Exogenous Insulin Antibody Syndrome (EIAS) Presenting in an Elderly, Long-Term Patient with Type 1 Diabetes Mellitus that Resolved with Low-Cost Outpatient Therapy with Mycophenolate Mofetil and Regular Insulin by Pump.

Exogenous insulin antibody syndrome (EIAS) has until recently been a rarely described complication of exogenous insulin therapy. EIAS results not only in hyperglycemia, but also in hypoglycemia and occasionally in ketoacidosis (DKA). The incidence of EIAS is increasing probably due to an overall increase in autoimmunity associated with the coronavirus disease 2019 (Covid-19) epidemic resulting in increasing binding of insulin by antibodies.

The potential for improved outcomes in the prevention and therapy of diabetic kidney disease through 'stacking' of drugs from different classes.

Aggressive therapy of diabetic kidney disease (DKD) can not only slow the progression of DKD to renal failure but, if utilized at an early enough stage of DKD, can also stabilize and/or reverse the decline in renal function. The currently recognized standard of therapy for DKD is blockade of the renin-angiotensin system with angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs). However, unless utilized at a very early stage, monotherapy with these drugs in DKD will only prevent or slow the progression of DKD and will neither stabilize nor reverse the progression of DKD to renal decompensation.

In praise of pioglitazone: An economically efficacious therapy for type 2 diabetes and other manifestations of the metabolic syndrome.

Pioglitazone improves glycaemic control, not only by lowering insulin resistance, but also by improving beta cell function. Because of the improved beta cell function the glycaemic control that occurs with pioglitazone is prolonged. Pioglitazone has positive effects not only on cardiac risk factors and surrogate measures of cardiovascular disease, it also lowers the incidence of cardiac events in patients with diabetes.

Management of the 'wicked' combination of heart failure and chronic kidney disease in the patient with diabetes.

Patients with type 2 diabetes are at an increased risk of developing heart failure and chronic kidney disease. The presence of these co-morbidities substantially increases the risk of morbidity as well as mortality in patients with diabetes. The clinical focus has historically centred around reducing the risk of cardiovascular disease by targeting hyperglycaemia, hyperlipidaemia and hypertension.

Heart failure and diabetes: Clinical significance and epidemiology of this two-way association.

People with type 2 diabetes (T2DM) and those with prediabetes have an increased risk of heart failure (HF). Longer duration of T2DM correlates with a greater risk of HF, but HF is also seen in patients with recent-onset diabetes. Insulin resistance is more likely to be present in patients with HF.

Detecting and treating the protean manifestations of diabetic autonomic neuropathy.

The manifestations of diabetic autonomic neuropathy (DAN) are protean and clinically involve multiple systems, including the cardiovascular system, the gastrointestinal system, the genitourinary system as well as the sweat glands (sudomotor dysfunction) and the gallbladder. In addition, cardiac autonomic neuropathy (CAN) is associated with a correctible inability to appreciate and correct hypoglycaemia. While not a clinical problem, pupillary involvement should be the clue and the catalyst to investigate for other manifestations of DAN.

Diabetic Mononeuropathies and Diabetic Amyotrophy.

This brief review describes the etiology, pathophysiology, clinical features, therapy and prognosis of the diabetic mononeuropathies and diabetic amyotrophy and neuropathic cachexia. Mononeuropathies include cranial neuropathies, of which the oculomotor nerve is most commonly affected, and are thought to be due to microvascular occlusion. Peripherally, entrapment neuropathies occur in both the upper and lower limbs and are due to compression of an already damaged nerve in anatomically restricted channels.

Combine and Conquer: With Type 2 Diabetes Polypharmacy Is Essential Not Only to Achieve Glycemic Control but Also to Treat the Comorbidities and Stabilize or Slow the Advancement of Diabetic Nephropathy.

The concept of polypharmacy in the type 2 diabetic patient is both historic and redundant. A combination of three or more medications usually at doses which are less than those utilized for monotherapy is efficacious not only in the therapy of hyperglycemia but also in the therapy of the comorbidities of hypertension and hyperlipidemia. In addition, multiple medications are now accepted as being necessary to reduce albuminuria and decelerate the decline in renal function in the patient with diabetic nephropathy.

Metformin-induced vitamin B12 deficiency can cause or worsen distal symmetrical, autonomic and cardiac neuropathy in the patient with diabetes.

Metformin blocks the absorption of vitamin B12 through a mechanism that has not been established but could be because of interference with the calcium-dependent binding of the intrinsic factor vitamin B12 complex to the cubam receptor in the terminal ileum. The subsequent deficiency of vitamin B12 may cause or accelerate distal symmetrical and autonomic neuropathy in the patient with diabetes. Several observational studies and meta-analyses have reported a significant association between metformin utilization and vitamin B12 deficiency.

Testosterone Deficiency is Not Protective Against the Development of Adenocarcinoma of the Prostate in a Type 1 Diabetic Patient.

We present a case of prostate cancer (PC) developing in a hypogonadal patient with well-controlled type 1 diabetes. The purpose of reporting this case is to emphasize that regular prostate examinations and prostate-specific antigen (PSA) measurements should be preformed in the diabetic male, even though the incidence of PC is lower in this group of patients. In addition, these examinations and tests need to be preformed even in the hypogonadal patient with diabetes since the presence of a low serum testosterone (T) level does not preclude the development of PC.

Are the Protean Effects of Pentoxifylline in the Therapy of Diabetes and Its Complications Still Relevant?

