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Slowly progressive type 1 insulin-dependent diabetes mellitus (SPIDDM), sometimes referred to as latent autoimmune diabetes in adults (LADA), is a heterogeneous disease that is often confused with type 1 and type 2 diabetes. As a result, there were few diagnostic criteria for this disorder until 2012, when the Japan Diabetes Society established criteria that could be used in clinical practice. A primary question is whether pathologic markers for type 1 or type 2 diabetes are present in the pancreas of patients with SPIDDM, because the phenotype of SPIDDM is similar to both type 1 and type 2 diabetes. Recent studies clarified pathologic findings in the pancreas of patients with SPIDDM, which included T-cell-mediated insulitis, a marker of type 1 diabetes; pseudoatrophic islets (islets specifically devoid of beta cells), another hallmark of type 1 diabetes; and a lack of amylin (ie, islet amyloid polypeptide) deposition to the islet cells, a pathologic marker of type 2 diabetes. In terms of preventing the loss of beta-cell function in patients with SPIDDM, several studies have shown that some drugs, including dipeptidyl peptidase-4 inhibitors, are effective. There is an increased need for early diagnosis of SPIDDM to preserve beta-cell function. This review presents updated findings on the pathogenesis and immunologic findings of the affected pancreas, diagnostic markers, risk factors for progression of beta-cell dysfunction, epidemiology, clinical features, diagnostic strategies, prevention strategies, and clinical options for patients with SPIDDM.

The severity of SDB is associated with albuminuria in patients with T2DM.

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Study Objectives: Although recent studies suggest that obstructive sleep apnea during rapid eye movement (REM) is associated with different cardiometabolic and neurocognitive risks compared with non-REM (NREM) sleep, there is no information on whether obstructive sleep apnea during REM and/or NREM sleep is independently associated with diabetic kidney disease (DKD). Methods: In this cross-sectional study, 303 patients with type 2 diabetes who were followed up at our diabetes outpatient clinic underwent all-night polysomnography. Logistic regression analysis was performed to determine the separate effects of obstructive sleep apnea during REM and/or NREM sleep (REM and/or NREM-apnea-hypopnea index [AHI]) and several other polysomnography parameters on DKD after adjustment for several known risk factors for DKD.

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Aims/Introduction: To investigate factors influencing glycemic control in diabetes mellitus complicated by autoimmune pancreatitis. Materials and Methods: This retrospective cohort study investigated 33 patients with diabetes mellitus complicated by autoimmune pancreatitis who had received steroid therapy at Toranomon Hospital between January 1, 2011, and December 31, 2020. The course of glycemic control at 12 months after starting steroids was classified into three groups: Improved, Unchanged, or Worsened. Factors affecting these groups were investigated. Furthermore, we created two scores: (1) time of diabetes mellitus onset and baseline body mass index; (2) time of diabetes mellitus onset and baseline C-peptide index. Diabetes mellitus occurring at the same time as autoimmune pancreatitis, body mass index ≥22 kg/m 2 , and C-peptide index ≥1.1 were each worth 1 point. Scores were summed and totals of 0-2 were compared between groups. Results: Ten patients were in the Improved group, 10 were in the Unchanged group, and 13 were in the Worsened group. The baseline body mass index and baseline Cpeptide index were lower in the Worsened group than in the Improved group (P < 0.05 each). In addition, the scores were lower in the Worsened group than in the other groups (P < 0.05). Conclusions: Patients with a lower baseline body mass index and a decreased baseline C-peptide index may experience worse glycemic control on steroid therapy.