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Biomedical subjects

V Hach-Wunderle

Publications and source records attributed to V Hach-Wunderle.

32 records · Page 2Linked to original sources
PubMed1993

[Disorders of the liberation of tissue-type plasminogen activator (t-PA) from the venous wall as a cause for recurrent thromboses].

The release of tissue-type plasminogen activator (t-PA) after venous occlusion was tested in 290 patients with venous thrombosis, at earliest three months after the last thrombo-embolic episode. In 37 patients (12.8%) the t-PA-activity was decreased. In 14 patients (4.8%) the defect was confirmed by control. A reduced release of t-PA was found in 4 patients, while 10 out of 14 patients had comparatively higher levels of plasminogen-activator-inhibitor (PAI-I).

Adult↗
PubMed1989

[Prevention of venous thromboses with oral anticoagulants].

Oral anticoagulants are effective for prophylaxis of venous thromboembolism. The therapy is usually monitored by the one-stage prothrombin time (Quicktest). The aim of anticoagulant therapy is to reduce the coagulability of blood into a so called therapeutic range within which the patient is protected against thrombosis while being exposed to a minimal risk of bleeding. The standardization of methods for the prothrombin time assay by the International Normalized Ratio is of further benefit for monitoring the therapy in the individual patient.

Administration, Oral↗
PubMed1989

Anti-A in factor VIII concentrate: a cause of severe hemolysis in a patient with acquired factor VIII:C antibodies.

The authors report a case of acute macrohematuria in a patient with spontaneously acquired antibodies against factor VIII:C. Severe hemolysis was observed under factor VIII concentrate therapy. In 4 batches of the factor VIII concentrate high titers up to 1:512 of 'immune' anti-A were found. Clotting factor preparations used for replacement therapy, therefore, should be investigated for iso-antibodies, at least in situations where an intensive infusion therapy is required.

ABO Blood-Group System↗
PubMed1988

Congenital deficiency of plasminogen and its relationship to venous thrombosis.

In a patient with deep venous thrombosis, plasma concentrations of coagulant and inhibitor proteins were normal except for moderate deficiency of plasminogen. Family studies revealed a similar deficiency in the mother and sister of the propositus. Evaluation of purified plasminogen demonstrated that it functioned normally. The patient represents our only example of plasminogen deficiency in 435 German individuals evaluated with a history of thromboembolism.

Blood Coagulation Disorders↗
PubMed1988

Congenital abnormal plasminogen, Frankfurt I, a cause for recurrent venous thrombosis.

A new abnormal plasminogen, Frankfurt I, has been identified in the plasma of a 42 year-old male patients who had recurring thromboses, thrombophlebitis and pulmonary embolism since his age of 29. Reduced functional and also slightly reduced antigen plasminogen concentrations were found in both the proposituts and his mother. Plasmin generation rates carried out by Streptokinase and Urokinase were also abnormal. The plasmin generated was very unstable in the absence of stabilizing ligands and/or substrates. Crossed immunoelectrophoresis of the purified Frankfurt I revealed a peak with normal size and shape, but displaced with respect to normal Glu-plasminogen toward the anode. Isoelectric focusing followed by zymography on an agarose-fibrin plate proved this observation but did not indicate a separation of the normal from the abnormal plasminogen molecular species, also, fewer bands were found in the abnormal plasminogen isozyme pattern. Kinetic studies of Frankfurt I Glu-plasminogen and plasmin showed that most of the functional abnormality is related to absence of active sites in half of the molecules.

Adult↗
PubMed1987

[Jellyfish poisoning].

While bathing in the Indian Ocean a 31-year-old German woman came into contact with a jelly-fish, probably of the species Chrysaora quinquecirrha. Initial signs were inflammatory cutaneous changes on the upper trunk, and both arms and feet. Over the next few days massive edematous swelling developed over the trunk, in addition to signs of arterial underperfusion in the hands and legs. Under treatment with urokinase and prostaglandin E1 the circulatory disorder in the feet completely disappeared. But the edema on the arms and hands got worse and huge bullae developed. On the assumption of a compartment syndrome a bilateral fasciotomy was performed. Wound healing proceeded normally. However, even after six months there remained extensive sensory and motor defects in both hands and arms.

Adult↗
PubMedDate not supplied

[Hemostatic changes in idiopathic venous thrombosis in childhood and adolescence].

