Health care services provided to type 1 and type 2 diabetic patients in Saudi Arabia

Objectives:

To assess health care services provided to type 1 and type 2 diabetic patients and diabetes health care expenditure in the Kingdom of Saudi Arabia (KSA).

Methods:

This study was part of a nationwide, household, population based cross-sectional survey conducted at the University Diabetes Center, College of Medicine, King Saud University, Riyadh, Kingdom of Saudi Arabia between January 2007 and December 2009 covering 13 administrative regions of the Kingdom. Using patients’ interview questionnaires, health care services data were collected by trained staff.

Results:

A total of 5,983 diabetic patients were chosen to assess health care services and expenditure. Approximately 92.2% of health services were governmental and the remaining 7.8% were in private services. The mean annual number of visits to physicians was 6.5±3.9 and laboratories was 5.1±3.9. Diabetic patients required one admission every 3 years with a mean admission duration of 13.3±28.3 days. General practitioners managed 85.9% of diabetic cases alone, or shared with internists and/or endocrinologists. Health care expenditure was governmental in 90% of cases, while it was personal in 7.7% or based on insurance payment in 2.3%.

Conclusion:

Health services and its expenditure provided to diabetic citizens in Saudi Arabia are mainly governmental. Empowerment of the role of both the private sector and health insurance system is badly needed, aside from implementing proper management guidelines to deliver good services at different levels.The health care system (HCS) in the Kingdom of Saudi Arabia (KSA) is growing at an annual rate of 2% to meet the increasing demand for health care services caused by increased population growth, and a surge in chronic non-communicable diseases.1 This has resulted in an increase in the total health care budget by more than 2 times; from 30 billion Saudi Riyals (SR) (US$8 billion) in 2008 to approximately SR69 billion (US$18.4 billion US dollars) in the year 2011 with a cumulative allocation of SR113 billion (U$30.13 billion) in 2010 and 2011; which accounted for 3.7% of the estimated country’s gross domestic product (GDP), which is one of the highest among Gulf Cooperation Council (GCC) countries.2 The Saudi health care system, which is ranked 26th among 190 countries by the World Health Organization (WHO),3 has a lower percentage of average expenditure in relation to the country’s GDP than many developed and developing countries.4 The government HCS in KSA is structured to deliver free health care services to Saudi citizens through various public hospitals and primary health care centers (PHCCs) including government health sectors, such as the Ministry of Health (MOH), Military Health Services and University Health Institutions. In addition to this, the private health care sector, through its clinics and hospitals, provided 31.1% of the total health care services in KSA in 2013.5 The real challenge facing the Kingdom’s HSC is the increased demands for hospital beds and medical personnel to meet international standards.6 The population ratio of physician and nurses in the Kingdom is lower than the global ratio being 9.4 physicians and 21 nurses per 10,000 of population versus 13 physicians and 28 nurses globally.7 This explains the current imbalance between the growth in HCS and the real medical needs of Saudi citizens.Diabetes mellitus, being the most prevalent chronic non-communicable disease in the Kingdom, has a significant effect on the country’s HCS and overall economy.8,9 This is proved by the fact that 25.4% of Saudi citizens older than 30 years of age have diabetes, which implies that there are approximately 1.5 million Saudi citizens suffering from this chronic disease.10 This is aside from the fact that more than 70% of known diabetic patients in the Middle Eastern countries have poorly controlled diabetes,11 associated with high rates of chronic complications that place greater pressure on health services and expenditure, where in 2013, it was estimated that the Middle East and North Africa (MENA) region spent US$13.6 billion on diabetes care with the spending per person with diabetes, where the spending in Saudi Arabia was US$934, which is far below other GCC such as United Arab Emirates (US$2,228), Qatar (US$2,199), and Kuwait (US$1,886),12 although we strongly believe that these figures are underestimated.Diabetic patients are currently managed at all health care levels, from primary to secondary and tertiary levels by general practitioners (GPs), internists, and endocrinologists.13 Since diabetes care involves many medical disciplines, such as ophthalmology, cardiology, nephrology and so forth, specialized diabetes clinics, and diabetes centers are needed to function as liaising bodies. Although health care needs for diabetic patients’ management at a global level have witnessed a clear shift to the primary from secondary and tertiary health care levels,14 diabetic patients in the Kingdom are still receiving services at secondary or even tertiary levels. Since there are no studies so far that have looked into the health care services provided to diabetic patients in KSA, the current study, as a part of the Saudi Abnormal Glucose Metabolism and Diabetes Impact (SAUDI-DM) survey,10 has investigated the current status of health care services provided to diabetic patients. This study aimed to assess the medical system providing care to diabetic patients, and methods of payment through a randomly selected cohort of diabetic patients at a country level.     

