Serum placental-like alkaline phosphatase levels and nicotine intake in smokers

Ellard, G. A.; Tucker, D. F.; Pookim, Y. L.; Wang, D. Y.; Barlow, Robert D.; Stone, R.

doi:10.1038/bjc.1988.198

Cited by 2 publications

(1 citation statement)

References 21 publications

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“…Simple and inexpensive colorimetric urine based methods have been developed for identifying smokers and quantifying their relative daily nicotine intakes using modifications of the Konig reaction to estimate nicotine together with all of its metabolites 9 . Such estimates agreed well with established methods for assessing nicotine intake based on serum or urinary cotinine level estimations using radio‐immunoassay or high pressure liquid chromatographic techniques 10–13 .…”

Section: Introductionmentioning

confidence: 72%

Smoking during pregnancy: the dose dependence of birthweight deficits

Ellard

Johnstone²,

Prescott

et al. 1996

BJOG

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Objective To assess whether a simple urine based estimate of relative daily nicotine intake could predict smoking related birthweight deficits more accurately than self‐reported cigarette consumption. Design Active smokers were identified by a simple qualitative colorimetric urine test procedure and their relative nicotine intakes assessed by determining the ratios of the urinary concentrations of nicotine plus its metabolites to creatinine using automated colorimetric methods. Setting A large teaching hospital. Participants Three thousand and thirty‐eight mothers from whom smoking histories had been elicited and who gave birth to live singleton babies after 28 weeks of gestation. Main outcome measures Birthweights (adjusted for maternal weight, maternal age, baby's sex, parity and length of gestation), maternal weight gains during pregnancy and placental weights. Results The adjusted birthweight deficits of babies born to proven active smokers averaged 226 g (95 % confidence interval 194 g to 258 g), but dose dependent effects were only apparent when nicotine intake was based on urinary nicotine metabolites/creatinine ratios. Among the smokers, adjusted birthweights fell linearly with increasing nicotine intakes but gave a predicted mean birthweight for nonsmokers that was 102 g (95 % CI 50 g to 154 g) lighter than that actually found (P < 0.0001). Maternal weight gains during pregnancy were substantially reduced in smokers and correlated more closely with urinary nicotine metabolite excretions than with reported daily cigarette consumptions. Placental weights were unaffected by smoking. Conclusions There was a closer dose‐effect relationship between birthweight deficits and urinary nicotine metabolites/creatinine ratios than with self‐reported daily cigarette consumptions. The influence of nicotine exposure on birthweight appears to be biphasic, with one mechanism operating at very low levels of tobacco smoke intake and the other causing seemingly linearly related effects over the whole range of nicotine intakes of active smokers. These findings support recent evidence that passive smoking can cause substantial birthweight deficits.

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Section: Introductionmentioning

confidence: 72%

Smoking during pregnancy: the dose dependence of birthweight deficits

Ellard

Johnstone²,

Prescott

et al. 1996

BJOG

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Interpretation and Clinical Significance of Alkaline Phosphatase Isoenzyme Patterns

Hoof

Broe

1994

Critical Reviews in Clinical Laboratory Sciences

197

141

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Alkaline phosphatase (ALP, EC 3.1.3.1) is a membrane-bound metalloenzyme that consists of a group of true isoenzymes, all glycoproteins, encoded for by at least four different gene loci: tissue-nonspecific, intestinal, placental, and germ-cell ALP. Through posttranslational modifications of the tissue-nonspecific gene, for example, through differences in carbohydrate composition, bone and liver ALP are formed. Nowadays, most commercially available methods for separating or measuring ALP isoenzymes are easy to perform and sensitive and allow for reproducible and quantitative results. As more isoenzymes and isoforms have been characterized, confusion has arisen due to the many different names they were given. For the sake of simplicity and because of structural analogies, we propose an alternative nomenclature for the ALP isoenzymes and isoforms based on their structural characteristics: soluble, dimeric (Sol), anchor-bearing (Anch), and membrane-bound (Mem) liver, bone, intestinal, and placental ALP. Together with lipoprotein-bound liver ALP and immunoglobulin-bound ALP, these names largely fit the many forms of ALP one can encounter in human serum and tissues. The clinically relevant isoenzymes are sol-liver, Mem-liver, lipoprotein-bound liver, and Sol-intestinal ALP in liver diseases, and Sol-bone and Anch-bone ALP in bone diseases. Many different isoenzyme patterns can be found in malignancies and renal diseases. This test provides the clinician with valuable information for diagnostic purposes as well as for follow-up of patients and monitoring of treatment. However, ALP isoenzyme determination will only provide clinically useful information if the patterns are correctly interpreted. In this respect, care should be taken to use the proper reference ranges, taking into account the age and sex of the patient. A normal total ALP activity does not rule out the presence of an abnormal isoenzyme pattern, particularly in children. Separating ALP into its isoenzymes adds considerable value to the mere assay of total ALP activity.

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Serum placental-like alkaline phosphatase levels and nicotine intake in smokers

Cited by 2 publications

References 21 publications

Smoking during pregnancy: the dose dependence of birthweight deficits

Smoking during pregnancy: the dose dependence of birthweight deficits

Interpretation and Clinical Significance of Alkaline Phosphatase Isoenzyme Patterns

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