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Biomedical subjects

W Luck

Publications and source records attributed to W Luck.

At least 55 records · Page 3Linked to original sources
PubMed1987

Nicotine and cotinine concentrations in the milk of smoking mothers: influence of cigarette consumption and diurnal variation.

The relationship between nicotine and cotinine concentrations in mother's milk (including 24 h profiles) and the number of cigarettes consumed was studied. A total of 206 milk samples were collected from 34 nursing, smoking mothers. The mothers were distributed into three groups: Group I (1-10 cigarettes/day), group II (11-20 cigarettes/day) and group III (21-40 cigarettes/day). Milk samples from all nursing periods of a 24 h interval were collected. Nicotine and cotinine concentrations were measured by specific gas chromatographic techniques. The average milk nicotine and cotinine concentrations over a 24 h interval in the three groups were as follows: group I, 18 +/- 16 and 76 +/- 33 ng/ml; group II, 28 +/- 21 and 125 +/- 60 ng/ml; group III, 48 +/- 25 and 230 +/- 62 ng/ml (means +/- SD). Over a time interval of 24 h the nicotine concentrations varied greatly in the milk of smoking mothers, while the cotinine concentrations remained relatively constant. Because of the great intra- and inter-individual variations in the nicotine concentrations, the influence of the number of cigarettes smoked on the nicotine concentration in milk was most apparent if nicotine concentrations were measured repeatedly over a prolonged time interval. Our results indicate that the exposure of the nursed infant to nicotine and cotinine via milk depends on the daily cigarette consumption but also on individual smoking habits; the time of smoking, smoking frequency prior to nursing, and the time interval between nursing and the last cigarette.

Circadian Rhythm↗
PubMed1987

Cadmium concentrations in milk and blood of smoking mothers.

Cadmium concentrations were measured by flameless atomic absorption spectrometry in blood and mature milk of 15 nonsmoking and 56 smoking mothers during the nursing period. Both blood and milk concentrations increased with increasing cigarette consumption. The median blood and milk concentrations in nonsmokers were 0.54 and 0.07 microgram/l, respectively; these values rose to 1.54 and 0.16 micrograms/l in blood and milk of mothers smoking more than 20 cigarettes per day. Milk concentrations of cadmium were approximately 10% of corresponding blood concentrations. The cadmium exposure of infants nursed by nonsmoking as well as by smoking mothers was far below the exposure of formula-fed infants or the provisional acceptable weekly intake level set by the WHO.

Adolescent↗
PubMed1986

Transcobalamin I as a "marker" for fibrolamellar hepatoma.

A 12 year old girl with a localised fibrolamellar hepatoma had a raised serum unsaturated vitamin B12 binding capacity (UBBC) and transcobalamin I (TCI) prior to complete resection and chemotherapy. Regular clinical and radiological follow-up detected no recurrence of her disease, but the UBBC and TCI slowly rose. Local recurrence and pulmonary metastases became detectable 2 1/2 years after diagnosis, 18 months after the UBBC and TCI level became elevated. Measurement of UBBC and TCI can help in the early detection of recurrence long before there is clinical or radiological evidence of recurrent fibrolamellar hepatoma.

Carcinoma, Hepatocellular↗
PubMed1985

Nicotine and cotinine concentrations in serum and urine of infants exposed via passive smoking or milk from smoking mothers.

The exposure of infants to nicotine via milk of smoking mothers or via inhaled side-stream smoke ("passive smoking") was evaluated. Newborn infants nursed by smoking mothers and unexposed to passive smoking showed measurable serum concentrations of nicotine (0.2 to 1.6 ng/ml) and its main metabolite, cotinine (5 to 30 ng/ml), and also excreted measurable amounts of nicotine and cotinine in their urine: the ratio of nanograms of nicotine/milligrams of creatinine (N/C ratio) ranged from 5.0 to 110 (median 14), and the corresponding ratio of nanograms of cotinine/milligrams of creatinine (C/C ratio) from 10 to 555 (median 110). Infants of the same age nursed by nonsmoking mothers did not excrete measurable amounts of the two substances except in one case. Older and non-breast-fed infants exposed only to passive smoking had N/C ratios in the range of 4.7 to 218 (median 35) and C/C ratios in the range of 117 to 780 (median 327 ng/mg). Infants exposed to passive smoking and to smoke via breast milk had N/C ratios in the range of 3.0 to 42 (median 12) and C/C ratios in the range of 225 to 870 (median 550). The significant serum concentrations and urinary excretion rates of nicotine in the breast-fed infants of smoking mothers suggest that nursing contributes to the nicotine exposure of these neonates. In older infants, the wide variation of cotinine excretion values did not allow separate evaluation of the two exposure routes.

Breast Feeding↗
PubMed1985

Extent of nicotine and cotinine transfer to the human fetus, placenta and amniotic fluid of smoking mothers.

