AbstractCOVID-19 may primarily cause respiratory symptoms but can lead to long-term effects known as long COVID. COVID-19-induced diabetes mellitus was reported in many patients which shares characteristics of types 1 and 2 (T1DM and T2DM). This study aims to identify and analyze the reported cases of new onset diabetes post-COVID-19 infection. Several databases were used to conduct a comprehensive literature search to target studies reporting cases of T1DM or T2DM post-COVID-19 infection. Screening, data extraction, and cross checking were performed by two independent reviewers. Only 43 studies met our inclusion criteria. Our results revealed that the overall prevalence of new onset diabetes post-COVID-19 was 1.37% with higher prevalence for T2DM (0.84%) as compared to T1DM (0.017%) while the type of diabetes was not reported in 0.51% of the cases. Several risk factors for developing diabetes post-COVID-19 infection were identified including the type of SARS-CoV-2 variant, age, comorbidities and the vaccination status. The direct viral attack of the pancreatic beta cells as well as inflammation and the anti-inflammatory corticosteroids were proposed as possible mechanisms of the COVID-19 induced diabetes. A multidisciplinary approach involving endocrinologists, primary care physicians, and infectious disease specialists should be implemented in the management of post-COVID patients to address both the acute and long-term complications, including metabolic changes and risk of diabetes.

Type 1 diabetes (T1D) is an autoimmune condition affecting approximately 1.5 million children and adolescents worldwide, with an incidence of approximately 2-3% each year and rising. During the recent COVID-19 pandemic, a significant increase in incidence of T1D in children and adolescents was observed in numerous countries worldwide, with an increased number of newly-diagnosed cases presenting with diabetic ketoacidosis. The increased frequency of T1D presenting with diabetic ketoacidosis has been attributed not only to the SARS-CoV-2 virus itself but also to the restrictions imposed by the pandemic. The shift to telemedicine and unwillingness to seek medical care due to fear of infection contributed to delayed diagnosis and more severe disease presentation. Furthermore, the periods of lockdown that were implemented during the pandemic presented multiple challenges for children and adolescents living with T1D and disrupted the management of their condition. Changes in physical activity and diet as well as shortage of medical supplies during that period have been linked to worsening of glycemic control, which were at least partly offset by increased parental involvement and use of telemedicine.

COVID-19 ranges from asymptomatic cases to severe disease with high mortality. Corticosteroids are crucial in treatment, reducing mortality and morbidity. However, the use of corticosteroids poses additional challenges in maintaining glycemic control in COVID-19 patients This study aims to eva-luate the impact of insulin requirement on mortality and morbidity in non-diabetic ICU patients and investigate its correlation with disease severity.

This retrospective cohort study included non-diabetic COVID-19 patients aged ≥ 18 years admitted to the ICU of Prof. Dr. Cemil Taşcıoğlu City Hospital (Turkey) between September 1, 2020, and May 31, 2021. Patients requiring ≥ 24 h of insulin therapy were compared with those who did not need insulin. Data on demographics, severity scores (SOFA, APACHE II, SAPS II), insulin initiation and duration, corticosteroid therapy, mechanical ventilation, antiviral and immunomodulatory treatments, laboratory markers, and infection parameters were analyzed. Mortality and incidence of new-onset diabetes mellitus within the first six months post-discharge were assessed. Statistical analyses were performed using SPSS v22.0, with p < 0.05 considered statistically significant.

Patients with insulin requirements had higher SOFA (p = 0.001), APACHE II (p < 0.001), and SAPS II (p = 0.041) scores, along with increased mechanical ventilation duration (p < 0.001). While corticosteroid type had no effect, > 1 mg/kg/day methylprednisolone or equivalent dexamethasone significantly increased insulin demand (p = 0.002). Among laboratory markers, only peak CRP levels were significantly higher in insulin-requiring patients (p = 0.001). ICU and total hospital stays were significantly longer in the insulin group (p < 0.001). Although in-hospital mortality was similar, 6-month mortality was significantly higher in insulin-requiring patients (p = 0.022). New-onset DM rates were 4.2% in the non-insulin group vs. 31.1% in the insulin group (p = 0.001).

Insulin requirement in non-diabetic COVID-19 ICU patients is a predictor of 6-month mortality. High-dose corticosteroids exacerbate glycemic dysregulation, increasing insulin needs. SARS-CoV-2-induced beta-cell damage and hyperinflammation-related stress hyperglycemia elevate the risk of post-discharge DM. Close monitoring and diabetes screening are essential in this population.

Background Despite being typically a viral respiratory disease, COVID-19 has harmful effects that go beyond the respiratory system. The endocrine system is particularly susceptible to damage due to the high expression of angiotensin-converting enzyme-2 receptors. This study evaluates glycemic status in survivors of COVID-19. Methodology In this prospective, observational study, 96 individuals were enrolled from the COVID-19 unit of Bangabandhu Sheikh Mujib Medical University (BSMMU). Mild and moderate COVID-19 patients were classified as non-severe, whereas severe and critical cases were classified as severe, following the WHO disease severity classification. Follow-ups were conducted at the post-COVID-19 clinic at BSMMU one and six months after diagnosis. Blood samples for fasting blood sugar and glycated hemoglobin measurements were collected within 24 hours of initial diagnosis and during each follow-up at the first and sixth months. Results Of the 96 participants, the non-severe and severe groups consisted of 49 (51%) and 47 (49%) participants, respectively. Among the participants, 62 (63.9%) were men, the mean age was 54.2 (15.9) years, and hypertension was the most common comorbidity (37, 38.5%). After six months, 12 new cases of diabetes (15.4%) were observed, with a male predominance (10, 62%). After adjusting for potential confounders, we found that severe COVID-19 was substantially linked to a higher risk of diabetes at six months (odds ratio = 5.5, 95% confidence interval, 1.1-27.7, p = 0.03). Conclusions The study findings showed a significant association between a higher frequency of diabetes and severe COVID-19.

Acute pancreatitis (AP) is a major health threat, with a high mortality rate in severe forms. Though alcohol and bile-induced factors are the most common causes, increasing evidence suggests that viral infections such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and human immunodeficiency virus (HIV) may also trigger AP development. Our study aims to explore this association in greater detail.

After the PROSPERO registration, we systematically searched PubMed, Embase, Cochrane Library, China Science and Technology Journal Database, China National Knowledge Infrastructure, and Wanfang Data Knowledge Service Platform in February 2023. We included studies with the following PECO framework: Population: AP patients, Exposure/Comparison: with/without virus infection, Outcome: mortality, severity, and complications of AP. Pooled odds ratios (OR) were calculated with 95 % confidence intervals (CIs).

