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Biomedical subjects

J Ahonen

Publications and source records attributed to J Ahonen.

At least 19 recordsLinked to original sources
PubMed2007

Premedication with controlled-release oxycodone does not improve management of postoperative pain after day-case gynaecological laparoscopic surgery.

BACKGROUND: Controlled-release (CR) oxycodone provides an option for the prevention of postoperative pain. We designed this randomized double-blinded placebo controlled study to evaluate the control of pain after premedication with CR oxycodone 15 mg in addition to ibuprofen 800 mg orally in day-case gynaecological laparoscopic surgery. METHODS: Sixty consenting patients were anaesthetized in a standardized fashion. Postoperative analgesia was provided by ibuprofen 800 mg twice a day in combination with fentanyl i.v. in the recovery room and normal-release (NR) oxycodone orally after the recovery room. The visual analogue scale (VAS) scores for pain and side-effects, and the amounts of postoperative analgesics were recorded for 24 h after discharge from the hospital. After a statistical analysis of the original study, we extended the study to investigate another 10 patients, who received CR oxycodone 15 mg orally in an open-labelled fashion 60 min before surgery. The plasma concentrations of oxycodone were measured from samples drawn before and 2, 4, 6 and 8 h after premedication. RESULTS: The amounts of fentanyl [100 microg (0-330) in the CR oxycodone group; 125 microg (0-330) in the placebo group], NR oxycodone, or the VAS scores for pain during the first 24 h after the discharge from the hospital did not differ after the premedication with CR oxycodone or placebo. In the extension study group, the peak plasma concentration (C(max)) of oxycodone was 10.0 (4.6-14.7) ng ml(-1), indicating possibly a sub-therapeutic level. CONCLUSION: Oral premedication with CR oxycodone did not improve management of postoperative pain after day-case gynaecological laparoscopic surgery.

Adult↗
PubMed2006

Response Entropy is not more sensitive than State Entropy in distinguishing the use of esmolol instead of remifentanil in patients undergoing gynaecological laparoscopy.

BACKGROUND: Monitoring of analgesia remains a challenge during general anaesthesia. Activation of Response Entropy (RE) to painful stimuli has been suggested to be a sign of inadequate analgesia. We evaluated the ability of RE to be more sensitive than State Entropy (SE) in measuring nociception in patients undergoing gynaecological laparoscopy. Our hypothesis was that while keeping SE at a predetermined level, RE would be higher in patients receiving a beta-blocking agent (esmolol) instead of an opioid (remifentanil) during a propofol/nitrous oxide anaesthesia. METHODS: Fifty-one women aged between 22-53 years were randomly assigned to receive esmolol (n=25) or remifentanil (n=26). SE was kept at 50+/-5. RE and SE were recorded at an interval of 30 s to 2 min and the areas under the RE and SE value-time curves (AUCRE and AUCSE) were calculated during the time of intubation and start of surgery as well as during the entire anaesthesia. The difference between RE and SE recordings in both groups was determined by subtracting the AUCSE from the corresponding AUCRE. Movements of the patients were recorded. RESULTS: No significant differences were detected in any of the several AUC values between the groups. The difference between RE and SE recordings was similar in both groups. Every patient in the esmolol group moved some time during the procedure interfering with surgery while no one in the remifentanil group moved. CONCLUSION: In patients undergoing gynaecological laparoscopic day-case surgery, RE seems not to be more sensitive than SE in guiding the use of opioids during general anaesthesia.

Adrenergic beta-Antagonists↗
PubMed2005

Recombinant factor VIIa for life-threatening post-partum haemorrhage.

The treatment of life-threatening post-partum haemorrhage (PPH) still remains challenging, and hysterectomy may be required to control the bleeding. We present 12 cases of severe PPH treated with recombinant factor VIIa (rFVIIa). We briefly describe the causes of the haemorrhage and the medical and surgical interventions before rVIIa administration. In 11 women there was a partial or good response to rFVIIa administration, while in one there was no response. In the four women undergoing a subsequent selective arterial embolization, the bleeding was significantly reduced although not completely stopped. From our experience with these 12 cases, and from previously reported cases, the use of rFVIIa may be of benefit in life-threatening PPH. However, treatment with rFVIIa, in addition to standard surgical and medical interventions, may not be definitive in every patient and a selective arterial embolization may be needed.

