COVID-19 and metabolic disease: mechanisms and clinical management.

Up to 50% of the people who have died from COVID-19 had metabolic and vascular disorders. Notably, there are many direct links between COVID-19 and the metabolic and endocrine systems. Thus, not only are patients with metabolic dysfunction (eg, obesity, hypertension, non-alcoholic fatty liver disease, and diabetes) at an increased risk of developing severe COVID-19 but also infection with SARS-CoV-2 might lead to new-onset diabetes or aggravation of pre-existing metabolic disorders.

Metabolic and Non-Metabolic Peripheral Neuropathy: Is there a Place for Therapeutic Apheresis?

As the rate of obesity and the incidence of diabetes mellitus have been increasing, diabetic neuropathy has become the most common cause of peripheral neuropathy in developed countries. In addition, a variety of pathogenetically heterogeneous disorders can lead to impairment of the peripheral nervous system including amyloidosis, vitamin deficiencies, uremia and lipid disorders, alcohol abuse, autoimmune and infectious diseases as well as exposure to environmental toxins. We have noted that a combination of these disorders may aggravate the manifestations of peripheral diabetic neuropathy, an effect, which is most pronounced when metabolic and non-metabolic pathologies lead to cumulative damage.

Current aspects in the pathophysiology and treatment of chronic wounds in diabetes mellitus.

Impaired wound healing is a frequent and very severe problem in patients with diabetes mellitus, yet little is known about the underlying pathomechanisms. In this paper we review the biology of wound healing with particular attention to the pathophysiology of chronic wounds in diabetic patients. The standard treatment of diabetic ulcers includes measures to optimize glycemic control as well as extensive debridement, infection elimination by antibiotic therapy based on wound pathogen cultures, the use of moisture dressings, and offloading high pressure from the wound bed.

Self-adjustment of insulin dose using graphically depicted self-monitoring of blood glucose measurements in patients with type 1 diabetes mellitus.

Background: There is a need for patients to be able to adjust their insulin doses accurately and independently during continuous subcutaneous insulin infusion (CSII) therapy in order to avoid glycemic excursions and improve glycemic control. Use of new technology has the potential to aid patients in visualizing their circadian patterns and improving their understanding of data provided by self-monitored blood glucose (SMBG) measurements.

Methods: A 24-week crossover study was performed in 25 patients with type 1 diabetes mellitus using CSII and SMBG.

Noninvasive management of the diabetic foot with critical limb ischemia: current options and future perspectives.

Foot ulcers are a major complication in patients with diabetes mellitus and involve dramatic restrictions to quality of life and also lead to enormous socio-economical loss due to the high amputation rate. The poor and slow wound healing is often aggravated by the frequent comorbidity of foot ulcers with peripheral arterial disease, making the treatment of this condition even more complicated. While the local treatment of foot ulcers is mainly based on mechanical relief and prevention or treatment of infection, improving perfusion of the impaired tissue remains the major challenge in peripheral arterial disease.

[Recent advances in type 2 diabetes mellitus].

Currently, the oral glucose tolerance test remains the "gold standard" for diagnosing type 2 diabetes, HbA (1c) being of subordinate value because of its limited diagnostic sensitivity. Fully evaluated risk scores and questionnaires are helpful in determining individual type 2 diabetes risk profiles and may prove valuable tools in preventing this type of diabetes. Genetic studies support our current understanding of the pathophysiology of type 2 diabetes.

Alcohol consumption and other psycho-social conditions as important factors in the development of diabetic foot ulcers.

Aims: To characterize bio-psycho-social factors, particularly mental disorders and self-harm behaviour, associated with the development of diabetic foot ulcers.

Methods: Two groups of diabetic patients with and without foot ulcers (n=47 in each group) with similar sex, age and diabetes duration were assessed for mental disorders using the Composite International Diagnostic Interview. Self-harm behaviour, quality of life, depressive symptoms and self-compassion were rated using different standard questionnaires.

Intermittent intravenous urokinase for critical limb ischemia in diabetic foot ulceration.

Patients with diabetic foot ulceration and critical limb ischemia have a high risk of major amputation, especially if limbs can not be revascularized. Urokinase is effective in improving microcirculation in critical limb ischemia and might improve outcomes. There are no data on the efficacy and safety of urokinase treatment (survival free of major amputation, ulcer healing and the rate of minor and major bleeding).

Heparin-induced Extracorporal LDL precipitation (H.E.L.P) in diabetic foot syndrome - preventive and regenerative potential?

Peripheral arterial disease is more aggressive in concomitant diabetes posing an increased risk for critical limb ischemia and subsequent limb loss. The majority of therapies available are not effective to prevent amputation in patients with severe disease. The current observational study reports the effect of the heparin-induced extracorporal LDL-precipitation (H.

Association of the calpain-10 gene with type 2 diabetes in Europeans: results of pooled and meta-analyses.

We conducted pooled and meta-analyses of the association of the calpain-10 gene (CAPN10) polymorphisms SNP-43, Indel-19 and SNP-63 individually and as haplotypes with type 2 diabetes (T2D) in 3237 patients and 2935 controls of European ancestry. In the pooled analyses, the common SNP-43*G allele was associated with modest but statistically significant increased risk of T2D (odds ratio (OR)=1.11 (95% confidence interval (CI), 1.

Influence of treatment with acarbose or glibenclamide on insulin sensitivity in type 2 diabetic patients.

Aim: The aim of our double-blind, placebo-controlled study was to compare the effect of acarbose and glibenclamide on the insulin sensitivity in type 2 diabetes.

Methods: We investigated 77 patients (mean age 58.7 years, mean BMI 27.

Cessation of insulin infusion at night-time during CSII-therapy: comparison of regular human insulin and insulin lispro.

Development of hyperglycemia with subsequent ketoacidosis is one of the potential risks of a sudden cessation of insulin delivery during continuous insulin infusion therapy with insulin pumps in patients with IDDM. To evaluate differences in the development of ketoacidosis after a sudden pump stoppage between regular human insulin and insulin lispro, we performed an open label randomized crossover investigation with 7 patients (6 male/1 female, mean age (SD: 40.9 +/- 12.

Hepatic function in a family with a nonsense mutation (R154X) in the hepatocyte nuclear factor-4alpha/MODY1 gene.

Maturity-onset diabetes of the young (MODY) is a genetically heterogeneous monogenic disorder characterized by autosomal dominant inheritance, onset usually before 25 yr of age, and abnormal pancreatic beta-cell function. Mutations in the hepatocyte nuclear factor(HNF)-4alpha/MODY1, glucokinase/MODY2, and HNF-1alpha/MODY3 genes can cause this form of diabetes. In contrast to the glucokinase and HNF-1alpha genes, mutations in the HNF-4alpha gene are a relatively uncommon cause of MODY, and our understanding of the MODY1 form of diabetes is based on studies of only a single family, the R-W pedigree.

An approach for identifying simple sequence repeat DNA polymorphisms near cloned cDNAs and genes. Linkage studies of the islet amyloid polypeptide/amylin and liver glycogen synthase genes and NIDDM.

Genetic factors contribute to the development of NIDDM, and genes involved in regulating pancreatic beta-cell function and insulin's effects on glucose metabolism are good candidates for being NIDDM susceptibility loci. However, testing candidate genes for linkage to NIDDM depends on the identification of highly informative DNA polymorphisms in or near the candidate locus. Here we describe an approach for identifying highly polymorphic markers near candidate genes that utilizes the emerging physical map of the human genome.