Nicotine and cotinine concentrations were measured in placental tissue during the first trimester, in amniotic fluid during the second trimester and in placental tissue and fetal serum at birth. These values were compared to the corresponding serum concentrations of the smoking mothers. Nicotine concentrations in the placentas (range 3.3-28 ng/g), in amniotic fluid (range 1.5-23 ng/ml) and in fetal serum (range 0.5-25 ng/ml) were all higher than the corresponding maternal serum values: amniotic fluid/maternal vein serum concentration ratio 1.54 +/- (SD) 0.27 (n = 23; week 16-24 of gestation), umbilical vein serum/maternal vein serum ratio 1.12 +/- 0.30 (n = 26; at birth); placental tissue/maternal vein serum ratio 2.58 +/- 1.30 (n = 17; at birth); these ratios were between 1.2 and 5 during week 10 of gestation (n = 3). The ratios did not depend on the time between the last cigarette smoked and sampling. Significant correlations were found between nicotine concentrations in amniotic fluid and maternal serum (r = 0.88), between fetal and maternal serum levels (r = 0.88) and between placental and maternal serum levels (r = 0.52). Cotinine concentrations in placental tissue (range 10-131 ng/g), amniotic fluid (range 5-188 ng/ml) and fetal serum (range 15-233 ng/ml) were lower than or similar to corresponding maternal serum levels. Our results indicate that the human fetus is exposed to higher nicotine concentrations that the smoking mothers.

Adolescent↗
PubMed1984

Valproic acid in the perinatal period: decreased maternal serum protein binding results in fetal accumulation and neonatal displacement of the drug and some metabolites.

The total concentrations of valproic acid were higher in cord serum than in the serum of epileptic mothers given this drug (fetal/maternal total concentration ratios 1.7 +/- 0.5). The maternal free fractions of VPA correlated with the fetal accumulation of the drug. The fetal/maternal free fraction ratios (0.47 +/- 0.24) correlated inversely with the fetal/maternal total concentration ratios. The free concentrations of VPA in fetal blood were similar to those in maternal blood. These results obtained in vivo were confirmed by an in vitro study in which the drug had been added to drug-free serum samples. The free fractions (x100) of VPA in the maternal serum at birth (27.3 +/- 6.3) were significantly higher than in the serum of adult controls (8.0 +/- 2.4) and in cord serum (11.8 +/- 1.3). The pattern of VPA metabolite binding in the three groups was similar to that of VPA, although an unsaturated metabolite (2-en) was bound to a much higher degree than VPA (greater than 98%). The high total drug load in the fetus was partially displaced from binding sites during the first few postnatal days. The free fractions of the drug and metabolites in the neonates were almost twice as high as those in the fetus at birth. The decreased protein binding of VPA in the mothers at birth and in the neonates during the first postnatal week was related to increased free fatty acid levels. VPA concentrations in mother's milk were much lower than the free concentrations in plasma milk/plasma ratios 0.025 +/- 0.01). In neonates, half-lives for VPA were prolonged (43 +/- 14 hours). Our results indicate that increased free fatty acid concentrations in the maternal blood at the time of birth result in partial displacement of VPA from maternal binding sites, additional placental transfer, and thus fetal accumulation of the drug. The high drug load in the fetus is subsequently partially displaced after birth, resulting in increased free fractions and free concentrations of VPA in the neonate.

Blood Proteins↗
PubMed1984

Decreased serum protein binding of diazepam and its major metabolite in the neonate during the first postnatal week relate to increased free fatty acid levels.

The protein binding of diazepam (D) and its major active metabolite N-desmethyl diazepam (DD) was investigated in vitro in the serum of 14 mothers at birth, 21 foetuses at birth, in 100 neonates between 1 and 11 days of age and in 16 control subjects. The free (unbound) fractions of D and DD in the foetus were similar to those in the controls, but lower than those in the mothers. During the first day of life the free fractions of D and DD doubled in the neonates and subsequently declined slowly to reach near control levels at 1 week of age. The sharp increase and slow decrease of the free fractions of D and DD during the first postnatal week was closely paralleled by sharply increasing and decreasing free fatty acid (FFA) concentrations. Bilirubin and albumin levels were of lower importance in regard to the protein binding of D and DD. These results indicate that the greatly increased FFA levels shortly after birth result in increased free fractions of D and DD. Because of the known immaturity of the neonatal hepatic elimination capacity, these elevated free fractions may result in elevated free concentrations of the two compounds, which may help to explain the adverse effects observed clinically in some D-exposed neonates.

Adult↗
PubMed1984

Nicotine and cotinine concentrations in serum and milk of nursing smokers.