Adult↗
PubMed2005

Effect of ciprofloxin on the pharmacokinetics of intravenous lidocaine.

BACKGROUND AND OBJECTIVE: Recent studies have suggested that cytochrome P-450 isoenzyme 1A2 has an important role in lidocaine biotransformation. We have studied the effect of a cytochrome P-450 1A2 inhibitor, ciprofloxacin, on the pharmacokinetics of lidocaine. METHODS: In a randomized, double-blinded, cross-over study, nine healthy volunteers ingested for 2.5 days 500 mg oral ciprofloxacin or placebo twice daily. On day 3, they received a single dose of 1.5 mg kg[-1] lidocaine intravenously over 60 min. Plasma concentrations of lidocaine, 3-hydroxylidocaine and monoethylglycinexylidide were determined for 11 h after the start of the lidocaine infusion. RESULTS: Ciprofloxacin increased the mean peak concentration and area under plasma concentration-time curve of lidocaine by 12% (range [-6] to+46%; P<0.05) and 26% (8--59%; P 0.01), respectively. The mean plasma clearance of lidocaine was decreased by ciprofloxacin by 22% (7--38%; P<0.01). Ciprofloxacin decreased the area under the plasma concentration-time curve of monoethylglycinexylidide by 21% (P<0.01) and that of 3-hydroxylidocaine by 14% (P< 0.01). CONCLUSION: The plasma decay of intravenously administered lidocaine is modestly delayed by concomitantly administered ciprofloxacin. Ciprofloxacin may increase the systemic toxicity of lidocaine.

Adult↗
PubMed2005

De novo seropositive rheumatoid arthritis during immunosuppressive treatment after kidney transplantation.

We detected de novo seropositive erosive rheumatoid arthritis (RA) in a patient seven years after successful cadaveric kidney transplantation (RTx). RA developed in spite of treatment with cyclosporine A (CyA), methylprednisolon (MP) and azathioprine (Aza), compounds often also used for treatment of active RA. Renal failure was due to diabetes mellitus (DM) nephropathy. Besides a slight increase in C-reactive protein (CRP) concentration two years after RTx, the clinical symptoms of RA were observed seven years after RTx. RA was confirmed by X-ray examination, isotopic skeletal scan and positive serum RA factor. After switching Aza to methotrexate (Mtx) treatment, his symptoms disappeared and CRP concentration returned to normal. Our patient had HLA DRB1 *0101, *0401 alleles and DQB1 *0501, *0302 alleles which have strong genetic association with both DM and RA. To our best knowledge, this is the first case in which de novo seropositive erosive RA developed while on treatment with triple immunosuppression after RTx. The immunosuppressive treatment probably masked the inflammation and symptoms of RA.

Adolescent↗
PubMed2004

No effect of cardiopulmonary bypass on hypnosis in patients anaesthetized with propofol and alfentanil.

BACKGROUND: The effect of cardiopulmonary bypass (CPB) on the level of anaesthetic depth has not been studied previously in a randomized way. METHODS: We assessed the effect of CPB on the propofol needed to maintain a fixed bispectral index score, and on the recovery from anaesthesia in 22 patients undergoing coronary artery bypass graft surgery with CPB (on-pump) compared with 18 patients operated on without CPB (off-pump). Anaesthesia was induced and maintained with propofol and alfentanil. Throughout the procedure, the infusion rate of propofol was adjusted to keep the BIS value at 40 +/- 5. RESULTS: With the off-pump technique, the duration of surgery and anaesthetic administration were significantly greater. The need for propofol in proportion to time was exactly the same in both groups. During anaesthesia and the first 3 h thereafter, the BIS recordings were similar in both groups. No differences were detected in the time to awakening or tracheal extubation. CONCLUSIONS: CPB does not affect propofol requirements or immediate postoperative recovery compared with the off-pump technique.

