PURPOSE: We present a case of ocular pathology linked to morbid obesity, emphasizing the role of systemic inflammation in ocular disease and clinical impact of weight loss. METHODS: We report the case of a 49-year-old man with morbid obesity and obstructive sleep apnea who underwent bilateral corneal transplants secondary to keratoconus. For 4 years, he had chronic bulbar hyperemia with progressive blood vessel growth across the graft-host junction, which was treated with chronic topical corticosteroids. Nine years after presentation, he also developed severe papilledema associated with idiopathic intracranial hypertension that proved recalcitrant to treatment with acetazolamide therapy and optic sheath fenestration. Concomitantly, the patient's proinflammatory markers (erythrocyte sedimentation rate, C-reactive protein) were consistently elevated. The patient underwent vertical sleeve gastrectomy, resulting in substantial weight loss. Clinical findings, treatment interventions, and outcomes were documented.Results: The patient experienced marked improvement in corneal graft health and resolution of papilledema following weight loss of 188 pounds. Systemic inflammatory markers, including erythrocyte sedimentation rate and C-reactive protein, also normalized. These findings suggest a correlation between adipose tissue mass and ocular inflammation. CONCLUSIONS: Our patient had rapid improvements in his ocular pathology that correlated with a notable reduction in body fat percentage. We propose that the immunological changes associated with obesity contributed to a proinflammatory ocular state that improved with weight loss. His case highlights that additional research is warranted to explore the etiopathogenic mechanisms of adipokines derived from white adipose tissue on major organ systems, including the eye.