Tag: Diabetes

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Severe COVID-19 increases risk of future cardiovascular events

Study: COVID-19 severity and risk of subsequent cardiovascular events. Image Credit: Yurchanka Siarhei / Shutterstock.com

To date, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is the virus responsible for the coronavirus disease 2019 (COVID-19), has infected over 603 million individuals and claimed more than 6.4 million lives worldwide.

About 30% of COVID-19 survivors continue to experience a wide range of persistent symptoms for several weeks since their initial diagnosis. This condition is commonly referred to as post-acute sequelae of SARS-CoV-2 infection (PASC) or “long COVID.”

Study: COVID-19 severity and risk of subsequent cardiovascular events. Image Credit: Yurchanka Siarhei / Shutterstock.com

Study: COVID-19 severity and risk of subsequent cardiovascular events. Image Credit: Yurchanka Siarhei / Shutterstock.com

Background

Even though multisystem inflammatory syndrome is the most common PASC syndrome in adults and children, a wide range of other symptoms, including sleep difficulties, persistent fatigue, type 1 diabetes, and neurological disorders, have been reported. The incidence of these symptoms varies from one person to another based on their demographic and clinical characteristics.

Several studies have indicated the manifestation of multiple cardiovascular complications, such as arrhythmia, hypertension, acute myocardial infarction, thromboembolism, and cerebrovascular accidents, in individuals who have recovered from COVID-19. However, a limited number of studies have confirmed that severe COVID-19 leads to a high risk of cardiovascular diseases.

A recent Clinical Infectious Diseases journal study determines the relationship between COVID-19 severity and risk of subsequent cardiovascular events (CVEs) in a large cohort.

Study findings

A retrospective cohort study was performed using nationwide health insurance claims data of adults from the United States Health Verity Real-Time Insights and Evidence database. Increased COVID-19 severity was found to enhance the risk of developing subsequent CVEs among individuals without a cardiac history in previous years. 

As compared to COVID-19 patients who required outpatient care, those who required hospital admission were more likely to experience CVEs. Among COVID-19 hospitalized patients, those admitted to the intensive care unit (ICU) were almost 80% more likely to develop CVEs than non-ICU hospitalized patients.

In fact, non-ICU hospitalized patients exhibited only a 28% possibility of experiencing CVEs thirty days after initial COVID-19 symptoms. Additionally, as compared to COVID-19 outpatients, hospitalized patients were more likely to be admitted for a CVE after recovering from COVID-19.

In younger adults, the incidence of cardiovascular sequelae was lower as compared to older adults. Aside from CVEs, other severe outcomes, such as thrombotic events and cerebrovascular accidents, were observed in patients who recovered from severe COVID-19. However, such observations were less likely in COVID-19 patients who required only outpatient care.

The study findings emphasize the importance of vaccination, as demonstrated by its ability to reduce severe disease. Similarly, prompt antiviral treatment of acute COVID-19 has been recommended, which would help reduce the possibility of transition to severe illness.

Both COVID-19 vaccination and timely therapeutic interventions would alleviate the risk of severe COVID-19 and subsequently decrease the possibility of experiencing CVEs.

The findings of the present study are consistent with previous research that has reported a higher incidence of myocarditis and pericarditis in patients who recovered from severe SARS-CoV-2 infection. Nevertheless, it was observed that elevated cardiovascular risk after acute infection may not be exclusive to COVID-19.

In fact, some other diseases that have been associated with an increased risk of long-term CVEs are influenza and pneumonia bacteremia. Additionally, 22-65% of sepsis survivors are at an increased risk of CVEs.

The underlying mechanism responsible for the increased risk of CVEs following SARS-CoV-2 infection has not been determined. SARS-CoV-2 infects cardiac myocytes through their interaction with the angiotensin-converting enzyme 2 (ACE-2) receptor, which might remain persistent; therefore, this interaction induces chronic inflammatory responses and subsequent tissue damage or fibrosis.

Another mechanism related to the development of CVEs following recovery from COVID-19 is an autoimmune response to cardiac antigens that causes delayed damage to cardiac tissues. Anti-heart antibodies also correlated with cardiovascular manifestation and COVID-19.

Viral toxicity is another possible mechanism that might cause long-term cardiac damage or thrombosis in vasculitis. However, in the future, more research is needed to confirm the mechanisms related to cardiac damage after SARS-CoV-2 infection.

