Background: Peripheral ulcerative keratitis (PUK) is a severe inflammatory ocular disease that can affect patients with a long history of rheumatoid arthritis (RA). The use of biotherapy has revolutionized the treatment of the RA and has provided encouraging outcomes especially in the treatment of PUK reported in few cases. In this article, we describe the case of two patients with the history of perforated corneal ulcer complicating RA treated successfully by biologic agents. Case presentation: Case 1: A 45-year-old woman was diagnosed for over 17 years with sero-positive RA refractory to conventional synthetic disease-modifying antirheumatic drugs (csDMARDs). She had received one cycle of Rituximab with clinical and biological failure. In July 2017, she presented an active RA flare with a painful left eye and a decreased visual acuity. Ocular examination revealed a corneal perforation in the left eye and a preperforation in the right eye. She received an emergency bolus of methylprednisolone 1 g/day during three consecutive days and was followed by Infliximab. After thirteen months, Infliximab was effective on the rheumatic disease and on the corneal involvement as it stopped its gradual perforation in the right eye, and stabilized corneal ulcer in the left eye. Case 2: A 68-year-old man had been diagnosed since 2010 with sero-positive RA refractory to csDMARDs complicated in July 2017 by corneal perforation in the right eye. He was hospitalized for his ocular involvement and his active RA. He received an emergency bolus of methylprednisolone 500 mg/day during three consecutive days and was followed by Rituximab. After six months, we observed the stabilization of the right eye corneal damage and the resolution of articular symptoms. Conclusions: Our cases suggest the efficacy of Infliximab (case 1) and Rituximab (case 2) as a treatment of this severe and destructive keratolysis of the cornea complicating an active RA allowing to plan corneal graft. This positive therapeutic response will contribute to increase literature reports of this therapy success.

No abstract

No abstract

S pondyloepiphyseal dysplasia tarda (SEDT) is a hereditary skeletal dysplasia caused by genes involved in bone growth and cartilage maintenance. The platyspondyly and the enlarged long bones characterize the disease due to abnormal enchondral ossification in the vertebral bodies and proximal epiphyses of long bones. These abnormalities and deformities lead to disproportionate dwarfism and expose patients to premature osteoarthritis in multiple joints. The major clinical importance of this rare disorder is its similarity to juvenile idiopathic arthritis, which has different prognosis and treatment. Clinical characteristics, typical radiological findings, dysmorphic features, and absence of synovial inflammation can aid in the exact diagnosis. 1 A few cases of SEDT have been described in the literature. We report clinical and radiological findings of a Moroccan adolescent with SEDT as the diagnosis.