Annals of internal medicine
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Three specific patterns of neurologic deficit were seen in a group of 52 patients with the idiopathic hypereosinophilic syndrome. Central nervous system dysfunction was seen in 7 patients (15%), 4 of whom had a distinctive encephalopathy characterized by behavioral disturbances and upper motor neuron signs. ⋯ Thus, a total of 65% of these patients had some neurologic dysfunction. Although the spectrum of neurologic disease is broad and includes very different manifestations, we conclude that distinct patterns of neurologic involvement are characteristic of this syndrome.
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Clinical, serologic, virologic, and immunologic evaluations for 31 adults with chronic illness and fatigue suggested that 23 had persisting Epstein-Barr virus infection. Among these 23 patients, cellular immune mechanisms were generally normal, but 4 had mild immunoglobulin deficiencies. However, 20 patients had abnormal serologic profiles specific for Epstein-Barr virus shown by significantly elevated titers of antibodies to the viral capsid antigen or early antigen, or by a deficiency of late-appearing antibodies. ⋯ Circulating interferon was not found in 18 patients tested, but the activity of 2-5 oligoadenylate synthetase, an interferon-induced enzyme, was increased in 5 patients studied. Of 19 patients, 18 had persisting suppressor T-cell activity typically found in patients recovering from acute infectious mononucleosis. We believe that the Epstein-Barr virus may be associated with chronic illness in adults.
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Randomized Controlled Trial Clinical Trial
Amplitude of ventricular fibrillation waveform and outcome after cardiac arrest.
The amplitude of ventricular fibrillation found initially in 394 patients was compared to clinical and logistical findings at the time of cardiac arrest. Peak-to-peak amplitude averaged 0.55 +/- 0.25 mV; a very low amplitude (0.2 mV or less) or "fine" fibrillation was present in 66 patients (17%). ⋯ Patient outcome related to amplitude even after adjusting for clinical history and logistical delays (p less than 0.005). We conclude that fine ventricular fibrillation is in part the result of delay in initiation of treatment, and that fibrillation amplitude is a powerful indicator of outcome after cardiac arrest.