Biomedical subjects
Publications and source records attributed to A Brunetti.
An enzymatic method for determination of Hg++ concentration is suggested. This method is based on the strong inhibitory effect of Hg++ on alcoholdehydrogenase (ADH). A correlation between per cent inhibition of ADH and [Hg++]/[ADH] was found. It was possible to determine [Hg++] in a range of values of [Hg++]/[ADH] from 1,58 to 72. A minimum Hg++ concentration of 3,3 X 10(-9) M was dosed.
Partial purification and characterization of a D-aminoacid oxidase from Octopus vulgaris hepatopancreas are described. An about 25-fold purification was achieved. The pH optimum was near to 9; molecular weight, determined by gel-filtration through G 200 Sephadex was approximately 55000; apparent Km was 10(-3)M. The enzyme showed great affinity for D-Ala and D-Val. Recovery of activity, due to pre-incubation with FAD was observed. The enzyme is strongly inhibited by benzoic acid and moderately inhibited by p-aminobenzoic acid.
Blood viscosity indices, fibrinolytic activity and other serum proteins related to haemocoagulation have been studied in 36 patients with multiple sclerosis. The whole blood viscosity was found to be increased in multiple sclerosis. The increase was caused by a decrease in erythrocyte deformability since plasma viscosity and haematocrit were normal. Plasminogen, fibrinogen and alpha 2 antitrypsin levels were found to be lower than normal. Such alterations were not observed in a group of patients with other non-immunological neurological diseases. In the latter group some coagulation indices were even higher than normal. The higher mean age of the pathological controls could explain the observed levels. The abnormalities observed in multiple sclerosis patients are considered to be a consequence of a non-specific activation of the coagulative system in a chronic immunological disease.
Several coagulative, fibrinolytic, and rheologic indices were studied in a large group of patients with acute myocardial infarction. The results were compared with those obtained in a normal control group. Changes of blood and plasma viscosity, fibrinogen, and fibrinolytic activity, compatible with a hypercoagulable state, were found in the immediate post-infarction period. However, elevated AT III levels as compared to control group were observed. This could be interpreted as a reactive response to the hypercoagulable state. Significant correlations could be observed between blood viscosity and Ht, plasma viscosity and fibrinogen, fibrinogen and fibrinolytic levels and between fibrinogen and ESR.
The authors describe a rare case of sigmoidovesical fistula due to a foreign body and giving trouble 30 years after the causative surgical procedure, namely an oopheroctomy. The cause of the fistula was apparently some suture material that had not been reabsorbed. Surgical excision of the fistula produced a complete recovery.
A study has been made of 31 patients with coronary heart disease where diagnosis had been clearly ascertained both from a clinical and strumental point of view. All patients had undergone aorto-coronary by-pass surgery. The controls of the parameters under observation (whole-blood and plasmatic viscosity, hematocrit, fibrinogen, euglobulin lysis, T protothrombin, T of partial thromboplastin, thromboelastogram antithrombin III, plasminogen, alfa2-macroglobulin and fractions C'3c, C'3c, C'4 of the complement) were carried out as follows: basic sample taken, I control (8th-10th day), II control (15th-20th day), III control (45th-50th day), IV control (85th-90th day) after surgical operation. A global examination of our results showed significant changes in the rheologic coagulative and fibrinolytic parameters after an aorto-coronary surgical operation. The slight tendency toward hypercoagulability met with in the basic blood sample (slight increase of whole-blood viscosity, hyperfibrinogenemy, inhibition of fibrinolytic activity) does not change significantly after surgical operation. This seems to indicate that the coronary by-pass does not in any way alter the evolution of arteriosclerosis.
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A Normotest (NT)-Thrombotest (TT) discrepancy is claimed to reflect the presence of coumarin-induced inhibitors or intravascular coagulation, or both. The results of this study indicate, however, that a significant NT-TT discrepancy is also present in all plasmas from patients who have congenital coagulation disorders of the prothrombin complex. None of these patients had received an anticoagulant or showed any sign of intravascular clotting; nevertheless the discrepancy observed was similar to that found in plasmas of coumarin-treated patients: average values were 0.437 and 0.450, respectively. As no inhibitor was present in the congenital coagulation disorders, except in hemophilia BM, the phenomenon does not appear to be specific for coumarin plasma. This indicates that the NT/TT discrepancy is a non-specific phenomenon that does not seem to provide any additional information about coumarin-treated patients compared with that obtainable by means of a simple prothrombin time test.
A case of urinary malakoplakia involving both ureters and the bladder is presented. Ultrastructural data relating to the ureteric lesion are illustrated. Pale, dark and intermediate cells were involved in the pathological process. Features common and specific for these three types of cell are described. Dark cells are thought to be of a histiocytic nature, while the others are of either histiocyte or urothelial origin. Cytoplasmic inclusions were abundant in all three types in the form of single-or multicentred multilamellar bodies. It was not clear whether these were the product of secretion or phagocytosis. Michaelis-Gutmann bodies, on the other hand, were found to be due to the deposition of needle-like crystals inside pre-existing multicentred multilamellar bodies. Pathogens could not be demonstrated for certain. It is felt, therefore, that the aetiology of malakoplakia must be considered as debatable. Biochemical and immunological research directed to the detection of a possible enzyme deficiency is suggested, along with further ultrastructural investigation of the histogenesis of the pale and intermediate cells.
