Case Report Seromuscular Colonic Flap for Intrapelvic Soft-Tissue Coverage: A Reconstructive Option for Plastic Surgeons When Traditionally Used Flaps Are Not Available

Background. Reconstruction of intrapelvic defects can be a challenging problem in patients with limited regional muscle flap options and previously resected omentum. In such situations, alternative methods of mobilizing vascularized tissue may be required. Methods. A case of a patient that underwent pelvic extirpation for recurrent rectal cancer who had limited donor sites for flap reconstruction is presented. The mucosa was removed from a blind loop of colon, and a pedicled seromuscular flap based on the colonic mesentery was placed into the pelvis for vascularized soft-tissue coverage and elimination of dead space. Results. The postoperative course was only complicated by a small subcutaneous fluid collection beneath the sacrectomy skin incision, which was drained with radiological assistance. The patient recovered without any major postoperative complications. Conclusion. Seromuscular colonic flap is a useful option for soft-tissue coverage after pelvic extirpation and should be considered by plastic surgeons when other reconstruction options are not available

A Novel Small Molecule 1,2,3,4,6-penta-O-galloyl-α-D-glucopyranose Mimics the Antiplatelet Actions of Insulin

BACKGROUND: We have shown that 1,2,3,4,6-penta-O-galloyl-α-D-glucopyranose (α-PGG), an orally effective hypoglycemic small molecule, binds to insulin receptors and activates insulin-mediated glucose transport. Insulin has been shown to bind to its receptors on platelets and inhibit platelet activation. In this study we tested our hypothesis that if insulin possesses anti-platelet properties then insulin mimetic small molecules should mimic antiplatelet actions of insulin. PRINCIPAL FINDINGS: Incubation of human platelets with insulin or α-PGG induced phosphorylation of insulin receptors and IRS-1 and blocked ADP or collagen induced aggregation. Pre-treatment of platelets with α-PGG inhibited thrombin-induced release of P-selectin, secretion of ATP and aggregation. Addition of ADP or thrombin to platelets significantly decreased the basal cyclic AMP levels. Pre-incubation of platelets with α-PGG blocked ADP or thrombin induced decrease in platelet cyclic AMP levels but did not alter the basal or PGE(1) induced increase in cAMP levels. Addition of α-PGG to platelets blocked agonist induced rise in platelet cytosolic calcium and phosphorylation of Akt. Administration of α-PGG (20 mg kg(-1)) to wild type mice blocked ex vivo platelet aggregation induced by ADP or collagen. CONCLUSIONS: These data suggest that α-PGG inhibits platelet activation, at least in part, by inducing phosphorylation of insulin receptors leading to inhibition of agonist induced: (a) decrease in cyclic AMP; (b) rise in cytosolic calcium; and (c) phosphorylation of Akt. These findings taken together with our earlier reports that α-PGG mimics insulin signaling suggest that inhibition of platelet activation by α-PGG mimics antiplatelet actions of insulin

Finerenone in the management of diabetes kidney disease.

People with type 2 diabetes are at risk of developing progressive diabetic kidney disease (DKD) and end stage kidney failure. Hypertension is a major, reversible risk factor in people with diabetes for development of albuminuria, impaired kidney function, end-stage kidney disease and cardiovascular disease. Slowing progression of kidney disease and reducing cardiovascular events can be achieved by a number of means including the targeting of blood pressure and the use of specific classes of drugs The use of Renin Angiotensin Aldosterone System (RAAS) blockade is effective in preventing or slowing progression of DKD and reducing cardiovascular events in people with type 2 diabetes, albeit differently according to the stage of DKD. However, emerging therapy such as non-steroidal selective mineralocorticoid antagonists (finerenone) is proven to lower blood pressure and further reduce the risk of progression of DKD and cardiovascular disease in people with type 2 diabetes. This consensus reviews current evidence and make recommendations for the use of finerenone in the management of diabetes kidney disease in the UK

