Prevalence and Associated Factors of Depression among Patients with Diabetes at Jazan Province, Saudi Arabia: A Cross-Sectional Study.

CONTEXT: Patients with diabetes mellitus (DM) have a poorer quality of life when compared with patients without DM. In fact, one in every five diabetic patients suffers from comorbid depression, which can lead to poor management, poor compliance with treatment, and low quality of life. Therefore, we assessed the prevalence of depression and identified its associated factors among diabetic patients at Jazan Province, KSA. METHODS AND MATERIALS: A cross-sectional study was conducted among 500 diabetic patients attending a diabetic center in addition to four primary healthcare centers. We used a simple Arabic translation of the Beck Depression Inventory (BDI II) tool to evaluate the depression level among the subjects. We also evaluated the frequencies of certain sociodemographic characteristics and clinical information. Moreover, we performed univariate and multivariate analyses to identify the potential risk factors using adjusted odds ratios (AORs). RESULTS: The prevalence of depression among DM patients was 20.6%. The majority of patients showed no depression (N = 285, 59.4%), one-fifth had mild depression (N = 96, 20.0%), some (N = 55, 11.4%) had moderate depression, and some had severe depression (N = 44, 9.2%). Depression was significantly more prevalent among uneducated patients (N = 27, 31.8%) (X2 = 17.627, P = 0.001) and patients with low monthly income (< 2500 SR/month) (N = 33, 22.8%) (X2 = 9.920, P = 0.019). Hypertension (AOR = 2.531, 95% CI [1.454, 4.406]) and ischemic heart diseases (AOR = 3.892, 95% CI [1.995, 7.593]) were considered as risk factors for depression among diabetic patients. CONCLUSIONS: Almost one in every five patients with DM is affected by depression coexisting with cardiovascular diseases. Therefore, screening for psychological problems, proper treatment, and educating patients with diabetes about DM self-management should be routine components of DM care.

Vascular endothelial growth factor improves functional outcome and decreases secondary degeneration in experimental spinal cord contusion injury.

Spinal cord injury leads to acute local ischemia, which may contribute to secondary degeneration. Hypoxia stimulates angiogenesis through a cascade of events, involving angiogenesis stimulatory substances, such as vascular endothelial growth factor (VEGF). To test the importance of angiogenesis for functional outcome and wound healing in spinal cord injury VEGF165 (proangiogenic), Ringer's (control) or angiostatin (antiangiogenic) were delivered locally immediately after a contusion injury produced using the NYU impactor and a 25 mm weight-drop. Rats treated with VEGF showed significantly improved behavior up to 6 weeks after injury compared with control animals, while angiostatin treatment lead to no statistically significant changes in behavior outcome. Furthermore, VEGF-treated animals had an increased amount of spared tissue in the lesion center and a higher blood vessel density in parts of the wound area compared with controls. These effects were unlikely to be due to increased cell proliferation as determined by bromo-deoxy-uridine-labeling. Moreover, VEGF treatment led to decreased levels of apoptosis, as revealed by TUNEL assays. In situ hybridization demonstrated presence of mRNA for VEGF receptors Flt-1, fetal liver kinase-1, neuropilin-1 and -2 in several important cellular compartments of the spinal cord. The different experiments indicate that beneficial effects seen by acute VEGF delivery was attributable to protection/repair of blood vessels, decreased apoptosis and possibly also by other additional effects on glial cells or certain neuron populations.

Neurotrophic factors and receptors in the immature and adult spinal cord after mechanical injury or kainic acid.

Delivery of neurotrophic factors to the injured spinal cord has been shown to stimulate neuronal survival and regeneration. This indicates that a lack of sufficient trophic support is one factor contributing to the absence of spontaneous regeneration in the mammalian spinal cord. Regulation of the expression of neurotrophic factors and receptors after spinal cord injury has not been studied in detail. We investigated levels of mRNA-encoding neurotrophins, glial cell line-derived neurotrophic factor (GDNF) family members and related receptors, ciliary neurotrophic factor (CNTF), and c-fos in normal and injured spinal cord. Injuries in adult rats included weight-drop, transection, and excitotoxic kainic acid delivery; in newborn rats, partial transection was performed. The regulation of expression patterns in the adult spinal cord was compared with that in the PNS and the neonate spinal cord. After mechanical injury of the adult rat spinal cord, upregulations of NGF and GDNF mRNA occurred in meningeal cells adjacent to the lesion. BDNF and p75 mRNA increased in neurons, GDNF mRNA increased in astrocytes close to the lesion, and GFRalpha-1 and truncated TrkB mRNA increased in astrocytes of degenerating white matter. The relatively limited upregulation of neurotrophic factors in the spinal cord contrasted with the response of affected nerve roots, in which marked increases of NGF and GDNF mRNA levels were observed in Schwann cells. The difference between the ability of the PNS and CNS to provide trophic support correlates with their different abilities to regenerate. Kainic acid delivery led to only weak upregulations of BDNF and CNTF mRNA. Compared with several brain regions, the overall response of the spinal cord tissue to kainic acid was weak. The relative sparseness of upregulations of endogenous neurotrophic factors after injury strengthens the hypothesis that lack of regeneration in the spinal cord is attributable at least partly to lack of trophic support.