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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atherogenesis is a disease of middle-sized and large-caliber blood vessels that can be divided into three major phases. The initial lesions of early atherosclerosis are characterized by the adhesion and subendothelial emigration of blood-borne monocytes, which differentiate into macrophages and provide the morphologic basis for the formation of foam cells and fatty streak lesions. These lesions are found in most children and teenagers in industrialized nations. The next key event in atherogenesis is the proliferation of smooth muscle cells within the intima and media, resulting in the gradual compromise of the vessel lumen. Myofibroblastic cells also contribute to lesion growth through the production of excessive amounts of extracellular matrix. Such lesions are clinically silent unless progression to the next phase continues: the lesions degenerate, forming a mostly necrotic "lipid core" consisting of extracellular lipid, cholesterol crystals, inflammatory cells and necrotic debris. A fibrous cap is formed which prevents the interaction of blood cells, particularly of platelets with the highly proaggregatory material found in the lipid core. However, continuous inflammatory activity and/or heightened mechanical stress (i.e., in hypertension) tends to weaken the fibrous caps. Eventually, plaque rupture ensues, platelets aggregate, and the lesions become clinically manifest in such dramatic events as myocardial infarction, stroke, or mesenteric ischemia. Research into lesion formation and progression is limited by the fact that lesions develop in silence over many decades and that animal models only incompletely model the situation in humans. Most currently debated concepts accept the "response to injury" hypothesis formulated by the late Russell Ross and the multi-factorial nature of atherogenesis. The discussion today circles around the relative contributions of low density lipoproteins (oxidized or enzymatically modified LDL?), the immune response (adaptive or innate?), infectious agents (CMV, Chlamydia pneumoniae?), and/or hereditary factors, to name only a few of the most widely debated concepts. Irrespective of the outcome of this pathomechanistic discussion, the knowledge of established risk factors (hypercholesterolemia, hypertension, diabetes, smoking, etc.) and protective interventions (lifestyle changes, physical exercise, "healthy" diets, effective dietary and pharmacologic control of hyperglycemia, blood pressure or hyperlipidemia) has helped to define atherosclerosis as a "new entity" that has little to do with the archaic concept of a "degenerative" vessel disease. The new concept takes us into the responsibility--puts us in charge of our own and our patients' cardiovascular risk--whether we like it or not. The smoking obese doctor no longer fits into the modern medical landscape.
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PMID:[Atherosclerosis--progression by nonspecific activation of the immune system]. 1197 79

This article offers an overview of the variety of pharmacologic treatments available to Type 2 diabetes patients. This surge of options has unfolded over the past 7-8 years, and has made the "one treatment fits all" approach an antiquated concept. A basic understanding of the complex physiology underlying Type 2 diabetes is addressed and is a prerequisite to understanding the mechanisms of the various medications. By grouping the oral agents for diabetes into physiologic categories, it is hoped that the reader will attain a clear image of these medications, both singularly and in combination.
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PMID:A new era in the pharmacologic management of type 2 diabetes. 1202 37

Fitting a Poisson model to national data on the incidence of type 1 diabetes mellitus (T1DM) under 5 years (1993-95) and to age-specific incidence data from three different German regions (age groups 0-4, 5-9, 10-14, 15-19 years, 1988-1995), national age-specific incidences of T1DM in childhood were estimated. From these the age-standardized national incidence and prevalence were derived for age groups 0-15 and 0-19 years. In 1993-95 the age-standardized national incidences (95% CIs) in the age groups 0-14 and 0-19 years were 14.2 (12.9-15.5) and 17.0 (15.2-18.8) per 100,000 person-years, respectively. The respective national prevalences were 86.7 (83.4-90.0) and 140.2 (134.3-146.1) per 100,000 persons. These estimates of the national incidence and prevalence of T1DM for the mid-1990s were about twofold higher than estimates from the former Eastern Germany in the late 1980s. This striking high frequency of T1DM in Germany has an important impact on clinical and economic aspects of diabetes care in childhood and adolescence.
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PMID:Incidence and prevalence of childhood type 1 diabetes mellitus in Germany--model-based national estimates. 1250 57