Association of total antioxidants level with glaucoma type and severity

Objectives:

To compare the mean total antioxidant status (TAS) among 3 glaucoma types, namely: pseudoexfoliation glaucoma (PEG), primary open angle glaucoma (POAG), and primary angle closure glaucoma (PACG), and study its potential association with various clinical glaucoma-parameters.

Methods:

In this case-control study, plasma samples were obtained between September 2013 and October 2014 from 340 glaucoma patients (PEG [n=54]; POAG [n=147]; PACG [n=139]), and 351 controls of matching age, gender, ethnicity, and 5 different systemic co-morbidities from King Abdulaziz University Hospital, Riyadh, Saudi Arabia. The TAS in all samples was determined by a colorimetric-based assay.

Results:

The mean±standard deviation of TAS was significantly lower among cases: 0.77±0.32 than controls: 1.1±0.22, p<0.0001. Moreover, the TAS levels were significantly different across the 3 types of glaucoma: 0.86±0.24 in PEG, 0.47±0.32 in POAG, and 0.98±0.41 in PACG (all p<0.0001). In addition, there was a significant correlation between TAS and age at onset (Pearson correlation coefficient [R] 0.17, p<0.0001), cup/disc ratio (R: -0.13, p=0.004), and number of anti-glaucoma medications (R: -0.16, p=0.001).

Conclusion:

Our findings provide evidence that plasma TAS levels are decreased in patients with glaucoma, more so in POAG and PEG than PACG, supporting the hypothesis that decreased antioxidative defense and/or increased oxidative stress may have a critical role in the pathogenesis of glaucoma.Glaucoma is a progressive optic neuropathy associated with optic nerve damage, and is one of the most leading cause of blindness worldwide.1 Elevated intraocular pressure (IOP) as a result of reduction in normal aqueous outflow is a major causal risk factor that is well supported by animal studies.2-4 Although IOP is considered a major risk factor for glaucoma,2,3 other concomitant factors affecting the pathophysiology of glaucomatous retinal ganglion cell (RGC) death include retinal ischemia,5 nutritional status,6 and oxidative stress.7 There is evidence of oxidative damage in ocular diseases, such as cataract and age-related macular degeneration.8 In addition, significant oxidative damage has been demonstrated in human trabecular meshwork (TM) cells of patients with glaucoma,7 causing elevated IOP and visual field damage.9 Furthermore, our previous studies have documented mitochondrial abnormalities10-12 (oxidative stress marker), and glutathione-S-transferase (antioxidant) gene (GST) polymorphisms to be associated with various types of glaucoma.13 It is clearly evident from the literature, and our own studies, that oxidative stress mechanisms play a critical role in the pathogenesis of glaucoma. Previous studies had demonstrated reduced total antioxidant capacity in aqueous humor and blood samples from patients with glaucoma.14-17 To evaluate the role of oxidative stress in different types of glaucoma we had previously investigated total antioxidants status (TAS) in the plasma of pseudoexfoliation glaucoma (PEG) patients,18 primary angle closure glaucoma (PACG) patients,19 and in the plasma of primary open angle glaucoma (POAG) patients.20 As an extension to these studies, here, we compare the mean TAS level among these 3 glaucoma types, and study the potential association between the TAS level and various clinical parameters important to each type of glaucoma.18-20     

Addressing the link between paraoxonase-1 gene variants and the incidence of early onset myocardial infarction

Introduction

The enzyme paraoxonase-1 (PON1) represents an endogenous defense mechanism against vascular oxidative stress, thereby contributing to the prevention of atherosclerosis. Several polymorphisms have been reported in the PON1 gene, including Q192R. PON1 phenotype is commonly expressed as the paraoxonase/arylesterase ratio (PON/ARE). The major aim of this study was to investigate the association between PON1 Q192R polymorphism, PON1 phenotypes and the incidence of early-onset acute myocardial infarction (AMI) in Egyptians.

