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Biomedical subjects

W Klockenbusch

Publications and source records attributed to W Klockenbusch.

18 recordsLinked to original sources
PubMed2004

Maternal posttraumatic stress response after the birth of a very low-birth-weight infant.

OBJECTIVE: For parents, the premature birth of a child represents a traumatic event for which they are poorly prepared. To date, the focus of scientific interest has been on maternal psychological stress responses, such as anxiety and depression, or on appropriate coping mechanisms, whereas only scant attention has been paid to the traumatic aspect of the maternal experience after very low-birth-weight (VLBW) birth. The present study is the first to investigate the posttraumatic stress response of mothers after the birth of a VLBW infant in a prospective longitudinal study. METHODS: Fifty mothers of VLBW infants were examined at four measuring time points (1-3 days pp, 14 days pp and 6 and 14 months pp) with respect to posttraumatic symptoms [Impact of Event Scale (IES-R)], psychiatric diagnosis (SKID I for DSM-IV) and the extent of depression [Beck Depression Inventory (BDI) and Montgomery Asberg Depression Scale (MADRS)] and anxiety [State-Trait Anxiety Inventory (STAI) and Hamilton Anxiety Scale (HAMA)]. The control group comprised a group of 30 mothers after the uncomplicated spontaneous birth of a healthy child. RESULTS: At all four measuring timepoints (except 6 months pp), the mothers of the premature infants recorded significantly higher values for traumatic experience and depressive symptoms and anxiety compared with the controls. In contrast to the mothers in the control group, the mothers of the premature infants displayed no significant reduction in posttraumatic symptoms (IES-total), even 14 months after birth. CONCLUSION: The results indicate that the situation of a mother who has given birth to a VLBW infant is a complex, with long-term traumatic event necessitating ongoing emotional support extending beyond the period immediately after the birth.

Adult↗
PubMed2004

Grief after termination of pregnancy due to fetal malformation.

Termination of pregnancy for fetal malformation is a traumatic event which any woman finds hard to withstand and which entails the risk of severe and complicated grieving. This paper presents three cases illustrating the trauma and coping mechanisms. Grieving continued for over 6 months in all cases and included pathological anxiety and depression. We offer advice and counselling to such women.

Abortion, Induced↗
PubMed2002

The conservative management of adnexal torsion--a case-report and review of the literature.

In clinical routine adnexal torsion tends to be subject to adnexectomy to prevent embolism of thrombosed ovarian veins and its sequelae. This therapeutic intervention can be derogatory especially for young women during the reproductive years. As seen in animal models with adnexal torsion, restitution of the adnexa next to reperfusion is possible until 36 h after interruption of venous and arterial blood perfusion. We report about the successful management of a case of adnexal torsion, which was detorsed laparoscopically. We also reviewed 214 cases with conservative management of adnexal torsions reported in the literature.

Abdominal Pain↗
PubMed2000

Prostacyclin deficiency and reduced fetoplacental blood flow in pregnancy-induced hypertension and preeclampsia.

BACKGROUND: Low endothelial generation of prostacyclin (PGI(2)) is a typical feature of pregnancy-induced hypertensive disorders. The aim of the current study was to establish whether changes in PGI(2) are accompanied by alterations in fetoplacental blood flow and to test the hypothesis that PGI(2) deficiency contributes to reduced fetoplacental perfusion in pregnancy-induced hypertension (PIH) and preeclampsia. METHODS: The study included 11 women with normal pregnancies, 12 with PIH/preeclampsia, and 7 with otherwise complicated pregnancies. Fetoplacental blood flow was assessed both by umbilical artery Doppler sonography measuring the resistance index (RI) and by means of neonatal birth weight. PGI(2) formation was measured in umbilical arteries prepared immediately after birth. PGI(2), RI and birth weight were correlated with and without correction for gestational age. Furthermore, data from patients with PIH/preeclampsia were compared with normal pregnancies as controls. RESULTS: A significant inverse correlation was found between umbilical PGI(2) formation and umbilical RI and between birth weight and RI, whereas PGI(2) and birth weight were directly related. Patients with PIH/preeclampsia showed reduced PGI(2) formation, markedly increased gestational age-corrected RI and significantly reduced percentile birth weight. CONCLUSIONS: These results provide evidence showing that PGI(2) is a relevant mediator of fetoplacental blood flow and suggest an important role of PGI(2) deficiency in PIH/preeclampsia.

6-Ketoprostaglandin F1 alpha↗
PubMed1999

[Early detection of pre-eclampsia within the scope of prenatal care].

