Background: COVID-19-induced hyponatremia is reportedly associated with pulmonary dysfunction, but mostly among Caucasians. Hence, the current study evaluated sodium status and its correlation with indices of pulmonary dysfunctions among Nigerians of Negroid race. Methods: This was a retrospectively-designed observational study. Data, all obtained at presentation, were acquired from medical records of 480 RT-PCR-confirmed COVID-19 patients managed at a COVID-19-designated treatment facility in Port Harcourt, Southern Nigeria. Analysis of acquired data was done by COVID-19 clinical grades and sodium status using descriptive and inferential statistics. Results: At presentation, hyponatremia and hypernatremia were observed in 47.7% and 1.0% of the entire studied cohorts (n=480), respectively. Both disorders (hyponatremia/hypernatremia) were mostly observed among the moderate, severe, and critical cases. Most hyponatremic cases (n=154;67.2%) and the entire hypernatremic cases (n=5;100%) were of mild grades. Hyponatremics had higher proportions of fever, breathlessness, confusion, and a higher burden of inflammatory markers which increased with worsening hyponatremic grade. Etiologically, hyponatremia was mostly associated with the syndrome of inappropriate anti-diuretic hormone secretion (SIADH) (n=132;56.7%). Among the hyponatremics, an inverse correlation existed between sodium and respiratory rate (RR), while a correlation existed between sodium and oxygen saturation (SpO2). Compared to mild hyponatremics, the moderate/severe hyponatremics had a greater risk of having RR>30 and SpO2 <95%.  Conclusion: Hyponatremia, mostly of mild grade, was common among the studied COVID-19 patients and was associated with indices of pulmonary dysfunctions, including disease severity, inflammatory markers, and SIADH. Hence, hyponatremia should be utilized to triage COVID-19 patients at presentation. However, further studies are recommended to verify these findings.

Background: Altered hepatobiliary status has been reported in association with COVID-19 which has been linked, with limited evidence, to the exaggerated COVID-19-induced hyper-inflammatory response. Hence, the current study evaluated hepatocellular status and its association with indicators of inflammation among COVID-19 patients. Methods: This study was conducted among the RT-PCR-confirmed and treatment-naïve COVID-19 patients in Port Harcourt, South-south Nigeria. Pre-medical/surgical data were retrieved retrospectively from archived patients’ case notes, medical review charts, nurses’ vital signs/medication sheets, and laboratory records at the center using validated data acquisition templates. All retrieved data were analyzed using standard protocols. Results: Among the 396 studied, 16.7% (n=66) had hepatobiliary pathologies. The majority of those with hepatobiliary pathologies had severe COVID-19 (93.3%). Patients with severe COVID-19 and concurrent hepatobiliary pathologies were mostly males and of older age. Cholestatic-specific pathology was the most common pattern observed among the general cases with hepatobiliary pathologies and among those having specific mild, moderate, and severe COVID-19. Among those with severe COVID-19, significant positive relationships were observed between markers of inflammation (Proclacitonin/C-reactive protein/D-dimer) and cholestatic-specific hepatobiliary markers (ALP/G-GT/TBil/CBil) (p<0.05), but not with the hepatocellular-specific markers (ALT/AST) (p>0.05). In contrast, no significant relationship existed between the relevant markers of inflammation and all the cholestatic/hepatocellular markers among those with mild and moderate COVID-19 (p>0.05). Conclusion: Hepatobiliary pathologies, mostly of cholestatic patterns, are frequent among the studied COVID-19 patients which were associated with inflammatory markers among those with severe disease. Therefore, hepatobiliary evaluation should be prioritized, especially among those with severe COVID-19.