Determinants associated with low dietary diversity among migrants to Morocco: a cross sectional study.

Low dietary diversity (LDD) is prevalent among vulnerable populations, posing a morbidity risk. Few studies have been conducted on the dietary diversity of migrants. The objectives of this study are to determine the prevalence of LDD among migrants in Morocco and the risk factors associated with it. In the Oriental region, we conducted a cross-sectional study with migrants between November and December 2021. The sampling method used was convenience sampling. A face-to-face, structured questionnaire was used to collect sociodemographic, behavioral, and clinical data. We calculated a dietary diversity score based on a 24-h food recall and assessed food intake. The risk factors associated with LDD were identified using multivariate logistic regression. A total of 445 migrants was enrolled. The prevalence of LDD was 31.7%. Risk factors associated with LDD were: being homeless (adjusted Odds Ratio (AOR) of 6.32; CI% [3.55-11.25]), a lack of social support (AOR of 2.30; CI% [1.33-03.98]), and low monthly income (AOR of 8.21; CI% [3.39-19.85]). Public policies must focus on social and environmental determinants. Nutrition training programs should be set up for the migrant population.

Uncontrolled blood pressure and its risk factors among hypertensive patients, Marrakech, Morocco.

Hypertension is a public health problem. Failure to control blood pressure figures is responsible for morbidity and premature mortality. This study aims to describe the characteristics of hypertensive patients followed at primary health care centers in Marrakech. Between May 2021 and December 2022, a cross-sectional study of 922 hypertension patients attending primary health care centers in Marrakech was done. To gather socio-demographic, behavioral, and clinical data, as well as hypertension treatment features and the care-patient-physician triad, a face-to-face questionnaire was employed. To identify risk factors associated with uncontrolled blood pressure, multivariate logistic regression was used. Uncontrolled blood pressure was found in 73.5% of people. The patients' average age was 63.4 ± 9.4 years (mean ± standard deviation), and 524 (77.3%) were women. Tobacco consumption (Adjusted Odd Ratio of 4.34; 95% CI [1.58-11.9]); lack of self-monitoring of hypertension (AOR of 1.69; 95% CI [1.14-2.52]); a family history of hypertension (AOR of 1.58; 95% CI [1.12-2.22]); overweight or obesity (AOR of 1.73; 95% CI [1.15-2.58]); and nonadherence to antihypertensive medication (AOR of 1.58; 95% CI [1.05-2.38]) were identified as risk factors for uncontrolled blood pressure. In hypertensive individuals, the percentage of uncontrolled blood pressure is considerable. It is essential to provide therapeutic education classes for hypertension patients in order to strengthen their power and autonomy in managing their hypertension.

The prevalence and risk factors for anxiety and depression symptoms among migrants in Morocco.

Humanitarian migration can result in mental health issues among migrants. The objective of our study is to determine the prevalence of anxiety and depression symptoms among migrants and their risk factors. A total of 445 humanitarian migrants in the Orientale region were interviewed. A structured questionnaire was used in face-to-face interviews to collect socio-demographic, migratory, behavioral, clinical, and paraclinical data. The Hospital Anxiety and Depression Scale was used to assess anxiety and depression symptoms. Risk factors for anxiety and depression symptoms were identified using multivariable logistic regression. The prevalence of anxiety symptoms was 39.1%, and the prevalence of depression symptoms was 40.0%. Diabetes, refugee status, overcrowding in the home, stress, age between 18 and 20 years, and low monthly income were associated with anxiety symptom. The associated risk factors for depression symptoms were a lack of social support and a low monthly income. Humanitarian migrants have a high prevalence of anxiety and depression symptoms. Public policies should address socio-ecological determinants by providing migrants with social support and adequate living conditions.

Disease burden among migrants in Morocco in 2021: A cross­sectional study.