Pregnancy-induced hypertension and preeclampsia account for about 25% of perinatal morbidity and mortality and are a leading cause of maternal death in developed countries. Consequently, early diagnosis of the disease seems very important. Numerous clinical and biochemical methods have been described and tested for the prediction of preeclampsia. The results of these studies are critically described here. In summary, no test presently available serve as a reliable early marker of developing preeclampsia. However, vaginal Dopplerultrasound may allow prediction as early as the 12th to 16th week of gestation. Moreover, methods detecting underlying mechanisms of the disease such as endothelial dysfunction and platelet activation, are being developed and might provide improved early identification of pregnant women at high risk.

Female↗
PubMed1996

Platelet PGI2 receptor affinity is reduced in pre-eclampsia.

Prostacyclin (PGI2) receptors were studied in platelet membrane preparations from women with normal pregnancy, pregnancy-induced hypertension (PIH) or pre-eclampsia. Patient groups showed no differences in gestational week at delivery. A markedly lower birth weight, however, was found in pre-eclampsia. No differences between groups could be detected in platelet PGI2 receptor number. In contrast, the binding affinity to the PGI2 mimetic iloprost was considerably reduced in pre-eclampsia, whereas receptor affinity between PIH and normal pregnancy did not differ significantly.

Adult↗
PubMed1994

Excretion of prostacyclin and thromboxane metabolites before, during, and after pregnancy-induced hypertension.

The aim of the present study was to assess whether changes in prostacyclin (PGI2) and thromboxane (TXA2) generation precede the manifestation of pregnancy-induced hypertension (PH). The metabolites 6-oxo-PGF1 alpha and TXB2 were measured in the urine of 69 randomly selected pregnant women from 16-20 weeks of gestation (wg) until delivery and more than 6 weeks postpartum. Between 16-20 and 21-24 wg 6-oxo-PGF1 alpha excretion did not change in patients who later developed PIH (n = 6) but increased significantly in the control group (n = 63). In contrast, a marked rise in TXB2 excretion was found in the PIH group but not in controls. Thereafter significant differences between both groups persisted from 25 wg until delivery. The 6-oxo-PGF1 alpha/TXB2 ratio was below the 10th percentile from 21-24 wg until delivery in patients with developing PIH. The excretion of both metabolites was substantially lower in the non-pregnant state without any difference between patient groups. These results show an altered urinary excretion of both 6-oxo-PGF1 alpha and TXB2 preceding the onset of the disease. A pathophysiological role of PGI2 deficiency and increased TXA2 formation in PIH appears substantiated.

6-Ketoprostaglandin F1 alpha↗
PubMed1993

Prostacyclin contributes to nitroglycerin-mediated relaxation of human umbilical arteries.

This study compared the action of nitroglycerin (GTN) and linsidomine (SIN-1) on vessel tone and prostacyclin (PGI2) production of human umbilical arteries in vitro. GTN-induced vessel relaxation was significantly attenuated by indomethacin pretreatment. This was associated with a significant inhibition of the fourfold stimulation of PGI2 release by GTN. No such effects were seen with SIN-1. We concluded that GTN-induced PGI2 release contributed to the vasodilatory action of organic nitrates in the fetoplacental circulation.

Epoprostenol↗
PubMed1992

Prostacyclin rather than nitric oxide lowers human umbilical artery tone in vitro.

This study was designed to determine vasodilator activities of two endothelium-derived relaxing factors: prostacyclin (PGI2) and nitric oxide (NO) in human umbilical arteries. Isolated vessel segments were contracted by submaximal concentrations of serotonin and bradykinin. These contractions were enhanced after inhibition of prostaglandin formation by the cyclooxygenase inhibitor indomethacin and after removal of the endothelium, both resulting in a pronounced decrease in PGI2 formation. Contractions remained unchanged after treatment of the vessels with nitro-L-arginine, a selective inhibitor of endogenous NO biosynthesis. The efficacy of inhibition of NO biosynthesis was established by a more than 60% reduction in cyclic GMP accumulation. Even inhibition of stimulated NO formation by histamine did not change vascular tone. These data suggest that PGI2 rather than NO is an endothelium-derived relaxing factor in human umbilical arteries.

Arginine↗
PubMed1992

Any physiological role for prostacyclin in regulation of fetal vessel tone?

This study investigates the contribution of endogenous prostacyclin and nitric oxide (NO) for maintenance of umbilical artery tone in vitro. Treatment with indomethacin as well as removal of the endothelium was followed by contractions of umbilical arteries and a reduced formation of prostacyclin. In contrast, vessel tone was not affected by inhibition of NO synthesis, using nitro-L-arginine. Thus, prostacyclin rather than nitric oxide appears to be the endogenous endothelium-derived factor in the umbilical circulation that is involved in regulation of vessel tone.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

[The value of functional tests in diagnosis of prolactinoma].