Altogether, 29 cohorts with 2,295,172 patients were identified for the meta-analysis and 858 cases for the qualitative synthesis. Patients with concurrent SARS-CoV-2 infection and AP exhibited heightened odds of in-hospital mortality (OR: 3.15, CI: 2.08-4.76), and necrosis (OR: 1.83, CI: 1.13-2.97). Mild AP was less prevalent in the SARS-CoV-2 group (OR: 0.37, CI: 0.14-0.97) compared to moderately severe and severe AP together. Contrarily, no evidence was found that concomitant HIV infection elevated in-hospital mortality (OR: 1.12, CI: 0.92-1.37) or sepsis occurrence (OR:1.21, CI: 0.41-3.59).

Patients co-diagnosed with AP and SARS-CoV-2 infection require heightened attention due to an increased risk of mortality and complications. No evidence was found that HIV infection elevated the risk of a more severe outcome.

To improve medical care and rehabilitation algorithms for patients affected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), it is important to evaluate and summarize the available data on the effect of coronavirus infection (COVID-19) on the endocrine system. The purpose of this review was to study the effect of COVID-19 on the endocrine system. The scientific novelty of this study is the evaluation of the effect of coronavirus infection on the endocrine system and the potential effect of hormones on susceptibility to COVID-19. The results of this review show that the endocrine system is vulnerable to disorders caused by COVID-19, mainly thyroid dysfunction and hyperglycemia. The information in the published literature mentioned here contains some unclear aspects and contradictory data, but much remains to be studied and clarified regarding the impact of COVID-19 on the endocrine system. In particular, this concerns the study of the hyperglycemic status of patients who have had coronavirus infection, which is extremely important for the future metabolic health of COVID-19 survivors. This review contributes to the scientific discourse by systematically synthesizing disparate studies to identify patterns, gaps, and emerging trends in the literature concerning the effects of COVID-19 on the endocrine system. By integrating these findings, this study offers a novel perspective on potential hormonal interactions influencing COVID-19 susceptibility and outcomes, proposing new hypotheses and frameworks for future research.

Propofol, a commonly used agent for short- and long-term sedation, is associated with acute pancreatitis. The main indirect mechanism of propofol-associated acute pancreatitis is by inducing hypertriglyceridemia. Patients with severe coronavirus disease 2019 (COVID-19) pneumonia often require prolonged mechanical ventilation and sedation. We examined the incidence rate of acute pancreatitis among critically ill adults with COVID-19 pneumonia on mechanical ventilation receiving propofol. In addition, we attempted to determine cutoff levels of serum triglycerides and doses of propofol that are predictive of propofol-associated acute pancreatitis.

This was a multicenter retrospective cohort study using a large dataset of hospitalized patients with COVID-19. The collected data included the number of days on propofol, cumulative doses of propofol, peak levels of serum triglycerides, serum lipase levels, and abdominal imaging findings. We used receiver-operating characteristic analysis in conjunction with Youden's index to identify the optimal thresholds for propofol administration parameters and levels of triglycerides that would provide maximal sensitivity and specificity for predicting acute pancreatitis.

Out of 499 critically ill patients with COVID-19 pneumonia, 154 met the inclusion criteria. Six (4%) patients had suspected acute pancreatitis based on elevated serum lipase levels. Cutoff values greater than 688 mg/dL for peak level of triglycerides, 4.5 days on propofol, 3007 mg/day for average daily propofol dose, and 24 113 mg for cumulative propofol dose were associated with high risk of suspected acute pancreatitis. The negative predictive values for suspected acute pancreatitis using these cutoffs ranged from 98% to 100%.

Propofol use in critically ill COVID-19 patients is associated with a low incidence rate of acute pancreatitis. We identified cutoff values for serum triglycerides and cumulative propofol dose that are linked to higher risk of propofol-associated pancreatitis. More research is needed to examine the true incidence of propofol-associated pancreatitis and help develop optimal cutoff values for certain parameters to help guide safe propofol administration.

Bakground: The mortality rate from community-acquired pneumonia (CAP) or coronavirus disease 19 (COVID-19) is high, especially in hospitalized patients. This study aimed to assess the disturbances of glucose and lipid metabolism with in-hospital complications and short-term outcomes for patients with pneumonia with different etiologies. Methods: This observational study comprised 398 patients divided as follows: 155 with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pneumonia, 129 participants with viral CAP, and 114 with bacterial pneumonia. Results: Fasting plasma glucose (FPG) at admission and glycemic variation during hospitalization was linked with acute kidney injury (AKI) in bacterial CAP. Compared with a value <110 mg/dL for FPG at admission, levels between 110 and 126 mg/dL are associated with mortality in both COVID-19 (OR = 3.462, 95% CI: 1.275-9.398, p = 0.015) and bacterial CAP participants (OR = 0.254; 95% CI: 0.069-0.935, p = 0.039), while a value ≥126 mg/dL was linked with mortality only in patients with SARS-CoV-2 (OR = 3.577, 95% CI: 1.166-10.976, p = 0.026). No relation between lipid biomarkers and complications or in-hospital outcomes was observed in all three participant groups. Conclusions: Patients with bacterial CAP are more prone to developing AKI due to increased FBG at admission and glycemic variations during hospitalization, while elevated FBG values at admission are associated with mortality in both COVID-19 and bacterial CAP.

The pandemic COVID-19 (coronavirus disease 2019) is caused by the severe acute respiratory syndrome corona virus 2 (SARS-CoV-2), which devastated the global economy and healthcare system. The infection caused an unforeseen rise in COVID-19 patients and increased the mortality rate globally. This study gives an overall idea about host-pathogen interaction, immune responses to COVID-19, recovery status of infection, targeted organs and complications associated, and comparison of post-infection immunity in convalescent subjects and non-infected individuals. The emergence of the variants and episodes of COVID-19 infections made the situation worsen. The timely introduction of vaccines and precautionary measures helped control the infection's severity. Later, the population that recovered from COVID-19 grew significantly. However, understanding the impact of healthcare issues resulting after infection is paramount for improving an individual's health status. It is now recognised that COVID-19 infection affects multiple organs and exhibits a broad range of clinical manifestations. So, post COVID-19 infection creates a high risk in individuals with already prevailing health complications. The identification of post-COVID-19-related health issues and their appropriate management is of greater importance to improving patient's quality of life. The persistence, sequelae and other medical complications that normally last from weeks to months after the recovery of the initial infection are involved with COVID-19. A multi-disciplinary approach is necessary for the development of preventive measures, techniques for rehabilitation and strategies for clinical management when it comes to long-term care.