The prevalence of inherited thrombotic syndrome in the general population appears to be higher than that of inherited bleeding disorders. The most important candidates for screening are patients with unexplained venous thromboembolism at ages of less than 40 years: In 18 children and adolescents suffering from "idiopathic" vein thrombosis laboratory screening has been performed: PT, PTT, TT, platelet count, spontaneous platelet aggregation, von Willebrand factor, fibrinogen, plasminogen, antithrombin III, protein C, C1-inactivator, alpha-1-antitrypsin, alpha-1-antichymotrypsin, alpha-2-antiplasmin and alpha-2-macroglobulin. Compared to an age matched healthy control group in children with idiopathic vein thrombosis we could demonstrate in vitro platelet activation with significant enhanced platelet aggregation and elevated levels of von Willebrand factor in the onset of the disease. Antithrombin III, protein C, alpha-2-antiplasmin and alpha-2-macroglobulin were significantly decreased. These changes turned to be normal in the following 6 to 9 months. PT, PTT, TT, platelet count, plasminogen, alpha-1-antitrypsin, alpha-1-antichymotrypsin and c1-inactivator showed no alterations compared to the control. Platelet activation and alteration of platelet function in vivo and in vitro is established to initiate thrombosis. The von Willebrand's VIII molecule is involved in this step. The decreased inhibitors of the hemostatic system antithrombin III and protein C in the onset period of thrombotic diseases are discussed to be an increased turnover, whereas the decreased levels of alpha-2-antiplasmin and alpha-2-macroglobulin might be a counter-regulation to the thrombotic event, showing an "activated" fibrinolytic system.

Adolescent↗
PubMedDate not supplied

Recombinant hirudin (lepirudin) provides safe and effective anticoagulation in patients with heparin-induced thrombocytopenia: a prospective study.

BACKGROUND: The immunological type of heparin-induced thrombocytopenia (HIT) is the most frequent drug-induced thrombocytopenia. This study evaluated the efficacy of recombinant hirudin (r-hirudin or lepirudin), a potent thrombin inhibitor, for anticoagulation in patients with confirmed HIT. METHODS AND RESULTS: Eighty-two patients in this prospective, multicenter study received 1 of 4 intravenous r-hirudin regimens: A1, HIT patients with thrombosis (n=51), 0.4-mg/kg bolus and then 0.15 mg. kg-1. h-1; A2, HIT patients with thrombosis receiving thrombolysis (n=5), 0. 2-mg/kg bolus and then 0.1 mg. kg-1. h-1; B, HIT patients without thrombosis (n=18), 0.1 mg. kg-1. h-1; and C, during cardiopulmonary bypass surgery (n=8), 0.25-mg/kg bolus and then 5-mg boluses as needed. Response criteria were increase in platelet count by >/=30% to >10(9)/L and activated partial thromboplastin time (aPTT) values 1.5 to 3.0 times baseline values achieved with a maximum of 2 dose increases. No placebo control was used for ethical reasons. Outcomes of a subset of r-hirudin-treated patients who met predefined inclusion criteria (n=71) were compared with those of a historical control group (n=120) for combined and individual incidences of death, amputations, new thromboembolic complications, and incidences of bleeding. Platelet counts increased rapidly in 88.7% of r-hirudin-treated patients with acute HIT. In regimens A1 and A2, the 25% and 75% quartiles of the aPTT were within the target range at all but 1 time point. The incidence of the combined end point (death, amputation, new thromboembolic complications) was significantly reduced in r-hirudin patients compared with historical control patients (P=0.014). During first selected treatment, the adjusted hazard ratio for r-hirudin patients versus historical control was 0.279 (95% CI, 0.112 to 0.699; P=0.003). Bleeding rates were similar in both groups. CONCLUSIONS: r-Hirudin treatment is associated with a rapid and sustained recovery of platelet counts, sufficient aPTT prolongations, and true clinical benefits for patients with HIT.

Adolescent↗
PubMedDate not supplied

Acute regional vascular insufficiency after jellyfish envenomation.

Three cases of jellyfish envenomation which occurred in the Indian Ocean and the Andaman Sea are reported. In each instance the stinging occurred on the upper extremities, and impaired the circulation to the stung limb(s), with absent distal arterial pulses, regional cyanosis, and the threat of distal gangrene. One of the patients is seriously and permanently handicapped, with bilateral upper-limb numbness and paresis; another patient has permanent sensory loss; the third patient, who also had brachial-artery narrowing that was demonstrated by angiography, made an uneventful recovery. The first two patients underwent surgical fasciotomy, whereas surgical exploration was performed on the third patient. Reduced blood flow in the major arteries of the limbs was observed directly in each case. Further, the arterial segment that primarily was affected, in each case, appeared to be that which underlay the actual site of the sting. All patients were young persons with no previous history of vascular disease. These cases corroborate the vascular and neurogenic injury, which previously have been reported in experimental animals and in human patients, that may result from jellyfish venoms.

Adult↗