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Biomedical subjects

G E Vogel

Publications and source records attributed to G E Vogel.

At least 19 recordsLinked to original sources
PubMed1996

Immunogenicity of an inactivated hepatitis A vaccine administered according to two different schedules and the interference of other "travellers" vaccines with the immune response.

A total of 2036 persons consulting vaccination centers in Germany were vaccinated with an inactivated hepatitis A vaccine (containing 720 ELISA units of antigen) either according to the standard schedule (two vaccinations given 4 weeks apart) or to an abbreviated schedule (two vaccinations given 2 weeks apart) in a controlled clinical study. The abbreviated schedule induced a similar rate of seroconversion and geometric mean antibody titre as compared to the standard schedule. The incidence of reactions reported after vaccination was similar in both groups. When other "travellers" vaccines were given simultaneously neither the immunogenicity nor the reactogenicity of the hepatitis A vaccine were influenced. These findings have considerable practical importance in the prevention of hepatitis A in travellers.

Adolescent↗
PubMed1986

The patient in shock--clinical picture and pathophysiology.

The diagnosis of hemorrhagic shock can be made on the basis of a good knowledge of the clinical picture of the bleeding patient. The necessary lab tests must be carried out over a period of time to establish their evolution and thus the degree of shock. At present, attention is being focused on the microcirculation. In shock, tissue is starved of oxygen and nutrients, resulting in the liberation by degenerating cell structures of numerous substances that have an effect on vascular tone. Decompensation is accompanied by consumption coagulopathy, which also has an influence on the microcirculation. The inhibitor potential is very important here. The patient must be out of shock before endoscopy can be considered.

Acidosis↗
PubMed1986

The treatment of consumption coagulopathy.

There has been a transformation in our views of consumption coagulopathy in recent years owing to the advances throughout intensive care. The findings about the importance of inhibitors in the coagulation system have resulted in new biochemical understanding. The aim nowadays is to diagnose the early phase of consumption coagulopathy-so-called hypercoagulability. It is possible in this phase to restore the balance by replacement of the inhibitor antithrombin III. This report deals with clinical observations.

Adolescent↗
PubMed1986

[New observations in a case of Cronkhite-Canada syndrome].

We report about a 76 years old patient with Cronkhite-Canada syndrome. The diagnosis has been found with the following clinical symptoms: diarrhea, anorexia, alopecia, and onychotrophia. Laboratory values: severe hypoproteinemia (total serum protein 4.3 g/dl, albumin 2.4 g/dl); endoscopical and radiological findings: a generalized polyposis which involved the whole intestine except the oesophagus. As far as we saw in our literature-overview of 55 patients with Cronkhite-Canada syndrome, this patient had for the first time a carcinoma of the urinary bladder and a Bricker operation 17 years before the onset of his disease. Further we remarked a lack in the resorption of the enterally administered thyroidal hormones. The progress was fatal despite a parenteral hyperalimentation and a treatment with antibiotics and glucocorticoids.

Aged↗
PubMed1983

Early treatment with AT III in acute liver failure.

In acute liver failure there is often evidence of consumption coagulopathy in addition to interference with the synthesis of coagulation enzymes. Seven patients in hepatic coma (Grade IV-V) were treated by baboon liver perfusion bypass. Replacement therapy with antithrombin III (AT-III) proved useful in the management of the consumption coagulopathy. In the course of further work antithrombin III replacement therapy was given to 13 patients with acute liver failure at an early stage, before they could lapse into deep coma. Six patients with a Colombi index (the sum of Factors II, V and VII) below 75% - an unfavourable prognostic sign - survived the episode of acute liver failure. Early replacement with antithrombin III can be used to treat the coagulation abnormalities which occur during acute liver failure and should gain time for liver cell regeneration to take place.

Acute Disease↗
PubMed1978

The conflict between anticoagulation and hemostasis during hemodialysis.

Anticoagulation with comparatively small amounts of heparin has been carried out in more than 3,000 acute and chronic hemodialysis procedures without problems. In a selected high risk group of postoperative and polytrauma patients no patient hemorrhages have occurred, nor have there been any clotting problems in the dialyser circuit. Studies to elucidate the underlying mechanisms of coagulation and anticoagulation in the extracorporeal environment have been performed. Minimal intermittent heparin administration based on plastic anticoagulation monitoring with the APTT method, has proven to be particularly safe.

Hemostasis↗
PubMed1977

[Hemodialysis without risk of hemorrhage. Introduction of an APTT bedside method for exact heparin monitoring--a review].

