The classification of diabetes mellitus and the tests used for its diagnosis were brought into order by the National Diabetes Data Group of the USA and the second World Health Organization Expert Committee on Diabetes Mellitus in 1979 and 1980. Apart from minor modifications by WHO in 1985, little has been changed since that time. There is however considerable new knowledge regarding the aetiology of different forms of diabetes as well as more information on the predictive value of different blood glucose values for the complications of diabetes. A WHO Consultation has therefore taken place in parallel with a report by an American Diabetes Association Expert Committee to re-examine diagnostic criteria and classification. The present document includes the conclusions of the former and is intended for wide distribution and discussion before final proposals are submitted to WHO for approval. The main changes proposed are as follows. The diagnostic fasting plasma (blood) glucose value has been lowered to > or =7.0 mmol l(-1) (6.1 mmol l(-1)). Impaired Glucose Tolerance (IGT) is changed to allow for the new fasting level. A new category of Impaired Fasting Glycaemia (IFG) is proposed to encompass values which are above normal but below the diagnostic cut-off for diabetes (plasma > or =6.1 to or =5.6 to <6.1 mmol l(-1)). Gestational Diabetes Mellitus (GDM) now includes gestational impaired glucose tolerance as well as the previous GDM. The classification defines both process and stage of the disease. The processes include Type 1, autoimmune and non-autoimmune, with beta-cell destruction; Type 2 with varying degrees of insulin resistance and insulin hyposecretion; Gestational Diabetes Mellitus; and Other Types where the cause is known (e.g. MODY, endocrinopathies). It is anticipated that this group will expand as causes of Type 2 become known. Stages range from normoglycaemia to insulin required for survival. It is hoped that the new classification will allow better classification of individuals and lead to fewer therapeutic misjudgements.

Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification of diabetes mellitus provisional report of a WHO consultation.

the growth of knowledge regarding the etiology and pathogenesis of diabetes has led many individuals and groups in the diabetes community to express the need for a revision of the nomenclature, diagnostic criteria, and classification of diabetes. As a consequence, it was deemed essential to develop an appropriate, uniform terminology and a functional, working classification of diabetes that reflects the current knowledge about the disease. (1)

Report of the expert committee on the diagnosis and classification of diabetes mellitus

So far in this course we have dealt entirely with the evolution of characters that are controlled by simple Mendelian inheritance at a single locus. There are notes on the course website about gametic disequilibrium and how allele frequencies change at two loci simultaneously, but we didn’t discuss them. In every example we’ve considered we’ve imagined that we could understand something about evolution by examining the evolution of a single gene. That’s the domain of classical population genetics. For the next few weeks we’re going to be exploring a field that’s actually older than classical population genetics, although the approach we’ll be taking to it involves the use of population genetic machinery. If you know a little about the history of evolutionary biology, you may know that after the rediscovery of Mendel’s work in 1900 there was a heated debate between the “biometricians” (e.g., Galton and Pearson) and the “Mendelians” (e.g., de Vries, Correns, Bateson, and Morgan). Biometricians asserted that the really important variation in evolution didn’t follow Mendelian rules. Height, weight, skin color, and similar traits seemed to

Human biochemical genetics

Objectives.This study attempts to develop a comprehensive set of comorbidity measures for use with large administrative inpatient datasets.Methods.The study involved clinical and empirical review of comorbidity measures, development of a framework that attempts to segregate comorbidities from other

https://czresearch.com/dropbox/Elixhauser_MedCare_1998v36p8.pdf

Comorbidity measures for use with administrative data.

