The American Society for Apheresis (ASFA) Journal of Clinical Apheresis (JCA) Special Issue Writing Committee is charged with reviewing, updating, and categorizing indications for the evidence-based use of therapeutic apheresis in human disease. Since the 2007 JCA Special Issue (Fourth Edition), the Committee has incorporated systematic review and evidence-based approaches in the grading and categorization of apheresis indications. This Seventh Edition of the JCA Special Issue continues to maintain this methodology and rigor to make recommendations on the use of apheresis in a wide variety of diseases/conditions. The JCA Seventh Edition, like its predecessor, has consistently applied the category and grading system definitions in the fact sheets. The general layout and concept of a fact sheet that was used since the fourth edition has largely been maintained in this edition. Each fact sheet succinctly summarizes the evidence for the use of therapeutic apheresis in a specific disease entity. The Seventh Edition discusses 87 fact sheets (14 new fact sheets since the Sixth Edition) for therapeutic apheresis diseases and medical conditions, with 179 indications, which are separately graded and categorized within the listed fact sheets. Several diseases that are Category IV which have been described in detail in previous editions and do not have significant new evidence since the last publication are summarized in a separate table. The Seventh Edition of the JCA Special Issue serves as a key resource that guides the utilization of therapeutic apheresis in the treatment of human disease. J. Clin. Apheresis 31:149-162, 2016. © 2016 Wiley Periodicals, Inc.

Guidelines on the Use of Therapeutic Apheresis in Clinical Practice—Evidence-Based Approach from the Writing Committee of the American Society for Apheresis: The Sixth Special Issue

Historically, nutrition principles and recommendations for diabetes and related complications have been based on scientific evidence and diabetes knowledge when available and, when evidence was not available, on clinical experience and expert consensus. Often it has been difficult to discern the level of evidence used to construct the nutrition principles and recommendations. Furthermore, in clinical practice, many nutrition recommendations that have no scientific supporting evidence have been and are still being given to individuals with diabetes. To address these problems and to incorporate the research done in the past 8 years, this 2002 technical review provides principles and recommendations classified according to the level of evidence available. It reviews the evidence from randomized, controlled trials; cohort and case-controlled studies; and observational studies, which can also provide valuable evidence (1,2), and takes into account the number of studies that have provided consistent outcomes of support. In this review, nutrition principles are graded into four categories based on the available evidence: those with strong supporting evidence, those with some supporting evidence, those with limited supporting evidence and those based on expert consensus.

Evidence-based nutrition recommendations attempt to translate research data and clinically applicable evidence into nutrition care. However, the best available evidence must still be moderated by individual circumstances and preferences. The goal of evidence-based recommendations is to improve the quality of clinical judgments and facilitate cost-effective care by increasing the awareness of clinicians and patients with diabetes of the evidence supporting nutrition services and the strength of that evidence, both in quality and quantity.

Before 1994, the American Diabetes Association’s (ADA’s) nutrition principles and recommendations attempted to define an “ideal” nutrition prescription that would apply to everyone with diabetes (3,4,5). Although individualization was a major principle of all recommendations, it was usually done within defined …

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Evidence-Based Nutrition Principles and Recommendations for the Treatment and Prevention of Diabetes and Related Complications

The purpose of this study was to determine whether the postponement of fatigue in subjects fed carbohydrate during prolonged strenuous exercise is associated with a slowing of muscle glycogen deple...

Muscle glycogen utilization during prolonged strenuous exercise when fed carbohydrate

Metformin has been the mainstay of therapy for diabetes mellitus for many years; however, the mechanistic aspects of metformin action remained ill-defined. Recent advances revealed that this drug, in addition to its glucose-lowering action, might be promising for specifically targeting metabolic differences between normal and abnormal metabolic signalling. The knowledge gained from dissecting the principal mechanisms by which metformin works can help us to develop novel treatments. The centre of metformin's mechanism of action is the alteration of the energy metabolism of the cell. Metformin exerts its prevailing, glucose-lowering effect by inhibiting hepatic gluconeogenesis and opposing the action of glucagon. The inhibition of mitochondrial complex I results in defective cAMP and protein kinase A signalling in response to glucagon. Stimulation of 5'-AMP-activated protein kinase, although dispensable for the glucose-lowering effect of metformin, confers insulin sensitivity, mainly by modulating lipid metabolism. Metformin might influence tumourigenesis, both indirectly, through the systemic reduction of insulin levels, and directly, via the induction of energetic stress; however, these effects require further investigation. Here, we discuss the updated understanding of the antigluconeogenic action of metformin in the liver and the implications of the discoveries of metformin targets for the treatment of diabetes mellitus and cancer.

Metformin—mode of action and clinical implications for diabetes and cancer

A healthful eating pattern, regular physical activity, and often pharmacotherapy are key components of diabetes management. For many individuals with diabetes, the most challenging part of the treatment plan is determining what to eat. It is the position of the American Diabetes Association (ADA) that there is not a “one-size-fits-all” eating pattern for individuals with diabetes. The ADA also recognizes the integral role of nutrition therapy in overall diabetes management and has historically recommended that each person with diabetes be actively engaged in self-management, education, and treatment planning with his or her health care provider, which includes the collaborative development of an individualized eating plan (1,2). Therefore, it is important that all members of the health care team be knowledgeable about diabetes nutrition therapy and support its implementation.

This position statement on nutrition therapy for individuals living with diabetes replaces previous position statements, the last of which was published in 2008 (3). Unless otherwise noted, research reviewed was limited to those studies conducted in adults diagnosed with type 1 or type 2 diabetes. Nutrition therapy for the prevention of type 2 diabetes and for the management of diabetes complications and gestational diabetes mellitus is not addressed in this review.

