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Biomedical subjects

G Lutze

Publications and source records attributed to G Lutze.

68 records · Page 4Linked to original sources

[Unusual joint complications in sickle cell anemia].

It is reported on the casuistics of a 23-year-old Lebanese who since his eighth year suffered from joint swellings and occasional attacks of jaundice. By the proof of false forms of erythrocytes and by the haemoglobin electrophoresis a homozygous sickle cell disease could be ascertained. Peculiarities of the clinical picture were among others changes of the bones of high degree (osteolyses of vertebral bodies, of the head of the right humerus and the heads of the two femurs) was well as of the knee-joints in form of ankyloses.

Adult↗

[Studies on the demonstration of a factor VIII or IX deficiency by means of partial thromboplastin time].

A report is presented on the performance of the correction of PTT by means of factor VIII and IX deficiency plasma, which may be used at least one year, when preserved in liquid nitrogen. The method allows reliable, qualitative statements to be made about disturbances in the area of the coagulation factors VIII, IX, XI and XII; the small amount of time required for preparing and carrying out these works representing an essential advantage.

Blood Coagulation Tests↗

Uber einen energieunabhängigen austausch der alkali-ionen Li(+), Na(+), K(+), Rb(+) und Cs(+) GEGEN H(+) in der membran intakter und desintegrierter rattenlebermitochondrien.

1. The energy-independent exchange of alkali metal cations against protons was investigated in intact and disintegrated mitochondria. The exchange is not specific for different alkali metal ions.2. In intact mitochondria the apparent K(m) for the energy-independent exchange range from 5 to 25 mM (Cs(+), Rb(+), K(+) 5-10 mM; Na(+) 15 mM; Li(+) 20 mM). At all ions studied the maximum release of protons was 15-20 nval/mg protein.3. In disintegrated mitochondria there are no differences between the alkali metal ions (apparent K(m) 30 mM; maximum H(+)-release 50 nval/mg protein).4. Directly accessible binding sites seem to exist in the outer membrane. Binding sites in the inner membrane are accessible only after disintegration, but not after addition of valinomycin + rotenone.

Journal Article↗

Uber die beziehungen zwischen einem energieunabhängigen K(+)-H(+)-austausch und der strukturellen integrität von mitochondrien und membranpartikeln.

Disintegration or altering of intact mitochondria or digitonin inner membrane + matrix particles causes an increase in K(+)-linked release of protons. This effect is not obtainable in the case of outer membranes. It is assumed, that also the inner membrane + matrix possesses exchange sites for K(+), which are freely accessible for the potassium ion if the structural integrity is damaged. The outer layer of inner membrane seems to be a barrier for the K(+)-movement.

Journal Article↗

Uber die lokalisation eines energieunabhängigen K(+)-H(+)-austausches in der aussenmembran von rattenlebermitochondrien.

The energy-independent K(+)-H(+)-exchange was measured in intact mitochondria and submitochondrial particles at different K(+)-concentration of the incubation medium. Correlation was found between H+-displacement and specific activity of monoamine oxidase. It is concluded, that the energy-independent K(+)-H(+)-exchange is localized in the outer membrane of mitochondria.

Journal Article↗

[Factor VIII inhibitors in patients suffering from severe haemophilia A: problems of "very low" responders].

Without recognition of any inhibitor until now, low concentrations of factor VIII inhibitors (< 1 Bethesda unit (BU)/mL plasma) can be occasionally measured in patients with severe haemophilia A. The existence of so-called "very low" responders is assessed contradictorily due to a methodically caused inhibitor increase. Plasma from 10 patients with severe haemophilia A was incubated with human plasma or animal plasma from pig, cattle, or cat and assayed for factor VIII inhibitors. No signs of inactivation could be detected in five specimen (0 BU/mL plasma). However, measurable signs of factor VIII inactivation (< 1 BU/mL plasma) did occur in the other five. Therefore, the existence of yet not defined unknown inhibitory substances in certain haemophilic plasmas must be assumed. They are directed against human factor VIII as well as partly against animal factor VIII. These "very low" inhibitors are not identical with factor VIII antibodies of "low" and "high" responding haemophiliacs. The clinical importance of "very low" inhibitors is insignificant because they do not tend to increase after exposure to factor VIII. In fact, a effect of factor VIII therapy is the neutralization of this kind of inhibitors.

Adolescent↗

[Postoperative haemorrhagia in a girl with congenital factor XI deficiency - successful treatment with desmopressin (DDAVP, Minirin(R))].

UNLABELLED: The rare factor XI deficiency is associated with different profuse bleeding without correlation to the severity of reduction of factor XI. Accordingly, traumata or surgical procedures may cause unexpected excessive bleeding in asymptomatic patients. After surgery of a nine-year-old girl with factor XI deficiency (8 per cent) profuse bleeding occurred which could only be stopped after infusion of desmopressin. After administration the factor XI activity was increased to 31 per cent, the factor VIII even to 290 per cent over the normal range. We suppose that the favorable clinical effectiveness is not only related to the increasing factor XI activity but also to the elevation of the factor VIII/von-Willebrand-complex. CONCLUSION: It is recommended to give desmopressin as firstline therapy of bleeding by factor XI deficiency since the only effective alternative such as substitution of factor XI by transfusion of fresh frozen plasma is associated with the risk of transmission of virus infections.

Child↗

[Severe acquired protein S deficiency with thrombophlebitis after febrile infection in a 7-year-old girl].

The importance of the anticoagulant properties of protein S is illustrated by the high incidence of thromboembolic events in individuals with protein S-deficiency. A 7 year old girl was hospitalized with purpura-like bruises and lesions on both thighs after she had suffered from febrile infection. A subsequently developing thrombosis of the left V. femoralis was treated successfully with urokinase. Haemostaseological investigations showed no signs of disseminated intravascular coagulation. However, isolated severe degradation or all protein S-components due to the presence of a circulating autoantibody to protein S was found. After several months the antibody was detectable not any more, activity and antigens of protein S were normal.

Bacterial Infections↗