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Biomedical subjects

J Conard

Publications and source records attributed to J Conard.

At least 127 records · Page 7Linked to original sources
PubMed1986

A new case of high-molecular-weight kininogen inherited deficiency.

A preoperative hemostasis study discovered a prolonged activated partial thromboplastin time in a 23-year-old Portuguese Caucasian woman without personal or past family history of hemorrhage or thrombosis. This was corrected by pooled plasma that excluded circulating anticoagulant. Activated partial thromboplastin time was prolonged whatever the activator, particularly ellagic acid, and was not corrected by prolonged kaolin incubation. Levels of factors VIII and XII were normal; factor XI and prekallikrein levels were either moderately low or normal according to activators and defective reagents used. High-molecular-weight kininogen (HMWK) level assessed by coagulation and immunological method was virtually nil. Fibrinolysis activity was normal before and after venous occlusion. The programmed operation was performed without any particular preparation and no complication arose. Family investigation found heterozygous HMWK deficiency in the proposita's father and three of her siblings.

Adult↗
PubMed1986

[Protein C].

Explore the source record for details and available documents.

Blood Coagulation↗
PubMed1986

Biological effects of estradiol-17 beta in postmenopausal women: oral versus percutaneous administration.

To determine whether the route of administration or the type of estrogen used in estrogen replacement therapy (ERT) is more important in avoiding effects on hepatic function, 24 postmenopausal women were studied before and at the end of 2 months of oral or percutaneous administration of the same estrogen, estradiol-17 beta (E2). The treatments studied were oral micronized E2, 2 mg/day (9 women); oral E2 valerate, 2 mg/day (5 women), and percutaneous E2, 3 mg/day (10 women). Specific plasma biological and biochemical markers of estrogenic action were evaluated, namely, E2, estrone (E1), LH, FSH, sex steroid binding protein (SBP), renin substrate, antithrombin activity, and lipoproteins (high density lipoprotein cholesterol, low density lipoprotein cholesterol, very low density lipoprotein triglycerides). Both oral and percutaneous administration of E2 increased plasma E2 levels up to midfollicular values and decreased LH and FSH levels into the same range. Oral administration of E2 led to substantial increases in plasma E1, SBP, renin substrate, and VLDL levels, whereas AT decreased significantly. Percutaneous administration of E2 led to a physiological plasma E1/E2 ratio and did not induce any change in hepatic proteins. These data suggest that the route of administration of E2 determines the biochemical response to ERT in postmenopausal women. SBP is the most sensitive marker of the liver action of estrogen, and triglycerides also are simple and useful markers for this effect. Percutaneous E2 therapy is an effective method of ERT, and has no measurable effects on hepatic markers of estrogen action.

Administration, Oral↗
PubMed1986

Contraception in hypertensive women using a vaginal ring delivering estradiol and levonorgestrel.

Contraception with a vaginal ring (CVR) that delivers estradiol and levonorgestrel was used during a mean of 15.6 menstrual cycles in 12 hypertensive women. Blood pressure (BP) was measured 5 times on each visit during 2 pretreatment control cycles; during the 1st, 2nd, 4th, 6th, and from the 9th to 12th cycles of CVR use; and again after a 1-month recovery period. No significant change in BP occurred during CVR use in any of the subjects. Plasma renin substrate and antithrombin III activity did not vary significantly, which suggests the utility of administering natural estradiol via the vagina, thus avoiding the first pass effect that occurs with oral contraceptives. Significant decreases in plasma sex hormone-binding globulin, cholesterol, high density lipoprotein cholesterol, phospholipids, and triglycerides occurred, indicating an androgenic effect of levonorgestrel. We conclude that the CVR is a method of contraception that does not elevate BP in hypertensive women.

Adolescent↗
PubMed1986

[Tissue plasminogen activator (t-PA) in myocardial infarction. Biological aspects].

A group of 37 patients with myocardial infarction less than 6 hours old was given 5,000 IU of heparin and 0.75 mg/kg of tissue plasminogen activator (rt-PA) (Group A, N = 18) or placebo (Group B, N = 19) intravenously over 90 minutes in a double blind study. Blood sampling was performed before, during and after treatment. The plasma rt-PA concentrations (micrograms/ml) of Group A were as follows: (Table: see text) The concentrations of plasminogen and antiplasmin have decreased significantly as did the fibrinogen level: a concentration of 1 g/l was observed in 7 cases during rt-PA therapy, lasting for 4 to 8 hours after the end of the infusion of rt-PA in 3 cases. The increase of FDP during rt-PA (m = 551 and 222 micrograms/ml at the 60th and 90th minutes) was relatively moderate considering the average level of defibrination (61%). No significant biological changes were observed in Group B. These results support those of our in vitro trials: at comparable thrombolytic activities, the reduction of plasma fibrinogen is less with rt-PA than with streptokinase (SK) or urokinase (UK). However, at concentrations 1 microgram/ml, rt-PA causes almost complete defibrination.