Aged↗
PubMed2004

Brain injury after adult cardiac surgery.

Despite remarkable progress in surgical, cardiopulmonary bypass and anaesthetic techniques during the last three decades, brain damage remains an important complication of adult cardiac surgery. Effective brain protection strategies are already implemented today, but ongoing research is needed to meet the challenges faced in operating on increasingly old and disabled patients. The incidence of brain injury may be reduced by modifying the surgical procedure according to carotid duplex scanning and epiaortic echocardiography, by using techniques to reduce microembolization during cardiopulmonary bypass and by optimizing patient temperature during and after surgery. Increased knowledge will aid in choosing the best procedure or combination of procedures in each case to ensure that risks do not outweigh benefits.

Adult↗
PubMed2003

Myocardial metabolism on off-pump surgery; a randomized study of 50 cases.

OBJECTIVE: To study the inflammatory reaction and myocardial metabolism in off-pump and on-pump coronary artery bypass patients. DESIGN: Fifty coronary artery bypass patients were randomized to off-pump or on-pump operations. Myocardial biopsies were taken to determine myocardial metabolism and inflammation (glutathione (GSH), superoxide dismutase (SOD) and myeloperoxidase (MP)) and plasma samples for indicators of oxidative stress (conjugated dienes (s-BDC), oxidative products of proteins (s-ox-Prot) and low-density lipoprotein (LDL)-total peroxyl radical trapping antioxidant potential (s-TRAP)). RESULTS: s-ox-Prot 10 min was 2.11 +/- 0.75 vs 2.69 +/- 0.60 (p = 0.014), s-TRAP 5 min was 861 +/- 180 vs 969 +/- 192 (p = 0.032) and s-TRAP 10 min 857 +/- 176 vs 985 +/- 166 (p = 0.011), GSH 10 min 0.55 +/- 0.19 vs 0.72 +/- 1.16 (p = 0.007) (off-pump vs on-pump). The monobasic (MB) fraction of the creatinine kinase 24 h after the operation was significantly lower in the off-pump group, 20.5 +/- 24.2 vs 61.8 +/- 84.6 (p = 0.023). CONCLUSION: GSH levels from the biopsies were increased in the perfusion group early in the reperfusion time showing that myocardial tissue was well protected and recovered more rapidly after cross-clamping than after the occlusion of the coronary arteries. However, release of creatinine kinase was lower in the off-pump group showing that cardiopulmonary bypass has more deleterious effects later after the operation.

Aged↗
PubMed2001

Soluble intercellular adhesion molecule-1 (sICAM-1) after kidney transplantation: the origin and role of urinary sICAM-1?

BACKGROUND: Intercellular adhesion molecule-1 (ICAM-1) binds to leukocyte adhesion receptors LFA-1 and MAC-1, and mediates leukocyte adhesion to target structures. During acute rejection there is increased expression of ICAM-1 in vascular and tubulointestial cells, and consequently accumulation of inflammatory leukocytes. Soluble ICAM-1 (sICAM-1) is released from ICAM-1 expressing cells and excreted into the surrounding fluid. Increased serum sICAM-1 levels are found in patients with acute rejections of various allografts, and high urinary levels in steroid resistant acute kidney allograft rejection. METHODS: Urinary excretion of sICAM-1 was measured by EIA in 136 kidney allograft recipients during the first 1-6 post transplant weeks: 30 patients developed acute rejection, and 106 patients had stable graft function. The molecular weight, binding to hyaluronan, and the origin of urinary sICAM-1 were studied. RESULTS: We show that urinary sICAM-1 circulates as a monomer with a molecular weight between 50 and 100 kD. It binds to immobilized, but not to circulating hyaluronan. About one week after transplantation the mean sICAM-1/creatinine ratio (306 ng/mmol) in transplanted patients was higher than in the healthy controls (167 ng/mmol, P<0.01), and remained basically unchanged during the follow-up in patients with stable graft function, whereas it increased in patients developing rejection, being about 2.5-fold above the initial level a few days before rejection (P<0.01). Urinary sICAM-1 did not correlate with the urinary albumin, whereas in patients developing rejection it correlated with urinary IL-2R (r=0.5146, P<0.001), a marker of lymphocyte activation. In the urinary sediment of rejecting patients ICAM-1 was demonstrated in the tubular epithelial cells, and in the macrophages. CONCLUSIONS: Increased urinary excretion of sICAM-1 was demonstrated in kidney transplanted patients a few days before acute rejection. It seems to originate from activated macrophages and/or from the tubular epithelial cells. The fact that urinary sICAM-1 is not bound to hyaluronan or to leukocytes suggests that it is not able to compete with membrane-bound ICAM-1 for these bindings, but may do so for the binding of activated macrophages.