The novel coronavirus strain SARS-CoV-2 triggered the COVID-19 pandemic with severe economic and social ramifications. As the pathophysiology of SARS-CoV-2 infection in the respiratory system becomes more understood, growing evidence suggests that the virus also impacts the homeostasis-regulating neuroendocrine system, potentially affecting other organ systems.

This review explores the interactions between SARS-CoV-2 and the neuroendocrine system, highlighting the effect of this virus on various endocrine glands, including the brain, hypothalamus, pituitary, pineal, thyroid, parathyroid, adrenal glands, pancreatic islets, gonads, and adipose tissue. The viral invasion disrupts normal hormonal pathways, leading to a range of endocrine disorders, immune dysregulation, and metabolic disturbances.

There is potential for SARS-CoV-2 to induce autoimmune responses, exacerbate existing endocrine conditions, and trigger new-onset disorders. Understanding these interactions is crucial for developing treatment strategies that address not only the respiratory symptoms of COVID-19 but also its endocrine complications. The review emphasizes the need for further research to elucidate the long-term effects of SARS-CoV-2 on endocrine health.

Environmental factors, in particular viral infections, are thought to have an important role in the pathogenesis of type 1 diabetes mellitus (T1DM). The COVID-19 pandemic reinforced this hypothesis as many observational studies and meta-analyses reported a notable increase in the incidence of T1DM following infection with SARS-CoV-2 as well as an association between SARS-CoV-2 infection and the risk of new-onset T1DM. Experimental evidence suggests that human β-cells express SARS-CoV-2 receptors and that SARS-CoV-2 can infect and replicate in β-cells, resulting in structural or functional alterations of these cells. These alterations include reduced numbers of insulin-secreting granules, impaired pro-insulin (or insulin) secretion, and β-cell transdifferentiation or dedifferentiation. The inflammatory environment induced by local or systemic SARS-CoV-2 infection might result in a set of signals (such as pro-inflammatory cytokines) that lead to β-cell alteration or apoptosis or to a bystander activation of T cells and disruption of peripheral tolerance that triggers autoimmunity. Other mechanisms, such as viral persistence, molecular mimicry and activation of endogenous human retroviruses, are also likely to be involved in the pathogenesis of T1DM following SARS-CoV-2 infection. This Review addresses the issue of the involvement of SARS-CoV-2 infection in the development of T1DM using evidence from epidemiological, clinical and experimental studies.

Cardiovascular disease (CVD) and cardiometabolic risk (CMR) are highly prevalent globally. The interplay between CVD/CMR and COVID-19 morbidity and mortality has been intensely studied over the last three years and has yielded some important discoveries and warnings for public health. Despite many advances in cardiovascular medicine, CVD continues to be the global leading cause of death. Much of this disease burden results from high CMR imposed by behaviors centered around poor nutrition related to lifestyle choices and systemic constraints. Increased CVD/CMR contributed to the COVID-19 pandemic's unprecedented wave of disability and death, and the current state of cardiovascular health been equated to a "Population Code Blue." There is an urgent and unmet need to reorient our priorities towards health promotion and disease prevention. This manuscript will review how nutrition and lifestyle affect outcomes in COVID-19 and how some interventions and healthy lifestyle choices can markedly reduce disease burden, morbidity, and mortality.

The objective of this study was to assess overall and segmented trends in the incidence of type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) in children and adolescents younger than 20 years, from 2002 to 2022.

This study used registry data on physician-diagnosed T1DM or T2DM from primary and secondary sources, covering the German federal state of North Rhine-Westphalia with 18 million inhabitants. The ages at T1DM and T2DM onset ranged from 0 to 19 and 10-19 years, respectively. The main outcomes were direct age- and/or sex-standardized incidence rates per 100,000 person-years (PYs) and trends estimated as annual percentage changes (APCs), both with 95 % confidence intervals. The segmented trends for subperiods were based on joinpoint regression models.

From 2002-2022, 17,470 and 819 persons had incident T1DM and T2DM, respectively. The total number of PYs was 73,743,982 for T1DM and 39,210,453 for T2DM, with a mean coverage rate of 98 % for T1DM and 90 % for T2DM. The standardized T1DM incidence increased from 17.6 [16.3;18.9} in 2002 to 33.2 [31.3;35.1] in 2022, with an APC of 2.7 % [2.3 %;3.1 %]. The standardized T2DM incidence increased from 1.3 [0.8;1.7] in 2002 to 2.8 [2.0;3.6] in 2022, with an APC of 6.4 % [4.9 %;8.0 %]. There were four different segmented trends for T1DM and T2DM, with the incidence peaking in 2021 and subsequently declining.

The incidence rates of T1DM and T2DM have increased over the past 20 years, with a wave-like pattern during the Covid-19 pandemic.

As the world population recovers from the COVID-19 infection, a series of acute sequelae emerge including new incident diabetes. However, the association between COVID-19 infection and new incident diabetes is not fully understood. We purpose to determine the risk of new incident diabetes after COVID-19 infection.

PubMed, Embase, and Cochrane Library were used as databases to search for cohort studies published from database inception to February 4, 2024. Two reviewers independently conducted the study screening, data extraction, and risk of bias assessment. A random-effects model was adopted to pool the hazard ratio (HR) with corresponding 95% confidence intervals (CI). Subgroup analysis was conducted to explore the potential influencing factors.

A total of 20 cohort studies with over 60 million individuals were included. The pooling analysis illustrates the association between COVID-19 infection and an increased risk of new incident diabetes (HR = 1.46; 95% CI: 1.38-1.55). In subgroup analysis, the risk of type 1 diabetes was HR=1.44 (95% CI: 1.13-1.82), and type 2 diabetes was HR=1.47 (95% CI: 1.36-1.59). A slightly higher risk of diabetes was found in males (HR=1.37; 95% CI: 1.30-1.45) than in females (HR=1.29; 95% CI: 1.22-1.365). The risk of incident diabetes is associated with hospitalization: non-hospitalized patients have an HR of 1.16 (95% CI: 1.07-1.26), normal hospitalized patients have an HR of 2.15 (95% CI: 1.33-3.49), and patients receiving intensive care have the highest HR of 2.88 (95% CI: 1.73-4.79).

COVID-19 infection is associated with an elevated risk of new incident diabetes. Patients ever infected with COVID-19 should be recognized as a high-risk population with diabetes.

https://www.crd.york.ac.uk/prospero, identifier CRD42024522050.

