COULD COVID-19 BE A HEMOGLOBINOPATHY?

The world is struggling to deal with the corona pandemic. Effective therapies are still awaited due to the lack of understanding of the pathophysiological mechanism of the disease. Bearing recent research and clinical observations in mind, the authors propose a novel physiological mechanism of COVID-19 and explain development of COVID-19 related acute respiratory distress syndrome (ARDS) secondary to COVID-19 related hemoglobinopathy. It is a consistent observation that the radiological picture of COVID-19 related ARDS bears more resemblance to high altitude pulmonary edema (HAPE) than typical ARDS. There has been great controversy regarding this proposed similarity. The main argument from those objecting to this comparison is that the etiology is hypoxia in case of HAPE and inflammation in COVID-19 related ARDS. We propose that considering the recent bioinformatics prediction models, COVID-19 might first infect red blood cells via CD147 and cause hemoglobin damage. The resulting hypoxemia may cause pulmonary hypoxic vasoconstriction leading to HAPE-like lung lesions. The now introduced alveolar hypoxia further exaggerates hemoglobinopathy hypoxemia leading to a vicious cycle. In this review, the authors recommend laboratory experiments to prove these hypotheses. The proposed physiological mechanism has significant therapeutic implications. If proven, the authors suggest the use of exchange transfusion as adjunct therapy and development of anti-CD147 drugs.

Impact of a Social Media Group Page on Undergraduate Medical Physiology Learning.

OBJECTIVE: To investigate the impact of associating classroom learning of medical physiology with a Facebook group page in an all-women medical college of a conservative small city in Pakistan. STUDY DESIGN: Qualitative interpretivist study using semi-structured interviews. PLACE AND DURATION OF STUDY: Women Medical College Abbottabad, Pakistan, from March to December 2014. METHODOLOGY: Aclosed Facebook study group was established at a local medical college in Pakistan. It was used to upload learning resources and initiate discussions, coordinated with classroom lectures of physiology. Thirteen semistructured interviews were conducted with volunteer students according to a standard protocol. RESULTS: Five major themes were identified. Facebook group is something new and exciting; it motivated self-study, research, collaborative learning and improved class attendance. Convenience of easily accessible resources allowed the students to concentrate on the lecture rather than note taking. It was easier to communicate with the instructor through Facebook than face to face. Lurkers were also learning. High achievers who had adapted to the current didactic system of teaching were less receptive of the collaborative learning and favored teaching geared towards exam preparation. CONCLUSION: Using social media for e-learning in undergraduate medical education can enhance the student learning experience, especially in resource-limited regions where Information and communication technology is not an integrated part of the teaching process.

SNP rs3088308 is a risk factor for poor lung function in healthy smokers.

OBJECTIVE: To see if single nucleotide polymorphisms of pulmonary innate immune molecule surfactant protein D were associated with poor lung function in smokers. METHODS: The study was conducted at Shaikh Zayed Hospital, Lahore, Pakistan, from April 2008 to August 2010, and comprised relatives and attendants of patients, as well as college and university students. Self-reported healthy smokers who demonstrated no airflow obstruction on spirometry were included. Deoxyribonucleic acid was extracted from their blood sample and genotyped for single nucleotide polymorphisms rs721917 and rs3088308 by polymerase chain reaction and restriction analysis. Serum was separated for measurement of surfactant protein D levels by a commercially available enzyme-linked immunosorbent assay based kit. Lung functions were compared between subjects possessing major and minor alleles using two-tailed Student's t-test. Multiple linear regression analysis was conducted to analyse the effect of age, smoking and the two single nucleotide polymorphisms on forced expiratory volume in 1 second. RESULTS: Of the 122 participants, all of whom were men, 98(80.33%) were smokers while 24(19.67%) had never smoked. Of the former, 90(91.84%) were current smokers and 8(8.16%) were ex-smokers. The overall mean age was 35.8±10.9 years. The mean surfactant protein D level was 121.4±61.6ng/ml. In case of rs3088308, all lung function variables were reduced in patients with a minor allele and the results for forced expiratory volume in 1 second (p=0.016), forced expiratory volume in 1 second (%) predicted (p=0.009), forced vital capacity (p=0.048) and forced vital capacity (%) predicted (p=0.048) were statistically significant. Age had the highest influence on lung function (p<0.001) followed by smoking status (p=0.04) and single nucleotide polymorphisms rs3088308 minor allele (p=0.04). CONCLUSIONS: Single nucleotide polymorphisms rs3088308 was found to modulate serum surfactant protein D levels and may be a risk factor for development of chronic obstructive pulmonary disease among smokers.

Serum surfactant protein D during acute exacerbations of chronic obstructive pulmonary disease.

BACKGROUND: There is a paucity of lung specific biomarkers to diagnose exacerbations of chronic obstructive pulmonary disease (COPD) and to track their progression. Surfactant protein D (SP-D) is a pulmonary collectin regulating the innate immunity of the lung and its serum expression is perturbed in COPD. However, it is not known whether serum levels change during exacerbations. We sought to determine whether serum SP-D levels are raised in COPD exacerbations. OBJECTIVES: To determine whether or not patients with exacerbations have elevated serum SP-D levels compared with asymptomatic controls, stable disease. STUDY DESIGN: case control study. METHODS: We measured serum SP-D levels from patients with stable COPD (n= 14), patients experiencing acute exacerbations (n=13) and in control subjects (n=54) using a specific immunoassay and compared the levels using analysis of variance. RESULTS: Serum SP-D levels were significantly increased in patients who experienced an acute exacerbation (227 +/- 120 ng/mL) compared to patients with stable disease (151 +/- 83 ng/mL) or control subjects (128 +/- 65 ng/mL; p=0.003). Serum SP-D levels were also found to be inversely related to various lung function parameters including FEV_{1}/FVC% predicted. CONCLUSIONS: Our study suggests that serum SP-D levels are increased in patients during exacerbations and may be a potential diagnostic biomarker for COPD exacerbations.