PubMed Health⌕ Search

Biomedical subjects

Lukas Hefler

Publications and source records attributed to Lukas Hefler.

At least 19 recordsLinked to original sources
PubMed2006

Genotype distribution of estrogen receptor-alpha, catechol-O-methyltransferase, and cytochrome P450 17 gene polymorphisms in Caucasian women with uterine leiomyomas.

OBJECTIVE: To evaluate the association between the presence of uterine leiomyomas and three functional single nucleotide polymorphisms (SNPs) of the estrogen receptor alpha (ESR1), catechol-O-methyltransferase (COMT), and cytochrom P450 17 (CYP17A) genes, which have been described to modify the estrogen metabolism. DESIGN: Prospective case control study. SETTING: Academic research institution. PATIENT(S): One hundred thirty women with clinically and surgically diagnosed uterine leiomyomas and 139 population controls. INTERVENTION(S): Peripheral venous puncture. MAIN OUTCOME MEASURE(S): Polymerase chain reaction and pyrosequencing were performed to genotype women with respect to the ESR1 IVS1-397 T/C (PvuII), COMT G158A, and the CYP17A 34T-->C SNPs. RESULT(S): Comparing women with uterine leiomyomas and controls, no statistically significant differences with respect to allele frequency and genotype distribution were ascertained for ESR1 IVS 1-397 T/C (PvuII) (P=0.9 and P=0.6, respectively), COMT G158A (P=0.3 and P=0.6, respectively), and CYP17A 34T-->C (P=0.1 and P=0.5, respectively). When all two-way interactions of investigated SNPs were ascertained, no significant interactions were observed. In a multivariate model, no SNP was significantly associated with leiomyomas. CONCLUSION(S): Carriage of the ESR1 IVS1-397 T/C (PvuII), COMT G158A, and the CYP17A 34T-->C SNPs is not associated with the susceptibility to uterine leiomyoma in a Caucasian population.

Adenine↗
PubMed2006

Impaired glucose tolerance is associated with changes in clinical and biochemical parameters in women with polycystic ovary syndrome.

BACKGROUND: To characterize the phenotype of women with polycystic ovary syndrome with and without impaired glucose tolerance by determining various polycystic ovary syndrome-associated clinical and laboratory parameters. METHODS: In a prospective clinical study, we evaluated a series of 102 Caucasian women with polycystic ovary syndrome. Women completed a detailed questionnaire and underwent a standardized oral glucose tolerance test. Various polycystic ovary syndrome-associated laboratory values such as hormonal and metabolic parameters were determined in these women and correlated to clinical data and the presence/absence of impaired glucose tolerance. Furthermore, the insulin resistance was calculated using the homeostasis model assessment index and correlated with clinical and biochemical parameters. RESULTS: Eighty-eight (86.3%) and 14 (13.7%) women were diagnosed as having non-impaired glucose tolerance and impaired glucose tolerance, respectively. Presence of impaired glucose tolerance was associated with an increased body mass index, increased body weight, elevated serum levels of bioavailable testosterone, insulin like growth factor-1, insulin, HbA1c, leucocytes, uric acid, alkaline phosphatase, hepatic C-reactive protein, and decreased serum levels of sex-hormone binding globulin. No association was ascertained with subfertility, hirsutism, and menstrual irregularities. We ascertained a positive correlation between the homeostasis model assessment index and body mass index, body weight, alkaline phosphatase, and hepatic C-reactive protein. CONCLUSIONS: Impaired glucose tolerance seems to be associated with a specific phenotype within polycystic ovary syndrome. This phenotype is more likely to present with biochemical parameters similar to an inflammatory reaction and a metabolic disorder.

Adult↗
PubMed2005

Clinical relevance of dominant-negative p73 isoforms for responsiveness to chemotherapy and survival in ovarian cancer: evidence for a crucial p53-p73 cross-talk in vivo.

