PubMed Health⌕ Search

Biomedical subjects

M De Kock

Publications and source records attributed to M De Kock.

At least 55 records · Page 3Linked to original sources
PubMed1995

Interactions between the lipophilic opioid sufentanil and clonidine in rats after spinal application.

BACKGROUND: Alpha2-adrenoceptor agonists, such as clonidine, can potentiate the analgesic properties of spinal opioids. In order to further extend this observation to highly lipophilic and potent spinally acting opioids, we tested the interactions between clonidine and sufentanil after both epidural and intrathecal administration in rats. METHODS: The rats were equipped with spinal catheters. Antinociceptive testing was performed with the Tail Withdrawal Reaction test. Dose-response functions of sufentanil, clonidine and combinations of clonidine plus sufentanil were determined. RESULTS: These indicated that 1) sufentanil, but not clonidine alone, results in a dose-related antinociception after both the epidural and the intrathecal route of administration; 2) In combination with normally inactive doses of sufentanil, the addition of clonidine results in activity; 3) In a particular dose-range of sufentanil, there is a direct relationship between the doses of sufentanil and clonidine needed to produce antinociception; 4) Even at very high doses of clonidine, a minimal amount of sufentanil is needed to produce antinociception and 5) At the conditions tested here, the contribution of clonidine is minimal at high, intrinsic active doses of sufentanil.

Analgesia, Epidural↗
PubMed1995

Can alpha 2-adrenoceptor agonists reverse or prevent tolerance to the antinociceptive activity of opioids in rats?

The present study was designed to investigate the possible role of some alpha 2-agonists in the phenomenon of tolerance to opioid-induced antinociception. To do so, the alpha 2-agonists were tested alone and in combination with opioids in naive and repeatedly fentanyl-treated rats in the tail withdrawal reaction (TWR) test. Under the treatment schedule used, rats became tolerant to fentanyl and cross-tolerance was observed with other opioids. The alpha 2-agonists alone were inactive in opioid naive and repeatedly fentanyl-treated rats. The potentiating interaction between the alpha 2-agonists and fentanyl in naive animals diminished considerably after the repeated fentanyl treatment. Adding an alpha 2-agonist to high doses of fentanyl during repeated treatment resulted in a complete tolerance to both compounds. Using lower, but equipotent antinociceptive drug combinations of alpha 2-agonists and opioids, resulted in less tolerance. Alpha 2-agonists are thus unable to directly overcome tolerance to the antinociceptive activity of fentanyl in tolerant animals. Nevertheless, by lowering the dose of the opioid for an equipotent antinociceptive activity, alpha 2-agonists are able to delay the onset of tolerance, probably based on the concept of opioid receptor sparing.

Adrenergic alpha-Agonists↗
PubMed1994

Potentiation of the analgesic properties of fentanyl-like opioids with alpha 2-adrenoceptor agonists in rats.

