Diabetes mellitus is a major independent risk factor for acute coronary syndrome (ACS). In addition, diabetic patients with ACS suffer from increased mortality compared to their nondiabetic peers. Driven by multiple pathophysiological disturbances, such patients are predisposed to a proinflammatory, prothrombotic state, which may lead to plaque rupture. To counteract this more complex biology, several therapies and strategies have emerged, with some having unique preferential benefits in this population. Antiplatelet agents such as aspirin and clopidogrel have long been standard of care. Dose adjustment of these therapies remains the subject of continued research. Along with medical therapy, ACS diabetic patients preferentially benefit from primary percutaneous intervention compared to fibrinolysis. However, with advances in reperfusion techniques, the optimal strategy has yet to be determined. With these differences in ACS treatment responses, diabetic individuals may not just be a high-risk group, but may actually constitute a fundamentally different population, requiring dedicated clinical trials and individualized treatment regimens.

The risk of cardiac device infection (CDI) is rising significantly, with several risk factors identified. The purpose of this study is to determine the rate of CDI at our center and to assess the associated risk factors, in order to define appropriate measures to prevent this complication. We retrospectively reviewed all cases of patients with CDI at St. George Hospital between February 1999 and July 2010. Each case was matched with three controls. We performed a descriptive and bivariate analysis to identify significant risk factors. Eighteen case patients and 54 control subjects met the inclusion criteria. An organism was recovered in 58 % of the cases. Significant risk factors included previous history of CDI (p < 0.001), recent manipulation (p < 0.001), trauma to the site of implant (p = 0.003), having a dual chamber/dual lead pacemaker (p = 0.002), and development of post-procedural hematoma (p = 0.012). Our findings complement the results of previous studies. We recommend a pre-procedural risk assessment and a thorough post-implantation follow-up to prevent the development of infective complications.

BackgroundPruritus is a common symptom in end-stage renal failure. Many patients suffer from this severe distressing symptom. Although several factors have been postulated to explain uremic pruritus, there is not any conclusive evidence for one of these factors.ObjectivesWe aimed to evaluate serum levels of brain-derived nerve growth factor (BDNF), neurotrophin-4 (NT-4), serum calcium, phosphors and parathyroid hormone in uremic patients with pruritus and without pruritus compared to control subjects.MethodsOne hundred twenty patients suffering from renal failure and 60 healthy subjects were included in the study. Serum BDNF and NT4 levels were determined by ELISA. The serum calcium, phosphorus, parathyroid hormone and hemoglobin were also evaluated.ResultsSerum BDNF was significantly higher in uremic patients with pruritus (P=0.0026) and uremic patients without pruritus (P=0.0294) than control subjects. In addition, NT-4 levels were significantly elevated in uremic patients with pruritus (P<0.0001) and uremic patients without pruritus than control subjects (P=0.0016). There was no significant difference of serum level of BDNF between uremic patients with pruritus and uremic patients without pruritus (P=0.1215). However, serum NT-4 was higher in uremic patients with pruritus vs nonpruritic uremic patients with a significant difference (P=0.0026). There was a positive significant correlation between serum level of NT-4 and severity of pruritus (P=0.024).ConclusionThe present study shows that NT-4 level is increased in the serum of uremic patients with pruritus and there was a significant correlation between NT-4 and severity of pruritus suggesting that NT-4 may have a role in uremic pruritus.

Anaphylaxis prevalence has increased within the last few years. This may be due to a marked increase in allergic sensitization to foods especially in the pediatric population, as well as to an increase in outdoor recreational habits and the availability of new biologic medications.  Furthermore, guidelines for the diagnosis of anaphylaxis have been published, thus facilitating the recognition of this disorder. Diagnosis of anaphylaxis is mainly based on history and clinical criteria of organ system involvement. The serum tryptase assay is now commercially available and may be a helpful diagnostic tool in certain clinical situations involving hypotension, but not in the context of food-induced anaphylaxis. Treatment of anaphylaxis mainly involves the use of epinephrine as a first line medication for severe manifestations followed by  symptomatic management of specific  symptoms, such as antihistamines for urticaria and albuterol for wheezing. Although commonly practiced, treatment with systemic corticosteroids  is not supported by evidence-based literature. Observation in a medical facility for 4-6 hours is recommended to monitor for late phase reactions, although these rarely occur. Education is an essential component of management of a patient with a previous history of anaphylaxis, emphasizing early use of epinephrine and providing a written action plan. Referral to a board-certified allergist/immunologist is recommended to determine  the cause of the anaphylaxis as well as to rule out other potential conditions. In this review, our main focus will be on the treatment and prevention of anaphylaxis while providing our readers with a brief introduction to the diagnosis of anaphylaxis, its prevalence and its most common causes.

Emphysematous gastritis is a severe and rare form of gastritis with characteristic findings of intramural gas in the stomach. It is an acute life-threatening condition resulting from gas-producing microorganisms invading the stomach wall. Early diagnosis and initiation of treatment with bowel rest, hydration, and intravenous broad-spectrum antibiotics is imperative for an effective outcome. Surgical intervention is reserved for perforations, peritonitis, strictures, and uncontrolled disseminated sepsis. We present a case of an 82-year-old female with prior history of colon and uterine cancer on remission treated with surgeries who presented with bilious vomiting, abdominal discomfort, and nausea. She was tachycardic and had a diffusely tender abdomen with rebound on examination. Her laboratory results including blood count, serum chemistry, and coagulation studies were normal. She was diagnosed with emphysematous gastritis based on the characteristic radiographic findings of intramural stomach gas and also the presence of gas in the portal venous system. It is important to differentiate emphysematous gastritis from gastric emphysema because of the difference in management and prognosis, as emphysematous gastritis has a worse outcome and requires aggressive management. Despite an anticipated poor prognosis due to the known grave outcomes of emphysematous gastritis, our patient was successfully managed with conservative treatment. We concluded that she developed emphysematous gastritis probably secondary to immunosuppression and possible mucosal tears from multiple bouts of vomiting. She had a stable hospital course and resolution with medical management most likely due to early diagnosis and initiation of appropriate treatment.