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J N Fiessinger

Publications and source records attributed to J N Fiessinger.

At least 145 records · Page 8Linked to original sources
PubMed1989

Variations of prothrombin time, factor VII and protein C with a single daily dose of acenocoumarol. Preliminary results.

In 11 patients on steady anticoagulation with a daily dose of acenocoumarol, prothrombin time, factor VII and protein C were measured 2 and 16 h after the daily intake of acenoumarol. Prothrombin time (expressed as International Normalised Ratio) increases significantly, factor VII and protein C decrease between the two samples. These results suggest that a daily dose of acenoumarol is associated with fluctuation of the anticoagulant effect.

Acenocoumarol↗
PubMed1989

Molecular characterization of antithrombin III (ATIII) variants using polymerase chain reaction. Identification of the ATIII Charleville as an Ala 384 Pro mutation.

The genes of seven structural mutants of antithrombin III (ATIII), presenting either defective serine protease reactivity or abnormal heparin binding, were analyzed. The polymerase chain reaction (PCR) was used to amplify the corresponding gene exon and the mutation was identified by either dot blot analysis using a battery of allele-specific oligonucleotide probes or sequencing. Variants Paris and Paris 2 were identified as Arg 47 Cys mutations, and Clichy, Clichy 2, and Franconville were found to be Pro 41 Leu mutations. All five are heparin binding-site variants. ATIII Avranches is an Arg 393 His mutation and ATIII Charleville is an Ala 384 Pro mutation. These two mutations impair the reactive site of the molecule. ATIII Charleville is a new mutation of the reactive center, as predicted by previous biochemical data. The position of this new mutation, together with the other previously described mutations of the reactive center, sheds light on the molecular function of this site in inhibiting thrombin. Finally, genomic amplification by PCR is a powerful technique for the fast identification of antithrombin III mutations and their homozygous/heterozygous status, and should be useful for predicting thrombotic risk.

Adult↗
PubMed1989

[Extratemporal Horton's disease: diagnosis using subclavian biopsy. 4 cases].

A histological diagnosis of Horton's disease was made in 4 patients with lesions of the axillary-subclavian arteries by biopsy of these vessels. Unilateral biopsy of the temporal artery, performed initially in 2 of these patients, during surgery in one and immediately after surgery in another, had been negative in 3 cases and insufficient for a diagnosis in 1 case. For temporal biopsy to be valuable, the arterial fragment resected must be long enough and serial histological sections must be performed to avoid false-negative results. It is only when these conditions are fulfilled that negative results may be considered. Horton's disease of the axillary-subclavian arteries is relatively frequent, and histological studies of these vessels have already been used to assert the diagnosis in case of negative or non-performed temporal biopsy, whether or not the arteriographic findings were suggestive of the disease. The indications for subclavian biopsy remain to be determined. It can be carried out for diagnostic purposes in case of clinically atypical suspected Horton's disease revealed by axillary-subclavian lesions and negative temporal biopsy, particularly when revascularization proves necessary.

Aged↗
PubMed1989

[Role of myocardium scintigraphy with thallium dipyridamole in the evaluation of arterial disease of the legs].

Thirty-eight consecutive patients with severe arterial disease of the lower extremities benefited from an exploration of the coronary reserve by myocardial scintigraphy with thallium dipyridamole. With this examination, it has been possible to screen 20 p. cent of asymptomatic patients and at least modify the perioperative treatment or even the very indication for surgery.

Adult↗
PubMed1989

[Effect of a single dose of nifedipine on the CO transfer capacity in patients with scleroderma].

The calcium antagonists are currently used in the treatment of Raynaud's syndrome for patients with scleroderma. The effect on the pulmonary vasculature in these patients is little understood. The study reported here is based on 15 patients with scleroderma. In each patient lung volumes, expiratory flow and transfer factor (DLCO) were carried out in a basal state and one hour after the administration of sub lingual nifedipine. Nine patients showed a diminution in the DLCO before taking the product but the mean variation after nifedipine was not significant. Different mechanisms may explain the absence of any effect: irreversible vascular disease or the absence of pulmonary arterial hypertension or hypoxic constriction, the latter conditions were previously associated with the efficacy of nifedipine. Thus it does not seem that nifedipine, in acute tests, has an effect on the pulmonary localisation of scleroderma, at least in the absence of pulmonary arterial hypertension.

Adult↗
PubMed1988

[Erythermalgia, rare acrosyndrome. 13 cases].