The pharmacology, clinical efficacy, adverse effects, drug interactions, and place in therapy of bitter melon are described. Bitter melon (Momordica charantia) is an alternative therapy that has primarily been used for lowering blood glucose levels in patients with diabetes mellitus. Components of bitter melon extract appear to have structural similarities to animal insulin. Antiviral and antineoplastic activities have also been reported in vitro. Four clinical trials found bitter melon juice, fruit, and dried powder to have a moderate hypoglycemic effect. These studies were small and were not randomized or double-blind, however. Reported adverse effects of bitter melon include hypoglycemic coma and convulsions in children, reduced fertility in mice, a favism-like syndrome, increases in gamma-glutamyltransferase and alkaline phosphatase levels in animals, and headaches. Bitter melon may have additive effects when taken with other glucose-lowering agents. Adequately powered, randomized, placebo-controlled trials are needed to properly assess safety and efficacy before bitter melon can be routinely recommended. Bitter melon may have hypoglycemic effects, but data are not sufficient to recommend its use in the absence of careful supervision and monitoring.
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PMID:Bitter melon (Momordica charantia): a review of efficacy and safety. 1262 17

In 103 children and adolescents aged 13.6+/-5.5 years with type I diabetes lasting for 5.9+/-3.1 years, we have retrospectively studied the frequency and circumstances of severe hypoglycemic episodes (coma and/or convulsions). There were 71 severe hypoglycemia during the 5 year follow-up period. One third of patients had one or more severe hypoglycemia during the 5 years, therefore 6.4% of patients had at least one severe hypoglycemia every year. 8.7% of patients had 3 or more hypoglycemia within 5 years. Both glycated hemoglobin and insulin dose were comparable in patients with, or without severe hypoglycemia. Only in one third of the hypoglycemic episodes an apparent cause was found. We conclude that, most often, severe hypoglycemia occur in diabetic children without an identifiable cause and without any direct relationship with the level of glycated hemoglobin (HbA1c).
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PMID:[Severe hypoglycemia in diabetic children and adolescents: frequency and circumstances of occurrence]. 1281 4

We herein report a case of aceruloplasminemia in a 27-year-old man who had a 10-year history of diabetes mellitus. The patient developed a convulsion, most likely as a result of hypoglycemia. Unexpectedly, this episode left him in a prolonged state of unconsciousness, which necessitated neurological testing and imaging. Brain MRI showed bilateral hypo-intensities in the basal ganglia and thalamus. Molecular analysis revealed a novel splicing mutation in the ceruloplasmin (CP) gene that would result in the skipping of exon 3 during transcription. This case suggests that diabetes associated with aceruloplasminemia can become manifest in the teens.
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PMID:Aceruloplasminemia with juvenile-onset diabetes mellitus caused by exon skipping in the ceruloplasmin gene. 1287 54

Prader-Willi syndrome (PWS) is a sporadic disorder of chromosome abnormalities with an estimated prevalence of 1 in 15,000. It mainly affects the central nervous system, and often involves the hypothalamus. Both general and regional anesthesia for these patients is difficult mainly due to morbid obesity. Other common problems include hypotonia, disturbance in thermoregulation, arrhythmia, cor pulmonale, diabetes mellitus, behavior problems, and convulsions. We report on 2 pediatric patients with PWS receiving general anesthesia. The first patient experienced life-threatening episodes of severe hypoxemia in the postanesthesia care unit (PACU) as well as in the pediatric intensive care unit (PICU). Nasal continuous positive airway pressure (CPAP) was suggested by the pediatric pulmonary medicine specialist, and thereafter the patient's condition improved. The clinical course of the second patient was uneventful except for transient intermittent episodes of bronchospasms during emergence. In addition, we discuss differences between these 2 cases and our strategy for the prevention of perioperative complications for PWS patients in the future.
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PMID:Anesthesia for pediatric patients with Prader-Willi syndrome: report of two cases. 1295 94

The chief dangers reported with some common drugs are reviewed. Hazards of antibiotic therapy include: the increasing incidence of sensitization to penicillin with occasional anaphylactic reactions; aplastic anemia with chloramphenicol, and the poor tolerance of infants for chloramphenicol; staphylococcal enterocolitis; unnecessary "prophylactic" use of antibiotics. Thiazide diuretics may precipitate potassium depletion, skin reactions, pancreatitis, blood dyscrasias, gout, diabetes mellitus and hepatic coma. Reserpine can increase gastric acidity, induce mental depression, and when used with digitalis lead to ventricular premature beats. Hydralazine may aggravate angina pectoris, cause tachycardia, and bring about a syndrome resembling disseminated lupus erythematosus. Guanethidine may result in loose stools, impotence, and postural hypotension. Hazards of phenothiazines include jaundice, parkinsonian states and tremors, convulsions, hypotension, and blood dyscrasias. The butanediols have numerous side effects including gastrointestinal, cutaneous and hypotensive reactions. Prolonged corticosteroid therapy introduces a new danger in surgical treatment. The progesterone-like drugs may induce masculinization of the female fetus.
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PMID:Dangers in the use of some potent drugs. 1398 37

