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Biomedical subjects

F Kunz

Publications and source records attributed to F Kunz.

11 recordsLinked to original sources
PubMed1992

Increased lipid binding to thrombi in coronary artery disease. Findings in patients without premedication in native (not anticoagulated) test systems.

Thrombi and clots were produced from native (i.e., not anticoagulated) platelet-rich and platelet-poor plasma from patients with coronary artery disease and control subjects who had not taken any medication known to influence plasma lipids, coagulation, or platelet aggregation. The clotting times were recorded, and the lipid content of clots, thrombi, platelets, plasma, and high density lipoprotein was analyzed. Thrombi produced from native platelet-rich plasma were 46% heavier in coronary artery disease patients and contained about 20% more phospholipids and free cholesterol and about twice the amount of triglycerides and esterified cholesterol in both absolute and relative amounts with respect to the corresponding lipids of plasma plus platelets. The elevated content of lipids not only increases the size of the thrombi but also changes their quality because of an increased content in plasmatic lipids, as platelets contain only trace amounts of triglycerides and cholesterol esters. In agreement herewith, fibrinogen and maximal amplitude on the thrombelastogram were increased in coronary artery disease patients, whereas the thrombus-forming time and clotting times of platelet-poor and platelet-rich plasma were shortened, indicating accelerated coagulation and activation of platelets. Analysis of these results suggests a disturbed interrelation in coronary artery disease between lipids and hemostasis, in which platelets, high density lipoprotein, and lipoproteins rich in triglycerides and cholesterol esters may play a role.

Blood Coagulation↗
PubMed1991

[An idiopathic floating left-ventricular thrombus].

Four weeks after appendicectomy a 28-year-old man developed dragging pains in the left calf. Left popliteal, posterior tibial and dorsalis pedis arteries could not be palpated. Angiography revealed an embolic occlusion of the left superior femoral artery at the level of the adductor canal. Echocardiography demonstrated a pedunculated left ventricular thrombus, 3.5 x 2.0 cm, as a possible source of the embolus. After successful trifurcation embolectomy and saphenous vein patch-plasty acenocoumarol, 4 mg/d and heparin, 3 x 7500 IU/d were administered. Because the thrombus failed to shrink, systemic thrombolysis, initially 750,000 IU streptokinase and 3000 IU heparin i.v., was begun. After five days the thrombus diameter had decreased to 0.7 cm. But because thrombus movement had increased, streptokinase was replaced by 70 IU/d ancrod i.v. The thrombus completely disappeared within two weeks. The patient was symptom-free during the period of anticoagulation with acenocoumarol. Six months later echocardiography confirmed the absence of thrombus in the left ventricle.

Acenocoumarol↗
PubMed1978

[Postoperative fructose infusion in a case of presumed hereditary fructose intolerance (author's transl)].

Hereditary fructose intolerance (HFI) was diagnosed in a 61 year-old male patient on account of liver dysfunction followed by prolonged shock immediately after the administration of a fructose and lactose infusion postoperatively. The diagnosis of HFI was based on an increased value of fructose, hypoglycaemia, lactic acidosis and diminution of the phosphate level in combination with the typical family history. The patient's children showed a normal reaction to fructose administration. The therapy included glucose, insulin and heparin administration, balance of acidosis and partial exchange of blood, which resulted in improvement in the glucose level, coagulation factors and acidosis, but could not prevent further liver damage and uraemia with a fatal outcome.

Acidosis↗
PubMed1978

Plasma lipids, coagulation factors, and fibrin formation after severe multiple trauma, and in adult respiratory distress syndrome.

Following severe multiple trauma, decreases were observed in a) Free cholesterol, b) Cholesteryl esters, c) Total phospholipids, and d) Lysolecithin. Comparatively slight changes in coagulation parameters did not differ regardless of whether pulmonary complications developed. In contrast, increased fibrin lipid complexing was more closely correlated with clinical data, because: a) Plasmatic lipids, particularly triglycerides complexed with fibrins, were elevated severalfold in patients with adult respiratory distress and fat embolism syndromes when compared with multiple trauma patients without pulmonary complications. This was independent of plasma lipid levels. b) Plasmatic triglycerides complexed with fibrins were significantly higher in patients who died than in those who survived. The considerable changes in the plasma lipid pattern following severe trauma suggest the presence of an abnormal lipoprotein with increased affinity to fibrin, thereby inhibiting fibrinolysis. This might well be one pathogenic mechanism in the development of post-traumatic respiratory distress syndrome.

Adult↗
PubMed1978

[Phospholipids].

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Animals↗
PubMed1975

[Lactacidaemia and disseminated intravascular coagulation associated with phenformin medication (author's transl)].

A patient with chronic active hepatitis developed vomiting, dyspnoea, tachycardia, diarrhoea and diffuse pains. For several years she had been treated with azathioprine and for a few weeks before admission with phenformin for mild diabetes. Laboratory examination revealed acute disseminated intravascular coagulation and lactacidaemia. Despite intensive treatment the patient died a few hours after admission, the post-mortem examination revealing diffuse pulmonary haemorrhages. The present case report and those published in the literature suggest that phenformin should not be given to diabetics who also have renal or hepatic disease. In any case, if phenformin is given, it should be stopped if hepatic, renal, infectious or thrombotic complications occur. In these cases and those of sudden unexplained deterioration in diabetics, hospitalisation is essential and lactic acid levels should be determined and coagulation tests performed.

Acidosis↗
PubMed1975

[The pattern of phospholipids during the course of delirium tremens (author's transl)].

Plasma phospholipids were examined in patients with delirium tremens in the acute phase of the disease and after recovery. The levels of lysolecithin, phosphatidylinositol, phosphatidylethanolamine, sphingomyelin and the total of phospholipids were decreased in comparison to normals. Phosphatidylethanolamine, phosphatidylinositol and the total phospholipids were diminished in comparison to patients with liver cirrhoses. Only in the plasma of patients with liver cirrhoses with bad prognosis (hepatic coma) similar low levels of total phospholipids were found. It is concluded from these results, that the synthesis of phospholipids is reduced during delirium tremens.

Alcohol Withdrawal Delirium↗