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Department of Rheumatology, Endocrinology and Nephrology, Faculty of Medicine and Graduate School of Medicine, Kita 14, Nishi 5, Kita-ku, Sapporo 060-8648, Japan
Department of Rheumatology, Endocrinology and Nephrology, Faculty of Medicine and Graduate School of Medicine, Kita 14, Nishi 5, Kita-ku, Sapporo 060-8648, Japan
Department of Rheumatology, Endocrinology and Nephrology, Faculty of Medicine and Graduate School of Medicine, Kita 14, Nishi 5, Kita-ku, Sapporo 060-8648, Japan
A 30-year-old woman manifested fatigue and high fever. She was diagnosed with antiphospholipid
antibodies positive-systemic lupus erythematosus (SLE), but she had never demonstrated
any serious organ involvements including nephritis and thrombosis, and had never received
immunosuppressants. Physical examination demonstrated costovertebral tenderness and
pyuria, and she was treated with cefaclor for uncomplicated pyelonephritis. After
ten days, she visited our emergency room with the same manifestations and was improved
equally by cefaclor. However, just after ten days, she was raced to our hospital again
with a shock state. She demonstrated costovertebral tenderness and pyuria with an
elevated level of procalcitonin. She was diagnosed with urosepsis despite undetectable
culture-proved bacteria, and was treated with meropenem and vancomycin, achieving
a clinical improvement. Computed tomography revealed calcified splenic atrophy which
was not observed a decade ago (Fig. 1). We diagnosed the patient with functional asplenia by autosplenectomy. She was finally
recovered with antibiotics and received vaccination for pneumococcus and Haemophilus influenzae type b to prevent further life-threating infection. Although we do not supply emergency
antibiotics, she is still infection-free.
Fig. 1Gradual progress of autosplenectomy. Computed tomography revealed (A) calcified splenatrophy in the lupus patient with
antiphospholipid antibody on axial and coronal planes (arrows), (B) as compared with
a decade ago (arrow).
