ABSTRACT
A case of beta-lactam antibiotic-induced pseudoporphyria is presented. A 24-year-old African American woman with systemic lupus erythematosus and end-stage renal disease on hemodialysis developed tense bullae on her forehead and cheeks after exposure to ampicillin-sulbactam and cefepime. Histologically, the lesions were similar to porphyria cutanea tarda, but without the associated porphyrin abnormalities. The lesions resolved spontaneously on cessation of the antibiotics.
Subject(s)
Ampicillin/adverse effects , Skin Diseases, Vesiculobullous/chemically induced , Sulbactam/adverse effects , Abdominal Abscess/complications , Abdominal Abscess/drug therapy , Anemia, Hemolytic, Autoimmune/complications , Anti-Bacterial Agents/adverse effects , Biopsy , Fallopian Tube Diseases/complications , Fallopian Tube Diseases/drug therapy , Female , Forehead , Humans , Kidney Failure, Chronic/complications , Kidney Failure, Chronic/therapy , Leukocyte Count , Lupus Erythematosus, Systemic/complications , Middle Aged , Ovarian Diseases/complications , Ovarian Diseases/drug therapy , Pruritus/chemically induced , Renal Dialysis , Sickle Cell Trait/complications , Skin/pathology , Skin Diseases, Vesiculobullous/pathology , Thrombocytopenia/complicationsABSTRACT
Proteoglycan accumulation within the arterial intima has been implicated in lipoprotein retention and in atherosclerosis progression in humans. Two commonly studied murine models of atherosclerosis, the apolipoprotein E (apoE)-deficient (apoE-/-) mouse and the low density lipoprotein receptor-deficient (LDLR-/-) mouse, develop arterial lesions similar to those of human atherosclerosis. However, specific proteoglycan classes that accumulate in lesions of these mice and their relation to the retention of specific apolipoproteins have not been previously determined. In this report, we characterized the distribution of proteoglycans (versican, biglycan, and perlecan) and apolipoproteins (apoB, apoA-I, and apoE) in proximal aortic lesions of chow-fed apoE-/- and LDLR-/- mice at 10, 52, and 73 weeks of age. We observed that similar to the apoE-/- mice, the LDLR-/- mice develop intermediate and advanced plaques within 52 weeks of age. Perlecan and biglycan (both are proteoglycans) appeared early in lesion development with distinct expression patterns as the plaques advanced. Versican, a major proteoglycan detected in human plaques, was mostly absent in both strains. ApoA-I and apoB were detected in early through advanced lesions in regions of proteoglycan accumulation in both strains. Our results indicate that proteoglycans may contribute to the retention of lipoproteins at the earliest stage of atherosclerosis in murine models of atherosclerosis.
