Browsing by Subject "Diabetes Mellitus"

Now showing 1 - 10 of 18
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    Case Presentation: Shoulder pain as a rheumatic manifestation of diabetes mellitus
    (Association of Kenya Physicians, 2007) Okanga, J. B.; Yossa, G. P.; Association of Kenya Physicians Scientific Conference (11th : Mar. 2007 : Eldoret, Kenya)
    Shoulder pain, a common musculoskeletal symptom, aetiologically is related to periarticular lesions mainly subacronial impingment (SAI) (90% adults). Articular lesions e.g. Synovvitis adhesive capsulitis (frozen shoulder) etc may be referred to the neck and humeral deltoid insertion. Referred pain from the cervical or thoracic spine, thoracic outlet or subdiaphramatic structures may manifest at the shoulder. Diabetes mellitus syndrome may be complicated by adhesive capsulitis more frequently than in the general population. A case is presented of a 52yr old house wife of high social standing, who has been followed up for 5yrs. Initially left shoulder pain but in the last 2yrs predominantly right shoulder pain, less involvement of the neck, right wrist and right foot. She has been under several clinicians with a frustration long list of probable diagnoses to her ailment. Diabetes mellitus was diagnosed in September 2005 and attacks related to hyperglycaemia/metabolic decompensation. The last attack was in January 2007 which necessitated hospitalization. A visiting rheumatologist confirmed "FROZEN SHOULDER" with diabetes mellitus. A multidisciplinary and multifactorial intervention aimed at multiple risk factors of diabetes syndrome is the way forward. Patient education/nutrition counseling and physiotherapy is the cornerstone of effective management.
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    Comment on Liu et al. Aberrant Expression of FBXO2 Disrupts Glucose Homeostasis Through Ubiquitin-Mediated Degradation of Insulin Receptor in Obese Mice. Diabetes 2017;66:689–698
    (American Diabetes Association, 2020-02) Wong, Siauyen; Nelson, Rick F.; Lu, Peiran; Paulson, Henry; Lin, Dingbo; Otolaryngology -- Head and Neck Surgery, School of Medicine
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    Correlates of depression among people with diabetes: The Translating Research Into Action for Diabetes (TRIAD) study
    (Elsevier, 2010-12) Waitzfelder, Beth; Gerzoff, Robert B.; Karter, Andrew J.; Crystal, Stephen; Bair, Mathew J.; Ettner, Susan L.; Brown, Arleen F.; Subramanian, Usha; Lu, Shou-En; Marrero, David; Herman, William H.; Selby, Joseph V.; Dudley, R. Adams; Department of Medicine, Division of General Internal Medicine, IU School of Medicine
    Aim The broad objective of this study was to examine multiple dimensions of depression in a large, diverse population of adults with diabetes. Specific aims were to measure the association of depression with: (1) patient characteristics
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    Diabetes and peripheral arterial disease in men: trends in prevalence, mortality, and effect of concomitant coronary disease
    (Wiley, 2009-08) Kamalesh, Masoor; Shen, Jianzhao; Biostatistics, School of Public Health
    BACKGROUND: Recent data on trends in diabetes mellitus (DM) prevalence and long-term effect on mortality in peripheral arterial disease (PAD) subjects is lacking. METHODS: All subjects discharged from any VA medical center between October 1990 to September 1997 with an International Classification of Diseases (ICD)-9 code for PAD and DM in the discharge summary were retrospectively identified. Demographic data were extracted from the database. Mortality data were obtained from the Beneficiary Information and Resource Locator. Outcome measures were age specific DM prevalence over time, and short-term and long-term mortality. RESULTS: Of 33, 629 patients with PAD, 9474 (29%) had DM. Diabetes mellitus subjects were less likely to be white and had more comorbidities. Mean length of hospital stay was greater for DM (22.3 d vs 18.7 days, P < 0.001). Mortality was higher for DM at 180 days (9.8% vs 8.4%, P < 0.001), 1 year (16.4% vs 13.7%, P < 0.001), and continues to increase at 8 years of follow-up. Logistic regression analysis showed no interaction between DM and coronary artery disease (CAD). CONCLUSIONS: Diabetes mellitus increases all-cause mortality in subjects with PAD starting at 6 months post-discharge and continues to be higher even at 8 years of follow-up. There was a lack of interaction of DM and CAD on mortality in this cohort of subjects with PAD.
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    Diabetes, Pancreatogenic Diabetes, and Pancreatic Cancer
    (American Diabetes Association, 2017-05) Andersen, Dana K.; Korc, Murray; Petersen, Gloria M.; Eibl, Guido; Li, Donghui; Rickels, Michael R.; Chari, Suresh T.; Abbruzzese, James L.; Medicine, School of Medicine
    The relationships between diabetes and pancreatic ductal adenocarcinoma (PDAC) are complex. Longstanding type 2 diabetes (T2DM) is a risk factor for pancreatic cancer, but increasing epidemiological data point to PDAC as also a cause of diabetes due to unknown mechanisms. New-onset diabetes is of particular interest to the oncology community as the differentiation of new-onset diabetes caused by PDAC as distinct from T2DM may allow for earlier diagnosis of PDAC. To address these relationships and raise awareness of the relationships between PDAC and diabetes, a symposium entitled Diabetes, Pancreatogenic Diabetes, and Pancreatic Cancer was held at the American Diabetes Association's 76th Scientific Sessions in June 2016. This article summarizes the data presented at that symposium, describing the current understanding of the interrelationships between diabetes, diabetes management, and pancreatic cancer, and identifies areas where additional research is needed.
