Featuring Trends in the Epidemiology of Lung Cancer Following the Publication of the National Cancer Strategy in Qatar.

OBJECTIVES: Qatar has witnessed significant reforms in its health care system, including the care of cancer patients. In 2011, the National Cancer Strategy was released with the aim to deliver a high standard of care to cancer patients across the country. We sought to investigate the featuring trends in the epidemiological and clinical characteristics of lung cancer in Qatar following the publication of the National Cancer Strategy. METHODS: We conducted a retrospective cohort study documenting the epidemiological and clinical characteristics of primary lung cancer cases in Qatar diagnosed from 1 January 2011 to 31 December 2018. RESULTS: The overall age-standardized incidence rate was 8.7 per 100 000 persons (11.6 per 100 000 and 5.4 per 100 000 persons for males and females, respectively). The one, three, and five-year overall survival rates were 67.0%, 48.0%, and 28.0%, respectively. The three-year overall survival rates for stages I, II, III, and IV were 97.0%, 78.0%, 52.0%, and 31.0%, respectively. The three-year survival rates for males and females were 43.0% and 64.0%, respectively (p = 0.029), for Qatari and non-Qatari nationals were 42.0% and 49.0%, respectively (p = 0.252), and for smokers and non-smokers were 39.0% and 69.0%, respectively (p ≤ 0.001). The overall age-standardized mortality rate was 5.5 per 100 000 persons. Adenocarcinoma was the most common histologic type. CONCLUSIONS: Despite the low overall lung cancer incidence rate in Qatar, there is a rise in the incidence among females when compared to previous studies. Qatar has favorable five-year lung cancer survival rates compared to many developed and neighboring countries. Policymakers in the country should consider the changing patterns in lung cancer incidence when planning future preventive strategies.

Frequency of Acute Kidney Injury in Patient Receiving Piperacillin - Tazobactam: A Hospital-based Study from Qatar.

BACKGROUND: several studies have been reported piperacillin-tazobactam (TAZ / PIPC)-associated AKI with various frequencies. The aim of this study was to determine the frequency of TAZ/PIPC- associated AKI among our patients and to identify the risk factors for this clinical entity. METHODS: this retrospective cross-sectional study was conducted at Hamad General Hospital; it involved adult patients who were admitted from January 2017 to December 2017. RESULTS: we involved 917 patients, of whom 635 (69.25%) were males and 282 (30.75%) were females. The mean age of the patients was 52 (SD 19) years, and 98 (10.7%) patients were diagnosed with AKI. The patients with AKI were significantly older than without AKI [59.71 (SD 19.79) versus 51.06 (SD 18.67); P <0.001]. After TAZ/PIPC initiation, the mean creatinine level in the AKI group was higher than the mean creatinine level in the non-AKI group, [158.91 (SD 81.93) versus 66.78 (SD 21.42); P<001]. The mean time of onset of AKI after PIPC/TAZ initiation was 4.46 (SD 3.20) (1-12 days). AKI was significantly associated with low mean serum albumin (P<0.001), high mean fasting blood glucose (P<0.001), coronary artery diseases (P<0.001), heart failure (P<0.001), liver diseases (P=0.047), diabetes mellitus (P=0.021) and hypertension (P<0.001). The in-hospital mortality was significantly higher in the AKI group [38.78% versus 5.13% in the non-AKI group; P<0.001], and only advanced age and heart failure were found as independent risk factors for TAZ/PIPC-associated AKI. CONCLUSION: TAZ/PIPC was significantly associated with AKI. Advanced age and heart failure were identified as independent risk factors for TAZ/PIPC-associated AKI.

Paroxysmal Nocturnal Hemoglobinuria with Glucose-6-Phosphate Dehydrogenase Deficiency: A Case Report and Review of the Literature.

In this study, we are describing a female patient with paroxysmal nocturnal hemoglobinuria (PNH) and glucose-6-phosphate dehydrogenase (G6PD) deficiency. Both diseases are known to cause hemolytic anemia that mediates the hemolysis of RBCs through several mechanisms. In PNH the hemolysis is mediated through complement activation and oxidative stress. G6PD enzyme is crucial in preventing damage to cellular structures caused by oxygen-free radicles. In G6PD deficiency the hemolysis is mediated through the oxidative stress created by oxygen-free radicles. Since both diseases mediate hemolysis through the oxidative stress, we hypothesize that both conditions have facilitated an effect on each other and this will reflect on the response to treatment, and this response to treatment could vary based on whether the two mutations occurred in the same gene or in two different X chromosomes. Having diagnosed PNH, the management is very expensive and not all the patients can afford it, especially our patient who is a maid by occupation. So, the real challenge in our case is to monitor her in subsequent visits and to plan the treatment keeping in mind her financial status.