The Effect of Obesity Management on Body Image in Patients Seeking Treatment at Medical Centers

treatment- seeking patients with obesity. We aimed to investigate the effects of obesity management on body image in patients with obesity attending Italian medical centers for weight loss programs. Research Methods and Procedures: A total of 473 obese patients seeking treatment in 13 Italian medical centers (80% females; age, 45.9 standard deviation 11.0 years; BMI, 36.8 5.7 kg/m2) were evaluated at baseline and after a 6-month weight loss treatment. Body uneasiness, psychiatric distress, and binge eating were tested by Body Uneasiness Test (BUT, Part A), Symptom CheckList-90 (SCL- 90), and Binge Eating Scale (BES), respectively. Results: At 6-month follow-up, the percentage weight loss was significantly higher in men (9.0 6.3%) than in women (6.8 7.3%; p 0.010). Both men and women had a significant improvement in BUT Global Severity Index and in all of the BUT subscales with the exception of the Compulsive Self-Monitoring subscale. Linear regression analysis selected baseline psychological and behavioral measures (global score of BUT and SCL-90) and improved psychiatric distress and binge eating as independent predictors of changes in basal body dissatisfaction in females, whereas in males, changes were associated only with baseline BUT-Global Severity Index score, binge eating, and its treatment-associated improvement. Pre-treatment BMI and BMI changes did not enter the regression. Discussion: Obesity treatment, even with a modest degree of weight loss, is associated with a significant improvement of body image, in both females and males. This effect depends mainly on psychological factors, not on the amount of weight loss

Dual Antiplatelet Therapy in Neuroendovascular Procedures

Dual antiplatelet therapy is currently used in clinical practice to prevent thrombotic events during and after neuroendovascular procedures. </p><p> Despite antiplatelet therapy, a significant number of patients show insufficient platelet inhibition, as measured by laboratory tests. These patients are at greater risk of developing thrombotic events than are patients sensitive to the treatment. This phenomenon is known as "antiplatelet drug resistance". The mechanisms that influence the individual response to antiplatelet therapy are not completely understood and are likely to be multifactorial. </p><p> Several platelet function tests have been developed to monitor antiplatelet therapy and may assist in adjusting it to improve outcomes in patients with antiplatelet drug resistance. Nevertheless, the optimal management for these patients has not yet been established. This chapter summarizes information on the available antiplatelet drugs currently used in neuroendovascular procedures, the commonly used tools for platelet function testing and the potential mechanisms underlying suboptimal platelet inhibition by aspirin and clopidogrel

Smoking cessation and body weight

A great attention is presently paid to smoking cessation and pharmacotherapy combined with counselling has been found to achieve the highest rate of smoking cessation. Smoking cessation is associated with weight gain and this may reduce compliance in a subset of smokers. In a previous research we evaluated the efficacy of a combined Group Counselling therapy and Bupropion therapy and we identified some outcome predictors.The aim of the present study is to evaluate the effects of smoking cessation on body weight during a one-year follow-up period. From January 2001 to December 2005, 587 volunteers (263 males and 324 females) who wanted to quit smoking were recruited by our unit. After an individual motivational interview subjects started a Six-week Group Counselling Program (SGCP) for smoking cessation and ten days before the “quitting day” were asked to begin a seven-week pharmacotherapy consisting of 300 mg Bupropion SR/daily (BT). Prior to admission to the program subjects were submitted to a physical examination by the medical staff and underwent a structured interview about their smoking history. The amount of exhaled CO was taken as a further measure of the smoking habit. Some psychometric instruments were administered: the Fagerström Tolerance Questionnaire (FTQ), the Severity of Dependence Scale (SDS) and the Three Factor Eating Questionnaire (TFEQ). Subjects were called in by counsellors after 3, 6 and 12 months to check their current smoking habit and body weight. Of the 229 subjects who accepted BT only 115 subjects completed the seven-week cycle of therapy (BT-COMP group) whereas the remaining 114 subjects discontinued medication (BT-NONCOMP group) but continued to attend SGCP. According to a previous report (3) both BT groups achieved a higher abstinence rate if compared to the sole SGCP. At the one-year follow-up abstinence rates were 65.4% and 47.4% in BT-COMP and BT-NONCOMP groups, respectively, whereas 39.7% was the quit rate of the SGCP sole group. We evaluated the increasing body weight in the three groups of subjects (SGCP only, BT-COMP e BT NONCOMP) according to gender and to the results of the one-year abstinence. Subjects who did not smoke after 12 months (nonS) are compared with those who were still smokers (S). Females and males non-smokers revealed - at five-week abstinence and at one-year follow-up - a weight gain significantly higher if compared with S of the same sex. Several different studies have shown that a great many people believe that smoking helps control weight and ex-smokers risk weight gain. Unfortunately, this widespread opinion is an accurate one and contributes to making difficult to quit this dangerous habit. Eating more food, particularly more sweet food, and a decrease in metabolic rate are the main causes. Our data suggest that seven-week BT is not a protective factor in increasing body weight. Regular aerobic exercise and nutritional counselling may be helpful to minimize weight gain after quitting smoking. Psychometric measures seem to be weak predictors of weight gain