PURPOSE: We aimed to determine the clinical role of the p53 family members p53 and p73 in the responsiveness to platinum-based chemotherapy and survival in ovarian cancer, considering their cross-talk and the p53 polymorphism at codon 72. EXPERIMENTAL DESIGN: A detailed analysis of p53 and p73 in a series of 122 ovarian cancers was done. We used a functional yeast-based assay to determine the p53 mutational status. Red yeast colonies, indicating mutant p53, were subsequently sequenced to determine the specific p53 alteration. p53 mutations were divided into two groups according to their previous characterization in the literature: those that efficiently inhibit transcriptionally active TAp73 function and those that do not. A p53 polymorphism at codon 72 was determined in corresponding normal tissue or blood of ovarian cancer patients. Isoform-specific p73 expression analysis using real-time reverse transcription-PCR has previously been done in the majority of ovarian cancers included in this study. In a retrospective chart review, responsiveness to chemotherapy was assessed, and survival data with long follow-up times were collected. RESULTS: Eighty of 122 (65.6%) of ovarian cancers harbored p53 mutations. p53 mutational status was an important determinant of responsiveness to platinum-based chemotherapy in all patients with a residual tumor of <2 cm in diameter after initial surgery (wild-type versus mutant, P = 0.029). In addition, p53 mutational status was a strong prognosticator for recurrence-free and overall survival (P < 0.0001 and P = 0.003, respectively) in univariate analyses. High expression levels of dominant-negative p73 isoforms (DeltaNp73 and DeltaN'p73) significantly correlated with chemotherapeutic failure (P = 0.048) and with worse recurrence-free and overall survival in patients with p53 mutant cancers (P = 0.048 and P = 0.005, respectively). Eight p53 mutations, present in 19 cases, were found that efficiently inhibit TAp73 (i.e., 175H, 220C, 245S, 245D, 248W, 248Q, 266E, and 273H). Patients with p53 mutations that efficiently inhibit TAp73 function had a significantly shorter overall survival than patients with p53 mutations of unknown effect on TAp73 (P = 0.044). The p53 polymorphism at codon 72 had no influence on responsiveness to chemotherapy or survival. CONCLUSION: We provide the first clinical evidence that dominant-negative p73 isoforms contribute to drug resistance in vivo, underscoring the importance of a p53-p73 cross-talk. NH2-terminally truncated p73 isoforms were of significant clinical effect by providing an additional unfavorable factor for response to platinum-based chemotherapy and survival in p53 mutant ovarian cancers.

Adenocarcinoma, Mucinous↗
PubMed2005

Polymorphisms of the Nos3 gene and unexplained late intrauterine fetal death.

OBJECTIVE: Genetic polymorphisms associated with vascular diseases have been proposed to be involved in the pathogenesis of late unexplained intrauterine fetal death (IUFD). The Nos3 gene is known to regulate vascular tone via the endothelial nitric oxide synthase/nitric oxide pathway. STUDY DESIGN: In a multicenter case-control study, we evaluated two Nos3 polymorphisms (exon 7 Glu298Asp and a 27bp-repeat in intron 4) in 92 women with IUFD and 92 healthy control women. RESULTS: The investigated Nos3 polymorphisms were not associated with the occurrence of IUFD. In the subgroup of pregnancies affected by IUFD, women with at least one mutant allele of the Nos3 intron 4 polymorphism were diagnosed with IUFD at a significantly earlier gestational age (31.8 [standard deviation (S.D.) = 4.9] weeks versus 34.6 [S.D. = 4.8] weeks, p = 0.02) and showed a significantly reduced birth weight (2113 g [S.D. = 1028] versus 1571 g [S.D. = 568], p = 0.03). CONCLUSION: We are the first to report on Nos3 polymorphisms and IUFD. While not being associated with the incidence of IUFD overall, the intron 4 Nos3 polymorphism might modulate the timing of IUFD in affected pregnancies.

Adult↗
PubMed2005

An Angiopoietin-2 gene polymorphism in unexplained intrauterine fetal death: a multi-center study.

OBJECTIVE: Angiopoietin-2 (Ang-2) is a potent regulator of angiogenesis and vascular tone. As vascular processes have been proposed to be involved in the pathogenesis of pregnancy associated complications such as late unexplained intrauterine fetal death (IUFD), we determined whether a common G/A polymorphism of the Ang-2 gene (ANGPT2) is associated with this condition. METHODS: In a multicenter case-control study, we evaluated the common G/A polymorphism within exon 4 of the ANGPT2 gene using PCR in 90 women with IUFD and 90 healthy women with at least one uncomplicated full term pregnancy and no history of IUFD. RESULTS: Genotype (p=0.2; OR=1.4 [0.8-2.6]) and allele frequencies (p=0.1; OR=1.4 [0.9-2.1]) of the ANGPT2 polymorphism did not differ between women with IUFD and healthy women. A multivariate regression analysis with smoking habits and preexisting diabetes as covariates did not change the results. CONCLUSIONS: We are the first to report on a common polymorphism of the ANGPT2 gene in patients with late IUFD. The investigated ANGPT2 poylmorphism does not seem to be a candidate gene for IUFD in Caucasian women.

