Amniotic fluid lysozyme activity in fetal distress.

Lysozyme activity was measured in amniotic fluid samples from 90 pregnant women with gestational age ranging from 30 to 41 weeks. Twenty-nine samples were from high-risk subjects with different pathologies and signs of fetal distress. The control group consisted of 20 normal and 41 pathological pregnant women, whose disorders included Rh isoimmunization, diabetes, systemic arterial hypertension and pre-eclampsia without signs of fetal distress. Amniotic fluid lysozyme levels in normal controls were similar to those detected in abnormal pregnant women without signs of fetal distress (means = 156.0 vs 131.8 micrograms/ml for 34-37 weeks of gestation), with a tendency toward higher values as pregnancy progressed to term (means = 182.1 vs 155.4 micrograms/ml for 38-41 weeks of gestation). Lysozyme levels were significantly lower in high-risk pregnant women with signs of fetal distress, regardless of neonate birth weight, than in subjects showing no such signs (means = 40.3 and means = 25.4 micrograms/ml at 34-37 and 38-41 weeks of gestation, respectively). These data support the possibility of using amniotic fluid lysozyme activity levels as an indicator of fetal distress.

Ammiotic fluid lysozyme activity in fetal distress

Lysozyme activity was m,easured in amniotic fluid samples from 90 pregnant women with gestacional age ranging from 30 to 41 weeks. Twenty-nine samples were from high-risk subjects with different pathologies and signs of fetal distress. The control group consisted of 20 normal and 41 pathological pregnant women, whose disorders included Rh isoimmunization, diabetes, systemic arterial hypertension and pre-eclampsia without signs of fetal distress. amniotic fluid lysozyme levels in normal controls were similar to those detected in abnormal pregnant women without signs of fetal distress (x = 156.0 vs 131.8 microng/ml for 43-37 weeks of gestation), with a tendency toward higher values as pregnancy progressed to term in high-risk pregnant women with signs of fetal distress, regardless of neonate birth weight, than in subjects showing no such sugns (x = 40.3 and x = 25.4 microng/ml at 34-41 weeks of gestation, respectively). These data support the possibility of using amniotic fluid lysosyme activity levels as an indicator of fetal distress

Frequency of selective IgA deficiency among Brazilian blood donors and healthy pregnant women.

Selective IgA deficiency (SIgAD) is the most common primary immunodeficiency, with frequencies ranging from 1:300 to 1:3,000 in populations surveyed in Europe and the US. In the present study we tested 11,576 clinically healthy persons (blood donors and pregnant women) for SIgAD (serum IgA less than 5 mg%). Serum samples were screened by double immunodiffusion with a sheep anti-human alpha-chain (minimal detection level of 30 mg%). Samples showing negative or doubtful reactions were submitted to the radial immunodiffusion test (minimal detection level of 0.5 mg%). For the samples with low or undetectable IgA levels, IgG and IgM concentrations were also determined. We found 12 individuals with SIgAD and 2 with deficiency of the 3 immunoglobulin classes. The prevalence of SIgAD in this Brazilian population (1:965) is equivalent to values reported for other countries.

Resistance to serum bactericidal activity distinguishes Brazilian purpuric fever (BPF) case strains of Haemophilus influenzae biogroup aegyptius (H. aegyptius) from non-BPF strains. Brazilian Purpuric Fever Study Group.

We studied the ability of normal human serum to lyse H. influenzae biogroup aegyptius (H. aegyptius) isolates recovered from patients with Brazilian purpuric fever (BPF clone) or non-BPF clone strains. BPF clone isolates, although similar to non-BPF clone isolates with regard to the ability to fix C3 to their surfaces, could be distinguished from non-BPF clone strains by their resistance to lysis in vitro following incubation with normal adult human serum.

Study of colostrum of a patient with selective IgA deficiency.

In a study of immunological factors in colostrum, we detected an 18-year old primipara with selective IgA deficiency and with a history of 3 previous hospitalizations for bronchopneumonia. Peripheral blood studies showed: IgG = 1240 mg%; IgM = 160 mg, and undetectable IgA on two different occasions. B lymphocyte measurement by immunofluorescence for membrane immunoglobulins, T lymphocyte determination by rosette formation with sheep red cells, and T lymphocyte determination with monoclonal antibodies of the Ortho series showed normal results. Salivary IgA was undetectable. The colostrum results were: undetectable IgA (mean, 19.2 g/l); IgM, 22,2 g/l (mean, 2.3 g/l); IgG, 1.3 g/l (mean, 0.7 g/l), and lysozyme, 214.2 mu/ml (mean, 157.1 mu/ml). The very high IgM levels detected in the colostrum of these patients are interpreted to be a compensatory factor for the lack of IgA.