Viral respiratory infections may precipitate type 1 diabetes (T1D). A possible association between the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for COVID-19, and the incidence of T1D is being determined. This study was carried out using Portuguese registries, aiming at examining temporal trends between COVID-19 and T1D.

Hospital data, comparing the incidence before and during the COVID-19 pandemic, from children and young adults diagnosed with new-onset T1D, was acquired beginning in 2017 and until the end of 2022. Data was obtained from nine different Portuguese hospital units. The impact of the COVID-19 pandemic, beginning in March 2020, was assessed comparing the annual numbers of new-onset T1D cases. The annual median levels of glucose, glycated hemoglobin (HbA1c) and fasting C-peptide at T1D diagnosis were compared. The annual number of diabetic ketoacidosis (DKA) episodes among new T1D cases was also assessed at two centers.

In total, data from 574 newly diagnosed T1D patients was analyzed, including 530 (92.3%) children. The mean ages for child and adult patients were 9.1 (SD 4.4) and 32.8 (SD 13.6) years, respectively. 57.8% (331/573) were male, one patient had unknown sex. The overall median (25-75 percentiles) levels of glucose, HbA1c and fasting C-peptide at diagnosis were 454 mg/dL (356-568), 11.8% (10.1-13.4) and 0.50 µg/L (0.30-0.79), respectively. DKA at T1D diagnosis was present in 48.4% (76/157). For eight centers with complete 2018 to 2021 data (all calendar months), no overall significant increase in T1D cases was observed during the COVID-19 pandemic, i.e. 90 cases in 2018, 90 cases in 2019, 112 in 2020 and 100 in 2021 (P for trend = 0.36). Two of the centers, Faro (CHUA) and Dona Estefânia (CHULC) hospitals, did however see an increase in T1D from 2019 to 2020. No significant changes in glucose (P = 0.32), HbA1c (P = 0.68), fasting C-peptide (P = 0.20) or DKA frequency (P = 0.68) at the time of T1D diagnosis were observed over the entire study period.

The T1D incidence did not increase significantly, when comparing the years before and during the COVID-19 pandemic, nor did key metabolic parameters or number of DKA episodes change.

The COVID-19 pandemic has revealed a bidirectional relationship between SARS-CoV-2 infection and diabetes mellitus. Existing evidence strongly suggests hyperglycemia as an independent risk factor for severe COVID-19, resulting in increased morbidity and mortality. Conversely, recent studies have reported new-onset diabetes following SARS-CoV-2 infection, hinting at a potential direct viral attack on pancreatic beta cells. In this review, we explore how hyperglycemia, a hallmark of diabetes, might influence SARS-CoV-2 entry and accessory proteins in pancreatic β-cells. We examine how the virus may enter and manipulate such cells, focusing on the role of the spike protein and its interaction with host receptors. Additionally, we analyze potential effects on endosomal processing and accessory proteins involved in viral infection. Our analysis suggests a complex interplay between hyperglycemia and SARS-CoV-2 in pancreatic β-cells. Understanding these mechanisms may help unlock urgent therapeutic strategies to mitigate the detrimental effects of COVID-19 in diabetic patients and unveil if the virus itself can trigger diabetes onset.

Investigate the effect of long-term COVID-19 on maternal and fetal complications. A retrospective cohort study was conducted. A total of 623 pregnant women who delivered in Kunming First People's Hospital from November 1, 2022 to July 31, 2023 were selected. By employing statistical methods, we compared the associations between maternal and fetal complications in pregnant women with acute COVID-19 during pregnancy, long-term COVID-19, and non-COVID-19 pregnant women. In the final 623 samples, there were 209 pregnant women with acute COVID-19, 72 pregnant women with long-term COVID-19, and 342 pregnant women without COVID-19. The epidemiological and clinical characteristics of all subjects were similar. Pregnant individuals who developed long-term COVID-19 during their pregnancy had an increased risk of experiencing gestational hypertension (OR 3.344, 95% CI 1.544-7.243), gestational diabetes mellitus (OR 2.301, 95% CI 1.290-4.102), and fetal intrauterine growth restriction (OR 2.817, 95% CI 1.385-5.952). Multivariate binary logistic regression analysis showed that this association remained consistent even after adjusting for confounders and performing subgroup analyses. Other maternal and fetal complications, such as premature rupture of membranes, preterm delivery, neonatal asphyxia, and transfer of neonates to NICU, did not exhibit statistically significant associations. After linear regression analysis, the platelet count (β: - 0.127, 95% CI - 0.001-0.000) of pregnant women with long-term COVID-19 was slightly lower than that of non-COVID-19 pregnant women, and the other coagulation parameters were not statistically significant. The incidence of gestational hypertension, gestational diabetes mellitus and fetal intrauterine growth restriction in pregnant women with long-term COVID-19 is significantly increased, but it does not further increase the coagulation status.

The interrelation between COVID-19 and various cardiovascular and metabolic disorders has been a critical area of study. There is a growing need to understand how comorbidities such as cardiovascular diseases (CVDs) and metabolic disorders affect the risk and severity of COVID-19.

The objective of this study is to systematically analyze the association between COVID-19 and cardiovascular and metabolic disorders. The focus is on comorbidity, examining the roles of CVDs such as embolism, thrombosis, hypertension, and heart failure, as well as metabolic disorders such as disorders of glucose and iron metabolism.

Our study involved a systematic search in PubMed for literature published from 2000 to 2022. We established 2 databases: one for COVID-19-related articles and another for CVD-related articles, ensuring all were peer-reviewed. In terms of data analysis, statistical methods were applied to compare the frequency and relevance of MeSH (Medical Subject Headings) terms between the 2 databases. This involved analyzing the differences and ratios in the usage of these terms and employing statistical tests to determine their significance in relation to key CVDs within the COVID-19 research context.

The study revealed that "Cardiovascular Diseases" and "Nutritional and Metabolic Diseases" were highly relevant as level 1 Medical Subject Headings descriptors in COVID-19 comorbidity research. Detailed analysis at level 2 and level 3 showed "Vascular Disease" and "Heart Disease" as prominent descriptors under CVDs. Significantly, "Glucose Metabolism Disorders" were frequently associated with COVID-19 comorbidities such as embolism, thrombosis, and heart failure. Furthermore, iron deficiency (ID) was notably different in its occurrence between COVID-19 and CVD articles, underlining its significance in the context of COVID-19 comorbidities. Statistical analysis underscored these differences, highlighting the importance of both glucose and iron metabolism disorders in COVID-19 research.

This work lays the foundation for future research that utilizes a knowledge-based approach to elucidate the intricate relationships between these conditions, aiming to develop more effective health care strategies and interventions in the face of ongoing pandemic challenges.

