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Biomedical subjects

A Abidia

Publications and source records attributed to A Abidia.

8 recordsLinked to original sources

The success of routine MRSA screening in vascular surgery: a nine year review.

AIM: Methicillin resistant Staphylococcus aureus (MRSA) infection in vascular patients is associated with increased morbidity and mortality. We investigated whether routine MRSA screening reduced complications related to MRSA infection. METHODS: Data was analysed for all MRSA positive (+ve) vascular patients admitted before (1996-2000) and after (2001-2004) routine MRSA screening was introduced. Outcome measures compared included wound infection, major limb amputation and mortality rates. RESULTS: There were 92 and 188 MRSA +ve patients in the pre- and postscreening periods, respectively. After the introduction of MRSA screening, MRSA wound infection in MRSA +ve elective admissions was significantly reduced from 55.6% (20/36) to 22.4% (15/67), (P=0.002, chi2 test); amputations were reduced from 27.8% (10/36) to 9% (6/67), P value 0.026, and mortality from 16.7% (6/36) to 9% (6/67), P value >0.05. In MRSA +ve emergency admissions wound infection was significantly reduced from 62.5% (35/56) to 43.8% (53/121), P value 0.042, amputations from 50% (28/56) to 38.8% (47/121), P value 0.26, and mortality from 25% (14/56) to 12.4% (15/121), P value 0.067. CONCLUSIONS: While the incidence of MRSA infection continues to rise, we have successfully demonstrated that MRSA screening identifies patients at risk of serious complications and is associated with a reduction in these complications following both elective and emergency surgery. Routine screening of all vascular admissions should be part of the strategy to combat MRSA infection.

Anti-Bacterial Agents↗

Surgery for deep venous incompetence.

BACKGROUND: Chronic deep venous incompetence (DVI) is caused by incompetent vein valves and/or the blockage of large calibre leg veins, with a range of symptoms including recurrent ulcers, pain and swelling. OBJECTIVES: To establish the effectiveness of various surgical procedures for treating DVI. SEARCH STRATEGY: Trials were identified through the Cochrane Peripheral Vascular Diseases Group's trials register, reference lists of relevant studies, and contact with principal investigators of identified trials and world experts in deep venous surgery. SELECTION CRITERIA: Randomised controlled trials of surgical treatment for patients with DVI. DATA COLLECTION AND ANALYSIS: Reviewers extracted data independently. Outcome measures included ambulatory venous pressure (AVP) and venous refill time (VRT). MAIN RESULTS: Three trials were included, one trial was excluded. Two trials compared external valvuloplasty using limited anterior plication (LAP) in combination with ligation (L) of incompetent superficial veins (L+LAP) against ligation only (L). The other trial compared external valvuloplasty and ligation (V+L) of incompetent superficial veins against ligation only (L). Trial participants had primary valvular incompetence with mild to moderate symptoms but no venous ulcers.L+LAP produced significant improvement in AVP: the mean difference between L+LAP and L groups was -15 mm Hg (95% confidence interval (CI) -20.9 to -9.0) at one year and -15 mm Hg (95% CI -21 to -8.9) at ten years.AVP values after surgery remained relatively high. Nine of eleven valves repaired remained competent after two years of follow up. No complications occurred. The overall mean score for clinical outcome was +2 (moderate improvement) in the L+LAP group compared with +1 (mild improvement) in the L group. Patients with deteriorating clinical dynamics over the five years preceding surgery had a significantly higher rate of improvement in clinical condition in V+L compared to L (81% versus 51%; p < 0.05) after seven years follow-up. Patients with stable preoperative clinical dynamics demonstrated a similar rate of improvement in both groups (96% versus 90%; p> 0.1). AVPs were not performed. REVIEWERS' CONCLUSIONS: These results indicate that ligation and valvuloplasty may have produced a moderate and sustained improvement for seven to ten years after surgery, in patients with mild to moderate DVI caused by primary valvular incompetence. However, there is insufficient evidence to recommend the treatment to this subgroup of patients, as the trials were small, used different methods of valvuloplasty and different methods of assessment.

Humans↗

Fluvastatin induces apoptosis of vascular endothelial cells: blockade by glucocorticoids.

Statins block de novo synthesis of cholesterol by inhibiting the enzyme, HMG CoA reductase. The product of this reaction, mevalonic acid, is also a precursor of isoprenoids, molecules required for the activation of signaling G-proteins, such as Ras. Signal transduction pathways involving Ras are important for cell survival and this may be why statins induce apoptotic death of several cell types. Given that statins are used to treat vascular disease, surprisingly no studies have been conducted on vascular endothelial cells. Here we show that fluvastatin (FS), at concentrations from 1-2 microM, blocks growth and induces apoptosis of the endothelial cell line, EA.hy 926. Considerable redundancy is known to exist in cell signaling and in vivo toxicity of FS might be prevented by other signaling pathways, like those activated by adrenal or sex steroids. RT-PCR analysis revealed the expression of the androgen and glucocorticoid receptor in EA.hy 926 cells. Although the androgen, dihydrotestesterone (DHT) had no effect, the glucocorticoid, dexamethasone (Dex), blocked FS-induced apoptosis. Cell cycle analysis revealed that 24 h exposure to FS prevented cells from leaving G(1) and 24-48 h later a marked sub-G(1) peak was observed. Dex was able to reduce the sub-G(1) peak, but it failed to block accumulation of cells in G(1), indicating that it's effect was specific for blockade of apoptosis, and not specific to an effect on FS alone. This study strongly suggests that glucocorticoids have a role to play in preventing vascular injury and they may provide the reason why statins are not inherently toxic to vascular endothelial cells, in vivo.