BACKGROUND: Data on the analgesic properties of alpha 2 agonists and their interactions with opioids are conflicting. Experiments were conducted in rats to evaluate whether various available alpha 2 agonists can potentiate the analgesic properties of opioids and to determine the route of administration needed for optimal interaction. METHODS: The tail-withdrawal reaction test was used as an analgesia assay. In separate experiments, the interactions between systemic (subcutaneous, intravenous, and intraperitoneal) and spinally (epidural and intrathecal) administered alpha 2 agonists and opioids were evaluated. The antagonism of medetomidine plus fentanyl with naloxone and/or idazoxan also was studied. RESULTS: All alpha 2 agonists tested, when injected subcutaneously with fentanyl, potentiated the opioid-induced analgesia. In terms of a reduction of the amount of fentanyl needed to produce a deep surgical analgesia (tail-withdrawal reaction latency > or = 10 s) over more than 2 h, the relative order of potency of the alpha 2 agonists tested was: medetomidine > dexmedetomidine > xylazine > clonidine > detomidine. For some of these alpha 2 agonists there was a biphasic effect: at the larger doses tested, a reduction in the fentanyl potentiation was present. The potentiation of the opioid activity with alpha 2 agonists was also demonstrated in terms of a longer duration of analgesia after combined treatment with fixed doses of opioids. The interaction between the alpha 2 agonists and the opioids remained present when a more profound criterion of analgesia (tail-withdrawal reaction latency > or = 30 s) was used. Furthermore, the interactions between the alpha 2 agonists tested and fentanyl or sufentanil appeared to be independent of the route of administration. Potentiations were observed after simultaneous subcutaneous injections of both groups of compounds, after the combination of intraperitoneal (alpha 2 agonist) plus subcutaneous (opioid), intravenous (alpha 2 agonist) plus epidural (opioid) and simultaneous epidural or intrathecal administrations. With regard to antagonism of the analgesic activity of combined treatment with alpha 2 agonists plus opioids, naloxone provided total antagonism, whereas the alpha 2 antagonist idazoxan overcame only the alpha 2 agonist-induced potentiation of fentanyl. CONCLUSIONS: The tested alpha 2 agonists can potentiate the analgesic properties of opioids, but they have no intrinsic antinociceptive effects on spinal reflexes on their own. The potentiating activities of the alpha 2 agonists could be measured both in terms of a reduction of the amount of opioid needed to reach a particular level of analgesia and in terms of a longer duration of analgesia with a fixed dose of the opioid. The potentiations were observed with various alpha 2 agonists and opioids and appeared independent of the routes of administration.

Adrenergic alpha-Agonists↗
PubMed1994

Laparoscopic antireflux surgery. What is real progress?

OBJECTIVE: The authors aim to substantiate, with objective arguments, potential advantages of laparoscopic versus open antireflux surgery in the light of the recent crude experience of the Louvain Medical School Hospital. METHODS: Seventy-two consecutive patients with disabling gastroesophageal reflux disease ([GERD], n = 56), symptomatic hiatal hernia without GERD (n = 5), or unsatisfactory outcome after unsuccessful antireflux procedure (n = 11) were operated on by laparotomy (n = 28), laparoscopy (n = 39), or thoracotomy (n = 5). The antireflux procedure was a subdiaphragmatic Nissen fundoplication (n = 60), an intrathoracic Nissen fundoplication (short esophagus, n = 3), a subdiaphragmatic 240 degrees fundoplication (severe motility disorders, n = 3), a Lortat-Jacob repair (hiatal hernia without GERD, n = 5), and a duodenal diversion (delayed gastric emptying, n = 1). RESULTS: Major postoperative morbidity included two pulmonary embolisms (one laparoscopy patient and one laparotomy patient), and one hemothorax (one thoracotomy patient). Mean hospital stay was 6.4 days for laparoscopy, 7.8 days for laparotomy, and 12.5 days for thoracotomy. Postoperative morphine consumption (patient-controlled analgesia) averaged 47 mg/48 hrs (laparoscopy) versus 46 mg/48 hrs (laparotomy with primary antireflux surgery) (p > 0.05). Although 93% of the laparoscopy patients returned to work within 3 weeks after surgery, 92% of the laparotomy and thoracotomy patients resumed their activity after more than 6 weeks. At follow-up, 87.5% of the patients were asymptomatic or had inconsequential symptoms, 9.8% had disabling side effects, and 2.7% had persistent or recurring esophageal symptoms. There were four parietal herniations, i.e., one incisional hernia and one recurrence of a repaired umbilical hernia in the laparotomy group, and two herniations of the wrap into the chest--probably related to a premature return to manual work--in the laparoscopy group. Three laparoscopy patients were dissatisfied with the esthetics of their scars. Lower esophageal sphincter pressure and esophageal acid exposure in the laparoscopy patients who were investigated were normal in 100% and 95%, respectively. CONCLUSIONS: Laparoscopy is a good approach for achieving successful antireflux surgery in selected cases. However, its fails to substantially reduce postoperative complication rate and discomfort, duration of the hospital stay, and the risk of esthetic sequela. Early return to work is questionable for manual workers. The subdiaphragmatic Nissen fundoplication is not an all-purpose antireflux procedure.

