Aims.This study assessed factors associated with glycemic control among Saudi patients with Type 2 diabetes mellitus (T2DM).Methods.We conducted an analytical cross-sectional study, which included a random sample of 288 patients with T2DM proportional to the diabetes population of each primary health care center in Jazan city, Kingdom of Saudi Arabia.Results.More than two-thirds (74%) of patients had poor glycemic control. Lack of education, polypharmacy, and duration of diabetes ≥ 7 years were significantly associated with higher glycated hemoglobin (HbA1c). Moreover, patients who were smoker or divorced were significantly more likely to have higher HbA1c. The patients who did not comply with diet or take their medications as prescribed had poor glycemic control. The study found lower HbA1c levels among patients who received family support or had close relationship with their physicians. Similarly, knowledgeable patients towards diabetes or those with greater confidence in ability to manage self-care behaviors had a lower HbA1c. In contrast, risk factors such as depression or stress were significantly correlated with poorer glycemic control.Conclusion.The majority of T2DM patients had poor glycemic control. The study identified several factors associated with glycemic control. Effective and tailored interventions are needed to mitigate exposure to these risk factors. This would improve glycemic control and reduce the risks inherent to diabetes complications.

We undertook enhanced surveillance of those presenting with respiratory symptoms at five healthcare centers by testing all symptomatic outpatients between November 2013 and January 2014 (winter time). Nasal swabs were collected from 182 patients and screened for MERS-CoV as well as other respiratory viruses using RT-PCR and multiplex microarray. A total of 75 (41.2%) of these patients had positive viral infection. MERS-CoV was not detected in any of the samples. Human rhinovirus (hRV) was the most detected pathogen (40.9%) followed by non-MERS-CoV human coronaviruses (19.3%), influenza (Flu) viruses (15.9%), and human respiratory syncytial virus (hRSV) (13.6%). Viruses differed markedly depending on age in which hRV, Flu A, and hCoV-OC43 were more prevalent in adults and RSV, hCoV-HKU1, and hCoV-NL63 were mostly restricted to children under the age of 15. Moreover, coinfection was not uncommon in this study, in which 17.3% of the infected patients had dual infections due to several combinations of viruses. Dual infections decreased with age and completely disappeared in people older than 45 years. Our study confirms that MERS-CoV is not common in the southwestern region of Saudi Arabia and shows high diversity and prevalence of other common respiratory viruses. This study also highlights the importance and contribution of enhanced surveillance systems for better infection control.

Background and Objectives: The link between celiac disease (CD) and type 1 diabetes (T1D) has been well-documented in the medical literature and is thought to be due to a shared genetic predisposition in addition to environmental triggers. This study aimed to determine the seroprevalence and biopsy-proven CD (PBCD) prevalence in individuals with T1D from Saudi Arabia and identify their clinical characteristics and the impact on glycemic control. Materials and Methods: A total of 969 children and adolescents with confirmed T1D were investigated. Prospective and retrospective data were collected to include clinical, anthropometric, and biochemical data. Total IgA and anti-TTG-IgA antibodies were screened to detect seropositive cases. Upper intestinal endoscopy and biopsy were performed to find BPCD. Results: The seroprevalence of CD was 14.6% (141/969), while BPCD prevalence was 7.5%. Females had a higher prevalence than males: 17.8% vs. 9.8%, p < 0.001. The CD group had lower HbA1c and more frequent hypoglycemia than the seronegative group. Conclusions: This study highlighted the high prevalence of CD in T1D Saudi patients. CD has multiple effects on glycemic control, growth, and puberty in children and adolescents with T1D. We emphasize the importance of early screening for CD at the time of diabetes diagnosis and periodically after that or if any atypical features present, especially anemia, growth delay, underweight, or frequent hypoglycemia.

Disordered eating behaviors (DEBs) in type 1 diabetes (T1D) have been studied globally in different age groups. However, there is no validated diabetes-specific questionnaire in the Arabic language for the screening of DEBs. This study aimed to translate the Diabetes Eating Problem Survey–Revised scale (DEPS-R) into the Arabic language and study its psychometric properties in adolescents with T1D. We adopted the forward–backward procedure to translate the DEPS-R questionnaire into Arabic. The validation study enrolled 258 Saudi adolescents with T1D aged 12–18 years who completed the Arabic DEPS-R questionnaire and the EAT-26. The Arabic DEPS-R showed good construct validity and reliability (Cronbach’s alpha = 0.86). The factor analysis revealed a three-factor structure of DEPS-R which explains 54.4 % of the variance. In total, 30.6% of the participants are at high risk for DEBs (DEPS-R score ≥ 20). The psychometric properties of the Arabic DEPS-R are satisfactory, consistent with the original scale and translations in other languages. These results support the validity of the Arabic DEPS-R for assessment of DEBs in the T1D Arabic population.

Familial partial lipodystrophies (FPLDs) are very rare inherited disorders characterized by partial loss of adipose tissue from the upper and lower extremities. At least seven subtypes of FPLD have been identified and are mostly dominantly inherited. FPLD type 3 is caused by mutations in the PPARγ gene, which encodes for the protein peroxisome proliferator-activated receptor gamma (PPARγ). We identified a Saudi female with PFLD3 presented with partial lipoatrophy, uncontrolled diabetes, severe hypertriglyceridemia, and recurrent pancreatitis. The clinical and biochemical findings in this proband were described before and after treatment with Pioglitazone in addition to the conventional treatment. DNA extraction and whole exome sequencing (WES) were performed to detect the variant. The mutant gene was subjected to Sanger analysis to confirm the results. We applied five specific computational prediction tools to assess the pathogenicity of variation, namely the MT, DANN, CADD, BayesDel, and fitCons tools. We assessed protein modeling and stability with the AlphaFold-generated structures for both wild-type and mutant proteins. Finally, we conducted molecular docking using the AutoDock Vina virtual docking. Upon whole exome sequencing, a c.1024C>T p.(Gln342Ter) missense mutation was detected in the PPARγ gene associated with FPLD3. This variant is a novel mutation that has not been described in all genome databases. Sanger analysis confirmed the heterogenicity and pathogenicity of this variant. All five computational prediction tools indicate that this variant is considered highly pathogenic. Our patient showed a dramatic response to Pioglitazone, a synthetic PPARγ agonist. From structural modeling, we found that the enhanced binding affinity of the mutant PPARγ protein to Pioglitazone likely improves the activation of PPARγ, enhancing its transcriptional activity and resulting in better clinical outcomes. These findings extend the spectrum of PPARγ mutations responsible for FPLD3 and highlight the potential for personalized treatment strategies based on genetic mutations.