ABSTRACT
BACKGROUND: While computed tomography (CT) exams are the major cause of medical exposure to ionising radiation, the radiation-induced risks must be documented. We investigated the impact of the cellular models and individual factor on the deoxyribonucleic acid double-strand breaks (DSB) recognition and repair in human skin fibroblasts and brain astrocytes exposed to current head CT scan conditions. METHOD: Nine human primary fibroblasts and four human astrocyte cell lines with different levels of radiosensitivity/susceptibility were exposed to a standard head CT scan exam using adapted phantoms. Cells were exposed to a single-helical (37.4 mGy) and double-helical (37.4 mGy + 5 min + 37.4 mGy) examination. DSB signalling and repair was assessed through anti-γH2AX and anti-pATM immunofluorescence. RESULTS: Head CT scan induced a significant number of γH2AX and pATM foci. The kinetics of both biomarkers were found strongly dependent on the individual factor. Particularly, in cells from radiosensitive/susceptible patients, DSB may be significantly less recognised and/or repaired, whatever the CT scan exposure conditions. Similar conclusions were reached with astrocytes. CONCLUSIONS: Our results highlight the importance of both individual and tissue factors in the recognition and repair of DSB after current head CT scan exams. Further investigations are needed to better define the radiosensitivity/susceptibility of individual humans.
Subject(s)
DNA Breaks, Double-Stranded , DNA Repair , Ataxia Telangiectasia Mutated Proteins/genetics , Ataxia Telangiectasia Mutated Proteins/metabolism , Fibroblasts/metabolism , Humans , Tomography, X-Ray ComputedSubject(s)
Calcinosis/complications , Hydroxyapatites/metabolism , Magnetic Resonance Imaging/methods , Sciatica/etiology , Calcinosis/diagnostic imaging , Diagnosis, Differential , Female , Humans , Middle Aged , Risk Assessment , Sciatic Nerve/physiopathology , Sciatica/diagnostic imaging , Severity of Illness IndexABSTRACT
Paroxysmal nocturnal hemoglobinuria (Marchiafava-Micheli disease) is a rare acquired clonal disorder of the hematopoietic cell, to a somatic mutation in the phosphatidylinositol glycan (PIG-A). The most frequent clinical manifestations are hemolytic crisis and venous thrombosis of the mesenteric, hepatic, portal or cerebral territories. We report a case of paroxysmal nocturnal hemoglobinuria with renal vein thrombosis, a rare complication of this disease.