Adult↗
PubMed1994

Intraoperative and postoperative analgesia using intravenous opioid, clonidine and lignocaine.

The postoperative analgesia afforded after colonic surgery by IV opioid, clonidine and lignocaine given intra- and postoperatively was evaluated. In a double-blind randomised trial, 80 male patients scheduled for colonic resection under general anaesthesia received fentanyl 5 micrograms.kg-1 at induction and another 4 micrograms.kg-1 before skin incision (group A) or fentanyl (same dose) plus clonidine 4 micrograms.kg-1 in 20 min + 2 micrograms.kg-1.h-1 (group B, C) or fentanyl plus clonidine (same dosage) plus lignocaine 2 mg.kg-1 before skin incision, repeated before peritoneal incision and retractor placement (group D). In the four groups, intraoperative boluses of fentanyl 2 micrograms.kg-1 were given in response to the painful stimulation of the procedure. Postoperative pain was managed with PCA delivering 2 mg morphine per request in group A, 1.5 mg morphine in group B, 1.5 mg morphine + 15 micrograms clonidine in group C and 1.2 mg morphine + 15 micrograms clonidine + 23 mg lignocaine in group D. Postoperative analgesia was assessed by recording the analgesic demands (met and unmet) and the dose of morphine delivered at 6, 12, 18, 24, 36 hours. Side-effects, pain and sedation analogue scores were also recorded. Analgesic demands and delivered morphine dose were reduced, at any time interval considered, in groups B, C, D, compared with A (P < 0.001). No differences were noted between the group B, C, D. Pain analogue scores were better in groups B, C, D compared with group A (P < 0.001). Sedation and side-effects were not increased in groups B, C, D.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Effects of intravenous clonidine on the secretion of growth hormone in the perioperative period.

Growth hormone (GH) improves the metabolic and immunitary parameters in the postoperative period. Clonidine, a central acting alpha 2-adrenoceptor agonist stimulates GH release and is currently used as a screening test for GH-deficiency. A continuous iv infusion of clonidine may lead to a sustained increase in GH secretion during the perioperative period. With institutional approval and after informed consent, 20 healthy (ASA 1) patients scheduled for functional middle ear surgery under deliberate hypotensive anesthesia were studied. The anesthetic technique consisted of isoflurane, fentanyl and atracurium. Patients were randomly assigned to two groups. In group 1, hemodynamic stabilisation was obtained with a loading dose of clonidine (4 micrograms.kg-1 in 30 min) and maintained with an infusion of 1 microgram.kg-1.h-1. In group 2, a loading dose of labetalol 0.2 mg.kg-1 was followed by an infusion of 0.1 mg.kg-1.h-1. These infusions were stopped 30 min. before the end of the procedure. GH and glucose concentrations were assayed before the induction of anesthesia, after the loading dose and every 30 min. during the procedure and after the recovery during 2 hours. Serum clonidine levels were assayed after the loading dose, 1 and 3 hours later. Somatomedin C (IGF-I) concentration was measured before the induction and in the first postoperative morning along with GH, glucose and clonidine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Clonidine combined with sufentanil and bupivacaine with adrenaline for obstetric analgesia.

