Coping with employment discrimination against diabetics: trends in social medicine and social psychology.

In many European countries, social-medical aspects in the management of diabetes mellitus are not satisfactorily respected. Our contribution reports a study addressing the impact of diabetes on the patient's career and daily work, in order to determine the extent to which diabetics are being discriminated against at work. Type I diabetics were questioned about their experience, and not on the objective burden. A questionnaire was developed to evaluate patients' social and employment problems. Few elements of an education program for Type I diabetes optimizing social skills (social competence) are demonstrated. In a group of 6-8 patients, assertive behavior in the work place is modelled (e.g., for hypoglycaemia, social phobia) by applying psychological methods (behavior modification role-playing). These methods can help diabetic patients to master their discrimination. They learn assertive behavior in social situations with superiors and colleagues and develop self-confidence (self-efficacy). This special education program supports Type I diabetics in coping with employment discrimination.

[Diagnosis of the diabetic metabolic status using fructosamine (and HbA1c) determination. The glycation quotient Glyc-Q, the glycation nomogram]. / Diagnostik der diabetischen metabolischen Situation mit Hilfe der Fructosamin- (und HbA1c-)Bestimmung. Der Glykierungsquotient Glyc-Q, das Glykierungsnomogramm.

The determination of fructosamine in serum is an accepted tool for the metabolic monitoring of diabetic patients. It provides an estimation of the glycemia state during the preceding 10 to 20 days. The turn-over of serum proteins is in general faster than that of hemoglobin. Therefore, fructosamine is faster responding than HbA1c to recompensation or fluctuations in glycemic control as observed in labile metabolic situations. On the other hand, under conditions of stable metabolic control fructosamine values correlate closely to HbA1c. The relation between the two parameters can be visualized in a nomogram of HbA1c, fructosamine and glucose or be expressed by a quotient (Glyc-Q = Fructosamine*2.2/HbA1c). A deviation from the stable metabolic situation (Glyc-Q = 100) reflects a trend in the recent development of glycemia: a Glyc-Q of greater than 120 is obtained in the state of decompensation, whereas in recompensation the Glyc-Q decreases significantly to values below 80. We propose to use the Glyc-Q in situations where a fast assessment of the glycemic state or an estimation of the development of glycemia within short intervals of observation are required.

[Microalbuminuria--an early marker of diabetic nephropathy]. / Mikroalbuminurie--ein früher Marker bei diabetischer Nephropathie.

The pathophysiological basis of microalbuminuria is outlined. In a preliminary study (n = 71) and a comprehensive retrospective study over 4 years in type I diabetics (IDDM) (n = 1470) and type II diabetics (NIDDM) (n = 2112), clinical and anamnestic data were compared and the blood pressure, protein excretion, and albumin concentration in the urine were recorded. Early recognition of microalbuminuria in diabetic nephropathy permits successful therapeutic intervention and thus a significant postponement of terminal renal failure.

[Fructosamine values in venous and capillary blood]. / Fructosamin-Werte in venösem und kapillarem Blut.

The determination of fructosamine could also be performed in serum obtained from capillary blood. The sample taking using micro sample carriers for capillary blood is more convenient for the patients. The described procedure is an alternative way suitable for the determination of fructosamine in ambulance and in doctor's office. Results obtained with uncoated micro carriers and capillary blood are in good agreement with fructosamine values from venous blood. However, the use of sample carriers coated with EDTA or heparin produced discrepant results.

Effects of ACE-inhibitors in hypertensive and normotensive diabetic patients with diabetic nephropathie.

