Asunto(s)
Vacuna BCG , Tuberculosis/diagnóstico , Humanos , Sensibilidad y Especificidad , Pruebas CutáneasRESUMEN
Little attention has been given to the question whether clinical heart failure can be a manifestation of hypocalcemia. A patient with hypoparathyroidism and heart failure prompted us to analyse the reports on this subject. The conclusion was that if associated with an underlying myocardial disease, hypocalcemia may be a rare contributing factor to hear failure. Hypocalcemic heart failure without coexisting heart disease has been suggested as a cause of hypotension in two special situations in which a sudden fall of serum ionized calcium is induced: massive transfusions of citrated blood and rapid correction of uremic acidosis. In addition to hypocalcemia and heart failure, our patient had exceptional repolarization disturbances: rate-dependent variation of T wave amplitudes during sinus arrhythmia and unexpected prolongations of the Q-T interval with attacks of ventricular tachycardia.
Asunto(s)
Insuficiencia Cardíaca/etiología , Hipocalcemia/complicaciones , Taquicardia/etiología , Adolescente , Electrocardiografía , Femenino , Corazón/diagnóstico por imagen , Corazón/fisiopatología , Humanos , RadiografíaRESUMEN
This paper reports an attempt to determine whether the short arm of one of the X chromosomes in XX males is longer than normal. In a blind study comparing coded photomicrographs of 15 G-banded mitoses from each of five XX males and five control females, the results were ambiguous and somewhat contradictory, but gave the impression of, or were compatible with, an XXp+ phenomenon in at least two of the five XX males. Measurements of the X chromosomes from the above cells and, in addition, from 15 mitoses from each of six XXY males, failed to disclose any XXp+ phenomenon. Statistical analysis indicated that in the five XX males there was no difference in the lengths of the two Xp arms. The reasons for the apparent discrepancy between the results of ocular inspection and measurement are discussed. The putative heteromorphism might be an alteration in shape, staining intensity, or position of bands, neither of which necessarily leads to an increase in length. We conclude that our results do not indicate any XXp+ phenomenon in the five XX males tested. However, the presence or absence of XXp+ is not in itself evidence for or against interchange betweenthe X and Y in the paternal meiosis. Our results emphasize that the etiology of XX males is likely to be heterogeneous.
Asunto(s)
Aberraciones Cromosómicas Sexuales/genética , Cromosomas Sexuales , Cromosoma X , Femenino , Humanos , Cariotipificación , Masculino , MitosisRESUMEN
Two healthy young women had an unexplained persistent elevation of aspartate aminotransferase (ASAT) activity. In both cases electrophoresis of serum ASAT isoenzymes displayed an abnormally moving fraction that comprised the whole serum activity, while liver and muscle revealed the normal cytoplasmic and mitochondrial isoenzymes. In the first case serum ASAT was found to be bound by serum IgG, in the second case the binding protein remained unidentified.
Asunto(s)
Aspartato Aminotransferasas/sangre , Adulto , Proteínas Portadoras/sangre , Reacciones Falso Positivas , Femenino , Humanos , Inmunoglobulina G/metabolismo , Isoenzimas/sangreRESUMEN
Two XX males who were second cousins are reported. A genetic mechanism producing maleness is suggested. The putative factor had been transmitted solely through males, which excludes the possibility of a heritable X-Y interchange. Recent reports on fluorescent Y chromatin in Sertoli cells of XX males prompted investigations into the fluorescence patterns of testicular cells. Sertoli cells from three XX males displayed brightly fluorescent spots, but it was concluded that they did not represent Y chromosomes. Evidence for this conclusion was obtained from the study of testicular fluorescence in XX, XXY and XY males. No visually detectalbe cytogenetic evidence for an increase in length or altered banding pattern of one of the X chromosomes was found in three XX males. We conclude that an autosomal gene is the most likely explanation of the male differentiation in the two XX males presented here.