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Biomedical subjects

Z Vorlová

Publications and source records attributed to Z Vorlová.

At least 19 recordsLinked to original sources
PubMed1995

[Results of induction therapy in newly diagnosed acute myeloid leukemias in study 911 at the Institute of Hematology and Blood Transfusion].

Thirty-seven patients with de novo acute myeloid leukemias were admitted to the Institute of Hematology and Blood Transfusion in Prague in February 1991-December 1993. Their age was 18-85 years with a median of 46 years. Two patients died on the day of admission, chemotherapy was initiated in 35 patients. Altogether 27 patients (77%) achieved complete remission (CR), i.e. 18 (81%) of 22 patients younger than 55 years and 9 (70%) of 13 patients older than 55 years. Only 7 (35%) of 20 patients achieved CR after a single therapy course 3/7 consisting of 3 doses of daunorubicin 45 mg/m2 on days 1, 3, 5 and cytosine arabinoside 150-200 mg/m2 every 12 hours for 7 days. However, 8 (61%) of 13 patients achieved CR after a single treatment course 4/7 with 4 doses of daunorubicin 45 mg/m2 on days 1, 3, 5, 7 and identical doses of cytosine arabinoside as in the 3/7 treatment. We used the course with 10 high-doses of cytosine arabinoside 2000 mg/m2 every 12 hours and daunorubicin 45 mg/m2 on days 4 and 5 (treatment HDAC/DNR) as the 1st, 2nd or 3rd induction therapy in 12 patients and 9 (75%) of them achieved CR. The treatment was associated with a high toxicity. An intensified therapy 3/7h similar to the 3/7 one but with the doubled dose of cytosine arabinoside 300-400 mg/m2 on days 5-7 was given to 5 patients as the 2nd induction but it did not improve the CR rate and it was associated with a high toxicity similar to the HDAC/DNR therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1994

[Late and slow diagnosis of acute promyelocytic leukemias--the main cause of early death].

Acute hypergranular promyelocytic leukemia (AML M3) belongs to malignant diseases leading very rapidly to death. Immediate treatment based on early diagnosis may cure one third of patients. The typical finding in peripheral blood of patients is pancytopenia with or without atypical promyelocytes. In published studies only 15-25% patients exhibit leukocyte counts above 10 x 10(9)/l. Five of our ten patients studied had leukocyte count above 10 x 10(9)/l. The difference might be in connection with late and slow diagnosis of AML M3. AML is not taken into consideration during medical examination even if the disease occurs in medical family. Thus we describe clinical signs of AML M3 that could be divided into three main groups: bleeding, infections and anemia. In patients with bleeding or anemia or with infections repeating within a short period or with an infection and concurrent signs of bleeding or anemia the complete blood cell count should be examined immediately. If blood cell count abnormalities are found the patient should be sent immediately to hematology unit for further examination and treatment. Early diagnosis enables to start "differentiation therapy" with all-trans retinoic acid that could be administered as monotherapy only in patients with leukocytes below 5 x 10(9)/l. Early diagnosis of AML M3 might ameliorate the fate of patients, since four of our five patients referred to us with elevated leukocyte counts expired in the first five days.

Adult↗
PubMed1994

[Changes in humoral pressor and depressor factors in essential hypertension during lisinopril therapy].