Diabetes mellitus (DM) is comprised of two predominant subtypes: type 1 diabetes mellitus (T1DM), accounting for approximately 5 % of cases worldwide and resulting from autoimmune destruction of insulin-producing β-cells, and type 2 (T2DM), accounting for approximately 95 % of cases globally and characterized by the inability of pancreatic β-cells to meet the demand for insulin due to a relative β-cell deficit in the setting of peripheral insulin resistance. Both types of DM involve derangement of glucose metabolism and are metabolic diseases generally considered to be initiated by a combination of genetic and environmental factors. Viruses have been reported to play a role as infectious etiological factors in the initiation of both types of DM in predisposed individuals. Among the reported viral infections causing DM in humans, the most studied include coxsackie B virus, cytomegalovirus and hepatitis C virus. The recent COVID-19 pandemic has highlighted the diabetogenic potential of SARS-CoV-2, rekindling interest in the field of virus-induced diabetes (VID). This review discusses the reported mechanisms of viral-induced DM, addressing emerging concepts in VID, as well as highlighting areas where knowledge is lacking, and further investigation is warranted.

The recent coronavirus disease 2019 (COVID-19) pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spurred intense research efforts to develop new materials with antiviral activity. In this study, we genetically engineered amyloid-based nanofibrils for capturing and neutralizing SARS-CoV-2. Building upon the amyloid properties of a short Sup35 yeast prion sequence, we fused it to SARS-CoV-2 receptor-binding domain (RBD) capturing proteins, LCB1 and LCB3. By tuning the reaction conditions, we achieved the spontaneous self-assembly of the Sup35-LCB1 fusion protein into a highly homogeneous and well-dispersed amyloid-like fibrillar material. These nanofibrils exhibited high affinity for the SARS-CoV-2 RBD, effectively inhibiting its interaction with the angiotensin-converting enzyme 2 (ACE2) receptor, the primary entry point for the virus into host cells. We further demonstrate that this functional nanomaterial entraps and neutralizes SARS-CoV-2 virus-like particles (VLPs), with a potency comparable to that of therapeutic antibodies. As a proof of concept, we successfully fabricated patterned surfaces that selectively capture SARS-CoV-2 RBD protein on wet environments. Collectively, these findings suggest that these protein-only nanofibrils hold promise as disinfecting coatings endowed with selective SARS-CoV-2 neutralizing properties to combat viral spread or in the development of sensitive viral sampling and diagnostic tools.

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease. Previous studies have primarily focused on the epidemiological and clinical characteristics of patients with SFTS, whereas pancreatic injury has received little attention. This study investigated the effects of pancreatic injury on the prognosis of patients with SFTS. A total of 156 patients diagnosed with SFTS between April 2016 and April 2022 were included in the analysis. Multivariate logistic regression analysis showed that pancreatic injury (odds ratio [OR] = 3.754, 95% confidence interval [CI]: 1.361-79.036, P = 0.024) and neurological symptoms (OR = 18.648, 95% CI: 4.921-70.668, P < 0.001) were independent risk factors for mortality. The receiver operating characteristic curve indicated that serum pancreatic enzymes were predictive of progression to death in patients with SFTS. The area under the curve (AUC) for amylase was 0.711, with an optimal cutoff value of 95.5 U/L, sensitivity of 96.4%, and specificity of 35.9%. Lipase had an AUC of 0.754, an optimal cutoff value of 354.75 U/L, sensitivity of 75%, and specificity of 67.2%. Thus, pancreatic injury was associated with a poor prognosis of SFTS and can be used as an important reference for SFTS determination and prognostic assessment.

Introduction: Although it has been observed that the triglycerides and glucose (TyG) index, a biomarker of insulin resistance, is associated with severity and morbidity by COVID-19, evidence is still scarce. Therefore, the objective of this study was to determine whether the TyG index is associated with both the degree of severity and mortality by acute respiratory distress syndrome (ARDS) in patients with COVID-19. Methods: Men and women aged 20 years or more with diagnosis of COVID-19 were included in a case-control study. Exclusion criteria were pregnancy, cancer, autoimmune diseases, autoimmune treatment, and incomplete data. Patients with severe COVID-19 ARDS were allocated into the case group, and those with mild or moderate COVID-19 ARDS in the control group. COVID-19 was defined by a positive reverse transcriptase-polymerase chain reaction test for SARS-CoV-2, and ARDS was defined according to the Berlin criteria. Results: A total of 206 patients were included and allocated into the case (n = 103) and control (n = 103) groups. The logistic regression analysis adjusted by age, sex, and body mass index showed that the TyG index is significantly associated with moderate [odds ratio (OR) = 6.0; 95% confidence interval (CI): 1.1-30.6] and severe (OR = 9.5; 95% CI: 2.4-37.5) COVID-19 ARDS, and death (OR = 10.1; 95% CI: 2.2-46.5). Conclusion: The results of our study show a significant and independent association of the TyG index with ARDS and mortality in patients with COVID-19.

Despite evidence demonstrating the risks of developing diabetes mellitus because of SARS-CoV-2, there is, however, insufficient scientific data available to elucidate the relationship between diabetes mellitus and COVID-19. Research indicates that SARS-CoV-2 infection is associated with persistent damage to organ systems due to the systemic inflammatory response. Since COVID-19 is known to induce these conditions, further investigation is necessary to fully understand its long-term effects on human health. Consequently, it is essential to consider the effect of the COVID-19 pandemic when predicting the prevalence of diabetes mellitus in the future, especially since the incidence of diabetes mellitus was already on the rise before the pandemic. Additional research is required to fully comprehend the impact of SARS-CoV-2 infection on glucose tolerance and insulin sensitivity. Therefore, this article delves deeper into the current literature and links the perceived relationship between SARS-CoV-2 and diabetes. In addition, the article highlights the necessity for further research to fully grasp the mechanisms that SARS-CoV-2 utilises to induce new-onset diabetes. Where understanding and consensus are reached, therapeutic interventions to prevent the onset of diabetes could be proposed. Lastly, we propose advocating for the regular screening of diabetes and pre-diabetes, particularly for the high-risk population with a history of COVID-19 infection.