Clonidine produces analgesia via a non-opioid mechanism and it may be used as an interesting adjuvant to local anaesthetics and opioids in obstetric analgesia. To examine the effects of the addition of clonidine to bolus injections of bupivacaine, adrenaline and sufentanil, we enrolled 50 women receiving extradural analgesia for vaginal delivery into a double-blind study. They were allocated randomly to two groups: group A received a 10-ml extradural solution of bupivacaine 12.5 mg combined with adrenaline 25 micrograms and sufentanil 10 micrograms; group B received the same solution with clonidine 30 micrograms. Each patient was allowed two subsequent injections of the chosen solution. Subsequently, if still in the first stage of labour, analgesia was augmented with additional 10-ml injections of bupivacaine 12.5 mg with adrenaline 25 micrograms, without sufentanil or clonidine. The latter solution was used for perineal analgesia in group A; clonidine 30 micrograms was added in group B. During the first and second stages of labour, there was no difference between the two groups in duration of analgesia after the first injection (142 min in group A; 127 min in group B), number of injections (1.8 in group A; 1.9 in group B) and the total bupivacaine requirements (33.9 mg in group A; 34 mg in group B). The quality of analgesia was evaluated as very good in both groups (23/25 in group A; 24/25 in group B). The degree of motor block or the frequency of other side effects were not enhanced by clonidine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Clonidine pretreatment reduces the systemic toxicity of intravenous bupivacaine in rats.

BACKGROUND: Clonidine prolongs the duration of sensory and motor block induced by bupivacaine, and this association, in constant infusion by the epidural route, is used for postoperative analgesia. After a near-fatal intravenous bolus of bupivacaine in dogs, clonidine improves ventricular electrophysiologic parameters, but probably worsens bupivacaine-induced bradycardia and depression of the myocardial contractility. The current study, using a rodent animal model, evaluated the influence of clonidine pretreatment on the systemic toxic effects of bupivacaine overdose induced by a constant intravenous infusion. METHODS: Twenty Wistar male rats were anesthetized with thiopental, and controlled ventilation was started with an equal mixture of O2 and N2O. Electrocardiogram (ECG), electroencephalogram (EEG), and invasive arterial blood pressure were continuously recorded. Clonidine (5 micrograms/kg) or saline was injected intravenously in a randomized fashion. After 15 min, an intravenous infusion of bupivacaine was started at 2 mg.kg-1 x min-1. The time of occurrence of the bupivacaine-induced toxic events was recorded and the doses were calculated. Ten (five in each group) additional rats, pretreated according to the same protocol, were killed at the time of the first dysrhythmia, for blood sampling and plasma bupivacaine concentration measurement. RESULTS: Clonidine reduced heart rate and arterial blood pressure before bupivacaine infusion (P < 0.05). The threshold doses at the first QRS modification (11.3 +/- 5.6 vs. 2.1 +/- 0.9 mg/kg) and the first dysrhythmia (40.6 +/- 15.3 vs. 8.48 +/- 3.7 mg/kg), the increase in EEG total spectral power (33.3 +/- 21.9 vs. 8.2 +/- 5.1 mg/kg), the 25 and 50% reduction in baseline mean arterial pressure and heart rate, the isoelectric EEG (58.6 +/- 14 vs. 22 +/- 6.6 mg/kg), and the final systole (99 +/- 16 vs. 51.8 +/- 14.5 mg/kg) were significantly greater in the clonidine group than in the saline group (P < 0.01). The time between the first dysrhythmia and 50% reduction of baseline mean arterial blood pressure was not different between the groups. In the additional series, the first dysrhythmia occurred later (10.9 +/- 4.5 vs. 3.2 +/- 1.0 min, P < 0.01) and plasma bupivacaine levels were greater (18.7 +/- 8.0 vs. 7.8 +/- 3.2 micrograms/ml, P < 0.01) in the clonidine group than in the saline group. CONCLUSIONS: In this model, clonidine given prophylactically delays the toxic manifestations of bupivacaine overdose and does not accentuate the subsequent hypotension.

Anesthesia, Epidural↗
PubMed1993

Intravenous or epidural clonidine for intra- and postoperative analgesia.

