The performance of rat liver and HEp-2 in the detection of antinuclear antibodies (ANA) was studied by two independent sites and compared against an ANA enzyme immunoassay (EIA) screen and EIA systems for the measurement of antibodies to double-stranded DNA (dsDNA) and ENA. Sixty-two sera from patients with connective tissue disease (CTD) and 398 from controls suffering from other disorders were included. The level of agreement was, for HEp-2 and rat liver (within one site), 82.0% (ANA positive/ANA negative) and 51.0% (ANA pattern); and for HEp2-and HEp-2 (between sites), 71.8 and 86.5%. On sera with the ANA homogeneous pattern, the measurement of anti-ENA EIA added little to the detection rate with anti-dsDNA EIA alone. On ANA speckled sera, the EIA reactivity depended on the reaction of the mitotic cells: while sera with positive mitoses reacted similarly to ANA homogeneous sera, in those with negative mitoses the measurement of anti-ENA added about 10% to the detection rate achieved with anti-dsDNA alone. The measurement of anti-Scl-70 and anti-Jo-1 did not markedly improve the positive rate with classical ENA (anti-SSA, -SSB, -Sm, and -RNP) alone, raising doubts about the cost efficiency of including these measurements in unselected sera. The ANA EIA identified patients with CTD at a rate similar to that for rat liver and HEp-2. However, up to 98% of the sera found to be negative by ANA EIA but positive by use of rat liver and HEp-2 were from controls. Thus, the ANA EIA may possible be used as an alternative screen, particularly in laboratories with a high frequency of sera from patients not suffering from CTD.

SUMMARY Thirteen newborn infants, 8 term and 5 preterm (gestational age 31 to 36 weeks), were treated for between 3 and 7 days with gentamicin and ampicillin or cloxacillin because of suspected bacterial infection. The dosage of gentamicin was carefully monitored by serum concentration assays. Urinary alanine aminopeptidase, urinary P2-microglobulin, serum urea, and serum f2-microglobulin were measured during and after the end of treatment to detect signs of renal toxicity. Levels of urinary aminopeptidase increased in 12 of them, indicating damage to the cells of the proximal tubuli. Changes in urinary 32-microglobulin followed the normal physiological course seen in neonates after birth. Serum levels of urea and 32-microglobulin did not indicate any drugassociated depression of glomerular filtration rate.In recent years it has been demonstrated that in most adults the kidneys are affected by therapeutic doses of gentamicin. After only one injection there is an increase in the urine of enzymes from renal tubular cells-for example, alanine aminopeptidase (AAP).' In many patients there is also an increase in the urinary excretion of ,B2-microglobulin, indicating a reduced reabsorptive capacity of the proximal tubuli.2 Moreover, a small but significant decrease of glomerular filtration rate (GFR), as measured by 51chrome-EDTA clearance, has been demonstrated.2 This decrease is accompanied by a significant increase in serum P2-microglobulin, but not in serum creatinine.Aminoglycoside-associated nephrotoxicity is considered to be rare in infants, but it is difficult to assess renal function and to determine which changes are drug associated and which are dependent on other factors.3 5 Clearance determinations may be difficult to perform in neonates. Serum urea, commonly used to approximate GFR, is influenced by the increased protein intake after birth.6 Furthermore, renal function in neonates alters according to gestational age6 and pronounced changes in both glomerular and tubular function occur after birth.6The aim of this study was to search for signs of renal toxicity in neonates treated with gentamicin. Levels of urinary AAP and urinary 3 2-microglobulin were used to evaluate effects on the proximal tubuli.

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The serum concentrations of total IgE were significantly raised in smokers compared to those who had never smoked @<0.005) among male patients with bronchial carcinoma, while no differences were found between smoking and non-smoking female bronchial carcinoma patients. The total IgE levels in male and female patients with nonmalignant pulmonary diseases were not correlated to smoking habits. No significant differences in the IgE levels were observed between smoking males subgrouped according to the WHO histological types of bronchial carcinoma. Males with carcinoma who had stopped smoking more than 10 years ago had significantly reduced IgE levels compared to male cancer patients continously smoking @ <0.01). These data, indicating that smoking is associated with elevated IgE levels in males with bronchial carcinoma, might suggest that smoking in certain, preferably male, individuals induces an impaired cellular immunity which is reflected by an enhanced IgE synthesis and a depressed resistance to carcinogens of tobacco smoke.