A summarized account of our experiences over 1 1/2 years is given, in relation to a minimum heparinisation technique during haemodialysis. This novel technique was made possible by the introduction of an APTT bedside method. In a comparison between the techniques employed so far for preventing a heparin-caused risk of haemorrhage and our method, the clear advantage of our method was apparent. In addition to a discussion of our methods, we describe the cases treated so far. The amounts of heparin required for dialysis are so small that a necessary coagulation can occur even in a part of the organism where there is a danger of haemorrhage. Thereby it was possible to extend the range of indication for haemodialysis substantially. By using minimum heparinisation, it is possible to perform an immediate postoperative haemodialysis. The healing of wounds, which is impaired in cases of renal insufficiency, may be improved by early dialysis without the risk of haemorrhage. Our results show that the minimum heparinisation signifies a decisive achievement in acute dialysis therapy.

Acute Kidney Injury↗
PubMed1977

[Heparin dosage in chronic hemodialysis (author's transl)].

Over a period of 10 months hemodialyses in 20 patients with chronic renal failure were performed with a 40% lower heparin-dose. Blood coagulation was controlled from the activated partial thromboplastin time (APTT). There were no unfavourable side-effects, also the effectivity of the hemodialyses was not changed. However, we measured a significant increase in the hemoglobin-concentration and in the packed cell volume. Bleeding from the punctures was significantly shortened.

Adult↗
PubMed1977

[Theoretical basis and practical carrying out of an APTT control test for exact heparin monitoring (author's transl)].

We presented in this journal (Med. Klin. 71 [1976], 116), a procedure how to avoid hemorrhage risks due to heparine giving during hemo-dialyses. In this presentation is found the theoretical basis of the "minimal heparinisation". The practical carrying-out of the APTT (Activated Partial Thromboplastin Time)-control test as demonstrated by the 1200 bedside test cases, was done in order to give the personal without lab experience a practical guideline in the hand.

Blood Coagulation Tests↗
PubMed1977

[Uremic tendencies for hemorrhage and hemodialysis].

By means of a simple heparin test which reflects the actual processes in the contact of the blood with heterogeneous surfaces we can securely regulate the heparinisation in each phase of the dialysis, which, as I tried to explain, brings considerable consequences for the clinic.

Acute Disease↗
PubMed1977

Artificial organ support strategies in combined renal, circulatory, pulmonary and liver failure.

Within recent years we have significantly broadened the indication for the treatment of acute renal failure in intensive care patients, even in the presence of multiple organ failure. This was made possible by: 1. safe heparinization of the extracorporeal circulation while avoiding bleeding tendencies 2. hemofiltration of patients threatened by pulmonary complications early during renal failure and 3. the simultaneous use of various special intensive care measures. By this approach we have succeeded in a number of cases to break the chain of complications leading to multiple organ failure and death.

Acute Kidney Injury↗
PubMed1976

[Control of the heparin induced bleeding risk in haemodialysis patients (author's transl)].

Partial-Thromboplastin-Time (PTT) has been used as a bedside-method to control the dosage of heparin in haemodialysis patients at a high bleeding risk. The practical procedures and the advantages of the method as compared to current coagulation controls are outlined. As a result a technique of "minimal intermittent heparinization" has been developed which effectively prevents bleeding in the heparinized patient on haemodialysis.

Blood Coagulation Disorders↗
PubMedDate not supplied

Idiopathic hemochromatosis in a 45-year-old infertile man.

The clinical manifestations of primary or idiopathic hemochromatosis include mainly hepatomegaly, diabetes mellitus, and hypogonadism. Most investigators postulated that the hypogonadism is caused by pituitary dysfunction and that the deposition of iron in the testes is of little importance. We found not only pituitary failure in a 45-year-old man with idiopathic hemochromatosis (low LH and FSH levels, no response to GnRH) but could also detect by light microscopy deposition of iron in capillary endothelial cells and in the perivascular space of the testicular tissue. Electron microscopic study of tissue from the testes showed intracytoplasmic hemosiderin deposits in capillary endothelial cells. Abundant lipofuscin granules were present in Sertoli cells and Leydig cells. The serum testosterone levels were also lowered. In our opinion, the androgenic deficiency in idiopathic hemochromatosis is not only caused by pituitary failure but also by testicular dysfunction due to deposits of hemosiderin and lipofuscin in the testes.

Chorionic Gonadotropin↗