The metabolic syndrome

The Health Care Financing Administration (HCFA) publishes hospital mortality rates each year. We undertook a study to identify characteristics of hospitals associated with variations in these rates. To do so, we obtained data on 3100 hospitals from the 1986 HCFA mortality study and the American Hospital Association's 1986 annual survey of hospitals. The mortality rates were adjusted for each hospital's case mix and other characteristics of its patients. The mortality rate for all hospitalizations was 116 per 1000 patients. Adjusted mortality rates were significantly higher for for-profit hospitals (121 per 1000) and public hospitals (120 per 1000) than for private not-for-profit hospitals (114 per 1000; P less than 0.0001 for both comparisons). Osteopathic hospitals also had an adjusted mortality rate that was significantly higher than average (129 per 1000; P less than 0.0001). Private teaching hospitals had a significantly lower adjusted mortality rate (108 per 1000) than private nonteaching hospitals (116 per 1000; P less than 0.0001). Adjusted mortality rates were also compared for hospitals in the upper and lower fourths of the sample in terms of certain hospital characteristics. The mortality rates were 112 and 121 per 1000 for the hospitals in the upper and lower fourths, respectively, in terms of the percentage of physicians who were board-certified specialists (P less than 0.0001), 112 and 120 per 1000 for occupancy rate (P less than 0.0001), 113 and 120 per 1000 for payroll expenses per hospital bed (P less than 0.0001), and 113 and 119 per 1000 for the percentage of nurses who were registered (P less than 0.0001).

Hospital characteristics and mortality rates.

The importance of body fat distribution as a predictor of metabolic aberrations was evaluated in 9 nonobese and 25 obese, apparently healthy women. Plasma glucose and insulin levels during oral glucose loading were significantly higher in women with predominantly upper body segment obesity than in women with lower body segment obesity. Of the former group, 10 of 16 subjects had diabetic glucose tolerance results, while none of the latter group was diabetic. Fasting plasma triglyceride levels were also significantly higher in the upper body segment obese women. The site of adiposity in the upper body segment obese women was comprised of large fat cells, while in the lower body segment obese subjects, it was formed of normal size cells. In both types of obesity, abdominal fat cell size correlated significantly with postprandial plasma glucose and insulin levels. Thigh fat cell size gave no indication as to the presence of metabolic complications. Thigh adipocytes were also resistant to epinephrine-stimulated lipolysis, presumably due to an increase in alpha-adrenergic receptors. Thus, in women, the sites of fat predominance offer an important prognostic marker for glucose intolerance, hyperinsulinemia, and hypertriglyceridemia. This association may be related to the disparate morphology and metabolic behavior of fat cells associated with different body fat distributions.

Relation of Body Fat Distribution to Metabolic Complications of Obesity

Most epidemiologic studies which evaluate the association between obesity and disease consider only total adipose tissue and ignore its distribution. The present study used data from a national survey of women in TOPS (a weight reduction organization) in 1969. The purpose of this study was to evaluate the distribution of adipose tissue as a risk factor for disease using girth, height, and weight measurements in 21,065 women 40-59 years of age and 11,791 women 20-39 years of age. It was found that an index of body fat distribution, the ratio of waist girth to hip girth, was significantly associated with diabetes, hypertension, and gallbladder disease in women aged 40-59 and with menstrual abnormalities in women aged 20-39. Relatively more fat around the waist (as compared to hips) was associated with higher disease prevalence even among women with comparable total body fat. These findings suggest that indices based only on weight and height may not adequately characterize the risks associated with obesity.

The association of girth measurements with disease in 32,856 women

Data from 932 patients with leukemia who received bone marrow transplants were analyzed to determine factors associated with an increased risk of developing interstitial pneumonitis. Interstitial pneumonitis developed in 268 patients for a 2-year actuarial incidence of 35 +/- 4% (SD) and with a mortality rate of 24%. Six factors were associated with an increased risk: use of methotrexate rather than cyclosporine after transplantation (relative risk, 2.3; p less than 0.0002); older age (relative risk, 2.1; p less than 0.0001); presence of severe graft-versus-host disease (relative risk, 1.9; p less than 0.003); long interval from diagnosis to transplantation (relative risk, 1.6; p less than 0.002); performance ratings before transplantation of less than 100% (relative risk, 2.1; p less than 0.0001); and high dose-rates of irradiation in patients given methotrexate after transplantation (relative risk, 3.2; p less than 0.03). The risk of developing interstitial pneumonitis ranged from 8% in patients with none of these adverse risk factors to 94% in patients with all six. These findings may help to identify patients at high risk for this complication.

Arthur J. Hartz

Papers

Hospital characteristics and mortality rates.

Relation of Body Fat Distribution to Metabolic Complications of Obesity

The association of girth measurements with disease in 32,856 women

Interstitial pneumonitis after bone marrow transplantation. Assessment of risk factors.

Relationship of obesity to diabetes: Influence of obesity level and body fat distribution