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© 2022 The AuthorsObjective and aims: Acute pancreatitis in inflammatory bowel disease occurs mainly as an extraintestinal manifestation or a side effect of medications. We aimed to investigate the prognostic factors and severity indicators of acute pancreatitis and the treatment of patients with both diseases. Design: We performed a matched case-control registry analysis of a multicentre, prospective, international acute pancreatitis registry. Patients with both diseases were matched to patients with acute pancreatitis only in a 1:3 ratio by age and gender. Subgroup analyses were also carried out based on disease type, activity, and treatment of inflammatory bowel disease. Results: No difference in prognostic factors (laboratory parameters, bedside index of severity in acute pancreatitis, imaging results) and outcomes of acute pancreatitis (length of hospitalization, severity, and local or systemic complications) were detected between groups. Significantly lower analgesic use was observed in the inflammatory bowel disease population. Antibiotic use during acute pancreatitis was significantly more common in the immunosuppressed group than in the non-immunosuppressed group (p = 0.017). However, none of the prognostic parameters or the severity indicators showed a significant difference between any subgroup of patients with inflammatory bowel disease. Conclusion: No significant differences in the prognosis and severity of acute pancreatitis could be detected between patients with both diseases and with pancreatitis only. The need for different acute pancreatitis management is not justified in the coexistence of inflammatory bowel disease, and antibiotic overuse should be avoided.

2-es típusú cukorbetegségben a vércukorszint növekedésével párhuzamosan, progresszív módon nő a mikro- és makrovaszkuláris szövődmények kialakulásának kockázata. A szövődmények megelőzéséhez és a halálozás csökkentéséhez alapvető fontosságú a cukorbetegség korai felfedezése és a megfelelő glikémiás kezelés mielőbbi megkezdése; ez utóbbi a betegség korai szakaszában egyénre szabott, szoros HbA1c-célérték (

Supplemental material, sj-docx-1-tag-10.1177_17562848231177151 for Microscopic colitis is a risk factor for low bone density: a systematic review and meta-analysis by Anett Rancz, Brigitta Teutsch, Marie Anne Engh, Dániel Sándor Veres, László Földvári-Nagy, Bálint Erőss, Nóra Hosszúfalusi, Márk Félix Juhász, Péter Hegyi and Emese Mihály in Therapeutic Advances in Gastroenterology

Összefoglaló. A Nemzetközi Diabetes Szövetség (International Diabetes Federation, IDF) legutóbbi becslése szerint napjainkban több mint 600 000, 15 év alatti 1-es típusú cukorbeteg gyermek él a világon, az új esetek száma pedig évi 98 200-ra tehető. Az elmúlt évtizedekben az 1-es típusú diabetes incidenciája világszerte jelentősen nőtt ebben a korosztályban: Európában az 1989 és 2013 közötti periódusban átlagosan évi 3,4%-kal, ami 20 éven belül a betegek számának duplázódását vetíti előre a kontinensen. Az epidemiológiai vizsgálatok kezdete óta nyilvánvaló, hogy a gyermekkori kezdetű, 1-es típusú diabetes előfordulási gyakorisága széles határok között ingadozik, amit egyaránt befolyásolnak geográfiai és klímaviszonyok, etnikai és demográfiai hatások. Bár az 1-es típusú cukorbetegség kialakulása során az autoimmunitás primer kockázati tényezője a genetikai háttér, mégsem a genetikai terheltség populációszintű fokozódása okozza az incidencia robbanásszerű növekedését, hanem a környezeti tényezőknek a betegség penetranciáját megváltoztató hatása. A környezeti hatások oki tényezőkként, akcelerátorokként és védőfaktorokként is hozzájárulhatnak mindehhez, sőt akár a betegség patogenezisében egyszerre több ponton, több mechanizmussal is részt vehetnek. Ugyanakkor a nemzetközi kutatások ellenére a legnépszerűbb háttérelméletek (például vírusinfekció, higiéniahipotézis, bélmikrobiom, áteresztő bél, D-vitamin-hiány) máig nem szolgálnak kielégítő magyarázattal az epidemiológiai észlelések többségére (például földrajzi régiónként jelentősen eltérő incidenciaértékek, geográfiai „forrópontok”, az új esetek megjelenésének szezonális ingadozása, az incidenciacsúcsok ciklicitása). Összefoglalónk célja a gyermekkori 1-es típusú diabetes epidemiológiájára vonatkozó aktuális adatok és háttérelméletek áttekintése. Orv Hetil. 2021; 162(1): 13–22. Summary. According to the latest report of the IDF (International Diabetes Federation), more than 600 000 children under the age of 15 years are living with type 1 diabetes in the world and the number of new cases is estimated to be 98 200 annually. In recent decades, a significant increase in the incidence has been observed globally: during 1989–2013, the annual rate of increase was 3.4% in Europe, suggesting a doubling in the number of patients within approximately 20 years on the continent. The wide variation in incidence has been well documented by epidemiological studies and influenced by geographical and climatic conditions, ethnic and demographic factors. Although the genetic background is the primary risk factor for beta-cell autoimmunity, such dynamic changes in incidence are more likely to be associated with the higher environmental pressure than the increase in genetic load at population level. Environmental factors can also contribute to the pathogenesis of type 1 diabetes as accelerators, causal or protective factors, moreover may even be involved at several points and with several mechanisms at the same time. However, despite the extensive international research on environmental factors, the most popular hypotheses associated with them (e.g., virus infections, hygiene hypothesis, intestinal microbiota, leaky gut, lack of vitamin D) have not yet provided a satisfactory explanation for most epidemiological observations (e.g., geographically significant variability of incidence rates, geographical “hotspots”, seasonal fluctuations in new cases, cyclical trends of incidence peaks). In this article, recent data and hypotheses about the epidemiology of childhood type 1 diabetes are summarized. Orv Hetil. 2021; 162(1): 13–22.