BACKGROUND: Intravenous and epidural clonidine both produce postoperative analgesia. Several experimental reports demonstrate a spinal site of action for the analgesic effects of this alpha 2-adrenoceptor agonist. Therefore, the authors evaluated the clinical analgesic benefits of using clonidine, both intra- and postoperatively, by the epidural or the intravenous route. METHODS: Using a randomized prospective double-blind study design, 40 patients, between 18 and 50 yr of age, undergoing intestinal surgery under general propofol/nitrous oxide anesthesia, were enrolled. Before anesthesia, an epidural catheter was inserted at the L1-L2 interspace. At induction, a clonidine infusion was started at the doses of 4 micrograms/kg in 10 ml during 20 min, followed by 2 micrograms.kg-1 x h-1 (5 ml/h) during 12 h, either by the epidural (group 1) or by the intravenous (group 2) route. Intraoperatively, increased blood pressure and heart rate not responding to additional propofol bolus (0.5 mg/kg) was treated with a bolus of alfentanil (7 micrograms/kg). Postoperatively, morphine boluses (1.5 mg) were given through a PCA device according to the patient's need. Intraoperative analgesia was assessed by the alfentanil requirements. Postoperative analgesia was assessed by recording the morphine requirements, the visual analogue scale (VAS) at rest and after mobilization, and the patients' analgesia scale at 0, 3, 6, 12, 18, 24, and 36 postoperative hours. Sedation analogue scale and side effects were also recorded. Heart rate and blood pressure were particularly detailed during the first 2 h of the clonidine infusion. Plasma clonidine concentrations were measured after 20 min and 6, 12, and 24 h. RESULTS: Epidural clonidine significantly reduced the intraoperative alfentanil requirements (0.93 +/- 1.2 in group 1 vs. 2.4 +/- 1.8 mg in group 2). The postoperative morphine requirements were also reduced during the first 6 h (8.3 +/- 5.8 in group 1 vs. 17.8 +/- 13.4 mg in group 2). The VAS were comparable in both groups, despite the better patients' analgesia score reported in the epidural group during the first 12 h. There was no difference in sedation score at any time interval considered. Epidural and intravenous clonidine reduced heart rate and blood pressure to the same extent. The plasma clonidine concentrations were less in the epidural group only after the loading doses. CONCLUSIONS: Epidural clonidine reduces the intra- and early postoperative analgesic requirements when compared with the same dose given by the intravenous route. The side effects were similar with the two routes of administration.

Adolescent↗
PubMed1993

Intravenous clonidine does not promote hypoxemia or platelet aggregation in man.

This study was designed to evaluate hypoxemia and platelet aggregation in man following intravenous administration of clonidine. With Institutional approval and following informed consent, 20 patients (ASA I-II) without spontaneous or drug-induced coagulation disorder undergoing elective total hip replacement were studied. They were randomly divided into two groups. Group A (n = 10) received an IV loading dose of 4 micrograms/kg of clonidine in 30 minutes followed by an infusion of 1 microgram/kg/h till the end of the procedure. Group B (n = 10) received saline. Platelet aggregation was assessed before infusion and at the end of both the loading dose and the infusion. PaO2 was measured before anesthesia (FIO2 = 0.21), before femoral cementation (FIO2 = 0.40), 2 min. after prosthesis implantation (FIO2 = 1), before the end of the procedure (FIO2 = 0.40) and in the recovery room (spontaneous breathing with FIO2 = 0.21). Plasma clonidine levels were assessed at the end of both the loading dose and the infusion. At any time considered, no statistical differences were noted between the groups for platelet aggregation and PaO2. We conclude that intravenous clonidine does not clinically promote platelet aggregation nor hypoxemia in man.

Aged↗
PubMed1992

Central effects of epidural and intravenous clonidine in patients anesthetized with enflurane/nitrous oxide. An electroencephalographic analysis.