Obesity, diabetes mellitus (mostly type 2), and COVID-19 show mutual interactions because they are not only risk factors for both acute and chronic COVID-19 manifestations, but also because COVID-19 alters energy metabolism. Such metabolic alterations can lead to dysglycemia and long-lasting effects. Thus, the COVID-19 pandemic has the potential for a further rise of the diabetes pandemic. This review outlines how preexisting metabolic alterations spanning from excess visceral adipose tissue to hyperglycemia and overt diabetes may exacerbate COVID-19 severity. We also summarize the different effects of SARS-CoV-2 infection on the key organs and tissues orchestrating energy metabolism, including adipose tissue, liver, skeletal muscle, and pancreas. Last, we provide an integrative view of the metabolic derangements that occur during COVID-19. Altogether, this review allows for better understanding of the metabolic derangements occurring when a fire starts from a small flame, and thereby help reducing the impact of the COVID-19 pandemic.

Estimated age-adjusted comparative diabetes prevalence in adults (20-79 years) in Pakistan from the year 2011 to 2021.

As an increased body of COVID-19 related research is now available, it becomes apparent that the effects of COVID-19 extend beyond that of the respiratory system. Among others, the endocrine system is particularly vulnerable to perturbation from the COVID-19 infection. The present scoping review summarizes the bidirectional relationship between COVID-19 and endocrine system in children and adolescents, by describing both the possible susceptibility of children and adolescents without endocrinopathies to endocrine disorders following COVID-19 infection, but also the potential susceptibility to COVID-19 infection and severe infection, or the aggravation of endocrine dysfunction in patients with pre-existing endocrine diseases. Data suggest increased obesity and diabetes rates, as well as increased severity and frequency of diabetic ketoacidosis following COVID-19 infection. Conversely, patients with diabetes and obesity may experience a more severe course of COVID-19 infection. However, in the majority of cases, children and adolescents with well-managed and regulated endocrine disorders do not appear to be at increased risk of infection or severe infection from COVID-19. Thus, adhering to the appropriate "sick day management rules", maintaining adequate supply of medications and supplies, keeping close contact with the therapeutic team and seeking medical help without delay when needed, are the main recommendations for a safe outcome. Additional lessons learnt during the pandemic include the risk for mental health diseases caused by children's disrupted routine due to COVID-19 related protective measures and the importance of adopting alternative communication options, such as telehealth visits, in order to ensure uninterrupted endocrine care.

SARS-CoV-2 causes varied gastrointestinal symptoms. Cirrhosis patients face higher mortality rates from it, especially those with decompensated cirrhosis. This study examines SARS-CoV-2's impact on decompensation in previously compensated cirrhotic patients.

We analyzed the Global Collaborative Network, comprising 98 healthcare organizations across sixteen countries, using TriNetX's deidentified research database. Compensated cirrhosis patients were split into two groups: one with SARS-CoV-2-positive patients and another testing negative. Using a 1:1 propensity score matching model based on baseline characteristics and comorbidities, we created comparable cohorts. We then assessed decompensation, mortality, and GI bleed at 1 and 3 months.

Out of 252,631 identified compensated cirrhosis patients, 27.3% (69,057) tested SARS-CoV-2-positive, while 72.6% (183,574) remained negative. Post PSM, 61,963 patients were in each group. SARS-CoV-2-positive patients showed significantly higher decompensation rates (4.4% vs. 1.9% at 1 month; 6% vs. 2.6% overall). Rates of complications, like ascites, SBP, HE, and HRS, increased notably. Mortality (2.5% vs. 1.7% at 1 month; 3.6% vs. 2.7% at 3 months) and GI bleed (1.3% vs. 0.9% at 1 month; 1.9% vs. 1.2% at 3 months) were also elevated in SARS-CoV-2 patients.

SARS-CoV-2 increases decompensation over 2-fold in compensated cirrhosis patients and raises mortality and increases rates of complications at 1 and 3 months.

Early since the onset of the COVID-19 pandemic, the medical and scientific community were aware of extra respiratory actions of SARS-CoV-2 infection. Endothelitis, hypercoagulation, and hypofibrinolysis were identified in COVID-19 patients as subsequent responses of endothelial dysfunction. Activation of the endothelial barrier may increase the severity of the disease and contribute to long-COVID syndrome and post-COVID sequelae. Besides, it may cause alterations in primary, secondary, and tertiary hemostasis. Importantly, these responses have been highly decisive in the evolution of infected patients also diagnosed with diabetes mellitus (DM), who showed previous endothelial dysfunction. In this review, we provide an overview of the potential triggers of endothelial activation related to COVID-19 and COVID-19 under diabetic milieu. Several mechanisms are induced by both the viral particle itself and by the subsequent immune-defensive response (i.e., NF-κB/NLRP3 inflammasome pathway, vasoactive peptides, cytokine storm, NETosis, activation of the complement system). Alterations in coagulation mediators such as factor VIII, fibrin, tissue factor, the von Willebrand factor: ADAMST-13 ratio, and the kallikrein-kinin or plasminogen-plasmin systems have been reported. Moreover, an imbalance of thrombotic and thrombolytic (tPA, PAI-I, fibrinogen) factors favors hypercoagulation and hypofibrinolysis. In the context of DM, these mechanisms can be exacerbated leading to higher loss of hemostasis. However, a series of therapeutic strategies targeting the activated endothelium such as specific antibodies or inhibitors against thrombin, key cytokines, factor X, complement system, the kallikrein-kinin system or NETosis, might represent new opportunities to address this hypercoagulable state present in COVID-19 and DM. Antidiabetics may also ameliorate endothelial dysfunction, inflammation, and platelet aggregation. By improving the microvascular pathology in COVID-19 and post-COVID subjects, the associated comorbidities and the risk of mortality could be reduced.

Coronavirus disease 2019 (COVID-19) caused a severe epidemic due to severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Recent studies have found that patients do not completely recover from acute infections, but instead, suffer from a variety of post-acute sequelae of SARS-CoV-2 infection, known as long COVID. The effects of long COVID can be far-reaching, with a duration of up to six months and a range of symptoms such as cognitive dysfunction, immune dysregulation, microbiota dysbiosis, myalgic encephalomyelitis/chronic fatigue syndrome, myocarditis, pulmonary fibrosis, cough, diabetes, pain, reproductive dysfunction, and thrombus formation. However, recent studies have shown that naringenin and naringin have palliative effects on various COVID-19 sequelae. Flavonoids such as naringin and naringenin, commonly found in fruits and vegetables, have various positive effects, including reducing inflammation, preventing viral infections, and providing antioxidants. This article discusses the molecular mechanisms and clinical effects of naringin and naringenin on treating the above diseases. It proposes them as potential drugs for the treatment of long COVID, and it can be inferred that naringin and naringenin exhibit potential as extended long COVID medications, in the future likely serving as nutraceuticals or clinical supplements for the comprehensive alleviation of the various manifestations of COVID-19 complications.

