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Vitamin D toxicity is associated with accidental overdoses due to manufacturing or intake errors and its secondary hypercalcemia can result in severe morbidity. Although patients with cystic fibrosis are potentially at increased risk for this intoxication as prescription of vitamin D preparations is a common practice in this population, the frequency of such events is currently unknown. We performed a retrospective analysis of all the files of cystic fibrosis patients followed at the Cliniques universitaires Saint-Luc over a 10-year period, recording 25(OH)- and 1,25(OH)2vitamin D levels as well as demographic data, lung function tests, Pseudomonas aeruginosa infection and results from pharmacological analysis of magistral liposoluble vitamins preparations. A total of 244 patients were included in the study. 13 patients (5%) had serum vitamin D levels corresponding to vitamin D overdose. Patients who had experienced an overdose were more likely to be F508del homozygous or suffer from exocrine pancreatic insufficiency. 2 patients developed significant hypercalcemia necessitating monitoring and hospitalization. Errors in the preparation of magistral liposoluble vitamin pills were identified in several intoxicated patients. Retrospective assessment of the dosing errors with the local pharmacists showed that trituration and dosing errors were their most frequent causes. [ABSTRACT FROM AUTHOR]

Background: Hemophagocytic lymphohistiocytosis (HLH) is a rare and life-threatening syndrome that can occur either in genetically predisposed individuals (primary HLH) or in particular conditions in immunocompromised patients (secondary HLH). Secondary HLH is very rare among solid organ transplant recipients, especially in lung transplant recipients, for whom its prognosis is dismal. Case Report: We report an exceptional case of HLH occurring unusually late following lung transplantation. At 11 years after transplantation, the patient, aged 67 years, presented with pancytopenia, fever, hyperferritinemia, and hypertriglyceridemia, along with splenomegaly. Exhaustive serological and PCR tests ruled out active infection. Bone marrow aspirates showed signs of hemophagocytosis, and bone marrow biopsy was suggestive of posttransplant lymphoproliferative disorder (PTLD). Timely treatment with etoposide and corticosteroids led to a transient improvement in the patient's clinical condition, and rituximab was initiated as a treatment for PTLD. Unfortunately, pancytopenia persisted for weeks, and the patient died from refractory septic shock, despite appropriate intravenous antibiotics. Autopsy revealed lymphoid infiltration of the mediastinal lymph nodes, liver and bone marrow, with some lymphocytes expressing CD3. A final diagnosis of Ann-Arbor stage IV non-EBVmediated monomorphic T-cell PTLD was established. Conclusions: This case report highlights a very unusual and fatal presentation of HLH in a lung transplant recipient, secondary to a T-cell PTLD. Indeed, HLH is typically seen as infection-related and reported to occur in the initial months following transplantation. To date, no guidelines or consensus exist regarding the management of immunosuppression regimen in solid organ transplantation. [ABSTRACT FROM AUTHOR]