Adult↗
PubMed2005

An interleukin-6 gene promoter polymorphism and unexplained late intrauterine fetal death: a multicenter study.

OBJECTIVE: Interleukin-6 (IL-6)-mediated inflammatory processes have been proposed to be involved in the pathogenesis of pregnancy-associated complications such as late unexplained intrauterine fetal death (IUFD). Therefore we determined whether a common guanine/cytosine polymorphism at position -174 of the promoter of the IL-6 gene (IL6) known to affect in vivo protein activity can serve as candidate gene for this condition. METHODS: In a multicenter case-control study, we evaluated the IL6 promoter polymorphism by pyrosequencing in 92 women with IUFD. Ninety-four healthy women with at least one uncomplicated full-term pregnancy and no history of IUFD served as the control group. RESULTS: No significant association was found between the presence of at least one mutant allele of the IL6 promoter polymorphism (P = .2; odds ratio = 1.5 [95% confidence interval, 0.8-2.7]) and the incidence of IUFD. In women with IUFD, the presence of at least one mutant allele of the IL6 promoter polymorphism did not influence timing of fetal death (33.9 [5.1] gestational weeks vs 34.1 [4.9] gestational weeks, P = .8) or birth weight (2055 [1119] g vs 1963 [992] g, P = .7). CONCLUSION: To our knowledge, we are the first to report on a common polymorphism of the IL6 promoter gene in women with late IUFD. The investigated IL6 promoter polymorphism can not be seen as candidate gene for IUFD in Caucasian women.

Adult↗
PubMed2005

Ten polymorphisms of estrogen-metabolizing genes and a family history of colon cancer--an association study of multiple gene-gene interactions.

Estrogen replacement therapy is associated with a reduced risk of colon cancer. Therefore, we evaluated the following ten estrogen metabolism-associated single-nucleotide polymorphisms (SNPs) by sequencing-on-chip technology using solid-phase polymerase chain reaction (PCR) on oligonucleotide microarrays: catechol-O-methyltransferase (COMT) Val158Met G-->A, 17-beta-hydroxysteroid dehydrogenase type 1 (HSD17) vlV A-->C, cytochrome P-450 (CYP) 17 A2 allele T-->C, CYP1A1 MspI RFLP T-->C, CYP1A1 Ile462Val A-->G, CYP19 Arg264Cys C-->T, CYP19 C1558T C-->T, CYP 1B1 Leu432Val, CYP1B1 Asn453Ser, and estrogen receptor (ER) alpha IVS1 -401-->C in 76 patients with a family history of colon cancer and 722 healthy controls. Using stepwise logistic regression models, we found that none of the investigated SNPs is associated with a family history of colon cancer in a univariate and multivariate logistic regression model. In addition, when all two-way interactions of the investigated SNPs were ascertained, no significant interactions between SNPs were observed. In conclusion, we found no association between the carriage of one or multiple SNPs of the estrogen metabolism and a family history of colon cancer.

Adult↗
PubMed2005

Oral dydrogesterone treatment during the first trimester of pregnancy: the prevention of miscarriage study (PROMIS). A double-blind, prospectively randomized, placebo-controlled, parallel group trial.

OBJECTIVE: A planned study to test the hypothesis that dydrogesterone given during the first trimester of pregnancy can positively influence the immune system of women suffering from recurrent miscarriages and thereby lead to successful pregnancies. The primary objective is to show whether the administration of dydrogesterone during the first trimester of pregnancy increases the release of progesterone-induced blocking factor (PIBF) and causes a shift from Th-1 cytokines to Th-2 cytokines. Further objectives are an analysis of pregnancy outcome and to investigate the tolerability and safety of dydrogesterone use during pregnancy. METHODS: A prospectively randomized, placebo-controlled study of 20 mg dydrogesterone per day during the first trimester of pregnancy in women aged between 18 and 38 and with a history of idiopathic recurrent miscarriage. Start of treatment will be after ovulation. The study will be conducted in a two-stage adaptive design, starting with a sample size of 20 patients per treatment group. The concentrations of Th-1 and Th-2 cytokines in the serum and PIBF in the urine will be measured. Efficacy will be measured primarily by the ratio IFNgamma/IL-10. CONCLUSION: The results of this study will contribute to the discussion of a current concept of immunomodulation in pregnancy and potentially provide a treatment option for patients suffering from recurrent miscarriage.