Diagnosis and management of type 1 diabetes (T1D) have remained largely unchanged for the last several years. The management of the disease remains primarily focused on its phenotypical presentation and less on endotypes, namely the specific biological mechanisms behind the development of the disease. Furthermore, the treatment of T1D is essentially universal and indiscriminate-with patients administering insulin at varying dosages and frequencies to maintain adequate glycaemic control. However, it is now well understood that T1D is a heterogeneous disease with many different biological mechanisms (i.e. endotypes) behind its complex pathophysiology. A range of factors, including age of onset, immune system regulation, rate of β-cell destruction, autoantibodies, body weight, genetics and the exposome are recognised to play a role in the development of the condition. Patients can be classified into distinct diabetic subtypes based on these factors, which can be used to categorise patients into specific endotypes. The classification of patients into endotypes allows for a greater understanding of the natural progression of the disease, giving rise to more accurate and patient-centred therapies and follow-up monitoring, specifically for other autoimmune diseases. This review proposes 6 unique endotypes of T1D based on the current literature. The recognition of these endotypes could then be used to direct therapeutic modalities based on patients' individual pathophysiology.

Throughout the COVID-19 pandemic, there has been a notable increase in the incidence of new-onset diabetes and diabetic ketoacidosis (DKA). Simultaneously, children diagnosed with type 1 diabetes (T1D) have encountered difficulties in maintaining optimal blood glucose levels. The mechanisms underpinning these correlations still remain a puzzle. We reviewed the studies that examined changes in incidence during the pandemic. These studies utilized various metrics for comparison, which encompassed the timing of data collection, diagnostic criteria, as well as the numbers and incidence rates of diabetes and DKA. We found the incidence of diabetes and DKA was higher during the pandemic. As to mechanisms, the invivo and invitro study revealed the factors such as direct viral damage, metabolic dysfunction, and immune responses all attribute to the process of T1D after suffering from COVID-19. Furthermore, we provide some useful strategies to prevent and treat children suffering from diabetes and COVID-19.

Strong correlations have been observed between new-onset diabetes and COVID-19. Insights gleaned from clinical descriptions and basic research can offer valuable experience and recommendations for the treatment and prevention of diabetes during future pandemics.

The novel disease produced by SARS-CoV-2 mainly harms the respiratory tract, but it has shown the capacity to affect multiple organs. Epidemiologic evidence supports the relationship between Coronavirus Disease 2019 (COVID-19) and pancreatic and hepatic injury development, identified by alterations in these organ function markers. In this regard, it is important to ascertain how the current prevalence of non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) might affect COVID-19 evolution and complications. Although it is not clear how SARS-CoV-2 affects both the pancreas and the liver, a multiplicity of potential pathophysiological mechanisms seem to be implicated; among them, a direct viral-induced injury to the organ involving liver and pancreas ACE2 expression. Additionally, immune system dysregulation, coagulopathies, and drugs used to treat the disease could be key for developing complications associated with the patient's clinical decline. This review aims to provide an overview of the available epidemiologic evidence regarding developing liver and pancreatic alterations in patients with COVID-19, as well as the possible role that NAFLD/NASH might play in the pathophysiological mechanisms underlying some of the complications associated with COVID-19. This review employed a comprehensive search on PubMed using relevant keywords and filters. From the initial 126 articles, those aligning with the research target were selected and evaluated for their methodologies, findings, and conclusions. It sheds light on the potential pathophysiological mechanisms underlying this relationship. As a result, it emphasises the importance of monitoring pancreatic and hepatic function in individuals affected by COVID-19.

The global pandemic of coronavirus disease 2019 (COVID-19) poses a serious threat to human health, leading to a relatively high mortality in patients with severe or critical conditions in particular. Hyperglycemia is one of the high-risk factors for poor prognosis in these patients. Patients with COVID-19 are more likely to develop hyperglycemia, regardless of whether there is a previous history of diabetes mellitus. Glucocorticoid therapy is an important part of the anti-inflammatory regimen for COVID-19. However, the use of glucocorticoid significantly increases the occurrence of hyperglycemic events in COVID-19 patients, ultimately leading to poor prognosis. Timely monitoring of blood glucose and early intervention for hyperglycemia contribute to the improvement in the outcome of COVID-19 patients. In this paper, we comprehensively reviewed the potential mechanisms of COVID-19 and concomitant hyperglycemia. We reviewed the latest findings on the blood glucose management strategies for COVID-19 patients with concomitant hyperglycemia, aiming to optimize the management of hyperglycemia in COVID-19 patients and improve the outcome of the disease.

In the post-pandemic era, a wide range of COVID-19 sequelae is of growing health concern. However, the risks of digestive diseases in long COVID have not been comprehensively understood. To investigate the long-term risk of digestive diseases among COVID patients.

In this large-scale retrospective cohort study with up to 2.6 years follow-up (median follow-up: 0.7 years), the COVID-19 group (n = 112,311), the contemporary comparison group (n = 359,671) and the historical comparison group (n = 370,979) predated the COVID-19 outbreak were built using UK Biobank database. Each digestive outcome was defined as the diagnosis 30 days or more after the onset of COVID-19 infection or the index date. Hazard ratios (HRs) and corresponding 95% confidence intervals (CI) were computed utilizing the Cox regression models after inverse probability weighting.

Compared with the contemporary comparison group, patients with previous COVID-19 infection had higher risks of digestive diseases, including gastrointestinal (GI) dysfunction (HR 1.38 (95% CI 1.26 to 1.51)); peptic ulcer disease (HR 1.23 (1.00 to 1.52)); gastroesophageal reflux disease (GERD) (HR 1.41 (1.30 to 1.53)); gallbladder disease (HR 1.21 (1.06 to 1.38)); severe liver disease (HR 1.35 (1.03 to 1.76)); non-alcoholic liver disease (HR 1.27 (1.09 to 1.47)); and pancreatic disease (HR 1.36 (1.11 to 1.66)). The risks of GERD were increased stepwise with the severity of the acute phase of COVID-19 infection. Even after 1-year follow-up, GERD (HR 1.64 (1.30 to 2.07)) and GI dysfunction (HR 1.35 (1.04 to 1.75)) continued to pose risks to COVID-19 patients. Compared to those with one SARS-CoV-2 infection, reinfected patients were at a higher risk of pancreatic diseases (HR 2.57 (1.23 to 5.38)). The results were consistent when the historical cohort was used as the comparison group.

