There are reports of insulin overdose by injection, yet little is known regarding the potential harms of intentional oral ingestion of insulin. In this report, we describe a case of massive insulin ingestion and ensuing hypoglycemia. To our knowledge, there are no previously published cases of hypoglycemia caused by intentional insulin ingestion. A 51-year-old man intentionally ingested three 10-ml vials (total of 3000 units) of various insulins: one vial each of insulin aspart, lispro, and glargine. Four symptomatic hypoglycemic episodes, with blood glucose levels of 48, 25, 34, and 40 mg/dl, occurred approximately 1, 3, 4, and 5 hours, respectively, after ingestion. The hypoglycemia could not be explained other than the ingestion of the insulins. The patient was admitted for observation, and euglycemia occurred within 24 hours without any additional hypoglycemic episodes. Hypoglycemia treatment is reviewed in this case report, and factors that may affect systemic response of orally ingested insulin, including gastrointestinal absorption and insulin sensitivity, are discussed. In addition, the findings of our case report may provide useful insight into the development of novel oral insulin products that are currently in research. Despite poor bioavailability (1%) when taken orally, insulin may produce symptomatic hypoglycemia with a massive ingestion. Vigilant blood glucose monitoring, supportive care with glucose replacement therapy, and admission to the hospital for observation may be required.

EBV dosing achieved quick therapeutic anticoagulation with less bleeding compared to WB dosing in a veteran population. Due to the study's limitations, larger, randomized, comparative trials are needed to confirm our findings.

Ranolazine added to optimized doses of CADT demonstrated an improvement in angina symptoms when given to a veteran population with persistent CSA.

No abstract

Results from the trial by van Diepen and colleagues 1 found a statistically significant association between the diagnosis of heart failure (HF) and risk of orthopedic fracture in a large cohort of elderly patients with known cardiovascular disease. Although a pathophysiological link between HF and osteoporosis remains to be determined, the authors offer a potential cause beyond that of shared risk factors. The backbone of the proposed mechanism in HF is elevated aldosterone levels, which have been associated with increased urinary calcium and magnesium excretion, hyperparathyroidism, and diminished bone mineral density. One relationship that also deserves recognition is the association between HF, hyponatremia, and increased risk of falls and fractures.Hyponatremia in HF is relatively common with a prevalence of 20% in a large registry of over 48 000 HF patients. 2 Hyponatremia may reveal a more pronounced activation of the renin-angiotensinaldosterone system, sympathetic nervous system, and vasopressin release. 3 Therefore, hyponatremia may identify a population with a pathophysiological profile that differs from that of eunatremic HF patients. This population may be at an increased risk of falls and fractures.Hyponatremia has been associated with an increase in the risk of falls. In one case-control study of asymptomatic chronic hyponatremic patients, hyponatremia was associated with a higher incidence of falls, possibly as a result of gait and attention deficits. 4 Furthermore, the frequency of falls was the same regardless of level of hyponatremia, highlighting the observation that even mild hyponatremia (serum Na ϩ , 130 to 132 mmol/L) is linked to an increase in falls. In addition to evidence that illustrates an increased risk of falls, hyponatremia has been associated with an increased risk of fractures. One case-control study looked at the relationship between hyponatremia and bone fractures from incidental falls in elderly ambulatory patients. 5 In this study, hyponatremia (defined as serum Na ϩ Ͻ135 mmol/L) was associated with a greater than 3-fold increased risk of bone fracture after incidental fall (odds ratio, 3.47; 95% confidence interval, 2.09 to 5.79). The authors suggest that attention deficits and gait instability observed in elderly hyponatremic patients may explain the relationship between hyponatremia and bone fracture. This reaffirms the notion that hyponatremic patients represent a unique population that should not be overlooked, in particular when assessing outcomes that include fractures.Although the pathogenesis of hyponatremia in HF is usually multifactorial, the use of diuretics is most often implicated. In addition, patients with HF have an overstimulated renin-angiotensin-aldosterone system. Increased angiotensin II stimulates vasopressin release resulting in water resorption through increased production of aquaporin channels, ultimately causing hypervolemic hyponatremia.The trial by van Diepen and colleagues has provided the HF community with a valuable insight into the associatio...