Epidural clonidine produces regional anesthesia as well as sedation and a decrease in anesthetic requirements. To assess these effects, the electroencephalogram (EEG) was recorded after epidural or intravenous (iv) injection of clonidine during enflurane/N2O anesthesia. Eighteen ASA physical status 1 women undergoing vaginal hysterectomy were allocated randomly to receive epidural clonidine (8 micrograms.kg-1 in 4 ml over 2 min) and iv saline (10 ml over 14 min); or epidural saline (4 ml over 2 min) and iv clonidine (8 micrograms.kg-1 in 10 ml over 14 min); or epidural saline (4 ml over 2 min) and iv saline (10 ml over 14 min). The level of anesthesia was kept constant beginning 10 min before and until 44 min after epidural injection. EEG power spectral analysis was performed throughout the study period using a 2-min average of 8-9-s epochs. Clonidine significantly reduced EEG total power only after epidural administration (P less than 0.05). Relative power increased in the delta band in both the epidural and iv clonidine groups (P less than 0.001). The depression of the total EEG power after epidural injection could be explained neither by systemic absorption alone nor by hemodynamic variations. It may represent the contribution of the direct spinal action of this alpha 2-adrenergic agonist to general anesthesia.

Anesthesia, General↗
PubMed1991

Postoperative P.C.A. in abdominal surgery. Analysis of 200 consecutive patients.

Patient-Controlled-Analgesia (PCA) is becoming a standard in post-operative analgesia. This prospective study was designed to get more information on the safety and the efficiency of morphine PCA following abdominal surgery. Two hundred patients were enrroled Morphine requirements, number of unsatisfied demands, patients' satisfaction and side effects were recorded for 36 hours postoperatively. The mean morphine requirement was 23.2 mg for the first 12 hours, 22.2 mg for the next 12 hours and 16 mg for the last 12 hours. Female patients required significantly less morphine than male. Interestingly such difference was no more present for patients older than 60 years. The larger the morphine bolus dose, the greater the total amount needed without any better analgesia. A bolus dose of 1 mg seemed to be the best to be recommended. The variability in the number of unsatisfied demands (i.e. demands during the lockout interval) was quite large. The number of unsatisfied demands was not influenced by the size of the bolus dose. The patients' satisfaction was high: 60% enthusiastic, 36% satisfying, 4% negative. There was no difference in satisfaction linked to gender. On the other hand, a history of a previous surgery experience without PCA raised patients' satisfaction score. Side effects were uncommon. It is concluded that morphine PCA is an efficient and safe technique of post-operative analgesia in abdominal surgery.

Abdomen↗
PubMed1986

Alterations in myocardial metabolism and function at rest in stable angina pectoris: relations with the amount of exercise-induced thallium-201 perfusion defect.

The relation between the amount of exercise-induced ischemia and alterations in left ventricular (LV) function and metabolism at rest was studied in 18 coronary patients with stable angina pectoris. An ischemic defect area score was computed from quantitative exercise thallium-201 (Tl-201) scintigraphy; this estimation of the amount of ischemic myocardium was used to classify the patients in group I (n = 8; score less than 15%, mean 6.7 +/- 2.5%) and II (n = 10; score greater than 15%; mean 27.2 +/- 8.9%). Hemodynamics and metabolism were studied in basal state. No patient had anginal pain during the study, and the extent of angiographic coronary artery disease (CAD) was comparable in the two groups. Heart rate, aortic pressure, coronary blood flow, and myocardial oxygen uptake were also similar in both groups. However, ejection fraction was reduced in group II (51 +/- 13 vs 63 +/- 5%; p less than 0.01) and LV relaxation was impaired as shown by the increase in time-constant of isovolumic pressure fall (55 +/- 16 vs 44 +/- 6 ms in group I; p less than 0.05); the LV end-diastolic pressure was also increased in group II (19 +/- 8 vs 10 +/- 4 mmHg in group l; p less than 0.05). Furthermore, in group II, myocardial lactate uptake was reduced (4 +/- 19 vs 30 +/- 29 mumole/min in group I; p less than 0.01) and the productions of alanine and glutamine were augmented (-7.5 +/- 4.4 vs -4.6 +/- 1.6 mumole/min in group I; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Alteration of left ventricular diastolic filling in hypertensive patients: effects of nitrendipine and atenolol.