Our study provides insights into the association between COVID-19 and the long-term risk of digestive system disorders. COVID-19 patients are at a higher risk of developing digestive diseases. The risks exhibited a stepwise escalation with the severity of COVID-19, were noted in cases of reinfection, and persisted even after 1-year follow-up. This highlights the need to understand the varying risks of digestive outcomes in COVID-19 patients over time, particularly those who experienced reinfection, and develop appropriate follow-up strategies.

COVID-19 emerged in September 2020 as a disease caused by the virus SARS-CoV-2. The disease presented as pneumonia at first but later was shown to cause multisystem infections and long-term complications. Many efforts have been put into discovering the exact pathogenesis of the disease. In this review, we aim to discuss an emerging tool in disease modeling, organoids, in the investigation of COVID-19. This review will introduce some methods and breakthroughs achieved by organoids and the limitations of this system.

The pathogenesis of COVID-19 involves a complex interplay between host factors and the SARS-CoV-2 virus, leading to a multitude of clinical manifestations beyond the respiratory system. This chapter provides an overview of the risk factors, genetic predisposition, and multisystem manifestations of COVID-19, shedding light on the underlying mechanisms that contribute to extrapulmonary manifestations. The chapter discusses the direct invasion of SARS-CoV-2 into various organs as well as the indirect mechanisms such as dysregulation of the renin-angiotensin-aldosterone system (RAAS), immune response dysfunctions within the innate and adaptive immune systems, endothelial damage, and immunothrombosis. Furthermore, the multisystem manifestations of COVID-19 across different organ systems, including the cardiovascular, renal, gastrointestinal, hepatobiliary, nervous, endocrine and metabolic, ophthalmic, ear-nose-throat, reproductive, hematopoietic, and immune systems are discussed in detail. Each system exhibits unique manifestations that contribute to the complexity of the disease.

Coronavirus disease 2019 (COVID-19) was first reported in China at the end of 2019. Several case studies have documented a probable association between infection with severe acute respiratory syndrome corona virus 2 (SARS-CoV-2) and acute pancreatitis (AP). The objective of this study was to provide a complete analysis of existing literature that compares the clinical outcomes of AP in patients with COVID-19 and those without COVID-19. The intention was to further our understanding of the involvement of SARS-CoV-2 in the development of pancreatitis.

Between January 2019 and December 2022, we searched PubMed, Embase, Cochrane Library, Web of Science, and Scopus. Nine studies (3,160 patients) were included. In this meta-analysis, Stata 12.0. was utilized. The information provided in this study is presented following the MOOSE reporting checklist.

Mortality [odds ratio (OR) =3.95, 95% confidence interval (CI): 2.87, 5.43, P<0.001], intensive care unit (ICU) administration (OR =3.74, 95% CI: 2.26, 6.20, P<0.001), mechanical ventilation (OR =4.84, 95% CI: 2.14, 10.96, P<0.001), severe pancreatitis (OR =2.71, 95% CI: 1.04, 7.04, P=0.042), etiology of idiopathic and unknown (OR =4.75, 95% CI: 1.80, 12.56, P=0.002), necrotizing pancreatitis (OR =1.88, 95% CI: 1.28, 2.76, P=0.001), and length of hospital stay [weighted mean difference (WMD) =5.10, 95% CI: 2.79, 7.41, P<0.001] were more significantly increased in AP cases with COVID-19 than those without it.

In conclusion, the findings of this study indicate a potential worsening of AP outcomes in patients affected by COVID-19.

A 54-year-old man was admitted for fever and dyspnea. He presented with severe COVID-19 pneumonia and elevated amylase and lipase levels. He received treatment for COVID-19 and possible acute pancreatitis (AP). Although pneumonia and amylase levels improved, a high-grade fever persisted. On day 39, abdominal CT revealed heterogenous liquid and non-liquid components with a well-defined wall around the pancreas, and he was diagnosed with infected walled-off necrosis (WON) after AP. It was concluded to be associated with COVID-19 because there were no identifiable causes, such as alcohol consumption, gallstones, or other viral infections. The necrotic collection and fever improved after endoscopic transgastric drainage and necrosectomy. SARS-CoV-2 is becoming recognized as a new etiological infectious factor for AP, and COVID-19-associated AP shows higher severity and mortality. Clinicians should evaluate COVID-19 patients for concomitant AP, and if it is present, they should carefully monitor the development of local complications, including WON.

The coronavirus disease 2019 (COVID-19) pandemic became superimposed on the pre-existing obesity and diabetes mellitus (DM) pandemics. Since COVID-19 infection alters the metabolic equilibrium, it may induce pathophysiologic mechanisms that potentiate new-onset DM, and we evaluated this issue.

A systematic review of the literature published from the 1 January 2020 until the 20 July 2023 was performed (PROSPERO registration number CRD42022341638). We included only full-text articles of both human clinical and randomized controlled trials published in English and enrolling adults (age > 18 years old) with ongoing or preceding COVID-19 in whom hyperglycemia was detected. The search was based on the following criteria: "(new-onset diabetes mellitus OR new-onset DM) AND (COVID-19) AND adults".

Articles on MEDLINE (n = 70) and the Web of Science database (n = 16) were included and analyzed by two researchers who selected 20 relevant articles. We found evidence of a bidirectional relationship between COVID-19 and DM.

This link operates as a pathophysiological mechanism supported by epidemiological data and also by the clinical and biological findings obtained from the affected individuals. The COVID-19 pandemic raised the incidence of DM through different pathophysiological and psychosocial factors.

Aim: The aim of the research was to study the features of pancreatic exocrine insufficiency (EPI) in patients with nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes mellitus (DM) at COVID-19.

Materials and Methods: 72 patients with NAFLD and COVID-19 were examined. The patients have been divided into two groups: group 1 included 42 patients with NAFLD and insulin resistance (IR); group 2 consisted of 30 patients with NAFLD in the combination with type 2 DM. EPI was detected by 13С-mixed triglyceride breath test (13С-MTBT) in all the patients.

Results: The result of 13С-MTBT indicates EPI in the examined subjects of the 2 group. A significant decrease in the maximum concentration of 13СО2 between 150 and 210 min was also diagnosed in group 1 patients. research (up to 8.2 ± 0.9% - p < 0.05), however, the total concentration of 13СО2 at the end of 360 min. the study reached only 27.7 ± 1.1% (p < 0.05).

Conclusions: Based on the results of laboratory-instrumental methods of research, patients with NAFLD and type 2 diabetes with COVID-19 were diagnosed with severe EPI. The results of 13С-MTBT in NAFLD and IR with COVID-19 indicate a decrease in the functional reserves of the pancreas and the formation of its EPI.