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    An informatics approach to medication adherence assessment and improvement using clinical, billing, and patient-entered data
    (Oxford University Press, 2014-05) Dixon, Brian E.; Jabour, Abdulrahman M.; O’Kelly Phillips, Erin; Marrero, David G.; BioHealth Informatics, School of Informatics and Computing
    The aim of this study was to describe an integrated informatics approach to aggregating and displaying clinically relevant data that can identify problems with medication adherence and facilitate patient-provider communication about strategies to improve medication use. We developed a clinical dashboard within an electronic health record (EHR) system that uses data from three sources: the medical record, pharmacy claims, and a personal health record. The data are integrated to inform clinician-patient discussions about medication adherence. Whereas prior research on assessing patterns of medication adherence focused on a single approach using the EHR, pharmacy data, or patient-entered data, we present an approach that integrates multiple electronic data sources increasingly found in practice. Medication adherence is a complex challenge that requires patient and provider team input, necessitating an integrated approach using advanced EHR, clinical decision support, and patient-controlled technologies. Future research should focus on integrated strategies to provide patients and providers with the right combination of informatics tools to help them adequately address the challenge of adherence to complex medication therapies.
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    Mesenchyme homeobox 2 regulation of fetal endothelial progenitor cell function
    (2017-06-19) Gohn, Cassandra Rebekah; Haneline, Laura S.; Elmendorf, Jeffrey S.; Herring, B. Paul; Tune, Johnathan D.
    In the United States, 10% of pregnancies are complicated by diabetes mellitus (DM). Intrauterine DM exposure can have long-lasting implications for the fetus, including cardiovascular morbidity. Previously, we showed that fetal endothelial colony forming cells (ECFCs) from DM pregnancies have decreased vessel-forming ability and increased senescence. However, the molecular mechanisms responsible for this dysfunction remain largely unknown. The objective of this thesis was to understand how Mesenchyme Homeobox 2 (MEOX2) interacts with pathways that regulate cell cycle progression and migration, and how this interaction results in impaired vasculogenesis in DM exposed ECFCs. We tested the hypothesis that upregulated MEOX2 in DM-exposed ECFCs decreases network formation through impairments in senescence, cell cycle progression, migration, and adhesion. MEOX2 is a transcription factor which inhibits angiogenesis by upregulating cyclin dependent kinase inhibitors. Here, data show that nuclear MEOX2 is increased in DM-exposed ECFCs. Lentiviral-mediated overexpression of MEOX2 in control ECFCs increased network formation, altered cell cycle progression, increased senescence, and enhanced migration. In contrast, MEOX2-knockdown in DM-exposed ECFCs decreased network formation and migration, while cell cycle progression and senescence were unchanged. Adhesion and integrin expression defects were evaluated as mechanisms by which MEOX2 altered ECFC migration. While MEOX2-overexpression did not alter adhesion or cell surface integrin levels in control cells, MEOX2 overexpression in DM-exposed ECFCs resulted in an increase in α6 integrin surface expression. Similarly, MEOX2-knockdown in DM-exposed ECFCs did not alter adhesion, though did reduce α6 integrin surface expression and total cellular α6 mRNA and protein levels. Together, these data suggest that alterations in cell cycle progression and senescence are not responsible for the disrupted vasculogenesis of DM-exposed ECFCs. Importantly, these data suggest that altered migration may be a key mechanism involved and that altered cell surface levels of the α6 integrin may modify migratory capacity. Moreover, these data suggest that the α6 integrin may be a previously unrecognized transcriptional target of MEOX2. Ultimately, while initially believed to be maladaptive, these data suggest that increased nuclear MEOX2 in DM-exposed ECFCs may serve a protective role, enabling vessel formation despite exposure to a DM intrauterine environment.
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    Minireview: 12-Lipoxygenase and Islet β-Cell Dysfunction in Diabetes
    (The Endocrine Society, 2015-06) Tersey, Sarah A.; Bolanis, Esther; Holman, Theodore R.; Maloney, David J.; Nadler, Jerry L.; Mirmira, Raghavendra G.; Department of Pediatrics, IU School of Medicine
    The insulin producing islet β-cells have increasingly gained attention for their role in the pathogeneses of virtually all forms of diabetes. Dysfunction, de-differentiation, and/or death of β-cells are pivotal features in the transition from normoglycemia to hyperglycemia in both animal models of metabolic disease and humans. In both type 1 and type 2 diabetes, inflammation appears to be a central cause of β-cell derangements, and molecular pathways that modulate inflammation or the inflammatory response are felt to be prime targets of future diabetes therapy. The lipoxygenases (LOs) represent a class of enzymes that oxygenate cellular polyunsaturated fatty acids to produce inflammatory lipid intermediates that directly and indirectly affect cellular function and survival. The enzyme 12-LO is expressed in all metabolically active tissues, including pancreatic islets, and has received increasing attention for its role in promoting cellular inflammation in the setting of diabetes. Genetic deletion models of 12-LO in mice reveal striking protection from metabolic disease and its complications and an emerging body of literature has implicated its role in human disease. This review focuses on the evidence supporting the proinflammatory role of 12-LO as it relates to islet β-cells, and the potential for 12-LO inhibition as a future avenue for the prevention and treatment of metabolic disease.