Israel Medical Association Journal

Background: Dysphagia is a common disorder among the elderly population. As many as 50% of nursing home residents suffer from dysphagia. It is important to identify patients at increased risk for colonization of dental and denture plaque by pathogenic organisms for prevention of associated disease.

Objectives: To quantify the prevalence and evaluate the effect of dental and denture plaque colonization by Candida albicans in hospitalized elderly dysphagic patients as a complication of stroke, as well as the effect of systemic antimicrobial therapy on C. albicans colonization in these patients.

Methods: We evaluated dysphagia and antibiotic therapy as risk factors for dental and denture plaque colonization by C. albicans in elderly stroke rehabilitating patients with dysphagia, as compared to elderly non-dysphagic stroke and non-stroke rehabilitating patients on days 0, 7 and 14 following admission to the Fliman Geriatric Rehabilitation Hospital.

Results: The risk of C. albicans colonization of dental plaque was greater in dysphagic patients than in those without dysphagia on day 0 (50% vs. 21%, P = 0.076), day 7 (58 vs. 15.2%, P = 0.008) and day 14 (58 vs. 15.2%, P = 0.08). Similarly, patients on antibiotic therapy were at greater risk for C. albicans colonization of dental plaque on day 0 (56 vs. 11%, P = 0.002), day 7 (44 vs. 14.8%, P = 0.04) and day 14 (39 vs. 19%, P = 0.18). The risk of C. albicans colonization of denture plaque as opposed to dental plaques in non-dysphagic patients was significantly greater on day 0 (45.7 vs. 21.2%, P = 0.03), day 7 (51.4 vs. 15.1%, P = 0.0016) and day 14 (54.3 vs. 15.1%, P = 0.0007). Dysphagia did not increase the risk of denture plaque colonization by C. albicans.

Conclusiona: Both dysphagia and antibiotic therapy are risk factors for C. albicans colonization of dental plaque, and although dysphagia does not significantly increase colonization of denture plaque, denture wearers are at greater risk of such colonization.

Background: The external approach is the golden standard for sinonasal tumor removal but it is associated with several side effects, including facial scars, intracranial and extracranial complications, a long hospitalization period and high costs. Endoscopic sinus surgery enables resection of benign and selected malignant sinonasal tumors and has the advantages of no facial scars, better functional and structural preservation of the sinonasal complex, minimal trauma to surrounding tissue, a shorter hospitalization stay and lower costs.

Objectives: To evaluate the advantages and limitations of endoscopic resection of benign and malignant sinonasal tumors, their recurrence and complication rates.

Methods: The medical and radiology records of 56 patients who underwent endonasal endoscopic resection of benign and malignant sinonasal tumors between 1996 and 2003 were retrospectively reviewed. Tumors located in the center of the nose and sinuses were endoscopically resected.

Results: Six cases of malignant tumor and 50 cases of benign tumor underwent resection by ESS[1]. One of the patients with malignant tumor died, the remainder showing no evidence of disease on follow-up of 3–60 months (mean 26.8 months). Inverted papilloma was the most common benign tumor (40 patients). Seven patients (18%) had recurrence followed by endonasal resection. No major complications were recorded. Hospitalization stay was 2–7 days (mean 3.6 days).

Conclusions: Endoscopic resection of benign sinonasal tumors that are centrally located in the nose and sinuses should be considered before the external approach is used. In very carefully selected cases of malignant tumors ESS is oncologically acceptable, but more experience is needed for discerning the indications for endoscopic resection of malignant tumors. The complication rate for endoscopic resection is low, there are no facial scars, hospitalization stay is short, and costs are low.

The treatment of acute pain and anxiety in children undergoing therapeutic and diagnostic procedures in the emergency department has improved dramatically in recent years. The availability of non-invasive monitoring devices and the use of short-acting sedative and analgesic medications enable physicians to conduct safe and effective sedation and analgesia treatment. In today's practice of pediatric emergency medicine, sedation and analgesia has been considered as the standard of care for procedural pain. In most pediatric emergency departments throughout North America, "procedural sedation and analgesia" treatment is being performed by non-anesthesiologists (qualified emergency physicians and nurses). In 2003, the Israel Ministry of Health published formal guidelines for pediatric sedation by non-anesthesiologists; this important document recognizes for the first time the need for pediatric sedation and analgesia in the operating room. We describe the basic principles of procedural sedation and analgesia in children and urge physicians working in pediatric emergency rooms in Israel to expand their knowledge and be more involved in the treatment of pediatric procedural pain.

The 50th anniversary of the Israel Diabetes Association this year is a time less for celebration than for concern. The prevalence of diabetes is rapidly and alarmingly increasing in Westernized and developing countries around the world. Unfortunately, the majority of patients with diabetes do not meet their treatment goals – i.e., glucose, blood pressure or lipid levels. Moreover, our clinical experience and large longitudinal studies have taught us that the mean glucose levels of diabetic patients tend to increase over the years regardless of their treatment modalities. The appropriate answer to these somewhat frustrating data is that the medical community responsible for the integrated health of our diabetic patients – namely, physicians, researchers, nurses and dieticians – must use its combined resources and available therapeutic tools to optimize treatment for these patients. We should also deepen our understanding of the mechanisms underlying the various forms of diabetes and its complications in order to devise more efficient preventive measures for this prevalent devastating chronic disease.

This issue of IMAJ dedicated to diabetes provides some glimpses into these approaches. It contains relevant clinical management debates such as how and when insulin therapy should be instituted and which antihypertensive drugs are more appropriate in the treatment of diabetic nephropathy; a current state-of-the-art review of gestational diabetes as well as how to recognize and manage the diabetic Charcot foot. It exposes the reader to modern prevention strategies against type 1 and type 2 diabetes, to the search for alternative insulin-producing tissue, to advanced understanding of diabetic dermopathy, and more. It also includes selected abstracts of ongoing studies to be presented at the 2004 annual meeting of the Israel Diabetes Association. Most of all, the high quality of the clinical and basic research presented herein strengthens our hope for a better future for our diabetic patients.

Micha Rapoport MD (Guest Editor)

Department of Internal Medicine C and the Diabetes Service, Assaf Harofeh Medical Center, Zerifin, Israel

Editorial Committee

Hilla Knobler MD (Debate Editor)

Eleazar Shafrir PhD

Efrat Wertheimer MD PhD

Since both major forms of diabetes involve inadequate function of pancreatic beta cells, intensive research is ongoing to better understand how beta cells perform their complex role of secreting the hormone insulin in response to physiologic needs. Identification and characterization of pancreatic transcription factors has revealed that they play a crucial role not only in maintenance of mature beta-cell function but also at multiple stages in pancreatic development. Furthermore, recent reports have revealed their potential to convert non-beta cells into insulin-producing cells, which in some cases can function to ameliorate diabetes in experimental animals. The ability to translate these successes to the clinic will require a detailed mechanistic understanding of the molecular basis of action of these proteins. Specific gene regulation in beta cells involves the action of multiple transcription factors recruited to the promoter and functioning synergistically to activate transcription, in part through recruitment of co-activator proteins and components of the basal transcriptional machinery. In addition, the process involves modification of chromatin structure, the details of which are beginning to be elucidated. Our ability to modulate gene expression patterns may lead to developing ways to provide an unlimited supply of functional beta cells for transplantation, permitting a dramatic improvement in therapeutic options for diabetes.