Abortion, Habitual↗
PubMed2005

Polymorphisms within the interleukin-1 gene family and unexplained late intrauterine fetal death: a multi-center study.

PROBLEM: Interleukin-1 (IL-1) mediated inflammatory processes have been proposed to be involved in the pathogenesis of late unexplained intrauterine fetal death (IUFD). We determined whether common polymorphisms within the IL-1 gene locus can serve as candidate genes for this condition. METHOD OF STUDY: In a multi-center case-control study, we evaluated the -889 C/T polymorphism of the IL-1alpha gene (IL1A), the -511 C/T polymorphism of the IL-1beta promoter (IL1B promoter), the +3953 C/T polymorphism of IL-1beta exon 5 (IL1B exon 5), and a 86 base pair repeat in intron 2 of the IL-1 receptor antagonist gene (IL1RN) in 94 women with IUFD and 94 healthy controls using pyrosequencing. RESULTS: No significant associations were found between the presence of polymorphic alleles of IL1A (P = 0.9), IL1B promoter (P = 0.3), IL1B exon 5 (P = 0.9), and IL1RN intron 2 (P = 0.7) and the incidence of IUFD. In women with IUFD, polymorphisms were not associated with the timing of fetal death and birth weight. CONCLUSIONS: Polymorphisms within the IL1 gene family are not associated with the occurrence of IUFD overall and do not modulate the clinical characteristics of affected pregnancies in a large series of Caucasian women.

Female↗
PubMed2004

Genetic polymorphisms associated with thrombophilia and vascular disease in women with unexplained late intrauterine fetal death: a multicenter study.

OBJECTIVE: We determined whether gene polymorphisms associated with thrombophilia and vascular disease as etiologic factors were involved in the pathogenesis of pregnancy-associated complications. METHODS: We conducted a multicenter case-control study in which we studied 94 women with late unexplained intrauterine fetal death (IUFD) and 94 healthy women with at least one uncomplicated full-term pregnancy and no history of IUFD. We obtained blood samples from all subjects and analyzed their DNA for 12 common polymorphisms of thrombophilic and vascular genes (factor V Leiden, factor V H1299R, prothrombin G20210A, factor XIII V34L, MTHFR C677T, MTHFR A1298C, beta-fibrinogen-455 G to A, PAI-1 4G/5G, GPIIIa L33P, HFE C282Y, apolipoprotein B R3500Q, and apolipoprotein E2/E3/E4). RESULTS: We found no significant association between any of the polymorphisms investigated and IUFD. Subgroup analyses involving various combinations of polymorphisms and in which gestational age and fetal weight were corrected for also showed no significant results. CONCLUSIONS: Our data represent the largest study to date with respect to thrombophilic and vascular gene polymorphisms in IUFD. In accordance with others, we challenge the importance of thrombophilic and vascular gene polymorphisms in the pathogenesis of this condition.

Adult↗
PubMed2004

Polymorphisms of thrombophilic and vasoactive genes and severe preeclampsia: a pilot study.

OBJECTIVE: Carriage of thrombophilic and vasoactive polymorphic alleles has been associated with various pregnancy complications. The effect of carrying multiple polymorphisms is not known. We conducted a case-control study to determine the association between eight polymorphisms of thrombophilic and vasoactive genes and the risk of severe preeclampsia. METHODS: The following polymorphisms were analyzed by sequencing-on-chip-technology using solid-phase polymerase chain reaction on oligonucleotide microarrays: factor 5 (F5) Leiden, factor 2 (F2)-prothrombin G20210A, plasminogen activator inhibitor (PAI)-1 4G/5G, nitric oxide synthase (NOS) 3 T768C, NOS 3 Glu298Asp, angiotensinogen (AGT) Met235Thr, estrogen receptor (ER) alpha Pvu II, and mineralcorticoid receptor (MLR) Ser810Leu. The study comprised 24 patients with severe preeclampsia and 24 controls from a cohort of consecutive white women treated at the Obstetrics Department of the University of Vienna Medical School. Genotypes were correlated with clinical data. RESULTS: The investigated polymorphisms did not influence the risk of severe preeclampsia independently. When separately considering the simultaneous carriage of multiple thrombophilic or vasoactive polymorphisms, neither the combined carriage of thrombophilic polymorphisms (F5 Leiden, F2 G20210A, PAI-1 4G/5G), nor the combined carriage of vasoactive polymorphisms (NOS 3 T768C, NOS 3 Glu298Asp, AGT Met235Thr) conferred an increased risk of severe preeclampsia. Cumulative genotype frequencies for at least two homozygous mutant genotypes, however, were nine of 24 (38%) and two of 24 (8%) for the study and control groups, respectively (P <.05). All of these nine women with severe preeclampsia had at least two homozygous mutant genotypes of four polymorphisms, ie, F5 Leiden, NOS 3 T768C, NOS 3 Glu298Asp, or ER alpha Pvu II. CONCLUSION: Our data fail to document an independent significant influence of the investigated polymorphisms on the risk of severe preeclampsia. In an attempt to build a multigenetic model of severe preeclampsia, the combination of F5 Leiden, NOS 3 T768C, NOS 3 Glu298Asp, and ER alpha Pvu II was the most effective combination to predict the presence of severe preeclampsia in this small series of white women.