The present study in 37 hyperprolactinaemic patients was performed, to investigate the relationship between radiographic changes of the pituitary region and serum prolactin levels, clinical signs and the results of dynamic tests. Prolactin responsiveness after metoclopramide- and TRH-injection and the nocturnal profile of serum prolactin were examined in 25 women. The results of the dynamic tests did not correlate with the radiological diagnosis. However, serum prolactin concentrations correlated strongly with the radiographic evidence of a pituitary tumour. The results show, that prolactin stimulation tests and the evaluation of the nocturnal secretory pattern of prolactin are not useful for differentiating between adenoma and nonadenoma caused hyperprolactinaemia. However, determinations of prolactin serum levels are of great clinical importance in the diagnosis of prolactinomas.

Circadian Rhythm↗
PubMedDate not supplied

[Prevention of pre-eclampsia by low-dose acetylsalicylic acid--a critical appraisal].

Pre-eclampsia has been shown to be associated with platelet activation and excessive release of vasoconstricting thromboxane preceding the onset of the disease. Low-dose acetylsalicylic acid (ASA) substantially inhibits thromboxane formation and may thus prevent pre-eclampsia from developing. In agreement with this hypothesis early randomised trials reported on promising reductions in pre-eclampsia risk and possible fetal growth retardation. Subsequent multicentre trials during the nineties failed to confirm a large benefit, which may in part be explained by late initiation of treatment, low dosages, low patient compliance and wide inclusion of women with concomitant disorders such as chronic hypertension, diabetes mellitus and kidney disease. A recent systematic review of all randomised trials showed an acceptable safety profile and a significant but only moderate reduction in the risk of pre-eclampsia regardless of gestation at trial entry or dose of ASA. There is now growing evidence that the earlier ASA treatment is started, the greater the reduction in the risk of pre-eclampsia is. Moreover, ASA has much stronger effects at higher (80 - 150 mg/day) than at lower doses in the protection against pre-eclampsia and the prevention of severe fetal growth retardation. No clinically important effects, however, have been found in patients with chronic hypertension, kidney disease or diabetes mellitus. In contrast, low dose ASA (100 mg/day) might benefit women with unfavourable obstetric history, in particular those with severe fetal growth retardation or pre-eclampsia with onset at < 32 weeks. The crucial time for starting treatment may be before 16 weeks and daily ingestion before bedtime appears useful. To start low-dose ASA at 20 - 24 weeks gestation seems only justified in women with abnormal uterine Doppler flow.

Aspirin↗
PubMedDate not supplied

[The significance of eicosanoids in gestosis].

Eicosanoids, especially prostaglandins and other arachidonic acid metabolites, play an important role in gestosis. Experimental and clinical evidence suggest prostacyclin deficiency, enhanced platelet reactivity and increased production of thromboxane A2 as possible reasons for gestosis. In addition, pathological interactions between cyclooxygenase-derived products and the renin-angiotensin- and kallikrein-kinin systems may exist and contribute to hypertension and reduced fetoplacental blood flow. Moreover, pregnancy-induced hypertension appears to be also related to lipoxygenase products and enhanced lipid peroxidation. In general, little is known about the regulation of arachidonic acid metabolism in gestosis. It is also unknown whether altered activities of mediators and hormones are cause or effect of pregnancy-induced hypertension. This is particularly relevant to the site of eicosanoid formation, i.e. platelets, the trophoblast or endothelial cells. At this time, it is not possible to give therapeutical recommendations, which are specifically designed to correct changes in eicosanoid production in gestosis. Antihypertensive therapy alone is insufficient, particularly with regard to the fetal situation. Preventive treatment with low-dose acetylsalicylic acid may have a protective effect against pregnancy-induced hypertension. Presently, more selective antagonists of thromboxane generation and/or action are being developed and might provide fresh insights both into the pathology of the disease and improved drug treatment.

Eicosanoids↗
PubMedDate not supplied

[Thrombocyte prostacyclin receptors in gestational hypertension and pre-eclampsia].

OBJECTIVE: To determine prostacyclin (PGI2) receptor characteristics in pregnancies complicated by hypertension and to assess any relation to the clinical outcome. METHODS: Radioligand binding studies with [3H]-Iloprost were performed to measure receptor capacity (Bmax) and affinity (Kd-1) using platelet membranes from patients with preeclampsia, gestational hypertension or normal pregnancy. RESULTS: PGI2 receptor capacity did not differ between the patient groups. In contrast, PGI2 receptor affinity was diminished in gestational hypertension and considerably reduced in preeclampsia compared to normal pregnancy. A similar pattern was found in fetal growth (normal pregnancy > gestational hypertension > preeclampsia). Furthermore, the rate of low Apgar scores and acidosis was increased in preeclampsia. CONCLUSIONS: In preeclampsia reduced platelet PGI2 receptor affinity was found as well as poor pregnancy outcome in comparison with normal pregnancy, whereas these differences were less pronounced in gestational hypertension. This suggests a role of PGI2 and its receptor in gestational hypertension and in particular in preeclampsia.

Adolescent↗