Double-Blind Method↗
PubMed1986

[Uterine rupture causing acute defibrination syndrome. Apropos of 3 cases].

The authors report three cases of rupture of the uterus during delivery, complicated by an acute defibrination syndrome. Death resulted in two cases. The sequence of rupture of the uterus----shock----pathological condition of coagulation----great increase in the shock occurred in all three patients. This sequence could only be arrested in one of the three patients who had a total hysterectomy. Partial hysterectomy in the other two was ineffective. These three case histories suggest that total hysterectomy after even partial correction of the haemorrhagic state can be the best treatment in this very serious condition.

Adult↗
PubMed1986

[Resistance to vitamin K antagonists. 6 cases].

Haemorrhage is the most frequent complication of oral anticoagulant therapy (OAT) and a resistance to these drugs is rarely reported. The following classification of OAT resistance is proposed: primary or secondary resistance according to the delay of onset (at the initiation of therapy or later); selective or generalized according to the number of drugs involved (only one or several); absolute or relative as judged by the prolongation of the prothrombin time (absent or moderate). Six cases are reported and the mechanisms of resistance are discussed: no intake, variations in the vitamin K availability (diet, intestinal absorption and synthesis of vitamin K), variations in the pharmacokinetics of oral anticoagulants (drug interactions, abnormal hepatic metabolism) and variations in the receptor affinity (hereditary resistance). Resistance is often overcome by progressive increase of the doses of oral coagulant, or by changing drugs, to warfarin or coumadin (long acting drugs).

Adult↗
PubMed1986

[Constitutional protein C deficiency in 57 patients from 22 non-related families].

A congenital deficiency in protein C (physiological inhibitor of coagulation) was identified in 57 patients: the deficiency was quantitative (type I) in 20 families, qualitative (type II) in two families. The transmission was autosomal dominant in 21 families but was suspected to be recessive in one family: the 18 years old homozygous propositus has a severe deficiency (protein C = 16 p. 100): both parents are heterozygous (consanguinity was present) and 5 other family members with heterozygous deficiency are asymptomatic. In the 49 patients (25 women, 24 men) belonging to the 21 other families, 9 men and 4 women (27 p.100) are asymptomatic although precipitating factors had existed in 5 patients. In the remaining 36 symptomatic patients, a deep venous thrombosis was observed in 34, a pulmonary embolism in 18. Recurrent arterial thromboses were diagnosed in 3 patients. The first thrombotic episode was observed at the mean age of 27 +/- 11 years and a triggering factor was found in 26 patients (72 p. 100). Thrombosis was recurrent in 21 (60 p. 100). In the patients without oral anticoagulant treatment, mean protein C antigen concentrations were 47 +/- 9 p. 100 and mean protein C activity was 46 +/- 10 p. 100. In 4 patients with type II deficiency, protein C antigen levels were normal (113 +/- 15 p. 100), contrasting with decreased protein C activity (43 +/- 6 p. 100). Thirty-eight patients have been treated with oral anticoagulants and a skin necrosis developed in the homozygous patients only.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

[Treatment of deep venous thromboses with heparin. Therapeutic management and biological monitoring].

Heparin may be administered either prophylactically (to prevent postoperative thromboembolic complications) or therapeutically (when thrombosis has occurred) and the dosages are very different. In addition, low molecular weight heparins are now available, and usually reserved only for prevention of thrombosis. The biological monitoring of these different therapies has evolved, and in addition to the classical tests like the recalcified plasma clotting time or the APTT, it is now possible to use more specific tests like the amidolytic activity of anti-IIa or anti-Xa. None of the simple tests alone is satisfactory for the verification of the efficacy of the treatment on a formed thrombosis or for detecting patients at high risk of haemorrhage. At this present state of our knowledge, the association of two of the preceding tests is recommended as any discrepancy could lead to the detection of an associated, unrecognised abnormality such as a circulating anticoagulant factor or thrombocytopaenia. The monitoring of classical prophylactic treatment generally only requires a very limited monitoring.

Acute Disease↗