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Biomedical subjects

K J Matthes

Publications and source records attributed to K J Matthes.

At least 19 recordsLinked to original sources
PubMed2001

Protein Z.

Protein Z is a vitamin K-dependent protein. The first cases of protein Z deficiency were described in patients suffering from a bleeding tendency from otherwise unknown origin. Today, diminutions of protein Z seem to play a role not only in bleeding patients but also in patients with factor V Leiden mutation: Patients presenting with factor V Leiden mutation and low protein Z levels show earlier onset and higher frequency of thromboembolic events than do patients presenting with factor V Leiden mutation and normal protein Z levels. Thus, protein Z is a good example for the--at first sight--paradox action of coagulation proteins.

Adult↗
PubMed1997

What the neurosurgeon needs to know about the coagulation system.

Intracranial surgery is often complicated by thromboembolic events including the life-threatening pulmonary embolism. After head trauma and in patients with brain tumors disseminated intravascular coagulation (DIC) can occur, characterized by the triggering of the coagulation cascade and the depletion of coagulation factors which ultimately leads to bleeding. The identification of patients at high risk as well as the early diagnosis of hemostatic problems uses routine laboratory parameters such as partial thromboplastin time and prothrombin time reflecting the intrinsic and the extrinsic pathway of the coagulation respectively. Thrombin antithrombin III complexes (TAT) and prothrombin fragment 1 + 2 (F1 + 2) are further indicators of an activation of the coagulation whereas fibrinogen degradation products (FDP) refer to the fibrinolytic system. The basic principles of coagulation and fibrinolysis are summarized as well as the changes of laboratory parameters accompanying DIC, hypercoagulability and hyperfibrinolysis.

Blood Coagulation↗
PubMed1997

Coagulation alterations in patients undergoing elective craniotomy.

BACKGROUND: Thromboembolism remains a major problem in patients scheduled for craniotomy. The present study examined parameters of coagulation and fibrinolysis in 15 patients undergoing elective craniotomy in the perioperative period. METHODS: Plasma concentrations of thrombin antithrombin III complex (TAT), prothrombin fragment 1 + 2 (F1 + 2), and d-dimer were measured before and after induction of anesthesia, 60 minutes and 180 minutes after the beginning of surgery, and on the first postoperative morning. RESULTS: TAT, a marker of activation of coagulation, increased significantly (p < 0.05) from the preoperative measurements to the data obtained 60 minutes after beginning the surgery, reaching a maximum of 180 minutes after the start of surgery. F1 + 2, also indicating activation, showed a similar concentration time course with an intraoperative maximum. D-dimer, a marker of fibrinolysis, tended to increase slightly beginning 180 minutes after surgery with a maximum on the morning after surgery. Statistical significance for F1 + 2 and d-dimer was not found. CONCLUSIONS: This study showed a transient activation of coagulation with an intraoperative maximum in patients undergoing craniotomy. This result could be due to a liberation of thromboplastin from brain tissue.

Adult↗
PubMed1996

[The behavior of the activation parameters of plasma coagulation under HDR-afterloading therapy in patients with endometrial carcinoma].

BACKGROUND: In the radium era heparin prophylaxis was necessary to avoid thromboembolic events. Today with high-dose-rate (HDR) afterloading thromboembolic events are rare. Coagulation activation parameters were monitored during HDR afterloading to evaluate the necessity of heparin prophylaxis. PATIENTS AND METHODS: Twenty patients with uterine carcinoma and no postoperative tumor residuals were randomized before their first 10 Gy OD HDR-afterloading application. Ten patients received heparin prophylaxis, the other ten patients received no prophylaxis. Blood samples were taken before, immediately after, 6 and 24 hours after HDR afterloading. D-Dimer, TAT, and F 1 + 2 were measured. RESULTS: No significant activation of the coagulation system was observed over the investigated time period and no differences have been detected between both groups. None of the patients of either group developed thromboembolic complications. CONCLUSIONS: HDR afterloading has no direct influence on the plasmatic coagulation system. From this point of view heparin prophylaxis does not seem necessary.

Aged↗
PubMed1995

[Endemic sprue: its first diagnosis based on bleeding complications].