Conclusions

Due to the lack of a COVID-19-negative control group, the authors failed to quantify the elevated risk of CVEs in COVID-19 patients. The unwanted inclusion of patients with a history of CVEs could have overestimated the result as well. The impact of vaccination status on the incidence of CVE was not studied.

Despite these limitations, the present study strongly emphasized that patients who recovered from severe COVID-19 were at a greater risk of developing CVEs. As compared to COVID-19 patients who required outpatient care, those who were admitted to the ICU were at a higher risk of experiencing CVEs.

The importance of COVID-19 vaccination in preventing severe infection was strongly emphasized in this study.

Journal reference:

  • Wiemken, L. T., McGrath, L. J., Andersen, K. M., et al. (2022). COVID-19 severity and risk of subsequent cardiovascular events. Clinical Infectious Diseases. doi:10.1093/cid/ciac661.
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Impact of chronic hepatitis on cardiovascular events among type 2 diabetes patients in Taiwan pay-for-performance program – Scientific Reports

Research subjects

Patients with T2DM who joined the P4P from 2008 to 2010 were enrolled. Patients with a confirmed diagnosis of T2DM were defined as those who were hospitalized at least once or came in for outpatient visits at least three times within 1 year and had a primary or secondary diagnosis International Classification of Diseases (ICD) code “250,” “250.00,” or “250.02”38,39. Among them, patients with type 1 DM “250.x1” * or “250.x3;” gestational DM “648.0” or “648.8;” neonatal DM “775.1;” abnormal glucose tolerance test “790.2;” age < 20 years or > 100 years; and those who died within 1 year of joining P4P were excluded. Finally, 283,793 patients were included (Fig. 1). Based on the status of comorbid chronic hepatitis at enrollment, the patients were divided into four groups: no comorbid chronic hepatitis, named as “No chronic hepatitis”; comorbid liver B, named as “Hepatitis B” group; comorbid liver, named as “Hepatitis C” group; patients without viral hepatitis and with comorbid fatty liver were named as the “Fatty liver disease” group and were followed-up until the end of 2017. The “no comorbid chronic hepatitis” group was used as the reference group to analyze the correlation between different types of chronic hepatitis and the risk of cardiovascular disease.

Figure 1
figure 1

Flowchart for study subject selection. DM diabetes mellitus, P4P pay-for-performance, HBV hepatitis B virus, HCV hepatitis C virus.

Ethics statements

The National Health Insurance Research Database (NHIRD) is derived from Taiwan’s mandatory National Health Insurance program was established by the National Health Insurance Administration Ministry of Health and Welfare and maintained by the National Health Research Institute (NHRI). The patient identifications in the National Health Insurance Research Database have been scrambled and de-identified by the Taiwan government, and the database is commonly used for different types of research such as in medical, and public health fields. Thus, informed consent was waived by the Research Ethics Committee of the China Medical University, and the study protocol was approved by the research ethics committee of China Medical University and Hospital (IRB number: CMUH106-REC3-153) and was conducted in accordance with the principles of the Declaration of Helsinki.

Data sources

This retrospective cohort study analyzed data from the National Health Insurance Research Database of the “Applied Health Research Data Integration Service from National Health Insurance Administration”. The data included outpatient prescriptions and treatments, outpatient prescriptions and medical orders, inpatient medical expense lists, inpatient medical expense and medical order lists, insurance details of persons, major injury and illness, medical institution master files, diagnosis, and P4P education records.

Definitions of variables

Hepatitis B: Those with ICD-9 070.2, 070.20, 070.21, 070.22, 070.23, 070.3070.31, 070.32, or 070.33 or ICD-10 B16, B17.0, B18.0, B18.1, or B19.1 as the primary and secondary diagnosis during two outpatient visits or one hospitalization within 365 days of study enrollment.

Hepatitis C: Those with ICD-9 070.41, 070.44, 070.51, or V02.62 or ICD-10 B17.10, B17.11, B18.2, B19.20, B19.21, or Z22.52 as the primary and secondary diagnosis during two outpatient visits or one hospitalization within 365 days of study enrollment.