Pentoxifylline (Px) has protean effects that can be utilized in the therapy of diabetes and its complications. There have been well-documented but often inconclusive improvements in peripheral arterial disease, foot ulcers, peripheral neuropathy, nephropathy, retinopathy, ischemic heart disease and cerebrovascular disease. In addition, non-alcoholic steatosis and steatohepatitis, which are closely associated with insulin resistance and type 2 diabetes, have been shown to improve with pentoxifylline.

Alcohol Consumption as a Causator and/or an Accelerator of Neuropathy in People With Diabetes Is Regularly Overlooked.

Patients with diabetes and distal symmetrical polyneuropathy (DSP) are routinely evaluated for etiologies other than diabetes, including vitamin B12 deficiency, paraproteinemia, hypothyroidism and drug or autoimmune-induced neuropathy. However, the most common cause of DSP, next to that of diabetes, is alcohol intake, which is almost never evaluated. In addition to assessment of alcohol intake based on patient history, which often leads to an underestimation of alchohol intake, markers of a high alcohol intake (elevated liver enzymes, uric acid, triglycerides, low magnesium or low folic acid levels) should be obtained.

Development of Exogenous Insulin Antibody Syndrome in a Patient with Newly Diagnosed Type 1 Diabetes Successfully Treated with Oral Immunosuppressive Monotherapy.

Exogenous insulin antibody syndrome (EIAS), which rarely occurs in the patient with type 1 diabetes, results in antibody-induced insulin resistance, hyperglycemia, ketosis, ketoacidosis, and hypoglycemia when insulin is released from the saturated insulin antibodies. Recommended treatment regimens include glucocorticoids, immunosuppressants, and plasmapheresis. In the patient with type 1 diabetes, glucocorticoids may by inducing and/or worsening ketoacidosis be contraindicated.

Diabetogenic effects of cardioprotective drugs.

Drugs that protect against cardiovascular events in the patient with diabetes may also positively or negatively affect glycaemic control in the patient with established diabetes and may induce the development of diabetes in the predisposed patient. Mainly through increasing insulin resistance, beta-blockers, statins and high-dose diuretics have the potential to worsen glycaemic control. Dihydropyridine calcium channel blockers, low-dose diuretics, vasodilating beta-blockers, alpha-blockers and pitavastatin have little or no effect on glycaemic control.

Why Do Falls and Lower Limb Fractures Occur More Frequently in the Diabetic Patient and How Can They Be Prevented?

Due to primarily sarcopenia and hypoglycemia but also neuropathy, hypotension, analgesics and polypharmacy, there is an increased incidence of falls and hip fractures in both the type 1 and type 2 diabetic patient. Utilization of insulin, hypotensive drugs, analgesics and perhaps canagliflozin further increases the risk. Thiazolidinedione use may increase the risk of osteoporosis and fracture.

Stroke in the patient with diabetes (part 1) - Epidemiology, etiology, therapy and prognosis.

There is a higher incidence of stroke in both the type 2 diabetic and the non-diabetic insulin resistant patient which is accompanied by higher morbidity and mortality. The increase in the frequency of stroke is due to an increase in cerebral infarction, mainly lacunar infarcts, with the incidence of cerebral hemorrhage being less frequent. The major risk factors for stroke in the type 2 diabetic patient are age, hypertension, the number of features of the Metabolic Syndrome, the presence of diabetic nephropathy in both the type 1 and type 2 patient, the presence of peripheral and coronary artery disease and especially the presence of atrial fibrillation.

Stroke in the patient with diabetes (Part 2) - Prevention and the effects of glucose lowering therapies.

There is a higher incidence of stroke in both the type 2 diabetic and the non-diabetic insulin resistant patient which is accompanied by higher morbidity and mortality. Stroke primary prevention can be achieved by controlling atrial fibrillation and hypertension, and the utilization of statins and anticoagulant therapies. Utilizing pioglitazone and GLP-1 receptor agonists reduce the risk of stroke while the utilization of metformin, α-glucosidase inhibitors, DPP-4 and SGLT-2 inhibitors have no effect.

Case Report: Efficient Avoidance of Hospitalization for Diabetic Ketosis Utilizing Technosphere Inhaled Insulin.

We describe the use of inhaled insulin for the therapy of diabetic ketosis/ketoacidosis in a patient with type 1 diabetes. In this situation high insulin levels are needed to metabolize ketone bodies and avoid hospitalization. Technosphere inhaled insulin (TI) may be an alternative to subcutaneously injected fast-acting insulins, not only because of its rapid onset of action but also lack of stacking leading to late-onset hypoglycemia.

Heart failure in the patient with diabetes: Epidemiology, aetiology, prognosis, therapy and the effect of glucose-lowering medications.

In people with type 2 diabetes the frequency of heart failure (HF) is increased and mortality from HF is higher than with non-diabetic HF. The increased frequency of HF is attributable to the cardiotoxic tetrad of ischaemic heart disease, left ventricular hypertrophy, diabetic cardiomyopathy and an extracellular volume expansion resistant to atrial natriuretic peptides. Activation of the renin-angiotensin-aldosterone system and sympathetic nervous systems results in cardiac remodelling, which worsens cardiac function.

Atrial fibrillation and type 2 diabetes: Prevalence, etiology, pathophysiology and effect of anti-diabetic therapies.

New-onset atrial fibrillation (NAF) is increased in the type 2 diabetic patient because of the presence of the metaboli syndrome and increased sympathetic activity. This results in inflammation, endothelial dysfunction and myocardial steatosis which, in turn, lead to atrial fibrosis and dilatation. The end result is the development of structural and electrical atrial remodeling.