BACKGROUND: Morocco, traditionally an emigration country, has evolved into not only a transit country to Europe but also a country of residence for an increasing number of migrants, with 102,400 migrants in 2019. This is due to its geographic location, the induced effects of its "African policy," and the various laws adopted by Moroccan legislators in recent years. The purpose of this study is to determine the prevalence of communicable and noncommunicable diseases among migrants such as Hepatitis C virus (HCV), human immunodeficiency virus (HIV), diabetes, and hypertension. METHODS: We conducted a cross-sectional study in Oujda, Morocco, between November and December 2021. Face-to-face interviews with enrolled migrants aged 18 years and over, present in Oujda and attending an association, were carried out to collect socio-demographic data, lifestyle behaviors, and clinical parameters. Diabetes and hypertension were the primary outcomes. The Pearson's chi-squared test and the student's t-test were used to assess the bivariate associations between primary outcomes and categorical and continuous variables. In a multivariate model, we adjusted for predictors that were significant (p-value ≤0.05) in bivariate analysis to estimate Adjusted Odd Ratios (AOR) and 95% confidence intervals (CI). RESULTS: There were 495 migrants enrolled, with a male/female ratio of two and an average age of 27.3±11.5 years (mean±standard deviation), ranging from 18 to 76 years. Hepatitis C virus, human immunodeficiency virus, diabetes, and hypertension were found in 1%, 0.2%, 3.8%, and 27.7% of the population, respectively. Family history of diabetes was a risk factor for diabetes in the Oujda migrant population, with an Adjusted Odds Ratio (AOR) of 5.36; CI% [1.23-23.28]. Age (AOR of 1.1; CI% [1.06-1.13]) and African origin (AOR of 3.07; CI% [1.06-8.92]) were identified as risk factors for hypertension. CONCLUSION: Migrants in Oujda are healthy. The high prevalence of hypertension, as well as the presence of HCV and HIV positive cases, emphasizes the importance of routine screening for hypertension, HCV, and HIV in order to detect and treat these diseases as early as possible.

Prevalence and determinants of intercourse without condoms among migrants and refugees in Morocco, 2021: a cross-sectional study.

With the world's migratory flow, the risk of infection by the human immunodeficiency virus (HIV) among migrants is increasing. The prevalence of intercourse without condoms with a casual or commercial sex partner, a high-risk sexual behavior for HIV infection, is unknown among migrants. The purpose of this study was to determine the prevalence of intercourse without condoms among migrants and the risk factors associated with not using condoms. In Oujda, we conducted a cross-sectional survey of 416 sexually active migrants. We used a multistage sampling method. Face-to-face interviews were conducted with participants to collect socio-demographic information, disease perception, behavioral habits, sexual behavioral habits, and para-clinical parameters. A multivariate logistical regression analysis identified the risk factors associated with high-risk HIV sexual behaviors. The prevalence of intercourse without condoms with a casual or commercial sex partner was 72.8%, with a median age of 25.0 years, and 212 (69.9%) were males. The prevalence of HIV was 0.2%. Being homeless, having difficulty obtaining condoms, and only having a basic education were all risk factors for these sexual behaviors. Migrants with precarious living conditions are at increased risk of having intercourse without condoms. This group must be prioritized by strengthening public health programs targeting the health of migrants as well as the intervention of thematic non-governmental organizations. Vigilant monitoring of the HIV epidemic, with a focus on vulnerable populations, should be a high priority in Morocco.

A20/TNFAIP3 Increases ENOS Expression in an ERK5/KLF2-Dependent Manner to Support Endothelial Cell Health in the Face of Inflammation.

Rationale: Decreased expression and activity of endothelial nitric oxide synthase (eNOS) in response to inflammatory and metabolic insults is the hallmark of endothelial cell (EC) dysfunction that preludes the development of atherosclerosis and hypertension. We previously reported the atheroprotective properties of the ubiquitin-editing and anti-inflammatory protein A20, also known as TNFAIP3, in part through interrupting nuclear factor-kappa B (NF-κB) and interferon signaling in EC and protecting these cells from apoptosis. However, A20's effect on eNOS expression and function remains unknown. In this study, we evaluated the impact of A20 overexpression or knockdown on eNOS expression in EC, at baseline and after tumor necrosis factor (TNF) treatment, used to mimic inflammation. Methods and Results: A20 overexpression in human coronary artery EC (HCAEC) significantly increased basal eNOS mRNA (qPCR) and protein (western blot) levels and prevented their downregulation by TNF. Conversely, siRNA-induced A20 knockdown decreased eNOS mRNA levels, identifying A20 as a physiologic regulator of eNOS expression. By reporter assays, using deletion and point mutants of the human eNOS promoter, and knockdown of eNOS transcriptional regulators, we demonstrated that A20-mediated increase of eNOS was transcriptional and relied on increased expression of the transcription factor Krüppel-like factor (KLF2), and upstream of KLF2, on activation of extracellular signal-regulated kinase 5 (ERK5). Accordingly, ERK5 knockdown or inhibition significantly abrogated A20's ability to increase KLF2 and eNOS expression. In addition, A20 overexpression in HCAEC increased eNOS phosphorylation at Ser-1177, which is key for the function of this enzyme. Conclusions: This is the first report demonstrating that overexpression of A20 in EC increases eNOS transcription in an ERK5/KLF2-dependent manner and promotes eNOS activating phosphorylation. This effect withstands eNOS downregulation by TNF, preventing EC dysfunction in the face of inflammation. This novel function of A20 further qualifies its therapeutic promise to prevent/treat atherosclerosis.