NAFLD: Those with ICD-9 571.8, 571.9, or ICD-10 K74.4, K74.5, K74.60, K74.69, K76.0, K76.9, etc. as the primary and secondary diagnosis during two outpatient visits or one hospitalization within 365 days of study enrollment, and without the occurrence of a hepatitis B or C code, for whom the first hospital visit within 365 days was defined as the date of diagnosis. Patients with concurrent viral hepatitis and NAFLD were classified as having viral hepatitis.

Age-based categorization included 20–39, 40–54, 55–64, 65–74, and ≥ 75 years age groups. Monthly salary was divided into five grades, namely ≤ NTD 17,280, NTD 17,281–22,800, NTD 22,801–36,300, NTD 36,301–45,800, and ≥ NTD 45,801. Charlson comorbidity index was divided into 0, 1, 2, and ≥ 3 after excluding scores correlated with independent or dependent variables40.

The diabetes complications severity index (DCSI) was scored as 0, 1, and ≥ 2 points. The DCSI was calculated based on the classification and scoring method proposed by Young et al. If the patient had no complication, the score would be 0; for each complication, 1 point would be added; if the complication was serious, 2 points would be added. Based on this calculation method, the maximum score was 13 points41.

Cardiovascular disease: Those with ICD-9 398.91, 402.xx, 404.xx, 410.xx–414.xx, 422.xx, 425.xx or 428.xx, or ICD-10 I09.81, I11, I13, I20–I22, I24, I25, I40–I43, I50, R09.89, etc. as the primary and secondary diagnosis during two outpatient visits or one hospitalization within 365 days of study enrollment42.

Calculation of the coefficient of variation (CV% = standard deviation/mean) of HbA1c and fasting blood glucose: All measurements in the first year were used, and if the measurements were taken less than four times in the first year, measurements taken up to the second year were included. If measurements were taken less than four times in the 2 years, the patient would be excluded.

Adjusted CV = CV/√ (n/n − 1): When the examination data were limited, the examination times would affect the result of the CV. In this case, a relatively correct result of the CV with a reduced effect of the examination times could be obtained by correcting the examination times.

Analytical methods

Descriptive and inferential statistics were carried out according to the research objectives and framework. All research tests were based on a significance level of α = 0.05, and all statistical analyses were conducted using SAS software for Windows, version 9.4 (SAS Institute Inc., Cary, NC, USA). Descriptive statistics such as frequency, percentage, average, and standard deviation were used to describe the dependent and independent variables to be investigated in this study. This study adopted descriptive statistics to present the demographic characteristics, status of comorbidities, blood biochemical indicators, health status, economic factors, and medical care provider characteristics of patients with diabetes. The incidence of cardiovascular disease in patients with T2DM with chronic hepatitis per 1000 person-years was tested using univariate Poisson regression. The relative risks of cardiovascular disease in the four groups were calculated using a Cox proportional hazards model.

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Analysis finds little proof that testosterone treatment increases the risk of cardiovascular events

Analysis finds little proof that testosterone treatment increases the risk of cardiovascular events

Testosterone replacement therapy appears safe in the short-to-medium term to treat a condition caused by deficiency of the male sex hormone, according to the most comprehensive analysis of the treatment to date, published in The Lancet Healthy Longevity journal.

The findings suggest that men given testosterone to treat hypogonadism are at no greater risk of heart attack, stroke, and other cardiovascular events in the short-to-medium term than men who do not receive testosterone treatment.

Testosterone replacement therapy is the standard treatment for hypogonadism, which can cause sexual dysfunction, weakening of bones and muscles, and reduced quality of life. Risk factors for the condition include aging (as testosterone levels decline with age), obesity (BMI of 30 kg/m2 or above), and diabetes.

Despite being widely used, the cardiovascular safety of testosterone treatment has until now remained unclear due to inconsistent findings. This is because most previous clinical studies have relied on aggregate data, rather than individual participant data and have not published details of individual adverse events.

Prescribing of testosterone for hypogonadism is increasing globally, but conflicting messages about its safety may have led to many patients not receiving the treatment. Ongoing studies should help to determine the longer-term safety of testosterone but, in the meantime, our results provide much-needed reassurance about its short-to-medium term safety. Our findings could have important implications for the treatment of men with hypogonadism worldwide.”


Jemma Hudson, Study Lead Author, University of Aberdeen

The authors conducted a systematic review identifying 35 eligible clinical trials published since 1992, of which 17 provided individual participant data. A blinded analysis by two independent clinicians enabled the classification of every cardiovascular event, allowing for a more robust analysis of the cardiovascular safety of testosterone treatment.

