Diabetology International最新文献

Patients with non-diabetic hypoglycemia have a poorer prognosis than those with diabetic hypoglycemia. However, the factors associated with prognosis remain unclear. Therefore, this study aimed to identify the prognostic factors for non-diabetic hypoglycemia. This is a retrospective study of patients hospitalized for severe hypoglycemia with blood glucose ≤ 3.0 mmol/L (54 mg/dL) due to non-diabetic hypoglycemia between April 2008 and June 2023. Additionally, the underlying cause of hypoglycemia was identified, and the factors associated with mortality were examined. Of the 134 hospitalized patients, 126 were analyzed, excluding cases of multiple or scheduled hospitalizations. The most common causes of hypoglycemia were malnutrition (n = 79, 62.7%), alcohol intake (n = 27, 21.4%), and hypothermia (n = 27, 21.4%); 76 (60.3%) patients had multiple associated factors. Of the 126 patients, 52 died within 90 days. In the multivariate analysis, the estimated glomerular filtration rate (eGFR) (< 30 mL/min/1.73 m²) was independently associated with death [odds ratio (OR) 5.78, 95% confidence interval (CI) 1.69-19.8], whereas blood glucose (OR 0.95, 95% CI 0.92-0.99), serum albumin (OR 0.27, 95% CI 0.12-0.59), and alcohol intake (OR 0.03, 95% CI 0.004-0.34) were associated with survival. Moreover, age (OR 1.0, 95% CI 0.97-1.04) was not associated with death. Patients with non-diabetic hypoglycemia had a very high mortality. Low eGFR, blood glucose levels, and serum albumin levels at admission were associated with 90-day mortality, and alcohol intake was associated with survival.

Fulminant type 1 diabetes (FT1D) is a rapidly progressive form of diabetes in which the endogenous capacity to secrete insulin is depleted. The onset is unpredictable with conventional FT1D, and a few reports have tracked C-peptide in patients with conventional FT1D pre-onset. In this report, we present two typical cases of conventional FT1D where C-peptide was monitored from the onset of precursor symptoms to the development of diabetic ketoacidosis (DKA). Furthermore, we conducted a literature review and provide a detailed description of the process of C-peptide depletion in conventional FT1D. Case 1 involved a 72-year-old woman who initially presented with fever and fatigue. Case 2 involved a 45-year-old woman with fever, abdominal pain, and acute pancreatitis. In both cases, DKA developed five days after initial symptoms. A noteworthy observation in both cases was the drastic drop in C-peptide, which was detectable at initial presentation but depleted by the time of DKA diagnosis. These cases emphasize the importance of close follow-up of plasma glucose and serum C-peptide in cases presenting with infection and pancreatitis. Our literature review revealed that in conventional FT1D, endogenous insulin secretion becomes deficient in an average of 5.3 days. Regardless of any concomitant acute pancreatitis and/or pancreas enlargement, the period until endogenous insulin secretion became deficient showed no substantial variation. This result supports the concept that progression of conventional FT1D is more rapid than that of immune checkpoint inhibitor-related FT1D, which deplete insulin secretion in approximately 2 weeks.

Supplementary information: The online version contains supplementary material available at 10.1007/s13340-024-00755-0.

Purpose: A subpopulation of Japanese patients with type 2 diabetes mellitus (T2DM) who have elevated insulin clearance (IC) exists. We tested our hypothesis that it is possible to estimate IC using common and simple test results collected in routine clinical practice.

Methods: We recruited patients with newly diagnosed, treatment-naïve T2DM and measured the metabolic clearance rate of insulin (MCRI) determined by a hyperinsulinemic-euglycemic clamp examination. Multivariable regression analysis was performed with body mass index (BMI), serum uric acid (UA), and fasting plasma insulin (F-IRI) which were independently associated with IC increase in our previous reports as explanatory variables to calculate a prediction equation for MCRI.

Results: We enrolled 101 patients in this study. Because MCRI is not normally distributed, we calculated the logarithmically transformed estimated Log₁₀MCRI as a prediction formula for IC. Multivariable regression analysis showed that Log₁₀BMI (β =  - 0.3257, P < 0.001), UA (β =  - 0.1834, P = 0.0081), and Log₁₀F-IRI (β =  - 0.4367, P < 0.001) were significant independent factors for Log₁₀MCRI. The regression equation was as follows: estimated Log₁₀MCRI =  - 0.5421 × Log₁₀BMI - 0.0167 × UA - 0.1792 × Log₁₀F-IRI + 3.8251 (r = 0.7677, R ² = 0.5894, P < 0.001).

Conclusion: IC can easily be predicted using BMI, UA, and F-IRI which are common and simple test results collected in routine clinical practice.

