Diabetes and the Microcirculation
John H. Barker, Gary L. Anderson, Michael D. Menger in Clinically Applied Microcirculation Research, 2019
Damage to the microcirculation plays a central role in the development of the long-term complications of diabetes, leading to a specific microangiopathy characterized by basement membrane thickening in capillaries, arterioles, and venules. Although classically affecting the retina and kidney, the histological features of microangiopathy are apparent in a wide variety of other microvascular beds including skin, adipose tissue, and skeletal and cardiac muscle. In addition, it is increasingly recognized that microvascular abnormalities are involved in the development of neuropathy and diabetic foot ulceration. Microvascular disease is responsible for a substantial amount of morbidity in the non-elderly in Western countries, with diabetic retinopathy and nephropathy being the most common causes of blindness and renal failure, respectively. Foot ulceration is also a major problem, accounting for a large proportion of diabetes-related hospital admissions and bed occupancy. This chapter will outline the pathogenesis of these microvascular complications, their clinical manifestations in different tissues, and the potential treatment options available to minimize the impact of microvascular disease.
Research Models of Diabetes Mellitus
Grant N. Pierce, Robert E. Beamish, Naranjan S. Dhalla in Heart Dysfunction in Diabetes, 2019
Diabetes in the Chinese hamster is of genetic determination. Its symptoms appear at about 60 days of age, although this may vary with the subline of Chinese hamster studied.25 The animals are hyperglycemic, lean, hyperphagic, polydipsic, and glycosurie.14,25 Plasma insulin levels are depressed, normal, or elevated depending on the subline of hamster examined.25 Current sublines appear to have normal or elevated plasma insulin levels.14,15 Ketone bodies may be found in increased concentration in plasma samples from these animals.25 Plasma glucagon.4 and lipids6,26 are elevated whereas somatostatin levels are decreased.4 Nutritional and environmental manipulations can delay but not prevent the onset of diabetes in these animals.25,31 Complications which have been documented in the Chinese hamster affect the nerves, kidney, GI, and reproductive systems.5–11 Macroangiopathy.32 and microangiopathy have also been reported.33 Skeletal abnormalities have also been described.50 The disease is carried by at least four genes, two of which must be homozygous. The disease is normally progressive in nature.
Introduction
Emmanuel Opara in NUTRITION and DIABETES, 2005
While the risk of dying from acute complications of diabetes (sepsis, dehydration) has been reduced, the majority of patients with diabetes suffer from increased mortality and morbidity due to the vascular complications that develop within a variety of organ systems. Most vascular complications of diabetes mellitus are generally categorized as either microvascular or macrovascular problems; however, many patients with vascular disease have both kinds of vasculopathies, although to varying degrees [100]. Major risk factors for the progression of microangiopathy include poor glycemic control, a prolonged history of diabetes, and hypertension [101]. Those for macroangiopathy are aging, obesity, abnormal lipid metabolism, hypertension, and smoking [102].
Breaking Bad: a case of Lactobacillus bacteremia and liver abscess
Published in Journal of Community Hospital Internal Medicine Perspectives, 2019
Abdillahi M. Omar, Nastaran Ahmadi, Mutaz Ombada, Joseph Fuscaldo, Nazia Siddiqui, Myra Safo, Swaroopa Nalamalapu
The only identified known risk factor for our patient was his diabetes, which combined with lack of health insurance presented as uncontrolled diabetes. Diabetes mellitus is associated with two types of vascular disease. Non-occlusive microangiopathy, which is caused by increased vascular permeability and impaired autoregulation of blood flow involving the capillaries and arterioles. Macroangiopathy is associated with atherosclerotic lesions [21]. In addition, advanced glycation end products (AGEs) are responsible for glycosylation of basement membranes resulting in increased vascular permeability. Metabolic alterations in diabetes have also been reported to contribute in changes in endothelial cells. This is likely a factor in the higher susceptibility of diabetic patients to deadly complications of infectious diseases. This endothelial injury could be a possible route of bacterial translocation from normal flora to bacteremia and formation of liver abscess.
COVID-19 and the Ocular Surface: A Review of Transmission and Manifestations
Published in Ocular Immunology and Inflammation, 2020
Dawn Ho, Rebecca Low, Louis Tong, Vishali Gupta, Aravamudan Veeraraghavan, Rupesh Agrawal
To date, there is a scarcity of data about the intraocular manifestations of SARS-CoV-2 or CoVs in humans, although observational and experimental studies in animals have shown the involvement of the posterior segment. A recent study published in Lancet by Marinho et al. illustrated the presence of hyperreflective lesions at ganglion cell layer and also at inner plexiform layers (near papillomacular bundle) in all 12 patients in the case series from Brazil. In addition, some of the patients had features suggestive of retinal microangiopathy.37 Apart from conjunctivitis, feline coronaviruses were noted to cause granulomatous anterior uveitis, choroiditis with retinal detachment, and retinal vasculitis.12 Murine coronaviruses have been studied to induce retinitis, retinal degeneration, and optic neuritis.12 As the literature on human ocular CoV infection is still lacking, an understanding of the ocular manifestations of animal CoV infections may open insights into the spectrum of ocular diseases that CoVs can cause.
Caplacizumab: a change in the paradigm of thrombotic thrombocytopenic purpura treatment
Published in Expert Opinion on Biological Therapy, 2019
Maëlle le Besnerais, Agnès Veyradier, Ygal Benhamou, Paul Coppo
Thrombotic thrombocytopenic purpura (TTP) is a rare, life-threatening thrombotic microangiopathy with an average annual prevalence of about 10 cases/million people and an annual incidence of 1–2 new case/million people [1,2]. TTP results from systemic microvascular thrombosis and leading to profound thrombocytopenia, hemolytic anemia, and organ failure of varying severity [3,4]. Acquired, immune-mediated TTP (iTTP) is caused by a severe immune-mediated deficiency of ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) due to the presence of anti-ADAMTS13 autoantibodies that can be identified in 91% of adults with idiopathic TTP [5]. A deficiency in ADAMTS13 activity leads to an accumulation of ultra-large von Willebrand factor multimers (ULvWF) allowing unrestrained adhesion of von Willebrand factor (vWF) multimers to platelets and formation of platelet-rich microthrombi in small blood vessels with thrombocytopenia. Systemic microthrombi, by occluding vessels, result in microangiopathic hemolytic anemia, tissue ischemia [5,6] and organ dysfunction (typically the brain, the heart, and kidneys). If left untreated, iTTP is invariably fatal [7]. In patients who recovered from an iTTP episode, cognitive deficits, depression, arterial hypertension, autoimmune diseases, and a shortened life expectancy were also reported [3,8,9].
Related Knowledge Centers
- Aorta
- Common Carotid Artery
- Kidney Failure
- Microcirculation
- Retina
- Blood Vessel
- Atherosclerosis
- Brain
- Kidney
- Coronary Arteries