LETTERS
fluid C3 complement was 28 mg/dl with a serum C3 complement of 80 mg/dl. Examination of the synovial fluid under polarized light microscopy revealed multiple intracellular birefringent crystals. The crystals were small and the long axis could not be well determined, but they had the morphologic characteristics of calcium pyrophosphate crystals. The material was subjected to crystallographic analysis and found to contain microcrystalline uric acid and triclinic crystals of calcium pyrophosphate. (Crystallography was done by Louis C. Herring and Company, Orlando, FL.) Amorphous hydroxyapatite was also demonstrated. Treatment consisted of an injection of methylprednisolone into the knee and an addition of phenylbutazone 300 mg daily to her regimen. On this schedule she showed improvement of the knee effusion. In subsequent followup, the patient has been tapered off prednisone and started on hydroxychloroquine. She presently is maintained on only 200 mg hydroxychloroquine daily with no evidence of active disease.
Moidel and Good hypothesized that the rarity of coexistence of SLE and gout may be due to the disparity of the populations involved. In our patient, crystal deposition disease would not be expected as an etiology of acute monarthritis in a young woman. However, polarized light microscopy and crystallographic evaluation demonstrated that the acute synovitis of the knee in this patient was due to crystal deposition disease. This was detected only because the fluid was aspirated for symptomatic relief and examined routinely for crystals. In this case the determination that the acute monarthritis was due to crystal deposition precluded the necessity for more aggressive management of this patient's systemic lupus erythematosus. We must wonder whether crystal deposition disease may be misdiagnosed as flares of systemic lupus erythematosus in patients who also have that disease.