Researchers from the University of Modena and Reggio Emilia-Italy, the Policlinico of Modena-Italy and the University of Alberta-Canada have in a new study found that most Post COVID-19 hospitalized patients irrespective if they had moderate or severe COVID-19 disease will ultimately develop fatty liver disease.
A new initiative is underway to change the traditional definition of Non-Alcoholic Fatty Liver Disease (NAFLD) to Metabolic Associated Fatty Liver Disease (MAFLD), to reflect the cluster of metabolic abnormalities that may be more closely associated with cardiovascular risk.
Long COVID is a smoldering inflammatory condition, characterized by several symptom clusters.
The study team This aimed to determine the prevalence of MAFLD in patients with post-acute COVID syndrome (PACS) and its association with other PACS-cluster phenotypes.
The study findings were published in the peer reviewed journal: Oxford’s Open Forum Infectious Diseases. https://academic.oup.com/ofid/advance-article/doi/10.1093/ofid/ofac003/6501509
COVID-19 is a complex disease with long-term sequelae after the resolution of the acute phase . Several of the sequalae that may affect the quality of life and increase the risk of death of patients who survived an episode of COVID-19 have been grouped under the umbrella term of post-acute COVID syndrome (PACS).
A multitude of signs and symptoms affecting different organ systems have been described in the post-acute COVID state, and have been grouped qualitatively in clusters: neurocognitive (brain fog, dizziness, loss of attention, confusion), autonomic (chest pain, tachycardia, palpitations), gastrointestinal (diarrhea, abdominal pain, vomiting), respiratory (general fatigue, dyspnea, cough, throat pain), musculoskeletal (myalgias, arthralgias), psychological (post- traumatic stress disorder, anxiety, depression, insomnia), sensory (ageusia, anosmia, hearing loss) and dermatological (hair loss, skin rashes).
These clusters may carry a significant weight for society. Indeed, a pessimistic view argues that PACS may occur on a scale large enough to overwhelm the existing health care capacity and generate a ‖hidden public health disaster‖ .
Multiple simultaneously interacting and opposing factors are involved in the pathogenesis of PACS orchestrated in a delicate balance of pro- and anti-inflammatory responses . Although few biomarkers, mainly represented by cytokine signaling (the so-called cytokine storm), have been useful to predict outcome during severe COVID-19 pneumonia, in the post-acute phase the utility of these biomarkers is less clear.
A complex interplay of persistent inflammation, immunosuppression, and high catabolism may identify a set of immune-metabolic biomarkers associated with PACS .
Non-alcoholic fatty liver disease (NAFLD) has being classically described as a barometer of metabolic health [13,14] and carries a high risk of cardiovascular complications and mortality. Metabolic (dysfunction)-associated fatty liver disease (MAFLD), a recently proposed renaming of this disease state , describes a target organ damage bi-directionally associated with the metabolic syndrome .
Recent studies have proposed that MAFLD is an hepatic manifestation of a multisystem disorder, which is heterogeneous in its underlying causes, presentation, course and outcomes [13,17,18]. For the purpose of this paper, we will refer to MAFLD exclusively.
Numerous reports highlighted the negative impact of obesity, diabetes mellitus and MAFLD on the severity of SARS-CoV-2 infection [19–21]. We explored the prevalence of MAFLD in patients with PACS and its association with other PACS-cluster phenotypes.
We included 235 patients followed at a single university outpatient clinic. The diagnosis of PACS was based on ≥1 cluster of symptoms: respiratory, neurocognitive, musculoskeletal, psychological, sensory, dermatological. The outcome was prevalence of MAFLD detected by transient elastography during the first post-discharge follow-up outpatient visit. The prevalence of MAFLD at the time of hospital admission was calculated retrospectively using the hepatic steatosis index.
Of 235 patients, 162 (69%) were men (median age 61). The prevalence of MAFLD was 55.3% at follow-up and 37.3% on admission (p<0.001). Insulin resistance (OR=1.5, 95%CI: 1.14-1.96), body mass index (OR=1.14, 95%CI: 1.04-1.24), and the metabolic syndrome (OR=2.54, 95%CI: 1.13- 5.68), were independent predictors of MAFLD. The number of PACS clusters was inversely associated with MAFLD (OR=0.86, 95%CI: 0.76-0.97). Thirty-one patients (13.2%) had MAFLD with no other associated PACS clusters. All correlations between MAFLD and other PACS clusters were weak.