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At least 19 recordsLinked to original sources
PubMed1979

Ionization kinetics of the carbon acid phenindione.

The ionization kinetics of carbon acids are slow relative to those of classical acids and bases. Phenindione (2-phenyl-1,3-indandione) is a 1,3-diketone carbon acid of macroscopic experimental pKa 4.09 at 25 degrees and ionic strength 0.1. The ionization kinetics of phenindione were determined at an ionic strength of 0.1 and 25 degrees using stopped-flow spectrophotometry and a pH jump technique. A log k'obs-pH profile for the approach to the ionization equilibrium was determined, and a mechanism consistent with the profile was postulated. The percent enol versus diketo form of phenindione and the pKaenol and pKadiketo were calculated from the kinetic data. Phenindione acid deprotonation kinetics by various oxygen and nitrogen bases suggested that, with bases of pKa 4.7--8.5 and in the pH 5--8.5 range, the acidic phenindione proton as approximately 45% transferred in the rate-determining transition state.

Buffers↗
PubMedDate not supplied

[Acute nephritis and allergic vasculitis due to phenindione (author's transl)].

The authors report a case of acute nephritis which appears during a treatment with phenindione. The nephropathy described after this medication are now well known. Their manifestations are either a proteinuria associated or not with a nephrotic syndrome or an interstitial nephritis whose pronostic is reserved. In this observation the mechanism is different : the lesion is glomerular and complicates an allergic vasculitis which was secondary to the phenindione's therapy. The pronostic was good.

Acute Disease↗
PubMed1976

Bleeding from self-administration of phenindione: a detailed case study.

A young woman presented with a 2 year history of a severe bleeding disorder and marked deficiencies in all four vitamin-K-dependent factors. Metabolic studies with tracer doses of tritium-labelled vitamin K1 suggested that the patient might be taking an oral anticoagulant; and subsequently her plasma was found to contain a substance identical to phenindione in its spectrophotometric and chromatographic properties. The half-disappearance times of factors II, IX, X were measured after the administration of a concentrate of these factors and were found to conform with published figures. The concentrate controlled the patient's excessive bruising and prolonged skin and gingival bleeding. It would therefore seem that factor VII may not be essential in reversal of the bleeding disorder induced by anticoagulant overdose.

Adult↗
PubMed1976

The effect of different oral anticoagulants on diphenylhydantoin (DPH) and tolbutamide metabolism.

The effect of bishydroxycoumarin, phenprocoumon, warfarin and phenindione on the metabolism of diphenylhydantoin (DPH) and tolbutamide has been studied in 54 patients. The half-lives of DPH and tolbutamide in blood following i.v. injections were studied in 33 patients before and after one week of anticoagulant treatment. Bishydroxycoumarin increased the mean half-life values of DPH from 8.8 to 37.4 hours and of tolbutamide from 4.9 to 17.5. Phenprocoumon prolonged DPH half-life from a mean value of 9.9 to 14.0 hours but did not change the tolbutamide half-life. Warfarin and phenindione did not affect DPH or tolbutamide half-lives. Steady state concentration studies in 21 patients showed a rise in serum DPH during bishydroxycoumarin and phenprocoumon treatment but not during treatment with warfarin and phenindione. A rise in serum tolbutamide was noted during treatment with bishydroxycoumarin. These findings suggest that bishydroxycoumarin inhibits the betabolism of DPH and tolbutamide and that phenprocoumon inhibits DPH metabolism. No effect on DPH and tolbutamide metabolism could be demonstrated following administration of warfarin and phenindione.

Coumarins↗
PubMed1976

Drug induced interstitial nephritis, hepatitis and exfoliative dermatitis.

Acute interstitial nephritis associated with hepatitis, exfoliative dermatitis, fever and eosinophilia is uncommon. The syndrome has been described previously in association with phenindione administration, leptospirosis and heavy metal poisoning. Four cases are described, two of which were due to phenindione sensitivity. The other two patients had been exposed to a number of toxins including allopurinol, frusemide, chlorothiazide and methyldopa so that the exact aetiological agent is unclear. Interstitial nephritis should be considered as a cause of acute renal failure in patients with other features of drug hypersensitivity.