Drug non-adherence in hypertensive patients in Morocco, and its associated risk factors.

AIMS: Hypertension is a widespread public health problem; unfortunately, non-adherence to the treatment hinders the control of high blood pressure. Drug non-adherence is the degree to which a patient does not follow the prescription. We aimed to assess the extent of drug non-adherence among hypertensive patients treated in Meknes and identify risk factors associated with inobservance. METHODS AND RESULTS: Between November and December 2017, we conducted a cross-sectional study enrolling 922 hypertensive patients managed at Meknes's primary healthcare facilities (PHCF) using the multistage sampling method. We interviewed patients face to face to collect their socio-demographic characteristics, lifestyle behaviours, clinical parameters, and the relationship between the care system, the patient, and the physician. A multivariate logistic regression analysis highlighted the risk factors associated with drug non-adherence. The prevalence of drug non-adherence was 91% with a mean age of 61 ± 11 years (mean ± standard deviation) and a male/female ratio of 1/3. Risk factors associated with drug non-adherence were: (i) male sex [adjusted odds ratio (AOR) = 2.5, 95% confidence interval (CI) (1.26-5.10)]; (ii) monthly income per household <150$ [AOR = 4.47, 95% CI (1.22-16.34)]; (iii) monthly income per household 150-200$ [AOR = 4.44, 95% CI (1.04-18.93)]; (iv) bad relationship with the healthcare system [AOR = 2.17, 95% CI (1.29-3.67)]; and (v) uncontrolled blood pressure [AOR = 1.87, 95% CI (1.15-3.02)]. CONCLUSION: The prevalence of drug non-adherence is general among hypertensive patients in Meknes. Prevention should: (i) ensure the availability of adequate stocks of the anti-hypertensive drug at the PHCF; (ii) secure sufficient drug stocks to treat the poorest patients first; and (iii) improve blood pressure control in patients.

Epidemiological profile of methanol poisoning, El Hajeb, Morocco.

BACKGROUND: Methanol poisoning is of particular importance in low and middle-income countries. We reported on a methanol poisoning incident that occurred 22 May 2017, in El Hajeb (Morocco). AIMS: This study aimed to describe the extent of the intoxication, determine its source and implement the necessary preventative measures. METHODS: We conducted a cross-sectional survey. A standardized questionnaire including socio-economic data, clinical symptoms and time of use was administered face-to-face to cases of methanol poisoning. Biological samples were taken for toxicological analysis. Data were entered and analyzed on Epi Info version 7. RESULTS: Twenty-six cases of methanol poisoning were surveyed with a mean age of 39.7 (SD 11.1) years and a male/female sex ratio of 5.5. All intoxicated cases were of low socioeconomic status. The mean latency period between use and symptom onset was 1.5 (SD 1) days. Reported symptoms were mildly altered consciousness in 14 cases (53.8%), abdominal pain in 10 cases (38.5%), headache in 9 cases (34.6%), vomiting in 8 cases (30.8%) and coma in 7 cases (27.1%). Mortality was 65% and 4 cases developed blindness. Laboratory results confirmed the presence of methanol in the blood with values greater than 0.6 g/L. The dose of methanol in the associated bottle was 217 g/L. CONCLUSION: Public awareness of the dangers of methanol intoxication is important. Health professionals need to be aware of the clinical signs and what to do in the event of methanol poisoning.

Prevalence of uncontrolled blood pressure in Meknes, Morocco, and its associated risk factors in 2017.