A meta-analysis using individual participant data from 17 studies and a further meta-analysis integrating these data with the aggregate data provided by the 18 trials that did not provide individual participant data were performed.

Among the 17 trials with individual patient data, 1,750 participants received testosterone and 1,681 were given a placebo. The average length of testosterone treatment was 9.5 months. The average age of participants was 65 years, and most were white and did not smoke. Participants’ average BMI was 30 kg/m2, which is considered obese.

A meta-analysis showed there were 120/1,601 (7.5%) cardiovascular events in the testosterone group and 110/1,519 (7.2%) in the placebo group across 13 trials that provided this information. Patient age, smoking or diabetes status did not affect cardiovascular risk. Similarly, there was no significant difference in mortality rate between the testosterone group (6/1,621 deaths, 0.4%) and the placebo group (12/1,537 deaths, 0.8%) across the 14 trials that provided individual patient data on mortality, but only limited data were available.

The researchers also found that testosterone significantly reduced serum total cholesterol, high-density lipoprotein (HDL), and triglycerides compared with placebo. However, there were no significant differences in serum low-density lipoprotein (LDL), blood pressure, glycaemic parameters, diabetes incidence, and prostate adverse outcomes between the testosterone and placebo groups.

The meta-analysis that integrated individual participant data with aggregate data showed similar results.

The authors acknowledge some limitations to their study. There was little available data evaluating the cardiovascular safety of testosterone treatment beyond 12 months, and the very small number of deaths recorded during testosterone trials hampered the authors’ ability to analyze why they occurred.

However, the longer-term safety of testosterone treatment is currently being investigated in another clinical trial. While the meta-analysis of aggregate data showed similar results to the one involving individual patient data only, it cannot be ruled out with certainty that a high number of unreported cardiovascular events in the trials that did not provide individual participant data could alter the current conclusions.

Source:

Journal reference:

Hudson, J., et al. (2022) Adverse cardiovascular events and mortality in men during testosterone treatment: an individual patient and aggregate data meta-analysis. The Lancet Healthy Longevity. doi.org/10.1016/S2666-7568(22)00096-4

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Genetic Mapping Predicts Risk of Cardiovascular Events in People With Type 2 Diabetes

CVD, cardiovascular, heart MRI, cardiac

Risk scores based on genetic mapping were found to correlate with hypertensive blood pressure (BP) traits and an increased likelihood of adverse cardiovascular events, such as stroke, myocardial infarction, and cardiovascular death, in individuals with type 2 diabetes (T2D), according to results of a study published in Hypertension. The risk of adverse cardiovascular events in those with higher genetic risk scores were unchanged by intensive glycemic therapy approaches.

Researchers conducted a post hoc analysis of the National Institutes of Health’s ACCORD (Action to Control Cardiovascular Risk in Diabetes) trial (ClinicalTrials.gov Identifier: NCT00000620) to assess whether genetic variants influenced BP traits and adverse cardiovascular outcomes in individuals with T2D. Out of the 10,251 participants with T2D in the ACCORD trial, 6335 individuals had genetic data that were needed to calculate polygenic risk scores.

During the ACCORD trial, BP data were calculated using an average of 3 BP measurements with 5 minutes rest in between measurements. Overall, the median systolic blood pressure was 147 mm Hg, the median diastolic blood pressure was 83 mm Hg, and the median HbA1C was 8.1%.

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For the post hoc assessment, the researchers collected participant genotype data and compared these data with the Trans-OMICs Precision Medicine (TOPMed) Freeze 8 gene map, which consists of more than 1000 genetic variants known to affect blood pressure. The researchers calculated polygenic risk scores based on the number of matches between each participant’s DNA and the genetic variants known to influence BP. The greater the number of matches, the higher the risk score. The median polygenic risk score was 168.4 (range, 166.6-170.6).

After analyzing BP polygenic risk scores in relation to adverse cardiovascular outcomes, each degree of increase in the risk score was found to correlate with a 12% increased risk of cardiovascular events. Glycemic control therapy did not influence the BP polygenic risk scores, nor did it influence the primary outcome of cardiovascular risk prevention.

Study limitations included the pre-existing nature of the subset of participants available for analysis, as well as a lack of power to evaluate possible interactions due to the study’s post hoc design.