A grading system, developed by the ADA and modeled after existing methods, was utilized to clarify and codify the evidence that forms the basis for the recommendations (1) (Table 1). The level of evidence that supports each recommendation is listed after the recommendation using the letters A, B, C, or E. A table linking recommendations to evidence can be reviewed at http://professional.diabetes.org/nutrition. Members of the Nutrition Recommendations Writing Group Committee disclosed all potential financial conflicts of interest with industry. These disclosures were discussed at the onset of the position statement development process. Members of this committee, their employers, …

https://care.diabetesjournals.org/content/diacare/37/Supplement_1/S120.full.pdf

Nutrition Therapy Recommendations for the Management of Adults With Diabetes

The paper presents an analysis of clinical symptoms, signs and laboratory data of 330 diabetic patients who developed lactic acidosis after having been treated with biguanides (phenformin, buformin, metformin). From the review of the literature an attempt is made to find special features that predisposed patients to develop lactic acidosis such as accompanying illnesses and additional medications, to describe the course of illness and also the factors that influenced the prognosis. Of the patients that developed lactic acidosis 50.3% died. These patients were older, they suffered more frequently from cardiovascular shock, their acidosis was more severe, the whole blood lactate concentration was higher, and the degree of renal insufficiency was more advanced. From our observations we conclude that the treatment of diabetes mellitus with biguanides should be reserved for specially selected patients.

/pdf/lactic-acidosis-in-biguanide-treated-diabetics-a-review-of-3d5jqta51q.pdf

Lactic acidosis in biguanide-treated diabetics: a review of 330 cases.

Publisher Summary Triglycerides with the phosphatides, and the free and esterified cholesterol, make up the quantitatively most important lipid fractions of blood. Adipose tissue has the highest triglyceride content, between 60 and 85 %. The measurements of neutral fat by the determination of glycerol by chemical or fluorimetric methods require extraction and careful isolation of triglycerides followed by hydrolysis. In the enzymatic determination of triglycerides in blood serum or plasma, the isolation or purification of the triglycerides or the extraction of fat can be omitted. The glycerol present in serum, plasma, or Folch extracts of tissues before and after ethanolic-alkaline hydrolysis is converted to glycerophosphate and adenosine diphosphate (ADP) with ATPand glycerokinase. The ADP reacts with pyruvate kinase and added phosphoenolpyruvate to give that is reduced to lactate with NADH and lactate dehydrogenase.

Triglycerides and Glycerol Determination after Alkaline Hydrolysis

In order to define clinically relevant lactic acidosis, 12 biochemical variables, eight clinical symptoms and signs, leading diagnoses, and mortality were evaluated prospectively in approximately 2,000 unselected patients with internal diseases, consecutively admitted to the hospital. Patients with incomplete data sets were not considered. Of those patients who repeatedly were admitted to the hospital during the time of the study, only the first admission was included for statistical analysis. In addition to 11 definitions of lactic acidosis given in the literature, sequential cluster analyses of the biochemical variables were used to estimate the incidence of lactic acidosis in 1,467 patients. Depending upon which definition was used, 0.5-3.8% of all patients were classified as suffering from lactic acidosis, with a mortality rate ranging from 30-88%. From this study it is concluded that a limit of less than or equal to 7.35 for pH and of greater than 5-6 mmol/L for the concentration of lactate in whole blood will minimize false-negative or false-positive classifications.

Definition of Clinically Relevant Lactic Acidosis in Patients with Internal Diseases

To test the hypothesis that recurrent short-term hypoglycemic episodes may impair hormonal counterregulation, symptom awareness, and neurophysiological function during subsequent hypoglycemia, we examined two groups of IDDM patients ( n = 18), neither of whom exhibited signs of autonomic neuropathy. Two sequential euglycemic-hypoglycemic clamp studies were performed three days apart with stable glycemic plateaus of 5.6, 3.3, 2.2, and 1.7 mM, at which the patients9 awareness of and response to hypoglycemia was evaluated. In the intervention group ( n = 11), three short-term hypoglycemic episodes preceded the second clamp study. Counterregulatory hormones increased significantly during hypoglycemia, but adrenaline ( P P P P P P

Compromised Hormonal Counterregulation, Symptom Awareness, and Neurophysiological Function After Recurrent Short-Term Episodes of Insulin-Induced Hypoglycemia in IDDM Patients

Determination of the MB isoenzyme of creatine kinase in patients with acute myocardial infarction may be disturbed by the presence of macro creatine kinase. The relative molecular mass of this form of creatine kinase in human serum is at least threefold that of the ordinary enzyme, and it is more thermostable. Here we describe our method for determination of macro creatine kinases and an easy-to-perform test for differentiating two forms of macro creatine kinase, based on their distinct activation energies. The activation energies of serum enzymes are mostly in the range of 40-65 kJ/mol of substrate. Unlike normal cytoplasmatic creatine kinases and IgG-linked CK-BB (macro creatine kinase type 1) a second form of macro creatine kinase (macro creatine kinase type 2) shows activation energies greater than 80 kJ/mol of substrate. The exact composition of macro creatine kinase type 2 is still unknown, but there is good reason to believe that it is of mitochondrial origin.

M. Eggstein

Papers

Lactic acidosis in biguanide-treated diabetics: a review of 330 cases.

Triglycerides and Glycerol Determination after Alkaline Hydrolysis

Definition of Clinically Relevant Lactic Acidosis in Patients with Internal Diseases

Compromised Hormonal Counterregulation, Symptom Awareness, and Neurophysiological Function After Recurrent Short-Term Episodes of Insulin-Induced Hypoglycemia in IDDM Patients

Macro creatine kinase: determination and differentiation of two types by their activation energies.