Multidrug Resistance Protein-4 Influences Aspirin Toxicity in Human Cell Line

Overexpression of efflux transporters, in human cells, is a mechanism of resistance to drug and also to chemotherapy. We found that multidrug resistance protein-4 (MRP4) overexpression has a role in reducing aspirin action in patients after bypass surgery and, very recently, we found that aspirin enhances platelet MRP4 levels through peroxisome proliferator activated receptor-α (PPARα). In the present paper, we verified whether exposure of human embryonic kidney-293 cells (Hek-293) to aspirin modifies MRP4 gene expression and its correlation with drug elimination and cell toxicity. We first investigated the effect of high-dose aspirin in Hek-293 and we showed that aspirin is able to increase cell toxicity dose-dependently. Furthermore, aspirin effects, induced at low dose, already enhance MRP4 gene expression. Based on these findings, we compared cell viability in Hek-293, after high-dose aspirin treatment, in MRP4 overexpressing cells, either after aspirin pretreatment or in MRP4 transfected cells; in both cases, a decrease of selective aspirin cell growth inhibition was observed, in comparison with the control cultures. Altogether, these data suggest that exposing cells to low nontoxic aspirin dosages can induce gene expression alterations that may lead to the efflux transporter protein overexpression, thus increasing cellular detoxification of aspirin

Arachidonic acid-stimulated platelet tests: Identification of patients less sensitive to aspirin treatment

Serum thromboxane-B2 (TxB2), together with arachidonic acid (AA)-induced platelet aggregation, are, at the moment, the most used tests to identify patients displaying high on-aspirin treatment platelet reactivity (HAPR). Both tests are specific for aspirin action on cyclooxygenase-1. While the correlation between serum TxB2 assay and clinical outcome is established, data are conflicting with regard to aspirin treatment and a possible association with AA-stimulated platelet markers and clinical outcome. To understand such discrepancy, we performed a retrospective study to compare both assays. We collected data from 132 patients receiving a daily dose of aspirin (100 mg/day) and data from 48 patients receiving aspirin on alternate days. All Patients who received a daily dose of aspirin were studied for AA-induced platelet aggregation together with serum TxB2 levels and AA-induced TxB2 formation was also studied in 71 patients out of entire population. Consistent with recommendations in the literature, we defined HAPR by setting a cut-off point at 3.1 ng/ml for serum levels of thromboxane B2 and 20% for AA-induced platelet aggregation. According to this cut-off point, we divided our overall population into two groups: (1) TxB2  3.1 ng/ml. We found low agreement between such tests to identify patients displaying HAPR. Our results show that AA-induced platelet aggregation >20% identify a smaller number of HAPR patients in comparison with TxB2. A good correlation between serum TxB2 and arachidonic acid-induced TxB2 production was found (r = 0.76619)

Platelet activation and multidrug resistance protein-4 expression in children and adolescents with different subtypes of primary thrombocythemia

Article summary 1. MRP4 over expression may have a role to reduce aspirin action in primary thrombocythemia 2. Children and adolescents with MPLS505A hereditary thrombocytosis show a higher platelet reactivit

Nonsteroidal anti-inflammatory drugs in-vitro and in-vivo treatment and Multidrug Resistance Protein 4 expression in human platelets