Albuminuria↗
PubMed2001

Cyclosporine induces myocardial connective tissue growth factor in spontaneously hypertensive rats on high-sodium diet.

BACKGROUND: The introduction of cyclosporine (CsA) has led to an improvement in the prognosis of solid organ transplantation. However, drug-induced hypertension and nephrotoxicity, associated with the development of atherosclerosis and coronary heart disease, still worsen the long-term outcome of CsA-treated patients. Whether the CsA-induced myocardial changes are associated with the induction of connective tissue growth factor (CTGF), a recently found polypeptide implicated in extracellular matrix synthesis, is not known. METHODS: Spontaneously hypertensive rats (8-9 weeks old) were treated with CsA (5 mg x kg(-1) x d(-1) subcutaneously) for 6 weeks. The influence of angiotensin-converting enzyme inhibition (enalapril 30 mg x kg(-1) x d(-1) orally) and angiotensin-1 receptor blockade (valsartan 3 and 30 mg x kg(-1) x d(-1) orally) on CsA toxicity was also investigated. Myocardial morphology was examined, and vascular lesions were scored. Localization and the quantitative expression of CTGF, as well as collagen I and collagen III, mRNA were evaluated by in situ hybridization and Northern blot. RESULTS: CsA-induced hypertension and nephrotoxicity were associated with myocardial infarcts and vasculopathy of the coronary arteries. CsA increased myocardial CTGF, collagen I, and collagen III mRNA expressions by 91%, 198%, and 151%, respectively. CTGF mRNA expression colocalized with the myocardial lesions. Blockade of the renin-angiotensin system prevented vascular damage and the CsA-induced CTGF, collagen I, and collagen III mRNA overexpressions in the heart. CONCLUSIONS: CsA increases CTGF, collagen I, and collagen III mRNA expressions in the heart. The induction of CTGF gene is mediated, at least in part, by angiotensin II.

Animals↗
PubMed2001

No impact of a leucocyte depleting arterial line filter on patient recovery after cardiopulmonary bypass.

BACKGROUND: Contact of blood with foreign surfaces in the cardiopulmonary bypass (CPB) circuit induces an inflammatory response and immunosuppression which are associated with several organ dysfunctions following cardiac surgery. The aim of the present study was to evaluate clinical patient recovery after coronary artery bypass surgery (CABG) using CPB with leucocyte filtration or no arterial line filter. METHODS: Sixty patients scheduled for CABG were randomly assigned to undergo CPB with a leucocyte depleting arterial line filter (Pall LG6) or no filter. Total leucocyte count and platelet count were determined before and after CPB. Values for blood urea nitrogen, serum creatine, serum sodium and potassium, serum osmolality, urine creatine, urine sodium and potassium, and urine osmolality were recorded at baseline, at 6 h and 24 h after CPB, and on the 5th postoperative day. Complement status was evaluated by measuring the levels of C3 and C4 before surgery and 24 h after CPB. Need for postoperative inotropic support was recorded, as was oxygen index prior to and after tracheal extubation. Times to awakening and tracheal extubation were noted, as were length of stay at the intensive care unit (ICU) and the hospital. Amount of chest drainage until 24 h and need for red blood cell transfusions were recorded. RESULTS: The level of C3 at 24 h was significantly lower in LG6-patients, but no further differences were detected between the groups in any of the laboratory or clinical parameters except for greater chest drainage in LG6-patients. However, need for red blood cell transfusions was similar in both groups. CONCLUSION: Leucocyte filtration in our elective CABG patients did not have any impact on pulmonary gas exchange, need for postoperative inotropic support, length of postoperative mechanical ventilation, or length of ICU or hospital stay.

