Diabetic patients frequently develop a constellation of electrolyte disorders. These disturbances are particularly common in decompensated diabetics, especially in the context of diabetic ketoacidosis or nonketotic hyperglycemic hyperosmolar syndrome. These patients are markedly potassium-, magnesium- and phosphate-depleted. Diabetes mellitus (DM) is linked to both hypo- and hyper-natremia reflecting the coexistence of hyperglycemia-related mechanisms, which tend to change serum sodium to opposite directions. The most important causal factor of chronic hyperkalemia in diabetic individuals is the syndrome of hyporeninemic hypoaldosteronism. Impaired renal function, potassium-sparing drugs, hypertonicity and insulin deficiency are also involved in the development of hyperkalemia. This article provides an overview of the electrolyte disturbances occurring in DM and describes the underlying mechanisms. This insight should pave the way for pathophysiology-directed therapy, thus contributing to the avoidance of the several deleterious effects associated with electrolyte disorders and their treatment.

Spurious electrolyte disorders refer to an artifactually elevated or decreased serum electrolyte values that do not correspond to their actual systemic levels. When a clinician is confronted with a case of electrolyte disturbance, the first question should be whether it is an artifact. Spurious electrolyte disorders (pseudohyponatremia, pseudohypernatremia, pseudohypokalemia, pseudohyperkalemia, pseudohypomagnesemia, pseudohypophosphatemia, pseudohyperphosphatemia, pseudohypocalcemia and pseudohypercalcemia) are not infrequently observed in clinical practice. The recognition that an electrolyte disturbance may be an artifact may prevent inappropriate therapeutic interventions that could potentially have unfavorable outcomes. Clinicians must be alert to the possibility of spurious laboratory abnormalities when faced with conflicting laboratory values or measurements that are discordant with the clinical presentation. Moreover, in the presence of conditions that predispose to spurious electrolyte disorders, the normal measured electrolyte levels should raise the suspicion that true electrolyte disorders may be present.

Atherosclerotic cardiovascular disease (ASCVD) remains the major mortality cause in developed countries with hypercholesterolaemia being one of the primary modifiable causes. Lifestyle intervention constitutes the first step in cholesterol management and includes dietary modifications along with the use of functional foods and supplements. Functional foods enriched with plant sterols/stanols have become the most widely used nonprescription cholesterol-lowering approach, despite the lack of randomized trials investigating their long-term safety and cardiovascular efficacy. The cholesterol-lowering effect of plant-sterol supplementation is well-established and a potential beneficial impact on other lipoproteins and glucose homeostasis has been described. Nevertheless, experimental and human observational studies investigating the association of phytosterol supplementation or circulating plant sterols with various markers of atherosclerosis and ASCVD events have demonstrated controversial results. Compelling evidence from recent genetic studies have also linked elevated plasma concentrations of circulating plant sterols with ASCVD presence, thus raising concerns about the safety of phytosterol supplementation. Thus, the aim of this review is to provide up-to-date data on the effect of plant sterols/stanols on lipid-modification and cardiovascular outcomes, as well as to discuss any safety issues and practical concerns.

Background: Although a cholesterol-lowering diet and the addition of plant sterols and stanols are suggested for the lipid management of children and adults with familial hypercholesterolemia, there is limited evidence evaluating such interventions in this population. Objectives: To investigate the impact of cholesterol-lowering diet and other dietary interventions on the incidence or mortality of cardiovascular disease and lipid profile of patients with familial hypercholesterolemia. Search methods: Relevant trials were identified by searching US National Library of Medicine National Institutes of Health Metabolism Trials Register and clinicaltrials.gov.gr using the following terms: diet, dietary, plant sterols, stanols, omega-3 fatty acids, fiber and familial hypercholesterolemia. Selection criteria: Randomized controlled trials evaluating the effect of cholesterol-lowering diet or other dietary interventions in children and adults with familial hypercholesterolemia were included. Data collection and analysis: Two authors independently assessed the eligibility of the included trials and their bias risk and extracted the data which was independently verified by other colleagues. Results: A total of 17 trials were finally included, with a total of 376 participants across 8 comparison groups. The included trials had either a low or unclear bias risk for most of the assessed risk parameters. Cardiovascular incidence or mortality were not evaluated in any of the included trials. Among the planned comparisons regarding patients’ lipidemic profile, a significant difference was noticed for the following comparisons and outcomes: omega-3 fatty acids reduced triglycerides (mean difference (MD): −0.27 mmol/L, 95% confidence interval (CI): −0.47 to −0.07, p < 0.01) when compared with placebo. A non-significant trend towards a reduction in subjects’ total cholesterol (MD: −0.34, 95% CI: −0.68 to 0, mmol/L, p = 0.05) and low-density lipoprotein cholesterol (MD: −0.31, 95% CI: −0.61 to 0, mmol/L, p = 0.05) was noticed. In comparison with cholesterol-lowering diet, the additional consumption of plant stanols decreased total cholesterol (MD: −0.62 mmol/L, 95% CI: −1.13 to −0.11, p = 0.02) and low-density lipoprotein cholesterol (MD: −0.58 mmol/L, 95% CI: −1.08 to −0.09, p = 0.02). The same was by plant sterols (MD: −0.46 mmol/L, 95% CI: −0.76 to −0.17, p < 0.01 for cholesterol and MD: −0.45 mmol/L, 95% CI: −0.74 to −0.16, p < 0.01 for low-density lipoprotein cholesterol). No heterogeneity was noticed among the studies included in these analyses. Conclusions: Available trials confirm that the addition of plant sterols or stanols has a cholesterol-lowering effect on such individuals. On the other hand, supplementation with omega-3 fatty acids effectively reduces triglycerides and might have a role in lowering the cholesterol of patients with familial hypercholesterolemia. Additional studies are needed to investigate the efficacy of cholesterol-lowering diet or the addition of soya protein and dietary fibers to a cholesterol-lowering diet in patients with familial hypercholesterolemia.

Background: Hyponatremia is frequent in acute stroke patients, and it is associated with worse outcomes and increased mortality. Summary: Nonstroke-related causes of hyponatremia include patients’ comorbidities and concomitant medications, such as diabetes mellitus, chronic kidney disease, heart failure, and thiazides. During hospitalization, “inappropriate” administration of hypotonic solutions, poor solute intake, infections, and other drugs, such as mannitol, could also lower sodium levels in patients with acute stroke. On the other hand, secondary adrenal insufficiency due to pituitary ischemia or hemorrhage, syndrome of inappropriate antidiuretic hormone secretion, and cerebral salt wasting are additional stroke-related causes of hyponatremia. Although it is yet unclear whether the appropriate restoration of sodium level improves outcomes in patients with acute stroke, the restoration of the volume depletion remains the cornerstone of treatment in hypovolemic hyponatremia. In case of hyper- and euvolemic hyponatremia, apart from the correction of the underlying cause (e.g., withdrawal of an offending drug), fluid restriction, administration of hypertonic solution, loop diuretics, and vasopressin-receptor antagonists (vaptans) are among the therapeutic options. Key Messages: Hyponatremia is frequent in patients with acute stroke. The plethora of underlying etiologies warrants a careful differential diagnosis which should take into consideration comorbidities, concurrent medication, findings from the clinical examination, and laboratory measurements, which in turn will guide management decisions. However, it is yet unclear whether the appropriate restoration of sodium level improves outcomes in patients with acute stroke.