“These results invigorate the potential implications of [using] BP polygenic risk score in the primordial prevention of microvascular and macrovascular complications in T2D through early intensification of life-style measures such as healthy diet, exercise, smoking cessation, weight management, and BP control among those with high genetic risk,” the authors said.

This genetic risk assessment may especially benefit those with newly diagnosed T2D and those with prediabetes to encourage earlier adoption of a healthier lifestyle.

Reference

Parcha V, Pampana A, Bress AP, Irvin MR, Arora G, Arora P. Association of polygenic risk score with blood pressure and adverse cardiovascular outcomes in individuals with type II diabetes: insights from the ACCORD trial. Hypertension. Published online April 4, 2022. doi:10.1161/hypertensionaha.122.18976

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Risk for major adverse CV events elevated with type 2 diabetes, cognitive impairment

Hertzel C. Gerstein, MD, MSc

April 21, 2022

2 min read


Disclosures:
Gerstein reports receiving research grants from AstraZeneca, Eli Lilly, Merck, Novo Nordisk and Sanofi; receiving honoraria for speaking from Boehringer Ingelheim, DKSH, Eli Lilly, Novo Nordisk, Roche, Sanofi and Zuellig; and receiving consulting fees from Abbott, Covance, Eli Lilly, Hanmi, Kowa, Novo Nordisk, Pfizer and Sanofi. Please see the study for all other authors’ relevant financial disclosures.


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Adults with type 2 diabetes and cognitive impairment are more likely to experience major adverse cardiovascular events, stroke or CV mortality compared with those without cognitive impairment, according to study findings.

In an analysis of data from the REWIND trial, participants who scored 1.5 standard deviations below their country’s geometric mean on the Montreal Cognitive Assessment and the Digit Symbol Substitution Test were more likely to experience major adverse CV events, making cognitive impairment a potential predictor for CV health outcomes.


Hertzel C. Gerstein, MD, MSc

Gerstein is a professor and population health institute chair in diabetes research and care at McMaster University and Hamilton Health Sciences in Ontario, Canada.

“These findings highlight the relevance of cognitive function as an important risk factor for CV outcomes and suggest that patients with cognitive impairment should be offered proven cardioprotective therapies to mitigate their future risk of CV outcomes,” Hertzel C. Gerstein, MD, MSc, professor and population health institute chair in diabetes research and care at McMaster University and Hamilton Health Sciences in Ontario, Canada, told Healio.

Researchers collected data from 8,772 REWIND participants with type 2 diabetes who completed both the Montreal Cognitive Assessment and the Digit Symbol Substitution Test at baseline, 2 years, 5 years and their final trial visit. The Montreal Cognitive Assessment is a 30-item questionnaire assessing seven cognitive domains. The Digit Symbol Substitution Test presents nine symbols above blank squares, with a key corresponding each symbol to a number. Participants must place the correct number in each square in a spvan of 2 minutes. Scores on each test were standardized based on the participant’s country. Adults with a score 1.5 standard deviations below the mean score in their country were defined as having country-standardized substantive cognitive impairment. Those who had a mean score on both tests combined 1.5 standard deviations below their country’s mean were defined as having substantive cognitive impairment based on the geometric mean. Primary outcomes were incident major adverse CV events, incident stroke and CV mortality.

The findings were published in The Journal of Clinical Endocrinology & Metabolism.

Of the study cohort, 10.3% had substantive cognitive impairment and 6% had substantive cognitive impairment based on the geometric mean. Participants with substantive cognitive impairment did not have a significantly increased risk for major adverse CV events after adjusting for albuminuria, estimated glomerular filtration rate and retinopathy. However, in a fully adjusted model, those with substantive cognitive impairment based on the geometric mean had an increased risk for major adverse CV events compared with those without cognitive impairment (adjusted HR = 1.38; 95% CI, 1.09-1.77; P = .009).

Participants with substantive cognitive impairment (aHR = 1.35; 95% CI, 1.11-1.64; P = .002) and substantive cognitive impairment based on the geometric mean (aHR = 1.54; 95% CI, 1.22-1.93; P < .001) had an increased risk for either stroke or CV death compared with adults without cognitive impairment.

“These findings are consistent with other research suggesting that low cognitive scores on cognitive tests were a risk factor for a cardiovascular outcome,” Gerstein said. “This research extended those findings by using a composite measure of cognitive scores and prespecifying a threshold labeled substantive cognitive impairment. It also reported a novel way of combining the cognitive scores by calculating their geometric mean.”

