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Biomedical subjects

K Federlin

Publications and source records attributed to K Federlin.

At least 145 records · Page 8Linked to original sources
PubMed1992

Impairment of polymorphonuclear leukocyte function and metabolic control of diabetes.

OBJECTIVE: In this study, ingestion of Staphylococcus aureus and "bacteria killing" (BK) were measured to evaluate polymorphonuclear leukocyte (PMN) phagocytic functions and chemiluminescence response (CL) to phorbol-myristic acetate (PMA) as respiratory burst activity with regard to metabolic control parameters in diabetic patients. RESEARCH DESIGN AND METHODS: PMN phagocytic functions were assessed in 40 diabetic patients, all receiving insulin and in poor metabolic control, with 3H-thymidine-labeled Staphylococcus aureus in a modified radiometric assay. Bacteria killing was determined by pure-plate counting of surviving bacteria (colony-forming units [cfu]) and luminol-enhanced CL in response to PMA as a measure of respiratory burst. PMN function data were correlated to HbA1 as parameter of recent metabolic control. RESULTS: PMN of diabetic patients showed a significant reduction in Staphylococcus aureus (50.7 +/- 4.1%) and BK (29.4 +/- 4.2%) compared with healthy nondiabetic control subjects (76.6 +/- 4.6% and 16.3 +/- 3.1%, respectively, P less than 0.001), and PMN CL response was markedly reduced in diabetic patients also. Linear regression analysis showed a highly significant negative correlation of HbA1 versus Staphylococcus aureus (r = -0.67, P = 0.001) and a positive correlation for BK (r = 0.73, P less than 0.001). This was also true for CL, although this did not reach statistical significance (P = 0.06). CONCLUSIONS: The data obtained demonstrate impaired PMN phagocytic functions and CL response in diabetic patients. These findings suggest inhibitory effects of elevated glucose concentrations on PMNs, a possible role of protein glycosylation for impairing PMN function, thus contributing in part to altered host defense.

Adult↗
PubMed1992

[Expression of low-affinity Fc epsilon receptors on circulating monocytes in patients with inflammatory rheumatic diseases].

In patients with scleroderma, high proportions of circulating CD23+ monocytes could be detected by FACS analysis as compared with controls. Supernatants obtained from lymphocytes yielded high amounts of interleukin-4-(IL-4-)like activity. The results suggest that IL-4 contributes to monocyte activation in scleroderma. There were no correlations with serum IgE, or numbers of naive and memory-CD4+ lymphocytes.

Antigens, Differentiation, B-Lymphocyte↗
PubMed1992

Surgery, dopamine agonist therapy of combined treatment--results in prolactinoma patients after a 12 month follow-up.

In a non-randomized retrospective study n = 36 prolactinoma patients (n = 7 micro- and n = 29 macroadenomas) were evaluated before (E0), 4 (E1) and 52 weeks (E2) after applying 3 different treatment modalities: A dopamine agonist (DA) therapy (n = 14), B surgery as initial procedure (n = 12) and oral DA therapy, C DA preinjection, subsequent surgery (n = 10) and oral DA medication. T0 outline the effect of the 3 regimens upon serum prolactin (PRL) and tumour size reduction, clinical signs and symptoms, anterior/posterior pituitary lobe function and MRI/CT findings were evaluated in each patient at E0, E1 and E2. In group A, PRL normalization was achieved in n = 10 patients (71%), although the frequency of an empty sella was only one out of 12 macroprolactinoma patients (less than 10%). Patients of group C showed the lowest PRLE2 levels (32 +/- 11 ng/ml, normalization rate 60%), although not statistically significant when compared with the other groups (A: 41 +/- 28 ng/ml, B: 114 +/- 33 ng/ml, normalization rate 31%). According to MRI studies in groups B and C total removal was achieved in 33% and 50% of macroprolactinomas, respectively. The most favourable ratio of the leading pre/posttreatment signs and symptoms was observed in patients of group C. It was concluded that no superiority of either treatment regimen exists for prolactinoma patients. Each mode of therapy has its own benefits which may be applied to the different biological behaviour of a prolactinoma in the respective patient.

Adolescent↗
PubMed1992

Islet transplantation: clinical and experimental.

Experimental diabetes in rodents has been successfully treated by implantation of isolated islets using a syngenic system (Lewis rats). It is possible to reverse all diabetic symptoms of the animals and to prevent late complications in kidney, eye and nervous system. Although isolated islets are highly immunogenic in an allogenic system immuno-alteration techniques have been developed and succeeded in longterm survival after culture at low temperature (24 degrees C), UV-irradiation, cryopreservation, pretreatment with Ia-antibodies etc. Islet transplantation in larger animals and in man up to now has been less successful. Although in a few studies longterm survival of canine islets has been observed, other groups were less successful using dogs and pigs in auto- or allo-transplantation. In man there are reports from various institutions during the last fifteen years using adult or fetal islet material. Only in a few instances the patients came off insulin for some weeks or months. The reasons for this failure are probably manifold: low number of islets, impurity, long ischemia time before isolation, transplantation to inappropriate sites, impairment of engraftment in longterm diabetic recipients and recurrence of autoimmunity in transplanted islets. Further studies are necessary to overcome these barriers. Recent observations using a higher number of islets (> 500,000) and new immunosuppressive drugs (FK506) seem to be promising.