BACKGROUND: Uncontrolled high blood pressure (UBP) can lead to various cardiovascular complications causing an estimated nine million deaths per year worldwide. In Meknes, epidemiologic data on UBP are scarce, depriving programs from evidence-based information that would allow a better management of hypertension. Hence, we aimed to assess UBP prevalence in hypertensive patients treated in Meknes and identify UBP-associated risk factors. METHODS: Between November and December 2017, we conducted a cross-sectional study enrolling 922 hypertensive patients managed at Meknes's primary health care facilities using the multistage sampling method. We interviewed patients face to face to collect their socio-demographic-characteristics, lifestyle behaviours, clinical parameters and the triad care system-patient-physician. Another questionnaire was self-administered by physicians to characterize therapeutic inertia. A multivariate logistic regression analysis highlighted the risk factors associated with UBP. RESULTS: UBP prevalence was 73% with a mean age of 61±11 years (mean±standard deviation) and a male/female ratio of 1/3. Risk factors associated with UBP were: therapeutic inertia (adjusted odds ratio to other variables (AOR) = 18.2, 95% CI [8.35-39.84]), drug non-adherence (AOR = 1.8, 95% CI [1.07-3.04]), obesity/overweight (AOR = 1.6, 95% CI [1.03-2.58]), unemployment (AOR = 1.9, 95% CI [1.09-3.01]), low income (AOR = 2.6, 95% CI [1.01-6.86]), family history of hypertension (AOR = 1.5, 95% CI [1.07-2.08]) and male sex (AOR = 1.6, 95% CI [1.04-2.58]). CONCLUSION: UBP prevalence is high in Meknes. Prevention should firstly focus on raised awareness of hypertensive patients' self-care management. Secondly, health professionals should better comply to the guidelines of anti-hypertensive treatments. Lastly, health professionals should frequently be reminded to reach therapeutic goals to overcome therapeutic inertia.

A20-mediated modulation of inflammatory and immune responses in aortic allografts and development of transplant arteriosclerosis.

BACKGROUND: Transplant arteriosclerosis (TA) is the pathognomonic feature of chronic rejection, the primary cause of allograft failure. We have shown that the NF-κB inhibitory protein A20 exerts vasculoprotective effects in endothelial and smooth muscle cells (SMC), and hence is a candidate to prevent TA. We sought direct proof for this hypothesis. METHODS: Fully mismatched, C57BL/6 (H2) into BALB/c (H2), aorta to carotid allografts were preperfused with saline, recombinant A20 adenovirus (rAd.A20) or rAd.ß-galactosidase (ß-gal), implanted, harvested 4 weeks after transplantation, and analyzed by histology, immunohistochemistry, and immunofluorescence staining. We measured indoleamine 2,3-dioxygenase, interleukin-6, and transforming growth factor-ß mRNA and protein levels in nontransduced, and rAd.A20 or rAd.ß-gal-transduced human SMC cultures after cytokine treatment. RESULTS: Vascular overexpression of A20 significantly reduced TA lesions. This correlated with decreased graft inflammation and increased apoptosis of neointimal SMC. Paradoxically, T-cell infiltrates increased in A20-expressing allografts, including the immunoprivileged media, which related to A20 preventing indoleamine 2,3-dioxygenase upregulation in SMC. However, infiltrating T cells were predominantly T-regulatory cells (CD25+/Forkhead Box P3 [FoxP3+]). This agrees with A20 inhibiting interleukin-6 and promoting transforming growth factor-ß production by medial SMC and in SMC cultures exposed to cytokines, which favors differentiation of regulatory over pathogenic T cells. CONCLUSIONS: In summary, A20 prevents immune-mediated remodeling of vascular allografts, therefore reduces TA lesions by affecting apoptotic and inflammatory signals and modifying the local cytokine milieu to promote an immunoregulatory response within the vessel wall. This highlights a novel function for A20 in local immunosurveillance, which added to its vasculoprotective effects, supports its therapeutic promise in TA.

O-glycosylation regulates ubiquitination and degradation of the anti-inflammatory protein A20 to accelerate atherosclerosis in diabetic ApoE-null mice.

BACKGROUND: Accelerated atherosclerosis is the leading cause of morbidity and mortality in diabetic patients. Hyperglycemia is a recognized independent risk factor for heightened atherogenesis in diabetes mellitus (DM). However, our understanding of the mechanisms underlying glucose damage to the vasculature remains incomplete. METHODOLOGY/PRINCIPAL FINDINGS: High glucose and hyperglycemia reduced upregulation of the NF-κB inhibitory and atheroprotective protein A20 in human coronary endothelial (EC) and smooth muscle cell (SMC) cultures challenged with Tumor Necrosis Factor alpha (TNF), aortae of diabetic mice following Lipopolysaccharide (LPS) injection used as an inflammatory insult and in failed vein-grafts of diabetic patients. Decreased vascular expression of A20 did not relate to defective transcription, as A20 mRNA levels were similar or even higher in EC/SMC cultured in high glucose, in vessels of diabetic C57BL/6 and FBV/N mice, and in failed vein grafts of diabetic patients, when compared to controls. Rather, decreased A20 expression correlated with post-translational O-Glucosamine-N-Acetylation (O-GlcNAcylation) and ubiquitination of A20, targeting it for proteasomal degradation. Restoring A20 levels by inhibiting O-GlcNAcylation, blocking proteasome activity, or overexpressing A20, blocked upregulation of the receptor for advanced glycation end-products (RAGE) and phosphorylation of PKCßII, two prime atherogenic signals triggered by high glucose in EC/SMC. A20 gene transfer to the aortic arch of diabetic ApoE null mice that develop accelerated atherosclerosis, attenuated vascular expression of RAGE and phospho-PKCßII, significantly reducing atherosclerosis. CONCLUSIONS: High glucose/hyperglycemia regulate vascular A20 expression via O-GlcNAcylation-dependent ubiquitination and proteasomal degradation. This could be key to the pathogenesis of accelerated atherosclerosis in diabetes.