Material and methods

The study subjects consisted of 102 AMI patients and 72 age-matched healthy controls. Genotyping and enzyme activities were determined using PCR-RFLP and kinetic spectrophotometric assays, respectively.

Results

The genotype distribution for the PON1 gene was significantly different between AMI patients (QQ = 38.24%, QR = 49.02%, RR = 12.75%) and controls (QQ = 66.67%, QR = 25%, RR = 8.33%). Allele frequencies were also significantly different between patients (Q = 62.75%, R = 37.25%) and controls (Q = 79.17%, R = 20.83%). The genotypes QR and RR showed higher risk for AMI compared to the homozygous QQ (odds ratio (OR) = 3.231, p < 0.001). The average PON/ARE ratio in MI patients (1.187 ±0.1) did not differ significantly from controls (1.118 ±0.26). However, it showed a significant difference among different genotypes in both AMI patients (QQ = 0.91 ±0.11, QR = 1.09 ±0.11 and RR = 2.65 ±0.4) (p = 0.0002) and controls (QQ = 0.68 ±0.1, QR = 1.07 ±0.11 and RR = 4.89 ±2.84) (p < 0.0001).

Conclusions

PON1 192R allele represents an independent risk factor for early-onset AMI in Egyptians, and PON1 Q192R polymorphism modulates the paraoxonase phenotype.     

Discovery and antiproliferative evaluation of new quinoxalines as potential DNA intercalators and topoisomerase II inhibitors

In continuation of our previous work on the design and synthesis of topoisomerase II (Topo II) inhibitors and DNA intercalators, a new series of quinoxaline derivatives were designed and synthesized. The synthesized compounds were evaluated for their cytotoxic activities against a panel of three cancer cell lines (Hep G‐2, Hep‐2, and Caco‐2). Compounds 18b, 19b, 23, 25b , and 26 showed strong potencies against all tested cell lines with IC₅₀ values ranging from 0.26 ± 0.1 to 2.91 ± 0.1 µM, comparable with those of doxorubicin (IC₅₀ values ranging from 0.65 ± 0.1 to 0.81 ± 0.1 µM). The most active compounds were further evaluated for their Topo II inhibitory activities and DNA intercalating affinities. Compounds 19b and 19c exhibited high activities against Topo II (IC₅₀ = 0.97 ± 0.1 and 1.10 ± 0.1 µM, respectively) and bound the DNA at concentrations of 43.51 ± 2.0 and 49.11 ± 1.8 µM, respectively, whereas compound 28b exhibited a significant affinity to bind the DNA with an IC₅₀ value of 37.06 ± 1.8 µM. Moreover, apoptosis and cell‐cycle tests of the most promising compound 19b were carried out. It was found that 19b can significantly induce apoptosis in Hep G‐2 cells. It has revealed cell‐cycle arrest at the G2/M phase. Moreover, compound 19b downregulated the Bcl‐2 levels, indicating its potential to enhance apoptosis. Furthermore, molecular docking studies were carried out against the DNA–Topo II complex to examine the binding patterns of the synthesized compounds.     

Iron overload in non-transfusion-dependent thalassemia: a clinical perspective

Iron overload due to increased intestinal iron absorption represents an important clinical problem in patients with non-transfusion-dependent thalassemia (NTDT), particularly as they advance in age. Current models for iron metabolism in patients with beta (β)-thalassemia intermedia (TI) suggest that suppression of serum hepcidin results in increased iron absorption and release of iron from the reticuloendothelial system, leading to depletion of macrophage iron, relatively low levels of serum ferritin, and liver iron loading. The clinical consequences of iron overload in patients with NTDT are multifactorial and include endocrinopathy, bone disease, thromboembolism, pulmonary hypertension, cerebrovascular and neuronal damage, liver fibrosis or cirrhosis, and increased risk of hepatocellular carcinoma. Although serum ferritin levels correlate with liver iron concentration (LIC), they underestimate iron load in these patients compared with transfusion-dependent patients with equivalent LIC. Therefore, direct measurement of LIC is recommended with chelation therapy as indicated.