Biomedical subjects
Publications and source records attributed to E Dworzak.
In 50 patients, the majority of them suffering from parotid diseases, serum isoamylases were determined (salivary S-type and pancreatic P-type). After sialography, there was in most cases a slight increase in isoamylase level. Salivary amylase does not seem to be a suitable marker for parotid neoplasms.
Research during the last ten years into the pathophysiology of acute myocardial infarction (AMI) has made it gradually clearer that this is a phasic event. A number of independent authors have made this conclusion quite obvious. The authors of this review suggest that the alternating sequence of coronary spasm and dilatation should be described as the "thromboischemic reentry mechanism," which itself leads to waves of reperfusion, producing characteristic episodic changes in some of the parameters of AMI. The spasms are brought about by substances let loose from aggregating platelets. Metabolites released during the concomitant ischemia lead the vessel from spasm to dilatation. Following thrombolytic treatment, the 'staccato' signs of myoglobinemia disappear, because of the withdrawal of the spasmogenic products of the platelets. It could also be shown that the concentration of myoglobin in the serum as a result of the dilating effect of calcium antagonists is twice the mean maximum value that the myoglobin time curve would show without such treatment.
Evidence is presented for defective pyruvate dehydrogenase (EC 4.1.1.1) in leukocytes and muscle tissue from a 10-year old child with persistent lactic acidosis, suffering from myasthenia and growth retardation. The defect is expressed in vitro by a depressed stimulation of pyruvate dehydrogenase catalytic activity by exogenous phosphoprotein phosphatase, and in vivo by a lack of response to muscle work, in comparison with healthy controls. Pyruvate dehydrogenase activity is in the normal range when measured without addition of phosphoprotein phosphatase in cells obtained from the resting patient. The defect reported here represents a new, hitherto undescribed form of a pyruvate dehydrogenase deficiency. The insufficient catalytic activity explains the observed accumulation of pyruvate, lactate, oxaloacetate and alanine and the decrease of citrate concentration in the blood of this patient. Electron microscope studies of the muscle tissue show an enhanced number of enlarged mitochondria with bizarre shapes and high densities of cristae.
The authors report on their cases of parotid tumours between 1972-1982. Not only benign and malignant neoplasms but also inflammatory "tumours" were included, since they often exhibit signs of real neoplasms. The patient material and the results obtained agree well with the literature. The great value of computed tomography is underlined especially in cases with hidden parapharyngeal tumours. Hopefully, recently performed measurements of serum isoamylase will be a valuable diagnostic test for parotid diseases, particularly in differentiating between real neoplasms and chronic inflammatory diseases.
Close-meshed determinations of plasma myoglobin, creatine kinase, and its isoenzyme MB were carried out in nine patients admitted to the clinic less than 4 hours after the onset of symptoms in the course of acute myocardial infarction (AMI). Myoglobin clearly appears earlier (mean 2 hours and 30 minutes) in the plasma than creatine kinase (mean 4 hours and 15 minutes) and isoenzyme MB (mean 5 hours and 30 minutes after the onset of symptoms). During the first hours of AMI plasma myoglobin shows multiple peaks in all patients. Because this pattern is observed only with myoglobin but not with creatine kinase, it appears that myoglobin mirrors the early course of the necrosis more distinctly than creatine kinase. Plasma myoglobin was also found elevated after intramuscular injections and a high voltage accident. Myoglobinuria was not detectable after myocardial infarction.
In two siblings, brother and sister, with a history of bleeding Bernard-Soulier syndrome was diagnosed: The stronger affected sister showed a high percentage of giant blood platelets, an abnormal platelet spreading test and a defect in ristocetin and bovine fibrinogen-induced platelet aggregation. In addition, the content of platelet ATP, ADP and AMP was increased. As leucocyte counts were consistently decreased in the more seriously affected anaemic sister, repeated cytochemical examinations of the haemopoietic cells were carried out, revealing maturational defects in the whole haemopoietic system. Therapy with tranexamic acid reduced bleeding in the sister and she has not been anaemic since.
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A 51-year-old male patient with no history of musculo-skeletal or myopathic abnormalities, but suffering from manic-depressive psychosis, attempted suicide with an overdose of dolpersin hydrochloride (Mydocalm), dipenzepine hydrochloride (Noveril), meprobamate (Mepronox) and nitrazepam (Mogadon). He developed high fever, muscle rigidity, tachycardia, arrhythmias, hypotension and mottled cyanosis, symptoms well-known in persons with malignant hyperthermia, an autosomally inherited disease of skeletal muscle. There is also discussed the manifestation and the symptoms of an acute rhabdomyolysis. The diagnosis was confirmed by chemical pathological laboratory findings, including respiratory and metabolic acidosis, myoglobinaemia accompanied by myoglobin diuresis, and elevated creatine phosphokinase (CPK values up to 2790 U/l). Electron microscopic examination of muscle tissue revealed signs of myolysis and mitochondrial reactions with pleoconic hyperplasia. No inhalation anaesthetics or skeletal muscle relaxants, such as succinyl choline, were used in this case. Therefore, malignant hyperthermia might have been induced by a combination of drugs which were not known to induce this abnormal muscular reaction. However, the muscle relaxant effect of dolpersin hydrochloride may have acted as a possible inducer of the attack.
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Thymidine (TK) and deoxycytidine (dCK) kinase levels, chromosome counts and whole culture protein:DNA ratios have been determined in the TK- plasmodial strains of P. polycephalum--TU84 and TU63--and on several wild type (wt) plasmodial and amoebal strains from Wis 1 and Colonia backgrounds. It was found that (a) dCK levels and protein:DNA ratios were similar in all plasmodia, regardless of ploidy or genetic background; (b) TU84 and 63 were haploid; (c) TK specific activity was similar in all wt plasmodia but lower in amoebae; (d) TK activities of mutants and wt were approximately additive in heterokaryons. It was concluded that TK deficiency is due to a defect in a structural gene and that wt strains are TK+/TK+ and mutants hemizygous TK-.
The serum level of the myocardial-specific isoenzyme of creatine phosphokinase, CK-MB was determined in 50 patients with severe multiple injuries or following extensive surgery. It is concluded that whenever the proportion of CK-MB exceeds 10% of the total creatine phosphokinase activity myocardial damage has occurred, especially since equivalent ECG changes were registered in this group of patients.
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.
The paper deals with a new aspect in patients with polytrauma using a method to distinguish between myocardial or skeletal muscle damage. The isoenzyme CKMB of kreatine kinase is found to be characteristic for myocardial damage when increasing to more than 10% of the whole enzyme activity. It should be mentioned that this elevation is also seen in other disorders. Therefore the correlation to ECG changes is important in considering the diagnosis.
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