Pancreatic neuroendocrine tumors (PanNETs) are generally hypervascular and readily detectable on imaging tests. However, hypovascular PanNETs are clinically problematic, requiring multiple imaging tests and tissue analyses to differentiate them from pancreatic ductal cancers. A 41 year-old man presented with Whipple's triad; 72 h fasting test followed by glucagon challenge test suggested insulinoma. However, contrast-enhanced computed tomography image showed a 17 mm tumor with poor enhancement and unclear borders in the tail of the pancreas. Abdominal magnetic resonance imaging and contrast-enhanced endoscopic ultrasonography (EUS) indicated cystic degeneration and necrosis at the same site; EUS-guided fine-needle aspiration cytology indicated a PanNET Grade 1 tumor. Although the imaging was inconclusive, diazoxide treatment ameliorated the hypoglycemia-related symptoms and insulinoma was deemed likely; following tail pancreatectomy and splenectomy, the symptoms disappeared. Pathological examination revealed a tumor positive for insulin and classed as PanNET Grade 1 according to the 2019 WHO classification. The microvessel density (MVD) of the tumor was found to be as low as 3.9%, which may partly account for the inconclusive images. The present case was difficult to diagnose preoperatively due to hypovascularity on imaging because of reduced MVD. It is clinically important to evaluate MVD in cases of hypovascular PanNETs by multiple preoperative imaging studies to differentiate them from pancreatic cancers and to validate the findings by postoperative pathological analysis.

Type 1 diabetes (T1D) is characterized by the progressive destruction of insulin-producing beta cells in the pancreas. Despite improvements in insulin monitoring techniques, there remains no cure for T1D. Individuals with T1D require lifelong insulin therapy and some develop life-threatening complications. T1D is a complex, multifactorial, autoimmune condition. Understanding why people get T1D and how it progresses has advanced our knowledge of the disease and led to the discovery of specific targets that can be therapeutically manipulated to halt or reverse the course of T1D. Scientists investigating the potential of immunotherapy treatment for the treatment have recently had some encouraging results. Teplizumab, an anti-CD3 monoclonal antibody that has been approved by the FDA, delays the onset of clinical T1D in patients ≥ 8 years of age with preclinical T1D and improves beta cell function. Therapies targeting beta cell health, vitality, and function are now thought to be an essential component of successful combination therapy for T1D. The idea that the beta cells themselves may influence their own destruction during the development of T1D is a notion that has recently been gaining acceptance in the field. Researchers have recently made remarkable strides in beta cell replacement therapy and beta cell regeneration techniques. This review offers a detailed exploration of the pathophysiological mechanisms of T1D. It discusses the intricate interplay of factors leading to T1D development and the innovative approaches being explored to discover new treatments and a cure for the millions of people living with T1D worldwide.

We herein report a case of food-induced small bowel obstruction (FIBO) while using a glucagon-like peptide 1 receptor agonist (GLP1-RA), trying to lose weight due to distorted body image. The patient was a 30-year-old woman who was not obese (height 158 cm, weight 50 kg). She started taking an oral semaglutide, a GLP1-RA, and it was soon switched to weekly subcutaneous semaglutide because of ineffectiveness. More than 6 months after titrating up to 1.0 mg, she got drunk and chomped on a lot of scallops sandwiched between sheets of kelp, so-called "kobujime" in Japan, and half a day later complained of abdominal pain. Based on a finding of computed tomography at our emergency department, she was suspected of having a bowel obstruction and underwent laparoscopic surgery, which resulted in a diagnosis of small bowel obstruction by kelp. FIBO is rare, but it can become very severe once it happens. Although we cannot prove the direct pathophysiological effects of GLP1-RAs on FIBO in this particular case, GLP1-RAs have been reported to be one of the underlying risks of bowel obstruction based on epidemiological and basic research evidence; still, it is under-recognized. For example, the package inserts in Japan do not mention intestinal obstruction. We hope that the present report will prove helpful in paying attention to GLP1-RAs as a factor in bowel obstruction, including FIBO.

Type-1 diabetes is a multifactorial disease characterized by genetic and environmental factors that contribute to its development and progression. Despite progress in the management of type-1 diabetes, the final goal of curing the disease is yet to be achieved. To establish effective methods for the prevention, intervention, and cure of the disease, the molecular mechanisms and pathways involved in its development and progression should be clarified. One effective approach is to identify genes responsible for disease susceptibility and apply information obtained from the function of genes in disease etiology for the protection, intervention, and cure of type-1 diabetes. In this review, we discuss the genetic basis of type-1 diabetes, along with prospects for its prevention, intervention, and cure for type-1 diabetes.

Background and aims: To investigate the association between the frequency of intermittent-scanning continuous glucose monitoring (isCGM) and diurnal variation of time in range (TIR), time above range (TAR), and time below range (TBR), we performed a post hoc analysis of the ISCHIA study, a multicenter, prospective, open-label, randomized crossover study of patients with type 1 diabetes mellitus.

Method: Data of 93 people who completed the ISCHIA study were used. We calculated scan frequency, TAR, TIR, and TBR of four approximately 6-h intervals: 6:00-11:59 (morning), 12:00-17:59 (afternoon), 18:00-23:59 (evening), and 0:00-5:59 (night). The correlation between scan frequency and diurnal variation of CGM metrics was analyzed using nonparametric Spearman correlation analysis.

Results: More frequent scanning was associated with higher TIR in the afternoon (rho = 0.343, P < 0.001), evening (rho = 0.243, P = 0.019), and night (rho = 0.218, P = 0.036); furthermore, it was associated with lower TAR in the afternoon (rho = -0.275, P = 0.008) and TBR in the evening (rho = -0.235, P = 0.024). Concern about the effect of blood glucose fluctuation on social communication affected the number of scans during the day. Concerns about loneliness and hypoglycemia when alone also influenced the number of nighttime scans.

Conclusion: Scan frequency is influenced by psychological factors. Afternoon scans were associated with the highest increase in TIR and decrease in TAR. Evening scans were linked to a reduction in TBR.