Adult↗
PubMed2003

Biological markers in pT1 and pT2 ovarian cancer with lymph node metastases.

OBJECTIVE: A relatively high incidence of pelvic and paraaortic lymph node metastases is found in patients with pT1 and pT2 ovarian cancer. This paper investigates the clinicomorphological parameters and the expression of various biological markers in these tumors in order to define possible risk factors for lymphatic dissemination. METHODS: In a retrospective study we identified 51 patients with pT1 and pT2 ovarian cancer. All patients underwent total hysterectomy, bilateral salpingo-oophorectomy, omentectomy, and systemic pelvic +/- paraaortal lymphadenectomy. The incidence of lymph node metastases in these patients and the clinicomorphological parameters of their tumors were examined. Immunohistochemistry was used to determine the expression levels of the cell proliferation marker Ki-67, the cell adhesion molecules CD44s and CD44v6, and the oncoprotein HER2/neu of the tumors and their respective lymph node metastases. RESULTS: Lymph node involvement was found in 5 of 26 patients with pT1 ovarian cancer and in 6 of 25 patients with pT2 ovarian cancer. Serous adenocarcinoma was associated with a significantly higher incidence of lymph node metastases than other histological types (chi(2) = 4.7, P = 0.03). No correlation was found between tumor grade and the lymph node status. High Ki-67 expression was significantly correlated with spread to the lymph nodes (chi(2) = 4.2, P = 0.04), whereas expression of CD44s, CD44v6, and HER2/neu was not related to the lymph node status. Survival analyses showed no difference in disease-free and overall survival in patients with lymph node metastases compared to those without lymph node metastases. No association was seen among histological type, tumor grade, and immunohistochemically detected Ki-67, CD44s, CD44v6, and HER2/neu expression on the one hand and disease-free and overall survival on the other hand. CONCLUSIONS: Our data suggest that in early stage ovarian cancer the serous histological type and tumors showing a high Ki-67 expression carry a high risk of lymph node metastases. With respect to prognosis our data showed a minor role for Ki-67, CD44s, CD44v6, and HER2/neu expression and the occurrence of lymph node metastases in pT1 and pT2 ovarian cancer.

Adult↗
PubMed2003

Polymorphism of the interleukin-1beta gene and endometriosis.

OBJECTIVE: Experimental data indicate that interleukin (IL)-1 plays a role in the pathogenesis of endometriosis. We determined the genotype and the allele frequencies of the IL1B exon 5 polymorphism and the corresponding IL-1beta serum levels in women with endometriosis. METHODS: We genotyped 92 women with surgically and histologically confirmed endometriosis and 69 controls without history of endometriosis. Both groups were of middle European genetic background for the IL1B exon 5 polymorphism (at position +3954). Genotyping was performed by pyrosequencing. IL-1beta serum levels were analyzed by a commercially available enzyme-linked immunosorbent assay. RESULTS: Allele frequencies in women with endometriosis and controls were 76.6% and 76.8%, respectively, for the E1 allele (wild type) and 23.4% and 23.2%, respectively, for the E2 allele (polymorphic) (odds ratio 1.01; P > .99). The investigated polymorphism of the IL-1beta gene was not correlated with IL-1beta serum levels. CONCLUSIONS: We did not find an association between the IL1B exon 5 polymorphism, endometriosis, or increased serum IL-1beta levels.

Alleles↗
PubMed2003

Comparison of p53 mutational status with mRNA and protein expression in a panel of 24 human breast carcinoma cell lines.