Diabetic nephropathy leading to end stage renal failure with 30 to 40% cumulative incidence remains one of the great life threatening dangers for type I diabetics. Its natural history gets its impact due to the biochemical sequela of diabetic hyperglycemia such as polyol accumulation or glycation processes. Functional changes may be detected by microalbuminuria which in turn is followed by intraglomerular, intrarenal and finally systemic hypertension. Hypertension itself seems to be part of the self perpetuating process, and therefore antihypertensive treatment has been shown to be an effective area. Antihypertensive treatment by itself is effective in the slowing down of the decline of glomerular filtration rate, together with decreasing the amount of albumin excretion and, therefore, might be expected to be of value in prolonging the renal prognosis over a length of time. From the theoretical point of view the ACE inhibitors were looked upon as beneficial and therefore preferable as interventional tools because of their special effects of blood pressure redistribution within the glomeruli. Long term reports and a lot of short and intermediate term controlled studies were able to confirm the expected effects. Whether this is the case also in borderline hypertension or even in normotensive diabetics remains finally to be established. The question of long term effects such as survival rates and the superiority of antihypertensive treatments with beta blockers or drug combinations, or whether these results reflect merely their systemic blood pressure lowering effects remain finally to be elucidated.

The feedback between monitoring and improvement of quality of diabetes care.

The need for permanent, population-wide, improvement in metabolic care of diabetic patients is generally accepted. This paper highlights some related aspects which must be considered by any health care provider: (1) Monitoring metabolic or other variables in diabetic patients is an essential tool in routine metabolic care, where a "short feedback" between monitored data and medical or behavioral measures is permanently established by the patients themselves, the physicians, the nurses etc. (2) Quality insurance requires the closure of a "long feedback" between informations and interventions, such as conditions, tools, methods, used at the different levels of the care system, from the individual patient to a population scale. (3) Appropriate epidemiological studies are required to program and evaluate the effect of any activity aimed at insuring and maybe improving the quality of care of diabetic patients, especially if one considers the time required to reach "hard end-points" such as the evaluation of patient mortality or the outcome of children from diabetic mothers. (4) The knowledge of incidence and prevalence rates of diabetes and its complications, and of risk factors may stimulate the political and economical recognition of the importance of the disease by health care officials. (5) In this way, the medical recognition is also stimulated within the professional team responsible for the establishment of the "long feedback" of quality insurance at the level of a given method, of an individual patient or of a health care unit, and for the actual implementation of generally accepted knowledge, everywhere in routine care.

Non-specific viral infections as possible synchronising events of the manifestation of type 1 diabetes.

Four cases of simultaneous manifestation of Type 1 diabetes in two members of the same household are reported. In all cases, a flu-like infection preceded diabetes onset. Surprisingly, despite simultaneous development of insulin dependency, insulin requirements were strikingly different at 3 months in all cases. These observations suggest that increased insulin resistance during infection may cause insulin deficiency in individuals with widely varying residual beta cell activity.

Correlation of islet cell antibodies and HLA-DR phenotypes with diabetes mellitus in adults.

In a cross-sectional study, sera of 81 adult diabetic in-patients were tested for the presence of pancreatic islet cell antibodies (ICA), both IgG and complement-fixing. All patients had been well controlled initially with oral hypoglycaemic agents and therefore had been classified as having Type 2 (non-insulin-dependent) diabetes. However, 14 were subsequently classified as Type 1 (insulin-dependent) because they became insulin-dependent within 2 months of diagnosis. Ten of these patients (71%) were ICA-positive. Sixty-seven patients had been non-insulin-dependent for at least 1 year after diagnosis. Circulating ICA were present in 18 patients and 16 of these (89%) required insulin therapy. Secondary oral hypoglycaemic agent failure developed within a mean period of 3.7 years after diagnosis. In contrast, in the ICA-negative sub-group (n = 49) insulin treatment became necessary in 29 patients. Secondary oral hypoglycaemic agent failure of these patients had developed after a mean period of 8.4 years, which was significantly longer than in the ICA-positive patients (p less than 0.01). Complement-fixing-ICA were detected only in sera with an ICA-IgG titre of at least 8, and its prevalence was similar in the sub-groups tested, i.e., the Type 1 diabetic patients and the patients with secondary oral hypoglycaemic agent failure. With HLA-DR typing, a significant excess of the DR3 antigen and heterozygous DR3/DR4 phenotypes was found in ICA-positive patients with secondary oral hypoglycaemic agent failure and in the Type 1 diabetic patients, which was comparable with the frequencies reported in juvenile-onset Type 1 diabetes.