Issues around food in mixed families of adolescent girls with bulimia nervosa: A qualitative study with photo-elicitation.

OBJECTIVES: Bulimia nervosa (BN) is a common psychiatric disorder among adolescent girls with potentially significant complications. Family relationships play a major role in the development and progression of this disorder. Studies in migrant populations suffering from eating disorders show contrasting results depending on the generation of migrants: first generation migrants have fewer eating disorders than the native population, while the prevalence of this disorder is more important than the latter among second and third generation migrants. In our clinical experience, we have frequently encountered so-called "mixed" families, which are families composed of one migrant parent and one non-migrant parent. Research focusing on this kind of family is scarce which is why we chose to explore their dynamic. METHODS: This study explored the issues around food and family relationships of adolescent girls suffering from BN, a topic that, to date, has not yet been studied. Ten interviews were conducted with five adolescent girls with BN between the ages of 16 and 20 and their parents, using photo-elicitation to enrich the collected data. RESULTS: The results were organized around two axes: (1) identity issues around food, that is the assimilation process described by both parents and adolescents concerning family meals and food habits, and how the adolescents struggle to manage this interbreeding; and (2) transmission issues with the consequences the migrant parent has to deal with to transmit his/her cultural identity with food while being far away from the homeland, and the difficulties between this parent and his/her child to share this heritage. Both issues, identity and transmission, appear to be central among these families. CONCLUSIONS: Our results suggest a difficulty in mentalizing identity issues in adolescent girls; the function of appeasement around non-mentalized tensions was highlighted. In our opinion, in this particular context, BN acts as a means of expressing the difficulty of their mixed culture. This enables it to draw some clinical implications, especially using mentalization-based therapy which has already shown efficacy in adolescents with borderline personality disorder and ED.

[Quality assurance in drug treatment by prescription drug analysis in a psychiatric treatment facility]. / Démarche qualité dans le circuit médicament grâce à l'analyse pharmaceutique des ordonnances dans un établissement de soins psychiatriques.

This article reports pharmaceutical analysis of the medical prescription in a psychiatric hospital. This study estimates the impact of the pharmaceutical interventions on the security of the treatment prescribed. This pharmaceutical system is based on individual prescription and on pharmaceutical analysis of this document. This analysis consists in checking high dosage prescription, detecting drug interaction, omission or frank prescribing errors and providing pharmaceutical advice to the physicians. In 1997, hospital pharmacists have intervened in 510 prescriptions:--315 high prescribing dosages were checked. In 7.3 percent of these cases, an error of dosage was detected;--66 drug interactions were communicated. Thirteen interventions corresponded to a forbidden association according to the Vidal therapeutic register;--53 pharmaceutical advices were performed; 12 interventions were related to a physiological or a pathological characteristic of the patient which forbid the use of the treatment;--more over, 34 omissions or frank errors were detected through the medium of our interventions; 25 errors could be considered as clinically relevant. In conclusion, the interventions rate was estimated to 3.6% of the new prescriptions. In 14.1% of these cases, they appeared as clinically significant. These rates are lower than those described in the traditional global distribution for which pharmaceutical analysis is not performed. This report has underlined the interest of pharmaceutical care by analysing the medical prescriptions.

Differential effects of tyrosine kinase inhibitors on contraction and relaxation of the aortas of normotensive and hypertensive rats.

The contribution of tyrosine kinase activity to vasoreactivity in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats was investigated on isolated aortic preparations by the use of two tyrosine kinase inhibitors: methyl-2,5-dihydroxycinnamate (30 microM) and genistein (30 microM). The pretreatment of endothelium denuded aorta with methyl-2,5-dihydroxycinnamate reduced the sensitivity of the rings to noradrenaline to a larger extent in SHR than in WKY. The relaxing effects evoked by methyl-2,5-dihydroxycinnamate and genistein on the sustained contraction induced by endothelin-1 were also more pronounced in SHR denuded rings. Furthermore, in presence of methyl-2,5-dihydroxycinnamate, the endothelium-independent contractile responses to equipotent doses of cyclopiazonic acid were more depressed in SHR than in WKY. In WKY and SHR endothelium-intact aortas contracted with either phenylephrine or endothelin-1, carbachol and cyclopiazonic acid evoked endothelium derived relaxing factor (EDRF)/nitric oxide (NO)-dependent relaxations which were reduced by pretreatment of the rings with methyl-2,5-dihydroxycinnamate or genistein. These inhibitory effects were larger in WKY rings and more important on the cyclopiazonic acid response. In addition, sodium orthovanadate (30 microM) potentiated the noradrenaline-mediated contractions of endothelium-denuded SHR rings and reduced the cyclopiazonic acid-induced relaxation of endothelium-intact WKY rings. The present study suggests a regulatory role for tyrosine kinase in the smooth muscle contraction and the endothelium-dependent relaxation in WKY and SHR aortas and demonstrates the existence of a different relationship in the effect of tyrosine kinase inhibitors on vasoreactivity between SHR and WKY. We propose that an increase in the tyrosine kinase activity in SHR could lead to an enhanced reactivity of Ca2+-linked contractile mechanisms. In addition, our results suggest a link between the loss of tyrosine kinase activity and the altered endothelium-dependent relaxation associated with hypertension.