Analysis of 44 milk samples from 23 nursing smokers revealed that there was a linear correlation between nicotine concentrations in serum and in milk (r = 0.70). The nicotine concentrations in milk were considerably higher than the corresponding serum concentrations: milk/serum concentration ratio = 2.92 +/- 1.09; (n = 44). There was also a linear correlation between the cotinine concentrations in serum and in milk (r = 0.89). The cotinine concentrations in milk were lower than the corresponding serum concentrations: milk/serum concentration ratio = 0.78 +/- 0.19; (n = 44). The direct comparison between the half-lives of nicotine in serum and in milk was possible in five nursing smokers. The half-life of nicotine in milk was determined in four additional smoking mothers. The half-life of nicotine in milk t 1/2 = 97 +/- 20 min slightly exceeded the half-life of nicotine in serum t 1/2 = 81 +/- 9 min; the difference between these two values was not statistically significant (P greater than 0.05). Cotinine concentrations remained fairly consistent during a 4 h interval without smoking.

Breast Feeding↗
PubMed1983

Serum protein binding of diazepam, desmethyldiazepam, furosemide, indomethacin, warfarin, and phenobarbital in human fetus, mother, and newborn infant.

The protein binding of diazepam, desmethyldiazepam, furosemide, indomethacin, warfarin, and phenobarbital in maternal and fetal cord serum at the time of birth, and in serum of neonates between 1 and 11 days of age was studied. The protein binding of diazepam and desmethyldiazepam was higher in the fetus than in the mother, thus explaining the fetal cumulation of these drugs in vivo. After birth, both drugs were partially displaced from neonatal binding sites. The decreased protein binding capacity in the mother and the neonate related to increased free fatty-acid levels. The pattern of protein binding of warfarin in the groups investigated was a mirror image of those of diazepam and its metabolite. The protein binding of indomethacin progressively decreased in the neonate during the first two postnatal weeks, while that of furosemide remained at lowered levels throughout this time interval. The protein binding of phenobarbital was similar in the groups investigated. Our results suggest that drugs such as diazepam, which can be displaced from binding sites by free fatty acids, may cumulate in the fetus and may exhibit much decreased protein binding and possibly unexpectedly strong effects in the neonate after birth.

Blood Proteins↗
PubMed1981

Macrocytosis in alcohol-related liver disease: its value for screening.

The incidence of macrocytosis, defined as a mean corpuscular volume (MCV) of greater than 95 fl and large red cells on peripheral blood film, was determined in 303 alcoholics with liver disease (95 females: 208 males), 60 non-alcoholics with chronic liver disease (44 females: 16 males) and 35 control subjects (15 females: 20 males). Macrocytosis was found in 70.3% (213/303) of alcoholics with liver disease and in 23.3% (14/60) of non-alcoholics with liver disease, P less than 0.001. MCV values greater than 100 fl were seen in 49.5% (150/303) of alcoholics, but in only 3.3% (2/60) of non-alcoholics, P less than 0.001. Macrocytosis was more frequent in female, 86.3% (82/95) than in male alcoholics 63.0% (131/208), P less than 0.001. Serum folate values less than 3 microgram/l were found in 14.5% (44/303) of alcoholics and in 11.7% (7/60) of non-alcoholics. Low serum folate values were found in 18.3% (39/213) of alcoholics with macrocytosis and in 35.9% (28/78) of those with macrocytic anaemia. Twenty alcoholics with pre-cirrhotic liver disease were followed over three months. Macrocytosis was present in 85.0% (17/20) at the outset and in 40% (8/20) 3 months later. The changes in MCV were independent of alcohol intake and serum folate values. Macrocytosis is a useful diagnostic indicator of alcoholism. MCV values greater than 100 fl in patients with liver disease almost invariably indicate alcohol-related disease. In the short-term, changes in MCV are of little use in monitoring alcohol intake.

Anemia↗
PubMedDate not supplied

[The VIP-secreting tumor as a differential diagnosis of protracted diarrhea in pediatrics].

BACKGROUND: Vasoactive intestinal peptide (VIP) can be produced by mature neurogenic tumors. Pathologically elevated VIP plasma levels cause secretory diarrhea with excessive loss of water and electrolytes. Despite the clinical severity diagnosis of a VIP-secreting tumor is often delayed and subsequently its extirpation as the mainstay of therapy. PATIENTS: We report on two patients with ganglioneuroblastoma and secretory diarrhea. We contrast the case of a 13-month-old boy with advanced symptoms of secretory diarrhea, high VIP plasma levels, and late diagnosis to the case of a 14-month-old boy with mild secretory diarrhea and normal VIP plasma levels but positive proof of VIP in tumor tissue. Reviewing the literature we found 57 cases of pediatric VIP-secreting tumors. RESULTS: The clinical situation is characterized by the typical symptoms of secretory diarrhea with hypokalemia and metabolic acidosis. Histopathology predominantly reveals ganglioneuroblastoma or ganglioneuroma. The symptoms mostly stop after complete resection of the tumor whereas lack of resection is associated with elevated mortality rates. CONCLUSIONS: In case of prolonged therapy-resistant secretory diarrhea the existence of a VIP-secreting tumor should be considered. Diagnostic work-up should include the assessment of VIP plasma levels, catecholamines in urine, and appropriate imaging techniques in order to rule out or confirm the possibility of a VIP producing tumor.

Diagnosis, Differential↗