Use of the CO(2) laser (λ = 10.6 μm, continuous wave, defocused) is an established procedure for the treatment of premalignant lesions. Through employment of the sp-mode as well as scanners, thermal laser effects can be reduced but, on the other hand, a lesser degree of destruction of dysplastic cells could lead to an increased recurrence rate. The purpose of this study was to prospectively evaluate the recurrence rates resulting from different methods of CO(2) laser vaporization. From May 1995 to May, 2005, 145 patients with a total of 148 premalignant lesions of the oral mucosa were treated in a prospective clinical study. Sixty-two lesions in 62 patients were vaporized with the defocused CO(2) laser (group 1). In a further 45 lesions (43 patients, group 2), a scanner was additionally employed. In the remaining 41 lesions (40 patients, group 3), vaporization was carried out in the sp-mode in which the scanner was also used. In September, 2005, recurrence rates in the three groups were evaluated. Use of the scanner in sp-mode resulted in the most irregular tissue vaporization. This can be accounted for by the irregular paths of the laser beam and the pulsed delivery of the laser energy. Statistically significant lowest recurrence rates were yielded by the defocused cw-technique followed by the cw-scanner and the sp-mode. These results indicate that for CO(2) laser treatment of premalignant lesions of the oral mucosa, the best results can be achieved with the defocused technique. It may be assumed that other methods with lesser penetration of thermal effects (e.g. sp, scanner) do not reach the deeper-lying cells and, consequently, render higher rates of recurrence.

The increased incidence of infection in preterm neonates has been related in part to their relative deficiency of most complement components, because complement is known to participate in the defense against bacterial and viral infections. In a prospective study, complement activation products were determined in 52 preterm infants. Twenty preterm infants suffered from proven early onset infection, 11 infants were presumed to suffer from infection, which could not be confirmed. Twenty-one preterm infants without infection or perinatal asphyxia formed the control group. EDTA plasma was obtained within the first 6 h after birth, and follow-up examinations were done in 15 patients with proven infection during the next 24 h. The complement activation products C3a-desArg, C3bBbP, and sC5b-9 were measured with enzyme immunoassay systems. In preterm neonates with early onset infection, a significant elevation of C3a-desArg was found in the very early course of the disease. C3a-desArg generation resulted from alternative pathway activation as shown by a concurrent increase of C3bBbP concentration. In addition, significantly higher concentrations of sC5b-9 predicted infection in the first few hours after birth. Thus, despite very low levels of native complement proteins, preterm babies are able to generate remarkable amounts of activation products of the complement cascade. The elevation of these activation products preceded by hours significant changes of routine laboratory markers of infection, such as leukocyte count, differential blood count, and C-reactive protein. Thus they might help to identify preterm neonates with severe systemic infection earlier than other laboratory parameters.

Significance of increased serum gamma-glutamyltransjerase activity during long-term anticonvulsive treatment. Clinical and experimental studies. Neuropadiatrie 6: 77-89 (1975). In epileptic children on anticonvulsive treatment for at least 4 weeks, the following laboratory tests were performed and compared to age matched controls: serum activity determinations of gamma-glutamyltransferase (GGT), alanine (GPT) and aspartate aminotransferases, leucin arylamidase (LAP), alkaline phosphatase (AP), glutamate dehydrogenase (GLDH), and cholinesterase (CHE), determinations of fibranogen and clotting factors II, V, and VII, and of urinary D-glucaric acid excretion. Serum GGT activity was increased up to about 10 times above the upper limit of normal range (x + 2s) in 83 of 103 children, AP was enhanced in 26, CHE in 21, GLDH in 20, and GPT in 14 children (p< .05). Except for AP, the frequency of other increased serum activities was raised according to the degree of GGT enhancement. Clotting factor V was moderately elevated in 21°/o of those children, who had enhanced GGT activities (p < .05), no further significant deviation of any of the clotting factors was observed. In 17 children so studied the serum GGT activity was closely correlated to the urinary excretion of D-glucaric acid, an indicator of microsomal enzyme activity (r= + 0.67, p < .01). In phenytoin treated rats, given 100 mg/kg and 300 mg/kg, respectively, daily for 17-25 days, a dose dependent enhancement of liver and serum GGT was measured. This occured predominantly in total liver and in liver microsomes, less marked in the soluble liver fraction and in serum. An elevation of microsomal cytochrome P-450 in the liver was also found. It is concluded, that isolated enhancement of serum GGT activity during anticonvulsive treatment is not indicative of liver damage, but rather, of a clinically insignificant elevation of microsomal enzymes. Increased blood levels of other so-called liver enzymes and of clotting factors may be suggestive of more complex alterations of liver metabolism, the pattern of the laboratory findings being indicative of a clinically latent disturbance of excretory functions of the hepatobiliary system rather than of hepatic parenchymal damage. Enhancement of serum AP activity is primarily due to a disturbance in calcium metabolism.

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