ± 1 years. Ultrasound scans of the spleen were regularly performed. During this period of time, in concomitance with a relapse of lupus nephritis, in Case 4 autosplenectomy occurred. She underwent immunisation with a pneumococcal polysaccharide vaccine. The patient is now well with a low-dose prednisone, and she did not present infections. In the other subjects, the disease was inactive; none of them presented infections. To our knowledge, the association of splenic microcalcifications with a connective tissue disease has been described in only two reports.1,2 Due to the paucity of the disposable data, the pathogenesis of this rare condition can only be hypothesised. It is possible that splenic microcalcifications could be the late-end consequence of an immune-mediated inflammation of the arterial vessels probably linked to repeated flares of SLE.1,3 The link between SLE flare and spleen pathology seems more relevant in Case 4, in which autosplenectomy followed a relapse of lupus nephritis. As in two of our cases, splenic microcalcifications could be related to thrombotic microangiopathy, having thrombophilic factors (as aPL or LAC) a central role.4 Santilli, et al. revising the 18 cases with autosplenectomy described in the literature reported that autosplenectomy in SLE may be pathogenetically related to aPL because aPL was documented in most of the cases.4 Lupus (2009) 18, 570–571
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