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H Bechtold

Publications and source records attributed to H Bechtold.

10 recordsLinked to original sources
PubMed1992

[Ultrasonographic findings in varicose phlebitis of the great saphenous vein. Evidence of thrombus growth and detachment with asymptomatic lung embolism].

In five women (mean age 58 [31-74] years) with clinically diagnosed varicose phlebitis of the long saphenous vein appositional thrombus growth was demonstrated by serial ultrasonography (B-mode compression and colour-coded duplex sonography). In one patient the appositional thrombus was found to be free-floating as far as the common femoral vein, but this was not seen by phlebography. During therapeutic heparinization there was ultrasonographic evidence of softening and partial liquefaction of thrombus material in a cranial direction. There were no clinical signs of pulmonary embolism, but pulmonary perfusion scintigraphy demonstrated perfusion deficit characteristic of emboli. Four of the five patients had a surgical crossectomy and partial saphenous vein resection. The congruence between ultrasonographic and macro- as well as micropathological findings demonstrates the great value of B-mode and duplex ultrasound examination in the area of the epifascial veins. Ultrasonography should be performed in every case of varicose phlebitis of the large veins to exclude the presence of apposition thrombi.

Adult↗
PubMed1990

Lack of effect of cefixime on the metabolism of vitamin K1.

It seems that cephalosporins bearing a N-methyl-thio-tetrazole or a methyl-thiadiazole moiety in their molecule can cause hypoprothombinemia in patients via inhibition of the metabolism of vitamin K1 if they are in addition in a vitamin K1-deficient state. The authors therefore studied the effects of two different oral doses (200 and 400 mg) of the cephalosporin cefixime on the metabolism of vitamin K1 in healthy volunteers, because the accumulation of vitamin K1-2,3-epoxide in plasma is a sensitive marker of coumarin-like activity of drugs. The results indicate that the development of hypoprothrombinemia due to an impairment of the metabolism of vitamin K1 by cefixime seems unlikely because only trace amounts of vitamin K1-2,3-epoxide could be determined in the plasma of the subjects investigated.

Administration, Oral↗
PubMed1988

Mechanism of cephalosporin-induced hypoprothrombinemia: relation to cephalosporin side chain, vitamin K metabolism, and vitamin K status.

The mechanism of cephalosporin-induced hypoprothrombinemia has been investigated in hospitalized patients, with respect to cephalosporin structure, vitamin K metabolism, and vitamin K status. Cephalosporins containing side chains of N-methylthiotetrazole (latamoxef, cefmenoxime, cefoperazone, cefotetan, cefamandole) or methyl-thiadiazole (cefazolin) all caused the transient plasma appearance of vitamin K1 2,3-epoxide in response to a 10-mg intravenous dose of vitamin K1, whereas two cephalosporins without a heterocyclic side chain (cefotaxime and cefoxitin) did not. The plasma accumulation of vitamin K1 2,3-epoxide was qualitatively similar to, but quantitatively less than, that produced by the oral anticoagulant phenprocoumon. Patients eating normally had plasma vitamin K1 concentrations (176 to 1184 pg/mL) that were within the normal range (150 to 1550 pg/mL) and their clotting tests remained consistently normal for all antibiotics tested. Patients on total parenteral nutrition had lower plasma vitamin K1 concentrations (50 to 790 pg/mL) but normal clotting before starting antibiotic therapy. Of 19 parenterally fed patients, all seven treated with latamoxef developed hypoprothrombinemia, PIVKA-II and a decrease of protein C within four days whereas 12 patients treated with cefotaxime or cefoxitin showed no clotting changes. Latamoxef-associated hypoprothrombinemia was readily reversible by 1 mg of vitamin K1 given intravenously, but hypoprothrombinemia and sub-normal plasma vitamin K1 could recur within two to three days. The data suggest that NMTT-cephalosporins are inhibitors of hepatic vitamin K epoxide reductase and that a lower nutritional-vitamin K status predisposes to hypoprothrombinemia.

Adult↗
PubMedDate not supplied

Alteration of hemostasis associated with cefoperazone treatment.

21 Patients with normal and impaired renal function were given cefoperazone in a recommended dose of 4 g/day, irrespective of renal function. Platelet function and plasmatic coagulation were analyzed before and on day 7 of therapy. In patients with normal renal function on their usual diets, there was neither impairment of platelet function nor plasmatic coagulation. High serum antibiotic trough levels, prolongation of bleeding time and decreased vitamin K-dependent coagulation factors, as verified by the prolongation of prothrombin time and the appearance of descarboxyprothrombin, could be observed in those patients with impaired renal function whose insufficiency was far advanced and accompanied by a complex clinical picture. In this situation vitamin K deficiency may be due to poor oral intake, along with interference of hepatic vitamin K metabolism, showing an effect similar to that seen after coumarin therapy. Dosage reduction of the antibiotic in advanced renal failure and repeated control of prothrombin time is advised.

Adenosine Diphosphate↗