ABSTRACT
PURPOSE: To study the progression of visual acuity and visual function parameters in patients with optic neuritis (ON) treated with high-dose oral corticosteroid therapy. METHODS: This retrospective descriptive monocentric study included nine patients with ON treated with orally administered methylprednisolone at 1000 mg per day for three to five days. The follow-up visits were performed on day 4 (D4), day 15 (D15), day 30 (D30) and day 90 (D90) after treatment was begun. The initial examination (D0) and the follow-up visits included a visual acuity (VA) assessment according to the Early Treatment Diabetic Retinopathy Study scale, a contrast sensitivity test and a 30.2 automated visual field (Visual Field Index [VFI]). The overall subjective tolerance of the treatment was assessed by patients on a scale from 0 to 10. RESULTS: We observed an improvement of all parameters from D4. From D0 to D4, the average VA increased from 40.1 letters to 57.9 letters, the average VFI from 40.9% to 70.3% and the overall average contrast sensitivity from 7.7 dB to 11.3 dB. From D15 to D90, the average VA increased from 77 letters to 80.3 letters, the average VFI from 91.2% to 97.9% and the overall average contrast sensitivity from 15.4 dB to 16.7 dB. Four patients rated tolerance at 10 (excellent), three between 8 and 9, and two at 6. CONCLUSION: We demonstrated rapid improvement of visual function parameters in patients with ON after high-dose oral corticosteroids.
Subject(s)
Glucocorticoids/administration & dosage , Methylprednisolone/administration & dosage , Optic Neuritis/drug therapy , Visual Acuity/drug effects , Administration, Oral , Adult , Dose-Response Relationship, Drug , Drug Administration Schedule , Female , Humans , Male , Optic Neuritis/physiopathology , Remission Induction , Retrospective Studies , Time Factors , Treatment Outcome , Young AdultABSTRACT
BACKGROUND: Familial juvenile glomerulonephropathy (JGN) is reported in several breeds of dogs. The mode of inheritance and spectrum of pathological lesions vary among breeds. A progressive JGN was detected in a pedigree of French Mastiff (FM) dogs. OBJECTIVES: To describe clinical, laboratory, and histopathologic findings in related FM dogs suffering from progressive JGN and to determine the mode of inheritance of this condition. ANIMALS: Sixteen affected and 35 healthy related FM dogs METHODS: FM dogs < 24 months of age and diagnosed with chronic kidney disease with evidence of proteinuria entered the study. Clinical, laboratory, histopathologic findings, and pedigree data were recorded. RESULTS: Clinical signs were typical of progressive glomerulopathy with resultant renal failure. Increased blood urea nitrogen, creatinine and total cholesterol concentrations, and proteinuria were found in all patients. Affected dogs had abnormal kidney structure on abdominal ultrasound examination. Histopathologic examination revealed extensive cystic glomerular atrophy, glomerular hypercellularity, and capillary wall thickening without immune complex deposition when tested with immunohistochemistry or immunofluorescence. Electron microscopy did not disclose specific primary glomerular lesions. Mean age at death was 20 months and mean length of survival after diagnosis was 6 months. Both males and females from healthy parents were affected. An autosomal recessive mode of transmission is suspected, but a more complex mode of inheritance cannot be excluded. CONCLUSIONS AND CLINICAL IMPORTANCE: Progressive familial JGN occurs in FM dogs. Characterization of the pathogenesis and mode of inheritance of this disease warrants additional study.