Animals↗
PubMed1992

[Impaired induction of chemiluminescence and function of polymorphonuclear neutrophilic granulocytes in diabetes mellitus].

The aim of this study was to investigate PMN-chemiluminescence response as a measure of respiratory burst activity and the phagocytic PMN function "ingestion" with regard to metabolic control parameters in diabetes mellitus (d.m.) in comparison to healthy controls. Our findings demonstrated a significant reduction of chemiluminescence response and ingestion in diabetic patients compared to controls (p less than 0.01 resp.); further an inverse relation of metabolic control parameters in d.m. and PMN impairment, suggesting inhibitory effects on PMN function, thus leading or contributing at least in part to altered host defense.

Diabetes Mellitus↗
PubMed1992

[Reduced phagocytic capacity of circulating granulocytes in diabetes mellitus].

Impaired PMN function is regarded as a major cause for infectious complications in diabetes mellitus (d.m.). The aim of this study was to investigate the phagocytic PMN functions "ingestion" (IN) and "bacterial killing" (BK) with regard to metabolic control parameters and influences of variable glucose concentrations on these PMN functions in vitro. Our findings demonstrated a significant reduction of IN and BK in diabetic subjects compared to controls (p less than 0.001 resp.). The differences between type I and type II d.m. did not reach statistical significance. Linear regression analysis showed significantly negative correlations for fasting blood-glucose concentrations as well as glycosylated hemoglobin (HbA1) and IN (r = -0.34, p 0.03; r = -0.67, p = 0.001) and a highly positive for BK (r = 0.73, p = 0.0001). In vitro there was a significant decrease in IN and BK both in diabetic subjects and controls for glucose concentrations greater than 27.7 mmol/l (p = 0.01 resp.). These data clearly demonstrated impaired PMN ingestion and bacterial killing in diabetic patients, and the degree of PMN dysfunction is inversely related to the degree of metabolic control of diabetes. These findings suggest inhibitory effects of hyperglycemia on PMN functions, thus contributing at least partly to altered host defense in diabetes mellitus.

Blood Bactericidal Activity↗
PubMed1992

[Circulating CD8 as an indicator of inflammatory rheumatic disease].

An enzyme-linked immunoassay detecting soluble CD8 (s-CD8) was applied to study activation of CD8(+)-(suppressor/cytotoxic) T-cells in patients with rheumatic diseases. Compared with normals, s-CD8 levels were elevated in patients with rheumatoid arthritis, ankylosing spondylitis, and polymyositis. In contrast, low s-CD8 values were observed in patients with progressive systemic sclerosis/scleroderma. In systemic lupus erythematosus (SLE), s-CD8 values were correlated with C-reactive protein. This finding and an association with other parameters of clinical activity were confirmed by longitudinal studies. In summary, our findings support the view that implication of CD8(+)-T-cell activation is different in the pathogenesis of each rheumatic disease. Elevated s-CD8 indicates active disease, and can be used to monitor CD8(+)-T-cell activation in SLE while determination of s-CD8 seems to be of little clinical value in the other rheumatic diseases studied.

Adult↗
PubMed1991

Aminoguanidine treatment inhibits the development of experimental diabetic retinopathy.

Retinal capillary closure induced by hyperglycemia is the principal pathophysiologic abnormality underlying diabetic retinopathy, but the mechanisms by which this induction occurs are not clear. Treatment of diabetic rats for 26 weeks with aminoguanidine, an inhibitor of advanced glycosylation product formation, prevented a 2.6-fold accumulation of these products at branching sites of precapillary arterioles where abnormal periodic acid/Schiff reagent-positive deposits also occurred. Aminoguanidine treatment completely prevented abnormal endothelial cell proliferation and significantly diminished pericyte dropout. After 75 weeks, untreated diabetic animals developed an 18.6-fold increase in the number of acellular capillaries and formed capillary microaneurysms, characteristic pathologic features of background diabetic retinopathy. In contrast, aminoguanidine-treated diabetic animals had only a 3.6-fold increase in acellular capillaries and no microaneurysms. These findings indicate that advanced glycosylation product accumulation contributes to the development of diabetic retinopathy and suggest that aminoguanidine may have future therapeutic use in this disorder.

Animals↗