HISTORY AND CLINICAL FINDINGS: A 47-year-old man without previously known illness was admitted to hospital because of acute haematomas in the legs: the history revealed no cause. The pale-looking patient reported having large and foul-smelling stools once or twice daily. There were large haematomas and swellings on both legs. His general and nutritional state was reduced. "Bleeding of unknown origin" was suspected at this time. INVESTIGATIONS: Haemoglobin concentration was 5.6 g/dl, while iron was normal and ferritin reduced. Quick value was below 5%, activated partial thromboplastin time prolonged to 180 s. Vitamin A and E concentrations were reduced; coumarin derivatives were not demonstrated in blood. Abdominal ultrasonography showed clearly thickened intestinal walls. TREATMENT AND COURSE: Four units of erythrocyte concentrate were immediately administered, together with 2000 IU factors II, VII, X and anti-haemophilic factor B (PPSB), and 10 mg vitamin K intravenously. As intestinal malabsorption was suspected, a vitamin A absorption test was performed: it indicated malabsorption. Upper intestinal endoscopy showed coeliac disease, as did a biopsy. The patient's state quickly improved after he had been given vitamins A, D, E and K and put on a gluten-free diet. CONCLUSION: Coeliac disease can take a clinically unremarkable course for a long time and may finally become manifest through an isolated abnormality, such as bleeding.

Acute Disease↗
PubMed1995

Protein Z deficiency: a new cause of bleeding tendency.

Protein Z is a vitamin K-dependent plasma protein synthesized by the liver. Protein Z promotes the association of thrombin with phospholipid surfaces. So far, nothing is known about the clinical relevance of protein Z except alterations measured in patients under oral anticoagulant treatment. We propose that in protein Z deficiency a bleeding tendency might result because of the interaction of protein Z with thrombin on phospholipid endothelial surfaces. Therefore, we examined 36 patients with bleeding tendency of unknown origin, who were not under oral anticoagulant treatment and had normal liver synthesis function. Mean protein Z value of the patients with bleeding tendency was significantly diminished in comparison to the healthy control group. Twenty-one of the bleeding patients had lower protein Z levels than the lowest protein Z level of the control group. In conclusion, protein Z deficiency is described as a new type of bleeding tendency.

Adolescent↗
PubMed1991

Coagulation activation in liver diseases.

In liver disorders alterations of the coagulation system are mainly due to a reduced synthesis of coagulation proteins. In addition, an enhanced intravascular consumption of coagulation factors is discussed controversely in liver diseases. By measuring factor IXiAT- and TAT-complexes we tried to find out, whether coagulation activation in liver patients leads to activation of the complete coagulation cascade followed by DIC or whether in some diseases a futile partial coagulation activation develops. In all liver diseases examined, elevated factor IXiAT-complexes were demonstrated, while TAT-complexes were only elevated in chronic active hepatitis, metabolic decompensated liver cirrhosis and in patients suffering from end stage liver disease. We conclude that all liver diseases examined lead to an activation of the coagulation cascade. A complete activation followed by DIC only occurs in patients with very severe liver disorders.

Antithrombin III↗
PubMed1987

S protein/vitronectin in chronic liver diseases: correlations with serum cholinesterase, coagulation factor X and complement component C3.

S protein/vitronectin plays an important role as a regulatory component in the terminal steps of the complement- and coagulation cascades. In patients suffering from chronic liver diseases, plasma S protein concentration was measured and compared with changes in serum cholinesterase activity, coagulation factor X activity and complement component C3 concentration. Significant decreases of all these proteins were seen in liver cirrhosis. Changes in S protein concentration correlated closely with those of cholinesterase, factor X and complement C3. The data give support for the liver as the main organ of plasma S protein/vitronectin synthesis.

Adult↗
PubMed1986

Early detection of amatoxins in human mushroom poisoning.

Amatoxins were detected radioimmunologically as early as 90-120 min after ingestion in the gastric fluid and urine of a 15-year-old boy who tried to commit suicide by ingestion of wild mushrooms. This early detection of amatoxins in the urine is proof of rapid absorption from the intestinal tract and subsequent excretion by the kidneys in man.

Adolescent↗
PubMed1985

Parathion-provoked lethality in rats is reduced by diethyldithiocarbamate.