Whole saliva and plasma levels of clozapine and desmethylclozapine.

BACKGROUND: Therapeutic drug monitoring of clozapine as an aid in the treatment of schizophrenic states is commonly used in our hospital. OBJECTIVE: Development of a high-performance liquid chromatographic method for the determination of clozapine (CLZ) and its major metabolite desmethylclozapine (DMCLZ) in plasma and saliva, and investigation of the relationship between plasma concentrations of CLZ and DMCLZ and concentrations in saliva in patients treated with clozapine. METHODS: Subjects were either inpatients or outpatients with a DSM IV diagnosis of schizophrenia (n=34). Determination of CLZ and DMCLZ saliva concentrations appeared to be a satisfactory method to check compliance to treatment, particularly in outpatients. RESULTS: Mean CLZ and DMCLZ plasma concentrations were 432+/-264 ng/ml (+/-SD) (range 90-1310 ng/ml) and 257+/-144 ng/ml (range 55-580 ng/ ml), respectively. The CLZ/DMCLZ plasma ratio was equal to 1.7+/-0-5 (daily dosage 7.2+/-2.3 mg/kg, n=34). Mean CLZ plasma and saliva levels were 336+/-157 ng/ ml (range 90-580 ng/ml) and 159+/-86 ng/ml (range 40-364ng/ml), respectively (r=0.56, n=14). Mean DMCLZ plasma and saliva levels were 196+/-112 ng/ ml (range 55-481 ng/ml) and 109+/-67ng/ml (range 40-250ng/ml), respectively (r=0.73, n=14). Mean CLZ/DMCLZ ratios determined in plasma and saliva were 1.9+/-0.6 (range 1.0-3.4) and 1.7+/-0.6 (range 1.0-3.2), respectively (r=0.85, n=14). CLZ and DMCLZ saliva concentrations appear to be useful for checking compliance to treatment, in particular among outpatients.

Augmented endothelium-dependent contraction to angiotensin II in the SHR aorta: role of an inducible cyclooxygenase metabolite.

The purpose of this study was to investigate the mechanisms involved in the angiotensin II-induced increase in the contractile response of the hypertensive wall after prolonged incubation in the organ-bath buffer. In 5-h incubated rings, the contractile response to angiotensin II in aortic rings with endothelium from spontaneously hypertensive rats (SHRs) was markedly exaggerated in comparison to 2-h incubated rings. No such potentiation was observed in SHR rings after removal of the endothelium or in intact and denuded Wistar-Kyoto (WKY) rat rings. Aspirin and SQ29548 inhibited and cycloheximide and actinomycin D reduced the time-dependent enhanced response to angiotensin II in rings with endothelium from SHRs. In SHR rings with endothelium incubated for 2 h, the contractions caused by angiotensin II were potently inhibited by piroxicam but were unaffected by NS-398. Conversely, in rings incubated for 5 h, the hyperresponsiveness to angiotensin II was inhibited to a greater extent by NS-398 than by piroxicam. Piroxicam but not NS-398 had a further inhibitory effect on the residual angiotensin II-induced contraction in actinomycin D-treated rings incubated for 5 h. In conclusion, our study shows that long-term incubation leads to hyperresponsiveness to angiotensin II in SHR aorta with endothelium. The enhanced response is associated with the induced release of vasoconstrictor prostanoids sensitive to the inhibitory effect of NS-398, a preferential inhibitor of COX-2.

Role of endothelium in the endothelin-1-mediated potentiation of the norepinephrine response in the aorta of hypertensive rats.

OBJECTIVE: To investigate the role of the endothelium in the functional interaction between endothelin-1 and norepinephrine in the contractile response of aortas from Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). METHODS: Thoracic aorta rings with and without endothelium from SHR and from WKY rats were suspended in an organ bath to record the isometric tension. After an equilibration period of 120 min, the preparations with and without endothelin-1 were subjected to single and cumulative additions of norepinephrine in different experiments. To characterize the mechanisms involved in the interaction between endothelin-1 and norepinephrine, the aortic rings were pretreated with a cyclooxygenase pathway inhibitor (piroxicam, SO29548), an inhibitor of NO synthase [NG-nitro-L-arginine (NLA)], or selective endothelin receptor blockers (BQ-123 or BQ-788). In some experiments we examined the contractile responses to norepinephrine in aortas pretreated either with angiotensin II (AII) or with U46619, an agonist of prostaglandin H2-thromboxane A2 receptors. Finally, we examined the effect of the combination of calcium-entry blockade by administration of nifedipine and treatment with either endothelin-1 or U46619 on the norepinephrine reactivity. RESULTS: Administration of 3 x 10(-10) mol/l endothelin-1 potentiated the contractile response to norepinephrine in SHR aortas with endothelium, irrespective of whether they had been treated with NLA. No endothelin-1-mediated enhancement of the response to norepinephrine was observed in SHR denuded rings and in untreated and NLA-treated WKY rat aortas. All did not affect the response to norepinephrine in SHR rings with endothelium. The amplification by endothelin-1 of the response to (1-100) x 10(-9) mol/l norepinephrine was abolished by blockade of the cyclooxygenase pathway with piroxicam or SO29548. In WKY rat and SHR denuded aortas, 10(-8) mol/l U46619 potentiated the contractile responses to norepinephrine. Administration of 3 x 10(-6) mol/l BQ-123 abolished the increase in reactivity to norepinephrine evoked by endothelin-1 in intact SHR aorta, whereas 3 x 10(-6) mol/l BQ-788 failed to modify this potentiating effect. Administration of 10(-8) mol/l nifedipine inhibited the potentiation of the norepinephrine-induced contractions evoked both by endothelin-1 in SHR aortic rings with endothelium and by U46619 in SHR denuded rings. CONCLUSION: Our results show that a low concentration of endothelin-1 induced potentiation of the contractile response to norepinephrine in SHR aortas but not in WKY rat aortas. This response was endothelium-dependent. Furthermore, our study affords functional arguments that both endothelial and smooth muscle pathways are involved in the potentiating interaction. We propose that endothelin-1 stimulates the production of endothelium- and cyclooxygenase-generated vasoconstrictor factors, which in turn may serve directly as priming stimuli at the vascular smooth muscle level, to activate the Ca(2+)-signal pathway and consequently to increase locally the vascular sensitivity to norepinephrine.

