ABSTRACT
PURPOSE: To report a unique case of peripheral ulcerative keratitis secondary to hepatitis B virus (HBV)-associated cryoglobulinemia and vasculitis and its pharmacological and surgical treatment and 2-year follow-up. METHODS: A 52-year-old woman presented with unilateral eye pain and photophobia, arthralgia, remnants of a maculopapular rash, and subsequently facial numbness several weeks later. Her best spectacle-corrected visual acuity (BSCVA) in the affected eye was 20/80. Slit-lamp examination revealed severe superior corneal thinning without infiltrate. Corneal ulceration worsened until 10% of the cornea remained. Laboratory workup was positive for rheumatoid factor and revealed significantly decreased C4 complement, and HBV serology was positive. RESULTS: Clinical history, examinations, and laboratory results suggest HBV-associated cryoglobulinemia and vasculitis. Management included prednisone, cyclophosphamide, and mycophenolate mofetil for immunosuppression and tenofovir for HBV treatment. Conjunctival resection and a glue patch were used to reduce inflammation and stabilize corneal melt. BSCVA improved after treatment was initiated. Two years after initial presentation, her BSCVA is 20/30, significantly improved from her vision at presentation. CONCLUSIONS: Diagnosis of peripheral ulcerative keratitis requires thorough history and physical examinations given the numerous causes. Prompt treatment including immunosuppressive medication and, in this case, antiviral medication is crucial to preventing serious visual consequences including corneal perforation and blindness.
Subject(s)
Corneal Ulcer/etiology , Hepatitis B, Chronic/complications , Antiviral Agents/therapeutic use , Corneal Ulcer/drug therapy , Corneal Ulcer/surgery , Cryoglobulinemia/complications , Cryoglobulinemia/drug therapy , Cyclophosphamide/therapeutic use , Female , Glucocorticoids/therapeutic use , Hepatitis B, Chronic/drug therapy , Humans , Immunosuppressive Agents/therapeutic use , Middle Aged , Mycophenolic Acid/therapeutic use , Ophthalmologic Surgical Procedures , Prednisone/therapeutic use , Tenofovir/therapeutic use , Vasculitis/complications , Vasculitis/drug therapyABSTRACT
Prediabetes, a state of mild glucose intolerance, can persist for years before a sudden decline in beta cell function and rapid deterioration to overt diabetes. The mechanism underlying this tipping point of beta cell dysfunction remains unknown. Here, the furan fatty acid metabolite CMPF was evaluated in a prospective cohort. Those who developed overt diabetes had a significant increase in CMPF over time, whereas prediabetics maintained chronically elevated levels, even up to 5 years before diagnosis. To evaluate the effect of increasing CMPF on diabetes progression, we used obese, insulin-resistant models of prediabetes. CMPF accelerated diabetes development by inducing metabolic remodeling, resulting in preferential utilization of fatty acids over glucose. This was associated with diminished glucose-stimulated insulin secretion, increased ROS formation, and accumulation of proinsulin, all characteristics of human diabetes. Thus, an increase in CMPF may represent the tipping point in diabetes development by accelerating beta cell dysfunction.