A20 inhibits post-angioplasty restenosis by blocking macrophage trafficking and decreasing adventitial neovascularization.

OBJECTIVE: Neointimal hyperplasia is an inflammatory and proliferative process that occurs as a result of injury to the vessel wall. We have shown that the homeostatic protein A20 prevents neointimal hyperplasia by affecting endothelial cell (EC) and smooth muscle cell (SMC) responses to injury. In this work, we questioned whether A20 impacts other pathogenic effectors of neointimal hyperplasia including homing of monocyte/macrophages and EC/SMC precursors to the site of vascular injury, vascular endothelial growth factor (VEGF) secretion, and adventitial neovascularization. METHODS AND RESULTS: Carotid balloon angioplasty was performed on rat recipients of a bone marrow transplant from green fluorescent rats. Adenoviral delivery of A20 prevented neointimal hyperplasia and decreased macrophage infiltration. This was associated with decreased ICAM-1 and MCP-1 expression in vitro. Additionally, A20 reduced neovascularization in the adventitia of balloon injured carotid arteries, which correlated with fewer VEGF positive cells. CONCLUSIONS: A20 downregulates adhesion markers, chemokine production, and adventitial angiogenesis, all of which are required for macrophage trafficking to sites of vascular injury. This, in turn, diminishes the inflammatory milieu to prevent neointimal hyperplasia.

Microparticles from apoptotic monocytes induce transient platelet recruitment and tissue factor expression by cultured human vascular endothelial cells via a redox-sensitive mechanism.

Circulating microparticles derived from different types of blood cells have been reported to impair endothelial function and to induce pro-inflammatory and prothrombotic endothelial phenotypes. Although the number of monocyte-derived microparticles (M-MPs) is elevated in the blood of patients with various inflammatory conditions, their interaction with endothelial cells has been poorly investigated so far. In this study, we produced microparticles in vitro from apoptotic human monocytes and examined the effects of their interaction with cultured human umbilical vascular endothelial cells (HUVECs). We found that low concentrations of M-MPs induced the production of reactive oxygen species (ROS), mainly anion superoxide, by the endothelial cells. At sub-toxic concentrations, M-MPs induced a rapid expression of von Willebrand factor at the cell surface, which mediated the transient attachment of non-activated platelets to the endothelium in flow conditions. In parallel, M-MPs up-regulated the expression of functional tissue factor by the endothelial cells. ROS controlled these two major changes and the process involved the phosphorylation of p38 mitogen activated protein kinase. We conclude that M-MPs may contribute to thrombotic events by producing redox signalling in endothelial cells.

Microparticles from apoptotic vascular smooth muscle cells induce endothelial dysfunction, a phenomenon prevented by beta3-integrin antagonists.

Fragile atherosclerotic plaques are rich in apoptotic smooth muscle cells (SMCs) and macrophages, generating microparticules (MPs) which accumulate locally and may be released in blood in case of mechanical or spontaneous plaque disruption. Besides being highly procoagulant, this material may interact with downstream endothelium. Using a model of mouse aorta vaso-reactivity, we have investigated the effects of apoptotic MPs prepared in vitro from Fas-ligand sensitive SMCs. Short-term preincubation of aorta rings with the MPs dose-dependently reduced the vasodilatory response to acetylcholine dependent on the endothelium. This effect was prevented by the addition of abxicimab or eptifibatide, indicating a role for a beta3 integrin in this process. We further investigated its mechanism using cultured endothelial cells. The MPs were found to bind to the cells and to inhibit the production and the release of nitric oxide (NO) in response to bradykinin. This phenomenom was redox sensitive, independent of the generation of activated coagulation proteases, and was abrogated when the MPs were pretreated by trypsin. The metabolic effects of MPs were prevented by the addition of eptifibatide. Taken together, these results suggest a potential, platelet-independent, mechanism for the improvement of microvascular perfusion observed with beta3-integrin antagonists.