Visual impairment from fibrous dysplasia in a middle-aged African man: a case report

<p>Abstract</p> <p>Introduction</p> <p>Fibrous dysplasia is a benign tumour of the bones and is a disease of unknown aetiology. This report discusses a case of proptosis and visual deterioration with associated bony mass involving the right orbit.</p> <p>Case presentation</p> <p>A 32-year-old Nigerian man of Yoruba ethnic origin presented to the eye clinic of our hospital with right-eye proptosis and visual deterioration of 7-year duration. Presentation was preceded by a history of trauma. Proptosis was preceded by trauma but was non-pulsatile with no thrill or bruit but was associated with bony orbital mass. The patient reported no weight loss. Examination of his right eye showed visual acuity of 6/60 with relative afferent pupillary defect. Fundal examination revealed optic atrophy. Computed tomography showed an expansile bony mass involving all the walls of the orbit. The bony orbital mass was diagnosed histologically as fibrous dysplasia. Treatment included orbital exploration and orbital shaping to create room for the globe and relieve pressure on the optic nerve.</p> <p>Conclusion</p> <p>Fibrous dysplasia should be considered in the differential diagnosis of slowly developing proptosis with associated visual loss in young adults.</p

Rapidly progressive glomerulonephritis: A wild card manifestation of lupus nephritis

A significant proportion of individuals with systemic lupus erythematosus (SLE) will have clinical or laboratory evidence of renal involvement at some point in the course of their disease. Lupus nephritis (LN) is one of the more important systemic manifestations of SLE and although progression to end-stage renal disease (ESRD) is not usually the norm, a significant minority of patients will do so, some in a rather dramatic fashion. It is in such instances that LN constitutes a true nephrologic emergency. Gratifyingly, it is rarely a silent emergency and heightened awareness amongst clinicians about its unpredictable course should lead to earlier recognition and intervention. For this reason, a case of LN presenting with historical and histologic evidence of chronic kidney disease and superimposed, acute acceleration of renal function decline, leading rapidly to ESRD is reported here. A brief review of the literature surrounding the pathophysiologic mechanisms, clinicopathologic characteristics and current therapeutic approaches to LN is subsequently explored