Abstract: Introduction: Previous data showed bacterial infections among diabetic patients to be more serious and frequent, with higher mortality rates in comparison with non-diabetics. Recent investigations, however, are contradictory. Aim: The goal of our prospective, observational study was to compare patients hospitalized on a general medical ward due to community-acquired bacterial infections with type 2 diabetes mellitus (T2DM) to those of non-diabetics (K) by 1) infection localization, 2) spectrum of pathogens, 3) three-month mortality rates. Method: Patients were consecutively involved (T2DM: n = 205, K: n = 202). We characterized the infections, clinical parameters, mortalities of the two groups, and matched them to international data. Results: No difference regarding clinical details of the groups were found except for glycemic parameters and BMI. In the T2DM group the skin- and soft tissue- (37.1%), in the K patients respiratory infections (37.1%) were the most common, followed by urinary ones (31.2% and 31.7%, respectively). Skin- and soft tissue infection incidence among T2DM subjects were higher compared to international results (37.1% vs. 16%). Co-presence of Gram positive and Gram negative bacteria in the skin- and soft tissue infections (23/76 vs. 5/46, p = 0.0149), and polymicrobial origin in the urinary tract infections (34.0% vs. 15.1%, p = 0.0335) were found to be more frequent in T2DM than in K. No difference regarding mortality rates were detected. In T2DM the skin- and soft tissue while in the K group the respiratory infections had the most death counts. Conclusions: We found higher rates of skin- and soft tissue infections among T2DM patients hospitalized on a general medical ward compared to international data. In total we did not find difference regarding three-month mortality between the groups. Our results highlight the importance of primary prevention and shows its inadequacy concerning skin and soft tissue infections among type 2 diabetics in Hungary. Orv Hetil. 2019; 160(41): 1623–1632.

Összefoglaló. A Nemzetközi Diabetes Szövetség (International Diabetes Federation, IDF) legutóbbi becslése szerint napjainkban több mint 600 000, 15 év alatti 1-es típusú cukorbeteg gyermek él a világon, az új esetek száma pedig évi 98 200-ra tehető. Az elmúlt évtizedekben az 1-es típusú diabetes incidenciája világszerte jelentősen nőtt ebben a korosztályban: Európában az 1989 és 2013 közötti periódusban átlagosan évi 3,4%-kal, ami 20 éven belül a betegek számának duplázódását vetíti előre a kontinensen. Az epidemiológiai vizsgálatok kezdete óta nyilvánvaló, hogy a gyermekkori kezdetű, 1-es típusú diabetes előfordulási gyakorisága széles határok között ingadozik, amit egyaránt befolyásolnak geográfiai és klímaviszonyok, etnikai és demográfiai hatások. Bár az 1-es típusú cukorbetegség kialakulása során az autoimmunitás primer kockázati tényezője a genetikai háttér, mégsem a genetikai terheltség populációszintű fokozódása okozza az incidencia robbanásszerű növekedését, hanem a környezeti tényezőknek a betegség penetranciáját megváltoztató hatása. A környezeti hatások oki tényezőkként, akcelerátorokként és védőfaktorokként is hozzájárulhatnak mindehhez, sőt akár a betegség patogenezisében egyszerre több ponton, több mechanizmussal is részt vehetnek. Ugyanakkor a nemzetközi kutatások ellenére a legnépszerűbb háttérelméletek (például vírusinfekció, higiéniahipotézis, bélmikrobiom, áteresztő bél, D-vitamin-hiány) máig nem szolgálnak kielégítő magyarázattal az epidemiológiai észlelések többségére (például földrajzi régiónként jelentősen eltérő incidenciaértékek, geográfiai "forrópontok", az új esetek megjelenésének szezonális ingadozása, az incidenciacsúcsok ciklicitása). Összefoglalónk célja a gyermekkori 1-es típusú diabetes epidemiológiájára vonatkozó aktuális adatok és háttérelméletek áttekintése. Orv Hetil. 2021; 162(1): 13-22. Summary. According to the latest report of the IDF (International Diabetes Federation), more than 600 000 children under the age of 15 years are living with type 1 diabetes in the world and the number of new cases is estimated to be 98 200 annually. In recent decades, a significant increase in the incidence has been observed globally: during 1989-2013, the annual rate of increase was 3.4% in Europe, suggesting a doubling in the number of patients within approximately 20 years on the continent. The wide variation in incidence has been well documented by epidemiological studies and influenced by geographical and climatic conditions, ethnic and demographic factors. Although the genetic background is the primary risk factor for beta-cell autoimmunity, such dynamic changes in incidence are more likely to be associated with the higher environmental pressure than the increase in genetic load at population level. Environmental factors can also contribute to the pathogenesis of type 1 diabetes as accelerators, causal or protective factors, moreover may even be involved at several points and with several mechanisms at the same time. However, despite the extensive international research on environmental factors, the most popular hypotheses associated with them (e.g., virus infections, hygiene hypothesis, intestinal microbiota, leaky gut, lack of vitamin D) have not yet provided a satisfactory explanation for most epidemiological observations (e.g., geographically significant variability of incidence rates, geographical "hotspots", seasonal fluctuations in new cases, cyclical trends of incidence peaks). In this article, recent data and hypotheses about the epidemiology of childhood type 1 diabetes are summarized. Orv Hetil. 2021; 162(1): 13-22.

