RESUMO
Fatal hemolytic anemia developed in a 52-year-old woman who was treated with a cephalosporin, ceftriaxone. The patient's red cells (RBCs) were coated with C3, but no RBC-bound IgG, IgA, or IgM was detected. Her serum contained an antibody that did not react with cephalosporin-coated RBCs but reacted strongly with RBCs in vitro when her serum was added to drug and RBCs. This is the first case of immune hemolytic anemia associated with ceftriaxone, the first case of fatal cephalosporin-induced hemolytic anemia, and the second case in which a cephalosporin antibody showed in vitro and in vivo characteristics usually thought to be associated with the so-called immune complex mechanism.
Assuntos
Anemia Hemolítica/imunologia , Ceftriaxona/imunologia , Anemia Hemolítica/induzido quimicamente , Anticorpos/sangue , Ceftriaxona/intoxicação , Complemento C3/imunologia , Teste de Coombs , Eritrócitos/imunologia , Feminino , Humanos , Doenças do Complexo Imune/induzido quimicamente , Imunoglobulina G/imunologia , Imunoglobulina M/imunologia , Pessoa de Meia-IdadeRESUMO
Central neurogenic hyperventilation (CNH), for which there is no effective therapy, can eventually result in respiratory fatigue and death. This report describes a patient with CNH due to a brainstem anaplastic astrocytoma who also exhibited disturbances of sleep and ocular motor function. The CNH responded clinically to morphine sulfate and methadone. Analysis of ventilatory response to CO2 before and after morphine demonstrated a depression of ventilatory response (49 to 53% of baseline) and occlusion pressure response (35 to 50% of baseline) to CO2, with a requirement for high doses of naloxone (10 mg IV) to reverse the effect. Polysomnography revealed sustained hyperventilation, elevated O2 saturation, and low end-tidal CO2 throughout all stages of non-rapid eye movement (NREM) sleep, and absence of rapid eye movement (REM) sleep. Ocular motor evaluation disclosed absence of horizontal and reflexive saccades with compensatory head thrusts. Correlation of the clinical and physiologic data with the MRI abnormalities suggested that the lesion responsible for CNH in this patient might reside in the medial tegmental parapontine reticular formation. Since recurrent episodes of hyperventilation responded in a sustained fashion to IV and oral opiates, this treatment may warrant consideration in other patients with CNH.
Assuntos
Astrocitoma/complicações , Neoplasias Encefálicas/complicações , Movimentos Oculares , Hiperventilação/tratamento farmacológico , Morfina/uso terapêutico , Ponte , Respiração/efeitos dos fármacos , Sono , Adulto , Quimioterapia Combinada , Feminino , Humanos , Hiperventilação/etiologia , Hiperventilação/fisiopatologia , Metadona/uso terapêutico , Movimentos SacádicosRESUMO
1. The P50 of Cancer Magister hemocyanin in hemolymph was 40.0 mm at 25 degrees C, nmax = 3.9; at 14 degrees C, 15.0 mm and 3.4; and at 10 degrees C. 10.2 mm and 3.3. 2. In the absence of Ca2+ and Mg2+, the P50 at 25 degrees C was in the range of 150 to 250 mm, depending upon pH. 3. Our results show that temperature variation and pH variation may be important factors in the physiological regulation of oxygen delivery in this species. 4. The automatic recording device of Imai et al. (1970) previously used for the study of hemoglobins, was found to be eminently suitable for the study of O2 affinities of hemocyanins.
