Right lobe living-related liver transplantation in a Jehovah's Witness.
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Adolescent↗
Biomedical subjects
Pierre Damas
Publications and source records attributed to Pierre Damas.
Recurrent fatal drug-induced toxic epidermal necrolysis (Lyell's syndrome) after putative beta-lactam cross-reactivity: Case report and scrutiny of antibiotic imputability.
OBJECTIVE: A series of antibiotics may be responsible for toxic epidermal necrolysis. We report two successive episodes of toxic epidermal necrolysis in the same patient. Drug imputability criteria designate a cross-reactivity between two antibiotics of different chemical classes but sharing the beta-lactam ring in common. DESIGN: Descriptive case report and review of the literature. SETTING: Medical intensive care unit in a university medical center. PATIENT AND MAIN RESULTS: A 75-yr-old woman developed a first episode of toxic epidermal necrolysis (involving 40% of the body surface) after intake of cefotaxime, a third-generation cephalosporin. Perfusions of high-dose immunoglobulins rapidly improved the lesions, followed by partial reepithelialization in 5 days. Sepsis required the administration of meropenem, which is a carbapenem antibiotic. The epidermal destruction immediately recurred, with extension to previously uninvolved skin areas and fatal consequences. CONCLUSIONS: The beta-lactam ring present in cephalosporins and carbapenems represents the putative chemical structure responsible for the presently reported cross-reactivity to two antibiotics of different classes. Drugs having any chemical similarity to the initial culprit compound should be strictly avoided when possible in the management of toxic epidermal necrolysis.
Aged↗
Brain function in the vegetative state.
Positron emission tomography (PET) techniques represent a useful tool to better understand the residual brain function in vegetative state patients. It has been shown that overall cerebral metabolic rates for glucose are massively reduced in this condition. However, the recovery of consciousness from vegetative state is not always associated with substantial changes in global metabolism. This finding led us to hypothesize that some vegetative patients are unconscious not just because of a global loss of neuronal function, but rather due to an altered activity in some critical brain regions and to the abolished functional connections between them. We used voxel-based Statistical Parametric Mapping (SPM) approaches to characterize the functional neuroanatomy of the vegetative state. The most dysfunctional brain regions were bilateral frontal and parieto-temporal associative cortices. Despite the metabolic impairment, external stimulation still induced a significant neuronal activation (i.e., change in blood flow) in vegetative patients as shown by both auditory click stimuli and noxious somatosensory stimuli. However, this activation was limited to primary cortices and dissociated from higher-order associative cortices, thought to be necessary for conscious perception. Finally, we demonstrated that vegetative patients have impaired functional connections between distant cortical areas and between the thalami and the cortex and, more importantly, that recovery of consciousness is paralleled by a restoration of this cortico-thalamo-cortical interaction.
Cerebral Cortex↗