Platelet Multidrug Resistance Protein 4 (MRP4)-overexpression has a role in reducing aspirin action in patients after by-pass surgery. Aspirin induces platelet MRP4 over-expression, through megakaryocytes genomic modulation. Aim of our work was to verify whether other non-steroidal antiinflammatory drugs (NSAIDs) enhance platelet MRP4 expression and evaluate platelet function in patients who overexpressed MRP4. We evaluated MRP4-mRNA in a human megakacaryoblastic cell line (DAMI), treated with both COX-2 inhibitor (celecoxib) and traditional NSAIDs (diclofenac and naproxen). Osteoarthritis patients, who reported to take NSAIDs twice a week for at least four continuous weeks and a control population, who didn't take any drugs during the previous month, were enrolled. We evaluated platelet MRP4 amount, by both mRNA levels and protein expression (Western-Blot) and ADP induced platelet aggregation. DAMI cells treated with celecoxib, diclofenac, and naproxen showed a significant increase in MRP4-mRNA expression compared to the mock culture. Osteoarthritis patient platelets presented a higher expression of MRP4 (both at mRNA and protein levels) and an increase in ADP-induced platelet aggregation compared to the control population. NSAID treatment induced platelet MRP4 overexpression. Osteoarthritis patients, who overexpress MRP4, showed platelet hyper-reactivity. These evidences could explain in part the increased cardiovascular risk present during NSAID treatment.Platelet Multidrug Resistance Protein 4 (MRP4)-overexpression has a role in reducing aspirin action in patients after by-pass surgery. Aspirin induces platelet MRP4 over-expression, through megakaryocytes genomic modulation. Aim of our work was to verify whether other non-steroidal antiinflammatory drugs (NSAIDs) enhance platelet MRP4 expression and evaluate platelet function in patients who overexpressed MRP4. We evaluatedMRP4-mRNA in a human megakacaryoblastic cell line (DAMI), treated with both COX-2 inhibitor (celecoxib) and traditional NSAIDs (diclofenac and naproxen). Osteoarthritis patients, who reported to take NSAIDs twice aweek for at least four continuousweeks and a control population,who didn't take any drugs during the previous month, were enrolled.We evaluated platelet MRP4 amount, by both mRNA levels and protein expression (Western-Blot) and ADP induced platelet aggregation. DAMI cells treated with celecoxib, diclofenac, and naproxen showed a significant increase in MRP4-mRNA expression compared to the mock culture. Osteoarthritis patient platelets presented a higher expression ofMRP4 (both atmRNA and protein levels) and an increase in ADP-induced platelet aggregation compared to the control population. NSAIDtreatment induced plateletMRP4 overexpression. Osteoarthritis patients,who overexpressMRP4, showed platelet hyper-reactivity. These evidences could explain in part the increased cardiovascular risk present during NSAID treatment

Enhanced platelet MRP4 expression and correlation with platelet function in patients under chronic aspirin treatment

Platelet multidrug resistance protein4 (MRP4)-overexpression has a role in reducing aspirin action. Aspirin in vivo treatment enhances platelet MRP4 expression and MRP4 mediated transport inhibition reduces platelet function and delays thrombus formation. The aim of our work was to verify whether MRP4 expression is enhanced in platelets obtained from patients under chronic aspirin treatment and whether it correlates with residual platelet reactivity. We evaluated changes on mRNA and protein-MRP4 expression and platelet aggregation in four populations: healthy volunteers (HV), aspirin-free control population (CTR), patients who started the treatment less than one month ago (ASA< 1 month patients) and aspirinated patients who started the treatment more than two months ago (ASA> 2 months patients). In platelets obtained from ASA> 2 months patients, it was found a statistically significant MRP4 enhancement of both mRNA and protein expression compared to HV, CTR and ASA< 1 month patients. Platelets obtained from ASA> 2 months patients that present high levels of platelet MRP4, have higher serum TxB2 levels and collagen-induced platelet aggregation compared to patient with low levels of MRP4 in platelets. In addition collagen induced platelet aggregation is higher in in vitro aspirinated platelets obtained from patients with high levels of MRP4 patients compared to those obtained from patients with low MRP4 levels. We can assert that, in patients under chronic aspirin treatment, platelets that present high MRP4 levels have an increase of residual platelet reactivity, which is due in part to incomplete COX-1 inhibition, and in part to COX-1-independent mechanism