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E Pohanka

Publications and source records attributed to E Pohanka.

At least 55 records · Page 3Linked to original sources
PubMed1992

Increased levels of plasma amylin in advanced renal failure.

Amylin, a 37 amino acid polypeptide, has been suggested to play a prominent role in the pathogenesis of insulin resistance in type II diabetes mellitus. Various studies have demonstrated most recently that amylin is cosecreted with insulin. No data are available on the elimination of amylin from the circulation. We therefore tested plasma levels of amylin, insulin and C-peptide in 49 non-obese, non-diabetic patients (27 male/22 female) with various degree of renal impairment (Group A: CCr less than 20 ml/min, n = 20; Group B: CCr 20-89 ml/min, n = 18; and Group C: CCr greater than 80 ml/min, n = 9). We found a significant increase of plasma amylin when kidney function, expressed by creatinine clearance fell below 20 ml/min (17.9 +/- 1.7 vs. 12.2 +/- 0.8 vs. 8.8 +/- 1.2 pg/ml; p = 0.0005). Plasma amylin correlated closely with serum C-peptide (r = .764; p = 0.0001), and to a lesser extent with insulin (r = .595; p = 0.0001) underlining its postulated cosecretion with these peptides. The data indicate that amylin might be eliminated by renal mechanisms. Our data show that besides type II diabetes mellitus, advanced renal failure is another clinical situation with enhanced plasma amylin levels. Whether amylin plays any pathogenetic role in renal patients remains to be elucidated.

Amyloid↗
PubMed1990

Non-inherited maternal HLA antigens and protection against sensitisation.

To test the hypothesis that non-inherited maternal antigens (NIMAs), which reportedly afford protection against sensitisation by random transfusions, can provide protection against repetitive antigenic exposure of donor-specific transfusion (DST), 140 DST patients whose donors were mismatched for NIMAs and 71 whose donors were mismatched for non-inherited paternal antigens (NIPAs) were studied. The rate of sensitisation in the two groups of patients was similar (22.1% vs 15.5%). There was no difference in sensitisation to NIMAs and NIPAs between patients who received azathioprine and those who did not. The formation of donor specific HLA antibody was comparable in the two groups. After kidney transplantation there were no differences in 1-year graft survival or the incidence of rejection episodes. These findings suggest that NIMAs do not provide lifelong protection against subsequent repetitive antigen challenge and sensitisation.

Adult↗
PubMed1990

[OKT 3 treatment of kidney transplant recipients].

Anti-rejection therapy with the monoclonal antibody OKT 3 was effective in the treatment of acute rejection episodes in 66% (47/71) of OKT 3 treated kidney graft recipients. The success of OKT 3 therapy, however, appeared to be dependent on certain variables. Reversal of rejection differed significantly according to the indication, namely if patients were treated first line, as opposed to rescue therapy. Vascular components of rejection and/or severe interstitial rejection, as well as acute tubular necrosis were associated with a worse reversal rate. Non-responders to OKT 3 presented with significantly lower serum OKT 3 trough levels during the first three days of the treatment course. The presence of more than one of these risk factors was shown to decrease the reversal rate of rejection significantly. The variables appeared to exert their influence in an additive fashion. Administration of OKT 3 led to the induction of an acute phase reaction, which could be detected within one day after start of therapy. The incidence of both bacterial and viral infection was increased dramatically in OKT 3 treated patients as compared with graft recipients who were not treated with monoclonal or polyclonal antilymphocyte antibodies. The findings demonstrate that OKT 3 is of value in the treatment of acute rejection episodes but provide evidence of differential indications for OKT 3 therapy, which must be taken into account to optimize control of rejection and avoid unnecessary side effects where the drug is not indicated.

Antibodies, Monoclonal↗
PubMed1990

Influence of HLA phenotypes on the inhibition of in vitro alloreactivity by cyclosporine.

Interindividual variations in the immunosuppressive effect of Cyclosporine have been observed in clinical organ transplantation. Searching for an in vitro correlate we investigated a possible relation between inhibition of alloresponsiveness by CsA and the HLA phenotypes of the responder or stimulator in mixed lymphocyte reactions. Peripheral blood mononuclear cells from 28 healthy volunteers were used as responder or stimulator cells (gamma-irradiated) and the inhibitory effect of graded amounts of CsA was determined in 130 criss-cross combinations. Sensitivity of alloresponsiveness to the drug was expressed as the dose causing 50% inhibition (ED50) and was read from the inhibition curves generated after four-parameter logistic curve fitting. ED50 ranged from 0.35 ng/ml to 33.4 ng/ml and correlated only weakly with the magnitude of the response (r = 0.12). In MLC with HLA DR4-positive responder cells, ED50 was significantly lower (Pc = 0.0035, Kruskal Wallis) when compared with MLC with responder cells of other DR haplotypes. For HLA DR5-positive responder cells ED50 was significantly higher (Pc = 0.042) when compared with DR5-negative responder cells. No significant correlation between ED50 and any particular haplotype of the stimulator cells could be observed. Sensitivity to CSA did not differ in MLC with 1 or 2 mismatches in the HLA-DR locus. In summary, we found that sensitivity of in vitro alloreactivity was different for particular HLA DR phenotypes, which may have important implications for the immunosuppressive therapy of transplanted patients with cyclosporine.

Cyclosporins↗
PubMed1989

"Anti-idiotypic" antibodies to HLA in transiently sensitized DST patients.

To test the hypothesis whether "anti-idiotypic" antibodies (Ab2) were involved in the loss of sensitization following donor-specific blood transfusions (DST), we investigated nine potential kidney graft recipients who became transiently sensitized after DST. Inhibiting "anti-idiotypic" activity of post-DST sera was determined using a complement-dependent cytotoxicity inhibition assay. The follow-up after DST ranged from 9 to 66 months. The nine patients developed 12 different anti-HLA antibodies (Ab1). Inhibiting post-DST serum activity was found in relation to four of them, while enhancement of cell killing caused by post-DST sera was observed in relation to six anti-HLA antibodies. In two patients presenting with more than one anti-HLA antibody inhibition was found with only one of the antibodies, indicating that the blocking of Ab1 was specific for the respective antibody. Enhancement was associated with a significantly prolonged sensitization of the patients. On the average, 5.7 +/- 5.0 months were necessary before "anti-idiotypic" activity was developed after the loss of sensitization, whereas enhancement was found immediately thereafter. Testing by flow cytometry indicated that enhancing sera still contained subthreshold levels of Ab1. Our results indicate that DST can induce the development of "anti-idiotypic" antibodies following a short period of sensitization. This finding provides further evidence that anti-idiotypic antibodies might be relevant factors in the eventual disappearance of sensitization to HLA antigens.

Adult↗
PubMed1989

Secondary hypersplenism due to Caroli syndrome complicating immunosuppression in a renal allograft recipient.

The differential diagnosis of thrombocytopenia and leukocytopenia in renal allograft recipient can be troublesome. We report on a patient in whom the rare case of portal hypertension with secondary hypersplenism due to Caroli syndrome was detected to be the cause for the hematological disturbance. The management of the thereby complicated immunosuppressive regimen is discussed.

Adult↗