Therapeutic inertia is a substantial obstacle to the initiation of insulin therapy in people with uncontrolled type 2 diabetes (T2D). This effect has in part been perpetuated by concerns over the impact of a burdensome regimen and the increased risk of hypoglycemia and body weight gain often associated with insulin use. An effective, yet simple, less burdensome regimen with a lower risk of body weight gain and hypoglycemia compared with an insulin-only regimen, may help to address these concerns more effectively. We review the available clinical and real-world data on IDegLira, a once-daily, injectable, fixed-ratio combination of insulin degludec (degludec) and the glucagon-like peptide-1 receptor agonist (GLP-1RA) liraglutide, in people with T2D. Evidence from the comprehensive DUAL clinical trial program suggests an advantage of IDegLira over traditional insulin therapies in a number of clinical outcomes, including maintenance of glycemic control, achievement of glycemic targets, reducing the risk of hypoglycemia, and body weight loss. These findings were demonstrated in participants with T2D irrespective of prior GLP-1RA and insulin use. Furthermore, the individual components of IDegLira have confirmed safety (degludec) or significant benefit in terms of improvement of cardiovascular risk (liraglutide). As an injectable therapy that is simple to titrate, IDegLira has the potential to optimize the ability to achieve relevant glycemic targets, and offers a suitable treatment option for people with T2D requiring insulin therapy who are at risk of hypoglycemia or weight gain.

Abstract: Over the past decades the majority of genetic research focused on common diseases, and remarkable results were obtained for exploring the genetic background of type 1 diabetes. The classic linkage analyses and the modern genome-wide association studies demonstrated that the genetic background is the primary risk factor for beta-cell autoimmunity while the progression to clinical onset could be triggered by the genetic factors, epigenetic modifications of gene expression and environmental factors together. The new system biology concept can help to understand the mechanisms underlying the immune-mediated beta-cell destruction by generating networks based on data from whole genome scans, fine mapping and gene expression studies to develop targeted prevention and therapeutic strategies. In this paper, we discuss the present understanding of genetic factors which could initiate beta-cell autoimmunity (i.e. define the aetiology) and the genetic and epigenetic factors which might contribute to the progression to clinical disease in individuals with autoantibodies (i.e. define the pathogenesis). Orv Hetil. 2017; 158(44): 1731–1740.

Absztrakt

Bacterial infections are frequent and severe in patients with diabetes mellitus. Whether diabetes per se induces functional alterations in the complement system hampering activation during infection is unknown. We investigated key elements of the complement system during bacterial infections in patients with type 2 diabetes mellitus (T2DM) and compared them to non-diabetic (ND) individuals. Using a prospective design, we included 197 T2DM, and 196 ND subjects, all with clinical diagnosis of acute community-acquired bacterial infections. Functional activities of the ficolin-3-mediated lectin (F3-LP), mannose binding lectin-mediated lectin- (MBL-LP), classical (CP), and alternative pathways (AP), as well as concentrations of complement activation products C4d and sC5b-9 were determined. Functional in vitro activities of F3-LP and AP were significantly higher in T2DM than in ND subjects, (median 64% vs. 45%, p = 0.0354 and 75 vs. 28%, p = 0.0013, respectively), indicating a decreased in vivo activation and lack of consumption of F3-LP and AP in T2DM patients, whereas no difference in functional capacities of CP and MBL-LP were observed between T2DM and ND subjects. Diminished F3-LP and AP activation was most pronounced in diabetic patients with urinary tract infections with positive microbiological culture results for Escherichia coli bacteria. In the T2DM group 3-months mortality significantly associated with diminished F3-LP and AP, but not with CP activation. Concentrations of C4d and sC5b-9 were significantly lower in the T2DM than in ND patients. In conclusion, we found impaired F3-LP activation and lack of AP amplification during bacterial infections in patients with type 2 diabetes, compared to non-diabetic subjects, suggesting a diminished complement mediated protection to bacterial infections in T2DM.