Arterial hypertension is nowadays no longer considered an isolated disorder of blood pressure regulation but a multifactorial disease with metabolic and cellular deviations. From the therapeutic aspect of thus conceived hypertension today inhibitors of the angiotensin converting enzyme seem most promising. With regard to their assumed comprehensive effect, the authors investigated simultaneously selected pressor and depressor humoral indicators and other indicators in 21 hypertensive patients with stage I and II of essential hypertension before and after three-month treatment with an angiotensin converting enzyme inhibitor lisinopril (Prinivil, Merck, Sharp and Dohme) and compared them with findings in 21 normotensive healthy subjects. Hypertensive subjects before treatment had, as compared with normotensives, significantly lower urinary kallikrein (7.8 +/- 1.2 < 18.0 +/- 4.2 EU/24hr, a significantly higher basal plasma adrenalin (1.27 +/- 0.20 > 0.54 +/- 0.20 pmol/ml) and adrenalin after a glucose load (1.26 +/- 0.22 > 0.51 +/- 0.12) and a higher relative plasma viscosity (1.74 +/- 0.02 > 1.67 +/- 0.01). The two groups did not differ significantly as to the plasma renin activity, plasma aldosterone and fibrinogen concentration and the level of urinary prostaglandins per 24 hr: 6-keto-prostaglandin F1a, thromboxane B2 and prostaglandins E and F2a. The 75 g glucose load produced an increased plasma renin, aldosterone and noradrenaline activity in normotensives as well as hypertensives before and after lisinopril treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Factor VIII gene mutations and RFLP analysis in hemophilia A.

Hemophilia A is an X-linked bleeding disorder caused by a quantitative or qualitative defect of coagulation factor VIII. Since factor VIII has been cloned and several intragenic and linked DNA polymorphisms discovered, DNA analysis is an accepted and commonly used method for carrier testing in hemophilia A. Both a direct method using detection of mutation and an indirect method based on linkage between the disease and DNA polymorphism are used for this purpose. In this study, DNA samples of 110 hemophilia A patients from 99 families were screened for factor VIII gene mutation using Southern blot analysis; in seven families, mutations were detected. In 13 females from six families with identified mutation, the direct diagnosis of carriers was performed. Four intragenic (BclI, XbaI, BglI and MspI in F8C locus) and two linked polymorphisms (TaqI in DXS52 locus and BglII in DXS15 locus) were studied in members of 47 hemophilia A families. BclI-XbaI-BglI haplotypes were analyzed in 90 unrelated X chromosomes. Eighteen out of 31 females (58%) were heterozygous for at least one intragenic polymorphism, and 29 out of 31 females (94%) were heterozygous for at least one intra- or extragenic polymorphism tested. Carrier diagnosis was made in 15 out of 25 possible carriers (60%) based on intragenic and in an additional 3 out of 25 (12%) only on linked polymorphism.

DNA Mutational Analysis↗
PubMed1992

[Detection of carriers of hemophilia B].

Thirty-two families with haemophilia B were divided into sub-groups based on assessment of fIX:Ag, fIX:C and the thromboplastin time with bovine thromboplastin. In confirmed carriers from these families after assessment of fIX:Ag and, fIX:C the normal range of individual sub-groups of confirmed carriers was assessed and compared with values of fiX:Ag and fiX:C of the control group. It will be possible to use these groups after their extension to assess probable carriers in sub-groups CRM+ and CRM-. In the sub-group CRMR the only criterium of transmission is a reduced fIX:C level. A prolonged TP with bovine thromboplastin in families with BM haemophilia cannot be used to assess carriers.

Adult↗
PubMed1992

Factor VIII gene deletions in haemophilia A patients in Czechoslovakia.

Genomic DNA from 90 Czechoslovak haemophilia A patients from 81 pedigrees was analysed by Southern blotting and hybridization with factor VIII cDNA probes. Three partial deletions of the factor VIII gene were identified and characterized: a 4.8 kilobase (kb) deletion eliminating exon 10 in one patient with severe haemophilia A without inhibitor, a 6.1 kb deletion eliminating the 3' part of intron 13 and the 5' part of exon 14 in two related severe haemophiliacs, but only one of them produced inhibitor, and a 4.6 kb deletion eliminating the 3' part of intron 13 and the 5' part of exon 14 in a severe haemophiliac with high-titre inhibitor. Besides these three deletions, three different restriction site variants without apparent loss of DNA sequence were found.

Blotting, Southern↗
PubMed1990

Non-specific therapy of a hemorrhagic diathesis after a bite by a young Bothrops asper (barba amarilla): a case report.