Anticholesteremic Agents↗

The role of hyperbaric oxygen therapy in ischaemic diabetic lower extremity ulcers: a double-blind randomised-controlled trial.

OBJECTIVE: ischaemic lower-extremity ulcers in the diabetic population are a source of major concern because of the associated high risk of limb-threatening complications. The aim of this study was to evaluate the role of hyperbaric oxygen in the management of these ulcers. METHOD: eighteen diabetic patients with ischaemic, non-healing lower-extremity ulcers were recruited in a double-blind study. Patients were randomly assigned either to receive 100% oxygen (treatment group) or air (control group), at 2.4 atmospheres of absolute pressure for 90 min daily (total of 30 treatments). RESULTS: healing with complete epithelialisation was achieved in five out of eight ulcers in the treatment group compared to one out of eight ulcers in the control group. The median decrease of the wound areas in the treatment group was 100% and in the control group was 52% (p=0.027). Cost-effectiveness analysis has shown that despite the extra cost involved in using hyperbaric oxygen, there was a potential saving in the total cost of treatment for each patient during the study. CONCLUSION: hyperbaric oxygen enhanced the healing of ischaemic, non-healing diabetic leg ulcers and may be used as a valuable adjunct to conventional therapy when reconstructive surgery is not possible.

Aged↗

Statin-induced apoptosis of vascular endothelial cells is blocked by dexamethasone.

Statins block de novo synthesis of cholesterol by inhibiting the enzyme, HMG CoA reductase. The product of this reaction, mevalonic acid, is also a precursor of isoprenoids, molecules required for the activation of signalling G-proteins, such as Ras. Signal transduction pathways involving Ras are important for cell survival and this may be why statins induce apoptotic death of several cell types. Given that statins are used to treat vascular disease, it is surprising that no studies have been conducted on vascular endothelial cells. For this reason, we have tested the effect of fluvastatin (FS) on the endothelial cell line EA.hy 926. Here we show that FS, at concentrations from 1 to 2 microM, blocks growth and induces apoptosis of the endothelial cell line, EA.hy 926. As considerable redundancy exists in cell signalling pathways for cell survival, toxicity of FS under more physiological conditions might be prevented by pathways that do not require Ras, such as those activated by adrenal or sex steroids. To test this hypothesis, first RT-PCR analysis was performed for nuclear receptor mRNA expression. This revealed the presence of mRNA for the androgen receptor (AR) and glucocorticoid receptor (GR). The effect of the AR agonist, dihydrotestosterone (DHT), and the GR agonist, dexamethasone (Dex), was then tested. Whilst DHT (100 nM) had no effect on FS-induced cell death, Dex (1 microM) blocked FS-induced apoptosis. Cell cycle analysis revealed that 24 h exposure to FS prevented cells from leaving G(1) and 24-48 h later a marked sub-G(1) peak was observed. Dex was able to reduce the sub-G(1) peak, but it failed to reduce accumulation of cells in G(1). Further studies revealed that, in addition to blocking FS-induced apoptosis, Dex was able to block apoptosis of EA.hy 926 cells induced by serum deprivation, tumour necrosis factor-alpha, oxidants, DNA damage and mitochondrial disruption. This study strongly suggests that glucocorticoids have a role to play in preventing vascular injury and they may provide a reason why statins are apparently not toxic to vascular endothelial cells in vivo.

Androgen Receptor Antagonists↗

Surgery for deep venous incompetence.

BACKGROUND: Chronic deep venous incompetence (DVI) is a troublesome condition with a range of symptoms in the legs including recurrent ulcers, pain and swelling. It is caused by incompetent vein valves and/or the blockage of large-calibre leg veins. OBJECTIVES: To establish the effectiveness of various surgical procedures for treating DVI. SEARCH STRATEGY: Trials were identified from the Cochrane Peripheral Vascular Diseases Group's Specialised Trials Register, reference lists of relevant studies, and through contact with principal investigators of identified trials and world experts in deep venous surgery. SELECTION CRITERIA: Randomised controlled trials of surgical treatment for patients with DVI. Trials were selected by AA and checked by SCH. DATA COLLECTION AND ANALYSIS: The reviewers extracted the data independently. A variety of outcome measures were reported including ambulatory venous pressure (AVP) and venous refill time (VRT). MAIN RESULTS: Only one trial met the inclusion criteria, none was excluded. The trial compared external valvuloplasty using limited anterior plication (LAP) in combination with ligature of incompetent superficial veins (ligation and LAP) against ligation only. The trial participants had primary valvular incompetence with mild to moderate symptoms but no venous ulcers. Ligation and LAP produced significant improvement in AVP: the mean difference between the Ligation and LAP group and the Ligation only group was -15 torr (weighted mean difference [WMD] -20.9, -9.0, confidence interval [CI] 95% fixed) at one year and -15 torr (WMD -21, -8.9, 95% CI fixed) at two years. However, there was no statistically significant improvement in VRT, the mean difference between the groups at one year was 2 seconds (WMD -2.7, 6.7; 95% CI fixed) and at two years was 4 seconds (WMD -0.7, 8.7; 95% CI fixed). AVP values after surgery remained relatively high. Nine out of eleven valves repaired remained competent after two years of follow up. No complications occurred. The overall mean score for clinical outcome was +2 (moderate improvement) in the Ligation and LAP group. This compared with +1 (mild improvement) in the Ligation only group. REVIEWER'S CONCLUSIONS: The results of one small trial showed that ligation and LAP produced a moderate improvement for two years after surgery, in patients with mild to moderate DVI caused by primary valvular incompetence. However, there is not sufficient evidence to recommend the treatment to this subgroup of patients with DVI.

Humans↗