The diagnosis of erythermalgia, initially made in 27 patients between 1980 and 1986, was re-evaluated on the basis of 7 criteria. Three were major criteria: paroxysmal attacks, burning pain in the extremities and redness of the territory concerned during the attacks. The 4 minor criteria were: typical precipitating factors (exposure to heat, effort), typical relieving factors (exposure to cold, rest), elevated local temperature during the attacks and response of symptoms to acetylsalicylic acid. The diagnosis was deemed to be correct when the 3 major criteria and at least 2 of the minor criteria were present. Thirteen patients (8 women, 5 men) fulfilled these conditions. Nine of them had primary erythermalgia and in 4 patients the condition was consecutive to a myeloproliferative syndrome (thrombocytopenia in 2 cases, Vaquez' disease in 2 cases). These two forms differed on several points. Patients with secondary erythermalgia were older, some had unilateral disorders, and their symptoms were less intense; the syndrome always followed a favourable course and disappeared when the causative disease was cured; in 3 out of 4 cases erythermalgia disclosed a myeloproliferative syndrome. Patients with primary erythermalgia were younger, the syndrome was of longer duration and the symptoms always bilateral and sometimes severe; those who responded to acetylsalicylic acid had a favourable prognosis, but treatment was difficult in the others. Capillaroscopy is of little help to diagnose this syndrome; this is done on clinical grounds only and it is easy when the criteria, as defined in this study, are present. In every case, blood examination with platelet count and erythrocyte sedimentation rate is advisable.

Adult↗
PubMed1988

Antithrombin III Avranches, a new variant with defective serine-protease inhibition--comparison with antithrombin III Charleville.

A decreased plasma antithrombin activity in presence or in absence of heparin was discovered in a 47-year-old patient presenting with recurrent venous thromboembolism. The immunoreactive material (AT III-IR) was normal. The same biological abnormalities were found in two relatives of the patient, leading to the diagnosis of hereditary qualitative AT III deficiency. The propositus' AT III was coeluted with normal AT III from an heparin-sepharose column. An additional step of ion-exchange chromatography on a Mono Q column using a FPLC system (Pharmacia, St-Quentin en Yvelines, France) allowed the purification of a protein which was homogenous in SDS-10% polyacrylamide electrophoresis gel (PAGE). AT III purified from propositus' plasma, normal plasma and the plasma of the patient known to have an AT III variant with defective protease binding (AT III Charleville) were compared. The specific activities measured as heparin cofactor antithrombin or factor Xa inhibition in absence of heparin were decreased to half the normal value. Kinetic studies confirmed a decreased rate of thrombin inhibition for both abnormal AT III preparations. SDS-PAGE experiments performed in purified system and immunoblots obtained from plasma showed that the two variants have different behaviour: in the case of AT III Charleville thrombin induced an apparent 5 k delta increase in molecular mass, probably due to a conformational change. AT III Avranches did not form stoechiometric complexes with thrombin, but was unmodified by the protease.

Antithrombin III↗
PubMed1988

A study of fibrinogen and fibrinolysis in 10 adults with nephrotic syndrome.

In 10 patients with nephrotic syndrome (NS), the coagulation inhibitors, the fibrinolytic system and several functions of the fibrinogen-fibrin molecule were studied. Among the coagulation inhibitors, only antithrombin III (AT III) was found decreased and correlated with serum-albumin levels. Venous occlusion test provoked a normal tissue plasminogen activator (tPA) release in all patients. The plasminogen activator inhibitor (PAI) had an increased activity in 5 out of the 10 patients. Thrombin and reptilase times were found abnormal in most patients. The thrombin time (TT) prolongation correlated with serum albumin levels and was corrected by adding purified albumin. The fibrinogen was purified from each of the 10 patients' plasma. Only 2 of them showed abnormal polymerization in purified system, suggesting dysfibrinogenaemia. Other functions (thrombin binding, tPA stimulating activity, lysis by purified plasmin) were found normal except in one of the 2 patients with dysfibrinogenaemia whose fibrinogen lysis by plasmin was delayed. It is concluded that an abnormal fibrinogen molecule is not the most frequent explanation for thrombin time prolongation in NS.

Adult↗
PubMed1988

Association of inherited dysfibrinogenaemia and protein C deficiency in two unrelated families.

An inherited association of dysfibrinogenaemia and protein C deficiency was found in three members of the same family. The propositus was a 48-year-old man who suffered from severe and rapidly complicated atherosclerosis of the aorta and lower limbs arteries, which perhaps suggests that the association of these two molecular abnormalities may have enhanced the thrombotic process. The abnormal fibrinogen had a reduced ability to bind thrombin which may be thrombogenic. We found the same inherited association of dysfibrinogenaemia and protein C deficiency in a patient with venous thrombosis. The functional abnormality of the fibrinogen, which could have been responsible for thrombosis, was delayed proteolysis by plasmin. Not only fibrinogen, but also fibrin clots were resistant to plasmic degradation. These observations raise two questions: (1) Is the association of a protein C deficiency with a dysfibrinogenaemia fortuitous or the result of a common mechanism? (2) Is there a link between an increased thrombotic tendency and either both of the defects of haemostasis that we have found, or only one of them?

Adult↗