57 patients with cyanotic congenital heart diseases were studied. 39 patients presented t. of Fallot, 18 patients had patent ductus arterious with pulmonary hypertension and right to left shunt. The average whole blood viscosity in patients with t. of Fallot was 6.86+/-0.32 cps. This parameter was correlated with hematocrit, fibrinogen, euglobulin lysis time, pulmonary output, systemic output, and O2 saturation. The value of "r" resulted as statistically significant only for the correlation between viscosity and hematocrit and between viscosity and fibrinogen (t=13.22, p less than 0.0005; t=3.35, p less than 0.001 respectively). The average value of plasma viscosity in patients with t. of Fallot was 1.61+/-0.024 cps. The correlations of this parameter with fibrinogen, euglobulin lysis time, pulmonary output and systemic output did not result as statistically significant. The average fibrinogen value was 256.10+/-20.63 mg%, whereas that of euglobulin lysis time was 12,67+/-1.50 hours. In patients with patent ductus arteriosus the average blood viscosity was 6.65+/-0.56 cps. Such parameter was correlated with hematocrit, fibrinogen, euglobulin lysis time, pulmonary output, systemic output and O2 saturation. The value of "r" resulted as statistically significant only between blood viscosity and hematocrit and between blood viscosity and O2 saturation (t=9.30, p less than 0.0005; t=5.800, p less than 0.001 respectively). The average value of plasma viscosity was 1.61+/-0.04 cps. This parameter was correlated with fibrinogen, euglobulin lysis time, pulmonary output and systemic output. The correlation index "r" never resulted as statistically significant. The average fibrinogen value was 299.20+/-20.30 mg. The average euglobulin lysis time was 16.02+/-2.73 hours.
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The authors report of case of splenogonadic fusion in abdominal retention, revising the subject from the aetiopathogenetic and diagnostic point of view. It is emphasized that correct recognition of the lesion can obviate useless orchiectomies, preserving normal function of the testicle at least from the endocrinal standpoint.
Prothrombin (factor II) was assayed in a group of coumarin treated patients using the Echis carinatus venom as thromboplastin. The levels obtained were comparable to those observed using the classical one-stage method. A good correlation was in fact observed between the two methods. The levels observed by the Echis carinatus method were definitely lower than those obtained using two immunological methods indicating that Echis carinatus venom activated, in our system, only normal prothrombin. However, even the levels obtained immunologically were slightly decreased, regardless of the method used, as compared to pooled normal plasma. In congenital prothrombin deficiency (homozygotes and heterozygotes) the level obtained by the Echis carinatus method was comparable to that observed by the one-stage method. On the contrary, in a congenital dysprothrombinemia (prothrombin Padua) a normal level was observed whereas the one-stage and two-stage methods yielded constantly levels of about 50% of normal.
The behavior of K-test (Trypsin clotting time) has been studied in 38 patients on long-term coumarin therapy and in 19 patients with congenital coagulation disorders of the prothrombin complex. All coumarin treated patients showed a clear prolongation of the test. The results obtained were compared with the standard prothrombin time, the Hepato-Quick-test (P-P test) and the Factor II + X test values, observed in the same patients. A good correlation was observed in each instance. The highest correlation was observed between K-test and the Factor II + X test (r=+0,78;t=7,80;p less than 0.001). All congenital coagulation disorders of the prothrombin complex yielded a prolonged K-test value but for Factor VII deficiency. In three patients with this latter condition a perfectly normal value was obtained. The K-test together with the prothrombin time may be useful in the differential diagnosis of factor VII deficiency from factor X deficiency and from the factor X Friuli abnormality.
A case of classical factor X deficiency is reported. The propositus is a 28-year-old male who presented easy bruising, epistaxis, hematomas, hematuria and occasional hemartrosis since early childhood. The severely prolonged prothrombin time was corrected by normal serum but not by adsorbed normal plasma. The abnormality was not corrected by the plasma of a patient with factor X deficiency, but by the plasma of patients with factor II or VII deficiencies. Partial thromboplastin time, prothrombin consumption and the thromboplastin generation test were abnormal. The thromboelastogram showed a prolonged 'K' and 'r' together with a normal 'ma'. Factor X was very low (smaller than 1%). Platelet tests were normal. No factor X band or precipitates were seen on electroimmunoassay and on the cross-over electrophoresis. The non-consanguineous parents and several other members of the family were found to be heterozygotes.
Unrestrainable haematurias after supervoltage therapy of bladder tumours are a serious complication for the treatment. Excellent results were obtained by radical transurethral resection of the pathologically modified bladder mucosa. There is no bleeding and new mucosa with a particular appearance replaces the resected tissue. The histological findings and the results of the treatment confirm that the only cause of these haematurias is the presence of large newly formed vascular "lakes".
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