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.
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.
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