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Biomedical subjects

K Breddin

Publications and source records attributed to K Breddin.

At least 19 recordsLinked to original sources

[An epidemiologic study of the value and limits of physical therapy/exercise therapy in Fontaine stage II arterial occlusive disease].

Using a questionaire the members of the German Society for Angiology (DGA) were interrogated on the use of physical training for the treatment of peripheral arterial occlusive disease; from a total of n = 431 as much as n = 156 responded, i.e. making up a response of 36%. 104 of them conduct physical training either on their own or assign patients to it (67%). In most of the institutions exclusively walking/interval training (83%) or medical exercise (74%) are performed. In most cases the training is conducted by physiotherapeutists (71%). 13% of the patients are admitted exclusively to physical training, 34% undergo combined therapy, i.e. physical training and vaso-active medication. 22% receive mere medical, 31% surgical treatment. A general evaluation on the success of the different therapies applied turned out following frequency: 1. combined therapy (medical treatment/physical training); 2. surgical procedures as a therapeutic measure; 3. physical training; 4. medical treatment. A further study performed at three ambulatory centres offering physical training were to show what kind and to which extent such training is useful. In 34% of the cases (from a total of n = 201 patients with peripheral arterial occlusive disease in state II according to Fontaine) contraindications argue against the application of physical training. From a rest of 66% as much as 36% of the patients refuse to undergo physical training the reasons of which were stated with large transport distances and time problems. The remaining rest accepts the offer, although 24% attend such training only sporadically. The results show that mainly contraindications and insufficient patient compliance account for the fact that only one third of the patients attend physical training. The results are discussed and proposals are made to improve patient compliance.

Aged

Acquired disorder of platelet function associated with autoantibodies against membrane glycoprotein IIb-IIIa complex--1. Glycoprotein analysis.

A patient with idiopathic thrombocytopenic purpura developed after splenectomy a thrombasthenia-like severe haemorrhagic diathesis characterized by a normal or subnormal platelet count, prolonged bleeding time, strongly reduced platelet adhesion to glass and defective platelet aggregation in response to ADP and collagen. In contrast to hereditary thrombasthenia membrane glycoproteins (GP) IIb and IIIa were normally present in the patient's platelets. Immunoelectrophoretic analysis revealed an abnormal behaviour of the patient's GP IIb-IIIa complex. Autoantibodies against GP IIb-IIIa were detected in Triton-extracted washed platelets. Incubation of normal platelets with plasma from the patient resulted in a similar immunoelectrophoretic abnormality of the GP IIb-IIIa complex indicating that bound autoantibodies (IgG) are responsible for the abnormal immunoelectrophoretic behaviour of the patient's GP IIb-IIIa complex. Platelet fibrinogen was severely reduced similar to classical thrombasthenia suggesting that the GP IIb-IIIa complex is involved in platelet fibrinogen storage.

Autoantibodies

Fibrinogen does not protect von Willebrand factor against proteolysis by human cathepsin G.

The susceptibility of von Willebrand factor /vWF/ to digestion by human neutrophil cathepsin G in highly purified FVIII/vWF concentrate /BHS/ and in cryoprecipitate has been studied. In contrast to human neutrophil elastase, cathepsin G inactivates and degrades vWF not only in BHS but also in cryoprecipitate. Fibrinogen added in excess to purified FVIII/vWF concentrate does not protect vWF against cathepsin G proteolysis. Biological significance of this phenomena are discussed.

Cathepsin G

Effects of human elastase on von Willebrand factor in highly purified factor VIII concentrate and in cryoprecipitate.

The susceptibility of v. Willebrand factor (vWF) and F.VIII in virus-inactivated factor VIII/vWF concentrate (Behring-Haemate-HS (BHS] and in cryoprecipitate (Behring-Ristofact) to digestion by highly purified, cathepsin G free human neutrophil elastase (HNE) was compared. In Haemate-HS HNE induced a degradation of the vWF subunit. This reaction was dependent on time and enzyme concentration. It resulted in disappearance of large size vWF multimers, an anodal shift of vWF peak in crossed immunoelectrophoresis and a decrease of F.VIII:C and Ristocetin cofactor activities. In contrast in cryoprecipitate even high HNE concentration did not provoke changes of these parameters. Both Haemate-HS and Ristofact were free of alpha 1-proteinase inhibitor (alpha 1 PI) and alpha 2-macroglobulin (alpha 2 M) but they differed in the content of other contaminating proteins. In particular Haemate-HS was fibrinogen-free but Ristofact contained 6.6 mg/ml. Purified fibrinogen added to Haemate-HS was found highly effective in protecting vWF in Haemate-HS against the proteolytic degradation and loss of activity under the influence of HNE.

Factor VIII

Intravenous prostaglandin E1 versus pentoxifylline therapy in chronic arterial occlusive disease--a controlled randomised multicenter study.