Ambivalence related to potential lifestyle changes following preventive cardiovascular consultations in general practice: A qualitative study

<p>Abstract</p> <p>Background</p> <p>Motivational interviewing approaches are currently recommended in primary prevention and treatment of cardiovascular disease (CVD) in general practice in Denmark, based on an empirical and multidisciplinary body of scientific knowledge about the importance of motivation for successful lifestyle change among patients at risk of lifestyle related diseases. This study aimed to explore and describe motivational aspects related to potential lifestyle changes among patients at increased risk of CVD following preventive consultations in general practice.</p> <p>Methods</p> <p>Individual interviews with 12 patients at increased risk of CVD within 2 weeks after the consultation. Grounded theory was used in the analysis.</p> <p>Results</p> <p>Ambivalence related to potential lifestyle changes was the core motivational aspect in the interviews, even though the patients rarely verbalised this experience during the consultations. The patients experienced ambivalence in the form of conflicting feelings about lifestyle change. Analysis showed that these feelings interacted with their reflections in a concurrent process. Analysis generated a typology of five different ambivalence sub-types: perception, demand, information, priority and treatment ambivalence.</p> <p>Conclusion</p> <p>Ambivalence was a common experience in relation to motivation among patients at increased risk of CVD. Five different ambivalence sub-types were found, which clinicians may use to explore and resolve ambivalence in trying to aid patients to adopt lifestyle changes. Future research is needed to explore whether motivational interviewing and other cognitive approaches can be enhanced by exploring ambivalence in more depth, to ensure that lifestyle changes are made and sustained. Further studies with a wider range of patient characteristics are required to investigate the generalisability of the results.</p

Association of British Clinical Diabetologists and UK Kidney Association joint clinical practice guidelines for the pharmacological management of hyperglycaemia in adults with type 2 diabetes and CKD

A growing and significant number of people with diabetes develop chronic kidney disease (CKD) and diabetes related CKD is a leading cause of end-stage kidney disease (ESKD). People with diabetes and CKD have high morbidity and mortality, predominantly related to cardiovascular disease (CVD). Hyperglycaemia and hypertension are modifiable risk factors to prevent onset and progression of CKD and related CVD. Recent clinical trials of people with type 2 diabetes and CKD have demonstrated reduction in composite kidney endpoint events (significant decline in kidney function, need for kidney replacement therapy and kidney related death) and cardiovascular risk with sodium glucose co-transporter-2 (SGLT-2) inhibitors, non-steroidal mineralocorticoid receptor antagonists (nsMRAs) and glucagon-like peptide 1 (GLP-1) receptor agonists. The Association of British Clinical Diabetologists and UK Kidney Association Diabetic Kidney Disease Clinical Speciality Group have previously undertaken a narrative review and critical appraisal of the available evidence to inform clinical practice guidelines for the pharmacological management of hyperglycaemia in adults with type 2 diabetes and CKD. This 2025 abbreviated updated guidance from a multidisciplinary group of healthcare professionals from primary and secondary care settings summarises the key recommendations and recent evidence that has implications for clinical practice for health care professionals who treat people with type 2 diabetes and CK

Etiopathogenesis of type 1 diabetes mellitus: prognostic factors for the evolution of residual β cell function