Intoxication of male rats with 5 mg/kg parathion reduces survival to 15%. Diethyldithiocarbamate (DDC), known to inhibit mixed-function oxidase activity, has no effect on survival rate when this compound is used in a dosage of 300 mg/kg 45 min before or 10 min after parathion intoxication. However, when DDC and parathion are administered simultaneously, the rate of survival rises to 53%.

Animals↗
PubMed1984

Fructose 1,6-bisphosphatase in the diagnosis of chronic hepatitis. I. Activity measurements of fructose 1,6-bisphosphatase in human serum.

In this communication, we propose a method for the determination in human serum of fructose 1,6-bisphosphatase based on parallel measurements of enzyme activities in presence of 1-p-bromotetramisole oxalate and adenosine 5'-monophosphate. The employment of these specific inhibitors renders the discrimination between specific and non-specific activities feasible. A regression analysis identifies fructose 1,6-bisphosphatase (EC 3.1.3.11) as the origin of the specific and alkaline phosphatase (EC 3.1.3.1) as the source of the non-specific fructose 1,6-bisphosphate dephosphorylating activities. This procedure lends itself to the diagnosis using serum samples of 'piecemeal' necrosis in liver disease.

Adenosine Monophosphate↗
PubMed1984

Fructose 1,6-bisphosphatase in the diagnosis of chronic hepatitis. II. Classification of chronic hepatitis based on fructose 1,6-bisphosphatase and other laboratory data.

The histomorphology of typical liver cell necroses are here correlated with heterotope distributions of enzymes in liver parenchyma. A variety of findings indicate a congruence between gluconeogenetic areas of the liver and the typical pattern of 'piecemeal' necrosis. We therefore propose a diagnostic index based on fructose 1,6-bisphosphatase activity and the data from the clinical laboratory. This index makes it possible to distinguish between chronic persistent and chronic aggressive hepatitis.

Acute Disease↗
PubMed1984

[Insulin and C-peptide in chronic liver diseases during oral glucose tolerance testing].

Insulin and C-peptide in venous blood were determined during oral glucose tolerance testing in 59 non-manifest diabetics with histologically established chronic liver disease (fatty degeneration, chronic aggressive hepatitis, cirrhosis). Glucose tolerance was pathologic in 60-80% of patients. When compared to a control group patients with chronic liver disease showed significantly increased values of blood glucose (after glucose intake), of insulin and of C-peptide (fasting and after glucose intake). The C-peptide/insulin ratio, a measure of hepatic insulin degradation, was significantly decreased after glucose uptake. There were no significant differences of blood sugar, insulin and C-peptide among the various liver diseases. In chronic aggressive hepatitis and in cirrhosis the C-peptide/insulin ratio was partly significantly lower than in fatty degeneration. From the increased C-peptide values increased insulin secretion in chronic liver diseases can be deducted. In addition, the decreased C-peptide/insulin ratios show an impairment of insulin degradation in liver cirrhosis and other chronic hepatic diseases. However, in fatty liver degeneration this is clearly less pronounced than in more serious liver diseases.

C-Peptide↗
PubMed1982

Hyperinsulinemia in hepatic steatosis.

Blood glucose, serum insulin, C-peptide, free fatty acids and growth hormone were evaluated in 45 patients with histologically established hepatic steatosis after an oral glucose load (100 g). Glucose tolerance was impaired in 59 per cent of the patients. Significantly increased levels were found for blood glucose (fasting and after 60 and 120 min), insulin (after 60, 120 and 180 min), C-peptide (fasting and after 60, 120 and 180 min), and free fatty acids (fasting and after 60 and 120 min). Human growth hormone levels were not altered. After glucose administration the C-peptide/insulin ratio was significantly reduced in hepatic steatosis compared to controls. In patients with hepatic steatosis there were no differences between subjects with normal body weight or overweight nor between stadium I and stadium II ('alcoholic hepatic steatosis') concerning glucose, insulin, C-peptide, HGH and FFA levels in blood. We conclude, that hepatic steatosis is associated with relative insulin resistance to which elevated FFA may contribute. In addition, the decreased C-peptide/insulin ratios suggest an impaired hepatic insulin degradation as it was already described for more serious liver diseases.

Adult↗