Charcot osteoarthropathy (COA) is a potentially limbthreatening condition that mainly affects diabetic patients with neuropathy. In everyday practice, it presents as a red, hot, swollen foot, usually painless, and is frequently triggered by trivial injury. Its etiology is traditionally attributed to impairment of either the autonomic nervous system, leading to increased blood flow and bone resorption, or of the peripheral nervous system, whereby loss of pain and protective sensation render the foot susceptible to repeated injury. More recently, excessive local inflammation is thought to play a decisive role. Diagnosis is based on clinical manifestation and imaging studies (plain X-rays, bone scan, Magnetic Resonance Imaging). The mainstay of management is immediate off-loading, while surgery is usually reserved for chronic cases with irreversible deformities and/or joint instability. The aim of this review is to provide an overview of COA in terms of pathogenesis, classification and clinical presentation, diagnosis and treatment, with an emphasis on the high suspicion required by clinicians for timely recognition to avoid further complications.

We evaluated olfactory dysfunction in 154 adults (74 men, mean age 60.9 ± 11.9 years), of whom 119 had type 2 diabetes mellitus (T2DM). Olfactory function was assessed with “Sniffin’ Sticks.” A total Threshold-Discrimination-Identification (TDI) score was calculated. Type 2 diabetes mellitus, hypertension, and hyperlipidemia were associated with lower olfactory scores (all TDI scores <0.001). Age was negatively associated with odor threshold, odor identification, and TDI score (P = .009, <.001, and <.001, respectively). After adjusting for age, gender, body mass index, smoking, alcohol, diabetes, hypertension, hyperlipidemia, and cardiovascular disease, only T2DM and hypertension were associated with TDI score (R square = 0.281). Diabetic complications were associated with olfactory dysfunction (P = .006): TDI scores were lower in the presence of diabetic peripheral neuropathy (P = .017) and retinopathy (P = .047). In conclusion, T2DM and hypertension are independently associated with olfactory dysfunction while diabetic peripheral neuropathy and retinopathy are significantly associated with lower olfactory scores. The clinical relevance of these findings needs to be further examined.

Diabetic foot ulcer (DFU) is a well-known complication of diabetes and a significant burden on the national health systems. The neutrophil/lymphocyte ratio (NLR) and platelet/lymphocyte ratio are inexpensive and easily accessible biomarkers that have proved to be useful in several inflammatory, infectious and cardiovascular diseases. We carried out a comprehensive review examining the association of NLR and PLR with the onset and progression of DFU. PLR and NLR were significantly increased in patients with DFU, compared with a control group of T2DM patients without DFU, and correlate well with DFU severity, evaluated by Wagner and IWGDF grading scales. In patients with diabetic foot infections (DFI), elevated NLR and PLR were correlated with osteomyelitis, increased risk of amputation, and septic complications. The significance of the elevated value of these biomarkers in DFU is related to chronic hyperglycemia and low-grade systemic inflammation, atherosclerotic and vascular complications, and also the associated septic factor. Serial, dynamic follow-up can provide useful information in planning and monitoring DFU treatment, as well as in risk stratification of these vulnerable patients. Further randomized studies are needed to set the cut-off values with clinical significance.

The present review outlines the role of breastfeeding in diabetes. In the mother, breastfeeding has been suggested to reduce the incidence of type 2 diabetes mellitus, the metabolic syndrome and cardiovascular disease. Moreover, it appears to reduce the risk of premenopausal breast cancer and ovarian cancer. In the neonate and infant, among other benefits, lactation confers protection from future both type 1 and type 2 diabetes. Whether lactation protects women with gestational diabetes mellitus and their offspring from future T2DM remains to be answered. Importantly, for diabetic mothers, antidiabetic treatment itself may affect breastfeeding. There is not enough data to allow the use of oral hypoglycaemic agents. Therefore, insulin currently remains the optimal antidiabetic treatment during lactation. In conclusion, breastfeeding could be considered a modifiable risk factor for the development of diabetes and even a potential protective lifestyle measure from future cardio-metabolic and malignant diseases. Therefore, health care professionals should encourage both women with and without diabetes to breastfeed their children.

The present review outlines the various issues of breast pathology in diabetes. Diabetic mastopathy is an uncommon proliferation of fibrous tissue in the breast that mimics tumour. Breast arterial calcifications represent calcium deposits in the media of arterioles and are more frequently detected on mammograms of diabetic subjects. Importantly, type 2 diabetes mellitus (T2DM) has been associated with breast cancer, but the mechanism underlying this association is complex, since the two entities frequently co-exist and seem to share common aetiological factors and pathways. Furthermore, diabetes has been suggested to negatively affect breast cancer outcomes, but it is unclear whether better glycaemic control would ameliorate prognosis. Preliminary data suggest that antidiabetic treatment may also influence both the incidence and prognosis of breast cancer. However, available evidence is inconclusive and further research is needed. Therefore, treatment of diabetes should not be determined by its potential effect on breast cancer.

Evidence from large epidemiological studies has shown that obesity may predispose to increased Th2 inflammation and increase the odds of developing asthma. On the other hand, there is growing evidence suggesting that metabolic dysregulation that occurs with obesity, and more specifically hyperglycemia and insulin resistance, may modify immune cell function and in some degree systemic inflammation. Insulin resistance seldom occurs on its own, and in most cases constitutes a clinical component of metabolic syndrome, along with central obesity and dyslipidemia. Despite that, in some cases, hyperinsulinemia associated with insulin resistance has proven to be a stronger risk factor than body mass in developing asthma. This finding has been supported by recent experimental studies showing that insulin resistance may contribute to airway remodeling, promotion of airway smooth muscle (ASM) contractility and proliferation, increase of airway hyper-responsiveness and release of pro-inflammatory mediators from adipose tissue. All these effects indicate the potential impact of hyperinsulinemia on airway structure and function, suggesting the presence of a specific asthma phenotype with insulin resistance. Epidemiologic studies have found that individuals with severe and uncontrolled asthma have a higher prevalence of glycemic dysfunction, whereas longitudinal studies have linked glycemic dysfunction to an increased risk of asthma exacerbations. Since the components of metabolic syndrome interact with one another so much, it is challenging to identify each one’s specific role in asthma. This is why, over the last decade, additional studies have been conducted to determine whether treatment of type 2 diabetes mellitus affects comorbid asthma as shown by the incidence of asthma, asthma control and asthma-related exacerbations. The purpose of this review is to present the mechanism of action, and existing preclinical and clinical data, regarding the effect of insulin resistance in asthma.