For more information:

Hertzel C. Gerstein, MD, MSc, can be reached at gerstein@mcmaster.ca.


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Study provides new understanding of the earliest molecular events in Type 1 Diabetes pathogenesis

Study provides new understanding of the earliest molecular events in Type 1 Diabetes pathogenesis

For the first time, researchers have revealed that during the development of Type 1 Diabetes (T1D), when insulin-producing cells in the pancreas are under attack from T lymphocytes, the cells lining the pancreatic duct reprogram themselves in an attempt to suppress autoimmune T cell responses. This study is published today in Nature Metabolism.

The first events that occur in a patient heading towards Type 1 Diabetes, the events that trigger autoimmunity, have been difficult for researchers to pin down because of our inability to biopsy the pancreas, and the fact that clinical diagnosis is only made once massive beta cell destruction has occurred. That is why it is so important to develop a better understanding of the earliest molecular events in T1D pathogenesis, so we can uncover more about biomarker identification and disease prevention.”


Golnaz Vahedi, PhD, senior author, associate professor of Genetics and member of the Institute for Diabetes, Obesity and Metabolism, Perelman School of Medicine at the University of Pennsylvania

Autoimmune diseases, which affect as many as 23.5 million Americans, occur when the body’s immune system attacks and destroys healthy organs, tissues and cells. There are more than 80 types of autoimmune diseases, including rheumatoid arthritis, inflammatory bowel disease, and T1D. In T1D, immune cells called T lymphocytes attack and destroy insulin-secreting pancreatic beta cells and the pancreas stops producing insulin, the hormone that controls blood sugar levels.

“Although it might be an ultimately unsuccessful attempt of the pancreas to limit the adaptive T cell response responsible for destroying beta cells, this finding that the ductal cells are capable of playing this suppressive role towards autoimmune T cell responses is unprecedented,” said co-senior author Klaus Kaestner, PhD, the Thomas and Evelyn Suor Butterworth Professor in Genetics. “Our study shows that these cells, which had never previously been linked to immunity, may change themselves to protect the pancreas.”

Established in 2016, the Human Pancreas Analysis Program (HPAP) is supported by a $28 million grant from the National Institutes of Health with major contributions from Penn, the University of Florida and Vanderbilt University. The HPAP, which is co-directed by Kaestner and Ali Naji MD, PhD, the J. William White Professor of Surgical Research, started collecting pancreatic tissues from hundreds of deceased organ donors diagnosed with T1D. Because many T1D patients harbor beta cell autoantibodies called Glutamic Acid Decarboxylase (GAD) in their bloodstream years before clinical diagnosis, HPAP also collects samples from autoantibody-positive donors, who are at risk for developing T1D but have not received that diagnosis.

“Our study took those quality tissue samples and created high-resolution measurements of millions of cells from patients at various stages of T1D progression, resulting in a single-cell atlas of pancreatic islets,” said co-senior author R. Babak Faryabi, PhD, an assistant professor of Pathology and Laboratory Medicine and a core member of Epigenetics Institute at Penn.

Blood tests to check for levels of GAD are common for patients with, or at risk for, T1D, and doctors use it as a diagnostic tool. Another finding of this study is the new understanding of what is happening on a molecular level in the pancreas and how it correlates to the findings of the GAD test.

“Our study is the first to show that even when a person is not clinically considered to have T1D, high levels detected in their GAD test indicate large-scale transcriptional remodeling of their beta cells,” said Naji, a study co-senior author. “It solidifies to clinicians to closely monitor patients with increasing levels of GAD, as we now know what cellular and molecular changes are in motion in relation to those levels.”

Although researchers do not yet know whether these transcriptional changes are contributing to or are consequences of disease pathogenesis, the discovery of molecular phenotypic changes in pancreatic cells of autoantibody-positive individuals advances the understanding of early pancreatic changes occurring in T1D, and sets the course for continued research in this area.

Source:

University of Pennsylvania School of Medicine

Journal reference:

Fasolino, M., et al. (2022) Single-cell multi-omics analysis of human pancreatic islets reveals novel cellular states in type 1 diabetes. Nature Metabolism. doi.org/10.1038/s42255-022-00531-x.