Hemorrhagic diathesis developed 4 hr after a bite by one fang of a two-month-old specimen of Bothrops asper. Severe allergy to horse serum contraindicated the use of horse antivenom, and a substitution therapy was started 20 hr after the bite. During the following 4 days the patient was treated with infusions of 8 g human fibrinogen, 2500 U of cryoprecipitate, 1000 ml of human plasma and vitamin K in several portions. By means of plasmapheresis 1800 ml of plasma was exchanged. Until plasmapheresis on the third day the treatment resulted in short remission and diminution of the spontaneous bleeding, which ceased on the 5th day. Coagulation tests relevant to disseminated intravascular coagulation and consumption coagulopathy were performed for 12 days. Fibrinogen levels started to rise on the 8th day and normalized 12 days after the bite. Analysis of the venoms from juvenile and adult Bothrops asper snakes revealed that the former has a strong prothrombin-converting activity, the latter contained mainly a thrombin-like, fibrinogen-converting enzyme.

Age Factors↗
PubMed1988

Ecarin test in diagnosis of dicoumarol therapy, liver diseases and DIC.

The conversion of prothrombin by ecarin is independent of the presence of gamma carboxyglutamic residues on the N terminal of the molecule. Ecarin converts therefore also the acarboxylated precursor-PIVKA II. In a group of 347 patients under dicoumarol therapy of different intensity and duration PIVKA was detected in BaSO4 adsorbed PPP only in samples where prothrombin level (Quick's test) was lower than 50% of normal values. Increase in PIVKA did not correspond to the decrease of prothrombin. In some cases where the treatment was longer than two years no PIVKA was detected even when prothrombin was under 20%. This is explained by synthesis of partially carboxylated prothrombin molecules, which can be adsorbed. In liver diseases the ecarin test and Quick's time in native, untreated PPP showed about identical decrease of prothrombin level. This indicates that no PIVKA is released to plasma. The functional defect of the hepatocyte does not involve gamma carboxylation as long as vitamin K is provided. In patients with DIC ecarin test showed significantly higher level of thrombin activity than those obtained with Quick's test. It is known that during hypercoagulation stage of DIC prethrombin 1 and 2 are formed by the excess of thrombin. These split products of prothrombin are convertible by ecarin to meizothrombin 1 and 2. A positive ecarin test can be also due to acarboxylated precursors which are released during increased proteosynthesis triggered by consumption coagulopathy.

Diagnosis, Differential↗
PubMed1987

[Lyophilized plasmas for the control of thromboplastin time values and calibration of thromboplastins].

The paper deals with the production of normal and pathological plasmas for the calibration of thromboplastin. Calibration is performed according to WHO principles. We compared single charges of thromboplastin (Sevac, CSSR, human brain) with each other and a selected reference charge with British thromboplastin. Lyophilised reference plasmas produced (20-50 healthy blood donors) and plasmas taken from patients treated with coumarin derivates (single and mixtures) could replace their fresh equivalents which was confirmed by testing 4 different batches. The stability of these plasmas (for a time of at least 12 months) was proved by repeated checks. These plasmas also served as controls in other laboratories in Czechoslovakia.

Blood Coagulation Tests↗
PubMed1984

[Significance of the laboratory diagnosis of hypercoagulability].

Alterations characteristic of the hypercoagulation syndrome such as changes in fibrinogen content, in FDP concentration and platelet counts as well as the presence of fibrinogen complexes were demonstrated by laboratory findings in 175 patients with severe diseases and disturbances of haemostasis. Twenty per cent of the patients showed no clinical signs of disturbances of haemostasis, in 32.5 per cent pronounced venous thrombosis occurred, bleeding complications arised in 28 per cent and microthrombosis developed in 20 per cent. The different findings in the individual groups are assumed to be due not only to haemostatic factors but also to other ones.

Blood Coagulation Tests↗