Aged↗
PubMed2001

Effect of clarithromycin and itraconazole on the pharmacokinetics of ropivacaine.

In a double-blind, randomised, three-way cross-over study, eight healthy volunteers ingested daily for 4 days either 250 mg clarithromycin twice daily, 200 mg itraconazole once daily, or placebo. On day 4, each subject received a single dose of 0.6 mg kg-1 ropivacaine intravenously over 30 min. Ropivacaine and (S)-2',6'-pipecoloxylidide in venous plasma and urine samples were measured for up to 12 hours and 24 hours, respectively. There were no significant changes in the pharmacokinetic parameters of the parent ropivacaine after ingestion of clarithromycin or itraconazole. However, the peak plasma concentration and AUC of (S)-2',6'-pipecoloxylidide metabolite were significantly decreased in both the clarithromycin and itraconazole phases, compared with the placebo phase. The fraction of ropivacaine metabolised to (S)-2',6'-pipecoloxylidide excreted in urine was decreased in the itraconazole phase. Both clarithromycin and itraconazole inhibit the CYP3A4 mediated formation of (S)-2',6'-pipecoloxylidide from ropivacaine. With the doses used, itraconazole is a stronger inhibitor than clarithromycin. The interaction of clarithromycin with ropivacaine seems to be dose (concentration)-dependent.

Administration, Oral↗
PubMed2001

Drug interactions.

The prevalence of undesirable drug interactions is substantial but largely unknown. Although drug interactions are certainly an important cause of drug toxicity, their clinical significance may have been exaggerated. This review presents a brief overview of possible drug interactions.

Journal Article↗
PubMed2001

Effect of rifampin and tobacco smoking on the pharmacokinetics of ropivacaine.

OBJECTIVE: Our objective was to assess the effect of rifampin (INN, rifampicin) and tobacco smoking on the pharmacokinetics of ropivacaine. METHODS: A randomized, 2-phase, crossover study was performed in both a group of 10 healthy nonsmokers and a group of 8 healthy smokers. In both groups each subject ingested daily for 5 days either placebo or 600 mg rifampin. On day 6 each subject received intravenously over 30 minutes a single dose of 0.6 mg/kg ropivacaine. Ropivacaine, 3-hydroxyropivacaine (3-OH-ropivacaine), and (S) -2',6'-pipecoloxylidide (PPX) in venous plasma and urine were measured for up to 12 hours and 24 hours, respectively. Pharmacokinetic parameters were calculated with noncompartmental methods, and t tests were used for comparisons between the phases and between the smokers and nonsmokers. The electrocardiogram was monitored for 3 hours. RESULTS: There were no statistically significant differences in the area under the plasma concentration-time curve (AUC), plasma clearance (CL), or half-life (t(1/2)) of ropivacaine between the smokers and nonsmokers. However, smokers excreted in urine 31% more 3-OH-ropivacaine and 62% less PPX than nonsmokers did. Rifampin decreased the AUC of ropivacaine in nonsmokers by 52% and in smokers by 38%. In nonsmokers rifampin increased the CL of ropivacaine by 93% and shortened its t(1/2) by 25%. In smokers rifampin increased the CL of ropivacaine by 47% and shortened its t(1/2) by 20%. Rifampin decreased the urinary excretion of 3-OH-ropivacaine in nonsmokers by 74% and in smokers by 68%, and it increased the excretion of PPX by 97% and 158%, respectively. No clinically significant differences in the QTc times were found between the groups or treatments. CONCLUSIONS: Tobacco smoking increases the excretion of 3-OH-ropivacaine in urine, probably because of the increased cytochrome P450 (CYP) 1A2-mediated metabolism of ropivacaine, and decreases the excretion of CYP3A4-formed PPX in urine. Rifampin considerably increases the metabolism of ropivacaine to PPX and decreases the metabolism to 3-OH-ropivacaine in both nonsmokers and smokers.

Adult↗