[The role of hyponatremia in the rapid onset of coma after Cyclophosphamide]. / Rôle de l'hyponatrémie dans la survenue rapide d'un coma après Cyclophosphamide.

INTRODUCTION: Cyclophosphamide is an alkylating agent used in routine pulmonary practice, particularly in the management of connectivitis-related diffuse interstitial lung disease. Common side effects are gastrointestinal disorders and immunosuppression, and a sudden and exceptional adverse effect is severe hyponatremia. OBSERVATION: A 78-year-old female patient treated for NSIP-OP in the context of an anti-synthetase syndrome was treated with Cyclophosphamide 15mg/kg. Twenty-four hours after the end of the infusion, she was diagnosed at home in a coma with comitial seizures. Biological assessment revealed severe hyponatremia at 109 mmol/l with blood hypo-osmolarity. The patient's condition rapidly improved following correction of the ionic disorder. CONCLUSION: Hyponatremia induced by low-dose Cyclophosphamide is a rare but serious adverse effect that requires special attention.

Tumor suppressor TNFAIP3 (A20) is frequently deleted in Sézary syndrome.

Despite recent therapeutic improvements, the prognosis for patients suffering from Sézary syndrome (SS), a disseminated form of cutaneous T-cell lymphomas, is still poor. We identified bi- and monoallelic deletions of the tumor necrosis factor-α-induced protein 3 gene (TNFAIP3; A20) in a high proportion of SS patients as well as biallelic A20 deletion in the SS-derived cell line SeAx. Furthermore, we demonstrate that inhibition of A20 activates the NF-κB pathway thereby increasing the proliferation of normal T lymphocytes. On the other hand, the reconstitution of A20 expression slowed down the cell cycle in SeAx cells. Recently A20 inactivation has been reported in various B-cell lymphomas. In this study, we show that A20 is also a putative tumor suppressor in the T-cell malignancy-SS.