This study was undertaken to determine the chronic effects of a long-acting calcium-channel blocker (nitrendipine) on resting left ventricular filling abnormalities in ten patients with essential hypertension. Radionuclide left ventricular curves of these hypertensive patients were compared with the curves of twelve normal volunteers and of eight asymptomatic older patients. The curves were analyzed for ejection fraction, peak filling rate (normalized for end-diastolic counts and for stroke counts), time to peak filling rate and filling fraction in the first-third of diastole normalized for cycle length. Heart rate and ejection fraction were similar in both control groups and hypertensive patients before and after nitrendipine. Before nitrendipine, diastolic filling parameters were significantly different in the hypertensive patients as compared with the volunteers and with the asymptomatic aged patients: peak filling rate was lower, time to peak filling rate was longer and the first-third filling fraction was smaller. After six weeks of nitrendipine therapy, systolic and diastolic blood pressure decreased significantly. After nitrendipine, the time to peak filling rate decreased and the first-third filling fraction and the peak filling rate (normalized for stroke counts) increased significantly. The acute oral administration of 100 mg atenolol induced a further decrease in systolic blood pressure and a significant decrease in heart rate. The effect of combining nitrendipine and atenolol on diastolic indexes was a preserved effect on time to peak filling rate and on the first-third filling fraction. These results suggest that short-term therapy with nitrendipine improves early diastolic dysfunction in hypertensives: the addition of a beta-blocking agent further improved the early diastolic indexes.

Adult↗
PubMedDate not supplied

The paediatric liver transplantation program at the Université catholique de Louvain.

The Paediatric Liver Transplant Program at Saint-Luc University Clinics constitutes a substantial single centre experience, including 667 transplantations performed between March 1984 and April 2003, and the history of this program reflects the tremendous progress in this field since twenty years. Liver transplantation in children constitutes a considerable undertaking and its results depend on multiple, intermingled risk factors. An analysis of the respective impact of several surgical and immunological parameters on patient/graft outcome and allograft rejection after paediatric liver transplantation showed a significant learning curve effect as well as the respective impact of pre-transplant diagnosis on survival and of primary immunosuppression on the rejection incidence. The introduction of living related liver transplantation in 1993 not only permitted to provide access to liver replacement in as many as 74% more candidate recipients, but also resulted in better graft survival and reduced retransplantation rate. The results of a recent pilot study suggest that steroid avoidance is not harmful, and could even be beneficial for paediatric liver recipients, particularly regarding growth, and that combining tacrolimus with basiliximab (anti-CD25 chimeric monoclonal antibody) for steroid substitution appears to constitute a safe alternative in this context. The long-term issues represent the main future challenges in the field, including the possibility of a full rehabilitation through immunosuppression withdrawal and tolerance induction, the development of adolescence transplant medicine, and the risk of early atherogenesis in the adulthood.

Adolescent↗
PubMedDate not supplied

Adult liver transplantation at UCL: update 2002.

The authors present the results of a single centre study of 587 liver transplants performed in 522 adults during the period 1984-2002. Results have improved significantly over time due to better pre-, peri- and post-transplant care. One, five, ten and fifteen year actuarial survivals for the whole patient group are 81.2; 69.8; 58.9 and 51.2%. The high incidence of de novo tumors (12.3%), of cardiovascular diseases (7.5%) and of end-stage renal function (3.6%) should be further incentives to tailor the immunosuppression to the individual patient and to direct the attention of the transplant physician to the long-term quality of life of the liver recipient.

Adult↗