Type 1A diabetes mellitus (T1ADM) is a progressive autoimmune disease mediated by T lymphocytes with destruction of beta cells. Up to now, we do not have precise methods to assess the beta cell mass, "in vivo" or "ex-vivo". The studies about its genetic susceptibility show strong association with class II antigens of the HLA system (particularly DQ). Others genetics associations are weaker and depend on the population studied. A combination of precipitating events may occur at the beginning of the disease. There is a silent loss of immune-mediated beta cells mass which velocity has an inverse relation with the age, but it is influenced by genetic and metabolic factors. We can predict the development of the disease primarily through the determination of four biochemically islet auto antibodies against antigens like insulin, GAD65, IA2 and Znt8. Beta cell destruction is chronically progressive but at clinical diagnosis of the disease a reserve of these cells still functioning. The goal of secondary disease prevention is halt the autoimmune attack on beta cells by redirecting or dampening the immune system. It is remains one of the foremost therapeutic goals in the T1ADM. Glycemic intensive control and immunotherapeutic agents may preserve beta-cell function in newly diagnosed patients with T1ADM. It may be assessed through C-peptide values, which are important for glycemic stability and for the prevention of chronic complications of this disease. This article will summarize the etiopathogenesis mechanisms of this disease and the factors can influence on residual C-peptide and the strategies to it preservation

Current management of chronic kidney disease in type-2 diabetes-A tiered approach: An overview of the joint Association of British Clinical Diabetologists and UK Kidney association (ABCD-UKKA) guidelines.

A growing and significant number of people with diabetes develop chronic kidney disease (CKD). Diabetes-related CKD is a leading cause of end-stage kidney disease (ESKD) and people with diabetes and CKD have high morbidity and mortality, predominantly related to cardiovascular disease (CVD). Despite advances in care over the recent decades, most people with CKD and type 2 diabetes are likely to die of CVD before developing ESKD. Hyperglycaemia and hypertension are modifiable risk factors to prevent onset and progression of CKD and related CVD. People with type 2 diabetes often have dyslipidaemia and CKD per se is an independent risk factor for CVD, therefore people with CKD and type 2 diabetes require intensive lipid lowering to reduce burden of CVD. Recent clinical trials of people with type 2 diabetes and CKD have demonstrated a reduction in composite kidney end point events (significant decline in kidney function, need for kidney replacement therapy and kidney death) with sodium-glucose co-transporter-2 (SGLT-2) inhibitors, non-steroidal mineralocorticoid receptor antagonist finerenone and glucagon-like peptide 1 receptor agonists. The Association of British Clinical Diabetologists (ABCD) and UK Kidney Association (UKKA) Diabetic Kidney Disease Clinical Speciality Group have previously undertaken a narrative review and critical appraisal of the available evidence to inform clinical practice guidelines for the management of hyperglycaemia, hyperlipidaemia and hypertension in adults with type 2 diabetes and CKD. This 2024 abbreviated updated guidance summarises the recommendations and the implications for clinical practice for healthcare professionals who treat people with diabetes and CKD in primary, community and secondary care settings

Management of Hypertension in Patients With Diabetic Kidney Disease: Summary of the Joint Association of British Clinical Diabetologists and UK Kidney Association (ABCD-UKKA) Guideline 2021.

Diabetic kidney disease (DKD) accounts for >40% cases of chronic kidney disease (CKD) globally. Hypertension is a major risk factor for progression of DKD and the high incidence of cardiovascular disease and mortality in these people. Meticulous management of hypertension is therefore crucial to slow down the progression of DKD and reduce cardiovascular risk. Randomized controlled trial evidence differs in type 1 and type 2 diabetes and in different stages of DKD in terms of target blood pressure (BP). Renin-angiotensin blocking agents reduce progression of DKD and cardiovascular events in both type 1 and type 2 diabetes, albeit differently according to the stage of CKD. There is emerging evidence for the benefit of sodium glucose cotransporter 2, nonsteroidal selective mineralocorticoid antagonists, and endothelin-A receptor antagonists in slowing progression and reducing cardiovascular events in DKD. This UK guideline, developed jointly by diabetologists and nephrologists, has reviewed all available current evidence regarding the management of hypertension in DKD to produce a set of comprehensive individualized recommendations for BP control and the use of antihypertensive agents according to age, type of diabetes, and stage of CKD (https://ukkidney.org/sites/renal.org/files/Management-of-hypertension-and-RAAS-blockade-in-adults-with-DKD.pdf). A succinct summary of the guideline, including an infographic, is presented here