Effects of angiotensin I and angiotensin II in blood vessels: greater influence of converting enzyme activity in the rabbit basilar artery.

We investigated the constrictor effects of Angiotensin I (Ang I) and Angiotensin II (Ang II) on rabbit peripheral (aorta, carotid artery, mesenteric artery, saphenous artery) and cerebral (basilar artery) vessels and in rat aorta in functional organ bath studies. The effect of angiotensin converting enzyme (ACE) inhibition by captopril was also assessed in these preparations. Ang II elicited concentration-dependent contractions with comparable potency in rabbit and rat endothelium-free vascular rings (pD2 about 8.5) which indicates a lack of species and regional variation in the contractile responses to Ang II. The responses to Ang II were reduced by the presence of a functional endothelium in rabbit mesenteric artery and in rat aorta. Since ACE determines the plasma and tissue conversion of Ang I to active Ang II, we calculated the ratio R (EC50 Ang I-induced contraction: EC50 Ang II-induced contraction) as an indicator of the tissue ACE effectiveness. In the aorta without endothelium, Ang I was found to be much less potent than Ang II in the rabbit (R = 44) compared with the rat (R = 3.5). This species difference in the aortic conversion of Ang I to Ang II was confirmed by the use of captopril. Captopril (10(-6) M) shifted the Ang I concentration/ response curve by 2- and 14-fold to the right in rabbit and rat respectively. In other rabbit blood vessels, the rank order of potency to Ang I in endothelium denuded rings was basilar artery > > carotid artery > or = aorta > or = saphenous artery. In addition, the R value was the lowest for the basilar artery (R = 2.5). This is in agreement with the highest rightward shift (78-fold) of the Ang I concentration/response curve by captopril for basilar artery in comparison with only 3-, 8- and 3-fold shifts observed in carotid artery, saphenous artery and aorta respectively. In conclusion, our data provide evidence for a greater influence of ACE in rabbit basilar artery than in peripheral vessels.

[Role of endothelial nitric oxide synthases in the contractile response to angiotensin II of the aorta in rats. Wistar Kyoto and hypertensive rats]. / Rôle des oxydes nitriques synthases endothéliales dans la réponse contractile à l'angiotensine II de l'aorte de rat. Rats Wistar Kyoto et hypertendus.

Dysfunctions of EDRF/L-arginine-NO pathway have been demonstrated in genetic and experimental hypertension. NO is produced through the conversion of L-arginine to L-citruline by NO synthases (NOS) which exist at least in two isoforms. The first termed constitutive (NOSc) and located in the endothelium of the vascular wall results in the basal and stimulated NO production. The second termed inducible (NOSi), which produces large amounts of NO, can be expressed in both smooth muscle and endothelial cells. The aim of the study was to examine and compare in isolated aortic rings of WKY and SHR rats, the activity of the two isoforms of endothelial NO synthases and their influence on the constrictor response induced by angiotensin II. On phenylephrine preconstricted endothelium intact aortic rings (10(-6) M, WKY = 1.2 +/- 0.04 g; SHR = 1.2 +/- 0.07 g; n = 7), carbachol (10(-5) M) induced a greater relaxation in WKY (84 +/- 2.5%) than in SHR (63 +/- 8.5%) rat. This suggests the presence of a low NOSc stimulated activity in the hypertensive strain. When the incubation period was limited to 30 min after equilibration period, L-arginine (3.10(-4) M) did not induce relaxation. When the incubation period was prolonged (180 min), L-arginine induced a relaxation (WKY = 75 +/- 8%; SHR = 58 +/- 10%; n = 7). This relaxation was not observed in a medium containing actinomycin D (10(-6) M) or after endothelium removal, indicating the induction of an endothelial NOSi in the two strains.(ABSTRACT TRUNCATED AT 250 WORDS)