In a controlled multicenter study 70 patients with chronic arterial occlusive disease stage IV according to Fontaine's classification were randomised to treatment with prostaglandin E1 (PGE1) or pentoxifylline (PX), administered over 4 weeks. Parameters of effectiveness were the reduction of analgesics, the relief of rest pain according to an analogue scale, the improvement of the ulceration according to an ulcer score and the healing of necrotic area. The results show that both forms of treatment produced a significant reduction in analgesic consumption and rest pain. Moreover in both groups a significant reduction of the ulcer score and healing of the necrotic area were observed. Side effects occurred in six patients of the PGE1-group and in ten patients of the PX-group, which required premature discontinuation of treatment in four patients of the PX-group. The study also demonstrated that PGE1 is more effective in the treatment of severe arterial occlusive disease than PX. With respect to the analgesic consumption, the reduction of ulcer score and the healing of necrotic area a significant difference was found in favour of PGE1. In accordance the six months follow-up examinations showed a marked deterioration in the PX-group opposed to the PGE1-group. The intravenous application of PGE1 over a period of 4 weeks in patients with severe arterial occlusive disease seems to be an effective therapeutical principle.

Aged

Haemostasis during treatment with ciprofloxacin.

The effects of ciprofloxacin, a new quinolone derivative with high activity on gram-negative aerobic bacteria and gram-positive cocci, on haemostasis were investigated in 11 healthy volunteers. No influence on platelet function was detectable. In some cases a slight reduction in antithrombin III activity was observed at the end of the therapy. No other changes were evident in the plasma coagulation parameters.

Antithrombin III

Inhibition of platelet activation by 2-mercaptopropionylglycin in vitro and in vivo.

2-mercaptopropionylglycin (2-MPG), a cell membrane penetrating thiol, was evaluated for its antithrombotic potential using in vitro and in vivo tests. 2-MPG was found to inhibit agonist-induced platelet aggregation and serotonin release as well as prostaglandin/thromboxane synthesis in platelet-rich plasma. Administration of 2-MPG to rats resulted in an inhibition of laser-induced thrombus formation in mesenteric vessels. When plasma was incubated with 2-MPG and then used for determination of various standard coagulation parameters, significant prolongation of the clotting times were observed.

Animals

On the retraction of collagen and fibrin induced by normal, defective and modified platelets.

Fibrin clot retraction (FCR) and collagen gel retraction (CGR) were studied in patients with inherited platelet defects, i.e. in Glanzmann's thrombasthenia, Hermansky-Pudlak syndrome, May-Hegglin anomaly, giant platelet syndrome, as well as in patients with von Willebrand disease and factor XIII deficiency. FCR was abnormal only in thrombasthenia, while CGR was found to be reduced in 2 patients with Hermansky-Pudlak syndrome and in 4 out of 5 cases with von Willebrand disease. Both FCR and CGR were normal in May-Hegglin anomaly, giant platelet syndrome and severe factor XIII deficiency. In none of the examined bleeding disorders was a concomitant FCR and CGR reduction detected. Natural polyamines and anti-fibronectin antibodies did not affect platelet potency in FCR or CGR. Peroxidation of platelet membrane components by sodium periodate abolished the platelet-induced FCR and CGR. This effect was reversed by subsequent reduction by sodium borohydride.

Adolescent

[Primary thrombocyte reactions in hemostasis and thrombogenesis and the possibilities of influencing them by drugs].

The primary haemostasis begins with the activation of the thrombocytes. This activation is induced by nucleotides, by the haemostasis-activating factor existing in most tissues, by thrombin, collagen, adrenaline, serotonin and other activators. The activation is accompanied by an increased inclination of the thrombocytes to adhesion and aggregation. Morphologically activated platelets show appendices and become ball-shaped. These processes are reversible in vivo and in vitro. Medicaments inhibiting the function of the platelets were above all selected on account of their effect inhibiting the aggregation and were clinically tested. It is uncertain in what respect inhibition of the aggregation and inhibition of the thrombosis correlate. A technique for the judgement of the inhibition of the tissue extract-induced change of the form of thrombocytes is demonstrated as a method for the measurement of the activation of the platelets. Acetylsalicylic acid influences the aggregation of platelets by inhibition of the cyclooxygenase in the thrombocytes. This leads to an inhibition of the thromboxane synthesis in the platelets which lasts for days, since it is irreversible. The spontaneous change of the form of the thrombocytes and the tissue extract-induced change of the form of the platelets by acetylsalicylic acid are, however, influenced only for the duration of 6-10 hours.

Animals

[Prevention of postoperative thrombotic complications with heparin and dihydroergotamine. A randomized double-blind study].

In a randomized double-blind study of 660 patients with predominantly abdominal-surgical procedures the thrombosis-preventing effect of the following was compared: heparin 5000 (low-dose heparin), heparin 2500, a combination of heparin 2500 and 0.5 mg dihydroergotamine (HDHE 2500), 0.5 mg dihydroergotamine (DHE), and placebo. All preparations were administered three times daily. Radiofibrinogen test gave the following thrombosis incidence: heparin 5000-15.4%; heparin 2500-24%; HDHE 2500-13.2%; DHE-24.6%; placebo-28.9%. Bleeding complications, included postoperative blood loss (more than 500 ml), unusually marked bleeding from drains, seroma, wound haematoma, and re-operation. The rate of these complications was 18.5% with heparin 5000, 7.8% with placebo, 5.6% with DHE, 4% with heparin 2500 and 3.1% with HDHE 2500. The non-specific tolerance to the various preparations was good, especially in that there was no increased risk of coronary complications with HDHE or DHE, and there was no pointer to peripheral vasospasms. This study confirms the synergistic thrombosis-preventing effect of combined heparin-dihydroergotamine.

Abdomen