Hypoglycemia is a common complication of insulin therapy, particularly in the young. For children and adolescents with diabetes, the risk of hypoglycemia may not only prevent optimal glycemic control but can also add significantly to the psychosocial burden of the disease. Recently, surveys employing prospective monitoring techniques have allowed more precise information to be gained about rates of hypoglycemia, its clinical associations, and the impact of new therapies and technologies. A number of reports have estimated rates of hypoglycemic comas and convulsions to be approximately 20 events per 100 patient years in children on current conventional therapy. There is evidence that the introduction of new analog short- and longer-acting insulins and the more widespread use of continuous subcutaneous infusion therapies may allow improvements in glycemic control to occur without the usual increased rate of severe hypoglycemic episodes. The use of glucose sensor technology has brought into focus the widespread occurrence of asymptomatic hypoglycemia. Asymptomatic hypoglycemia has long been recognized, particularly at night, when the combination of excessive insulin action and suppressed counter-regulatory hormone responses put children at special risk of hypoglycemia. Hypoglycemia unawareness is common in the young and is associated with an increased risk of severe hypoglycemia. Whether episodes of severe hypoglycemia have long-term consequences is controversial. Early studies suggesting that the developing brain is sensitive to permanent neurological damage as a result of hypoglycemia have not been confirmed in more recent reports. Many studies have not found convincing evidence of neurological sequelae of the hypoglycemic events that are an inevitable complication of insulin therapy. The question, however, remains under active investigation. Continued prospective monitoring of hypoglycemia rates and consequences has become an essential component of diabetes management.
Pediatr Diabetes 2003 Sep
PMID:Hypoglycemia in children with type 1 diabetes: current issues and controversies. 1465 73

PCOS is a metabolic syndrome that exists throughout the world with much clinical heterogeneity. PCOS is now appreciated as encompassing two interrelated metabolic phenomena--insulin resistance and hyperandrogenism. Patients present with oligo-amenorrhea and clinical hyperandrogenism, and the diagnosis is based on clinical grounds with few laboratory tests necessary. Because patients are at higher than normal risk for diabetes, glucose intolerance, and hyperlipidemia, and perhaps at higher risk for coronary heart disease, newly diagnosed patients with PCOS should be evaluated for glucose intolerance and hyperlipidemia. The cornerstone of therapy today includes weight management, and further therapeutic intervention is focused on reproductive and cardiovascular health and treatment of insulin resistance. Clinical case continued The 17-year-old mentioned in the beginning of this article probably does have PCOS. She fits the clinical criteria: oligo-ovulation and hyper-androgenism (the acne and hirsutism). In addition, she is obese, which is also associated with PCOS. Her TSH and prolactin were normal, and as her presentation was not suggestive of an adrenal tumor or congenital adrenal hyperplasia (she had mild hirsutism, and those diagnoses are associated with more severe hyperandrogenism), no further laboratory evaluation was deemed necessary. Once the diagnosis was made, she was screened for lipid abnormalities and for glucose intolerance. Her LDL was 150, HDL 35; oral glucose tolerance test (OGTT) was normal. A pregnancy test was negative, and she was started on OCPs. Devoting herself to exercise and dietary change, she lost 10 pounds in her first 3 months after diagnosis. Her hirsutism and acne have improved with the OCPs and weight loss, and her menses are regular. She has elected to defer oral insulin sensitizers until her weight loss has stabilized. Findings PCOS is common in reproductive-aged women. Diagnosis is clinical and is supported by lab findings; there is significant clinical heterogeneity. Insulin resistance is likely central to the pathophysiology along with androgen excess. Health implications include infertility, diabetes, endometrial cancer, hyperlipidemia, and possibly coronary heart disease. Treatment is evolving and includes weight loss, OCPs, and insulin sensitizers.
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PMID:Polycystic ovary syndrome: a review for primary providers. 1502 92


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