We analyzed the p53 mutational status, mRNA and protein expression in 24 human breast carcinoma cell lines. Following measurement of their DNA content with flow cytometry, we ascertained the copy numbers of the centromere of chromosome 17 (cen17) and p53 with fluorescence in situ hybridization (FISH). A functional yeast assay (FASAY) was used to screen for inactivating mutations. Positive results were subsequently verified by DNA sequencing. Finally, we assessed the mRNA expression with a competitive reverse transcription-polymerase chain reaction (RT-PCR) assay and the protein expression with immunocytochemical staining, western blot, and quantitative flow cytometry. The DNA content of the cell lines ranged from 0.85 to 2.58. Nine cell lines had concordant copy numbers (between two and four) of p53 and cen17, whereas 12 had more, and three less cen17 than p53 copies. The FASAY was successful in all but one cell line and revealed the presence of mutated alleles in 16 of them, 13 cell lines expressed only the mutated, and three both the mutated and the wild-type alleles. The mutations were comprised of 11 missense, two nonsense, and three frameshift mutations. Immunocytochemical staining, western blot and quantitative flow cytometry yielded comparable p53 protein expression results. However, both the mRNA and the protein expression levels varied considerably in the different cell lines and no consistent pattern with regard to the respective p53 mutational status became evident. The results obtained in these breast carcinoma cell lines indicate that no clear-cut linear relationship exists between the p53 mutational status and the extent of its respective mRNA and protein expression. Therefore, direct DNA analyses and functional assays remain the only methods for the reliable detection of p53 mutations.

Breast Neoplasms↗
PubMed2003

Periurethral connective tissue status of postmenopausal women with genital prolapse with and without stress incontinence.

OBJECTIVE: Connective tissue consists mainly of collagen and structural glycoproteins and is considered an important factor of the supportive structures of the genitourinary region. Few data have been published as yet with respect to the role of connective tissue in pelvic floor relaxation and genuine stress incontinence (GSI). We compared periurethral connective tissue structures between continent and incontinent postmenopausal women with genital prolapse. METHODS: Twenty-nine women underwent pelvic floor reconstructive surgery (anterior colporrhaphy: n = 29, sacrospinous fixation: n = 12), with biopsies obtained from the periurethral region. Fifteen patients and 14 women were incontinent and continent, respectively. Tissue samples were investigated for localization and distribution of collagen (types I, III, IV, V, VI) and glycoproteins (fibronectin, laminin, vitronectin) using immunofluorescent microscopic techniques. RESULTS: Collagen types I, III, IV, V, and VI were found in all tissue samples. Compared with the continent women, the tissue samples of the incontinent women showed a significantly weaker immunohistochemical staining of type I, III, and VI collagen. No difference in staining patterns of collagen type IV and V, fibronectin, and laminin was observed between the two groups. Intact vitronectin was found in the periurethral tissues of all the continent women, whereas this glycoprotein was either absent or fragmented in the incontinent women. CONCLUSIONS: Our results indicate an altered metabolism of connective tissue in the periurethral region with a significant decrease of collagen and vitronectin expression in postmenopausal women with pelvic floor relaxation with and without GSI.

Aged↗
PubMed2003

Influence on fetal blood pH when adding amniotic fluid: an in vitro model.

OBJECTIVE: To assess the effect of contamination with amniotic fluid in different quantities on fetal capillary blood pH. DESIGN: In vitro model. SETTING: Department of Obstetrics, St Pölten Hospital. SAMPLE: Venous umbilical blood and amniotic fluid from 35 women who underwent amniotomy during labour. METHODS: Venous umbilical blood was mixed in vitro with amniotic fluid in diluted series (venous umbilical blood/amniotic fluid, 10:1 to 1:1). In every case two parallel runs of the dilution series in an inverted fashion were performed to rule out a possible time-dependent bias of the pH measurements. MAIN OUTCOME MEASURES: pH change in dilutions of umbilical venous blood with amniotic fluid: 10:1, +0.07 (0.02); 8:1, +0.08 (0.02); 6:1, +0.08 (0.03); 4:1, +0.07 (0.02); 2:1, +0.09 (0.03); 1:1, +0.12 (0.05); all P < 0.001. RESULTS: Amniotic fluid pH increases, whereas umbilical blood pH decreases slightly over time since collection. Dilutions of umbilical venous blood with amniotic fluid resulted in a significant pH rise. There was no significant difference between the two inversely performed dilution series. CONCLUSION: Amniotic fluid influences in vitro fetal venous blood pH immediately after contact. This observation indicates the possible masking of a fetus in distress by fetal scalp blood pH determination when amniotic fluid contaminates the sample.

Adult↗