Musa Norsyuhadah, Wan Azman Wan Norlina, Nazri Nor Amirah Mohammad, Tuan Ismail Tuan Salwani, Harun Azian, Yaacob Najib Majdi, Sulong Sarina, Sirajudeen K N S, Mat Mahaya Che, Zulkeflee Hani Ajrina
From the Department of Chemical Pathology, School of Medical Science, Health Campus, Universiti Sains Malaysia, Kelantan, Malaysia.
From the Hospital Pakar Universiti Sains Malaysia, Health Campus, Universiti Sains Malaysia, Kelantan, Malaysia.
Ann Saudi Med. 2025 Jul-Aug;45(4):225-234. doi: 10.5144/0256-4947.2025.225. Epub 2025 Aug 7.
Alpha-1 antitrypsin (A1AT) deficiency has been recognized as an adverse prognostic determinant in severe instances of COVID-19.
To determine the A1AT phenotypes and levels in individuals at various clinical stages of COVID-19 compared to healthy controls.
Case-control study.
Hospital Raja Perempuan Zainab II (HRPZ II) and Hospital Ampang, Malaysia.
The analysis included a total of 282 patients. We categorized 188 COVID-19 patients from two centres in Malaysia into two groups: mild to moderate (stages 1-3) and severe to critical (stages 4-5) and compared them with 94 healthy controls.
A1AT phenotypes and levels in different COVID-19 stages compared to healthy controls.
282 subjects.
The frequency (n) and percentage (%) in the control group, 88 (93.6) exhibited PiMM phenotypes, whereas 6 (6.4) displayed PiXM/PiYM phenotypes. Within the mild to moderate COVID-19 group, 88 (93.6) had PiMM phenotypes, 3 (3.2) featured PiXM/PiYM, and 1 presented PiBM phenotypes. Among severe to critical COVID-19 patients, the PiMM phenotype was identified in 61 (64.9) with 16 (17) having PiBM phenotypes, 4 (4.5) displaying PiCM, 2 (2.1) featuring PiXM/PiYM, and 1 (1.1) presenting PiEM phenotypes. Variants such as MS, MZ, S, and Z were undetected. However, 12 COVID-19 patient samples yielded inconclusive results. Median (IQR: 25th to 75th percentile) A1AT concentrations for controls were 1.8 (1.3-2.3) g/L, for mild to moderate cases 1.9 (1.2-2.6) g/L, and for severe to critical COVID-19 cases 2.1 (1.4-2.8) g/L.
This research identifies the PiMM phenotype as the predominant phenotype expression within the studied population. This prevalence underscores the potential role of genetic factors in determining the biological response to SARS-CoV-2 infection. The presence of another phenotype variant across the study population suggests a nuanced genetic landscape that warrants further exploration.
The absence of follow-up A1AT quantification and baseline measurements limits the assessment of disease progression. The isolectric focusing phenotyping technique used might have missed specific A1ATD variants.
α-1抗胰蛋白酶（A1AT）缺乏已被认为是重症新型冠状病毒肺炎（COVID-19）不良预后的决定因素。
确定COVID-19不同临床阶段个体的A1AT表型和水平，并与健康对照进行比较。
病例对照研究。
马来西亚拉贾佩empuan扎伊纳卜二世医院（HRPZ II）和安邦医院。
分析共纳入282例患者。我们将来自马来西亚两个中心的188例COVID-19患者分为两组：轻至中度（1-3期）和重至危重型（4-5期），并与94例健康对照进行比较。
与健康对照相比，不同COVID-19阶段的A1AT表型和水平。
282名受试者。
在对照组中，88例（93.6%）表现为PiMM表型，而6例（6.4%）表现为PiXM/PiYM表型。在轻至中度COVID-19组中，88例（93.6%）有PiMM表型，3例（3.2%）为PiXM/PiYM，1例为PiBM表型。在重至危重型COVID-19患者中，61例（64.9%）为PiMM表型，16例（17%）为PiBM表型，4例（4.5%）为PiCM，2例（2.1%）为PiXM/PiYM，1例（1.1%）为PiEM表型。未检测到MS、MZ、S和Z等变体。然而，12份COVID-19患者样本结果不确定。对照组A1AT浓度中位数（IQR：第25至75百分位数）为1.8（1.3-2.3）g/L，轻至中度病例为1.9（1.2-2.6）g/L，重至危重型COVID-19病例为2.
