Corticosteroid inhibition of the OKT3-induced cytokine-related syndrome--dosage and kinetics prerequisites

The data presented extend to a larger series of 27 consecutive renal allograft recipients treated prophylactically with OKT3 our previous observation that the acute OKT3-induced clinical syndrome is related to massive release in the circulation of some cytokines, among which are tumor necrosis factor and interferon gamma. In addition, a pilot randomized study was set up including 12 consecutive patients receiving high-dose corticosteroid treatment (0.5 g solumedrol) either before or at the same time as the first OKT3 injection. Results confirm that when corticosteroids are given in sufficient amount and, importantly, 1 hr before the first OKT3 injection, they significantly decrease the release of both tumor necrosis factor and interferon gamma. In addition, the pretreatment with corticosteroids may totally abolish the IL-2 release induced by OKT3. Given the key role the massive although transient cytokine release plays in determining the OKT3-induced acute syndrome, these results provide the biological basis supporting a precise kinetics of administration of high-dose corticosteroids to better decrease the severity of the clinical reaction.     

Excimer laser coronary angioplasty after primary unsuccessful PTCA]

Excimer laser coronary angioplasty is a new technique for ablation of coronary stenosis, however, the indications for its application are still controversial. We describe two male patients, 60 and 65 years old, who underwent unsuccessful balloon PTCA with a short, concentric and calcified coronary stenosis, although balloon inflation pressure was increased to a maximum in both cases. Excimer laser angioplasty following the failed procedures showed no evidence for tissue ablation angiographically, but a repeat attempt with balloon angioplasty was successful in both cases. Thus, laser angioplasty may be considered as an adjunct technique to balloon angioplasty after a failed PTCA in resistant, non-inflatable lesions.     

The anti-androgen flutamide in the treatment of prostatic hyperplasia]

The authors treated 23 benign prostatic hyperplasia (BPH) patients with antiandrogen flutamide. Half of the patients were treated with 500 mg, the another part with 750 mg flutamide for three months, and after 3 months brake again for 3 months. The decrease of the residual urine and an increase of the flow were observed. The subjective parameters were improved, too. In some patients side effects (gynecomastia, loss of appetite and potency) were observed. There was no different in the effect of the two doses.     

5-year experience with BCG immunoprophylaxis in superficial bladder cancer]

Our 5-year experience with BCG in the tumor stage pTis, pTa and pT1, G I-II shows a lasting remission of 88.5% (73%) in 78 (26) patients treated with BCG preparation Pasteur (Connaught) after transurethral resection. A complete remission in patients with carcinoma in situ (12 patients) could be found in 92%. The local and systemic side-effects, which are of limited duration, are tolerable, well treatable and fully reversible.     

Walk training and drug treatment in patients with peripheral arterial occlusive disease stage II. A review.

On the basis of the present studies physical therapy is the most effective basis therapy of peripheral arterial occlusive disease stage II according to Fontaine. The consequent integration of the patients into widespread vascular training groups would be desirable. All present studies with so-called vasoactive drugs led to a statistically significant increase in pain-free walking distance. This is especially true for the substances naftidrofuryl, pentoxifylline, and buflomedil. Nevertheless, these studies do not fully meet the standards set by the GCP or the FDA guidelines. It must also be said that the increase in walking distance by vasoactive substances is less pronounced than the effect obtained by walk training alone. Both the vasoactive therapy and controlled walk training aim at an increase in pain-free walking distance. It is, however, still unclear whether the modes of therapy described influence the primary disease. Angiographically controlled studies are momentarily not available.     

Recognition and killing of tumour cells expressing heat shock protein 65 kD with immunotoxins containing saporin.

The expression of heat shock proteins (HSP) of the 65 kD family (groEL) has been observed by flow cytometry using murine monoclonal antibody (MoAb) anti-HSP 65 kD (ML30) on the surface of B (Daudi) or T (H9) lymphoma cells, on a monocyte cell line (U937) and also on a primary culture of a human pancreatic carcinoma (HPC). Moreover, the MoAb ML30 was coupled to Saporin 6, a ribosome-inactivating protein recovered from the seeds of Saponaria officinalis, to kill HSP-expressing cells with a specific immunotoxin. An indirect method using first MoAb ML30 and then anti-mouse IgG1 immunotoxin was also performed. With this method a human serum positive for HSP65-antibodies was tested using anti-human IgG1 or IgM immunotoxins. All cell lines were inhibited when preincubated with the specific immunotoxin directed to HSP65 (ML30 SO6), although H9 cells were susceptible to immunotoxin only after thermal stress. Daudi and HPC cells were inhibited both after long-term culture and when freshly explanted from SCID mice. Proliferation of the U937 monocytic cell line, that constitutively expresses high levels of HSP65 on the surface (as determined by flow cytometry), was completely inhibited (100% inhibition) by the ML30 SO6. However, not all tumour cells constitutively express high levels of surface HSP65, as determined by cytometric analysis. For this reason it was not always possible to obtain complete inhibition of cellular proliferation.