Acute Disease↗
PubMed1975

Anticoagulant effect and plasma kinetics of fluorophenindione after a single dose in man.

After administration of a single loading dose (80 mg p.o.) of fluorophenindione, the prothrombin level decreased to 37% in 24 h, and the effect lasted for 48 h. Accordingly, fluorophenindione can be classified as an anticoagulant with an ""intermediate'' effect. Its elimination half-life was 31 h, which is longer than that of phenindione, because of the greater stability of the fluorinated derivate.

Administration, Oral↗
PubMed1979

Cimetidine: interaction with oral anticoagulants in man.

In 6 patients anticoagulated with warfarin, nicoumalone, or phenindione the addition of cimetidine prolonged the prothrombin-time (PT) by a mean of 12.6 s (range 5--23 s). In 7 volunteers taking daily subtherapeutic doses of warfarin the addition of cimetidine increased the PT from 19.4 to 22.9 s and the plasma-warfarin concentration from 0.96 to 1.76 microgram/ml. Cimetidine reduced the single-dose clearance of warfarin and antipyrine. The basis of the interaction between cimetidine and oral anticoagulants is probably inhibition of drug metabolism. Care should be exercised in concomitant therapy.

Acenocoumarol↗
PubMed1978

Immunologically mediated drug-induced acute renal failure.

(1) AIN is the most frequent pattern of drug-induced immunologically mediated renal injury. A number of drugs may be responsible for AIN, namely methicillin and other penicillin derivatives, rifampicin, phenindione and sulfonamides. Particular clinical and pathological features often suggest an immune pathogenetic mechanism. IgG anti-TBM and IgE antibodies have been found in only a few cases and it is likely that antibody-mediated and cell-mediated injury may operate in the same patient. (2) Only few examples of drug-induced vasculitis and glomerulonephritis are known, and the pathophysiology of this kind of renal damage is poorly understood.

Acute Kidney Injury↗
PubMedDate not supplied

[Oral aphthoid toxic dermatoses].

In a description of 4 cases (phenindione, 1 case; niflumic acid, 1 case; gold salts, 2 cases), the authors describe a new variety of oral toxicodermatitis characterized by an eruption of painful, infiltrated aphthoid ulcerations, not precededbybull ae, small (less than 1 cm), roundish, with a greyish yellow necrotic centre surrounded by an erythematous halo. Histological investigation reveals a compact, polymorphous inflammatory infiltrate with numerous polynuclear neutrophiles or, less commonly, eosinophiles some of which are in a state of pyknosis of leukocytoclasia, associated with phenomena of spongiosis or necrosis of the epithelium.

Adult↗
PubMed1978

[Acute renal insufficiency caused by phenyl-indane-dione. Apropos of 1 case].

One case of Phenindione (PID) adverse reaction is reported. The patient showed a typical picture of immunological reaction to the drug. In spite of severe bacteremia, she recovered. Only 33 cases of PID intolerance are reported in the literature. In all these patients, renal failure occurred. Superinfection is the most frequent cause of death. PID adverse reaction should be evoqued in the presence of signs such a fever, asthenia, anorexia and cutaneous reaction. The PID should be stopped immediatly but renal failure yet develops. During a PID treatment, frequent evaluation of blood azotemia, creatinine and proteinuria should be performed.

Acute Kidney Injury↗
PubMed1977

[Long-term anticoagulant therapy in subjects over 75 years of age. 100 cases].

100 patients (median age 79 years) were given anticoagulant therapy (ACT) for a period of time averaging 5 years 3 months (522 follow-up years).--Out of 3 522 Quick tests, converted into prothrombin times and all carried out in the same laboratory, the prothrombin time was at or less than 32% in 60.5%, and 34% in 69.6% of the tests.--The mean therapeutic doses were less than 27% of those for adults, and were decreased by 3 mg of phenindione per year over the age of 75, only the actively treated cases being retained.--The risks are the same as those for the middle-aged adult. They depend more on the quality of the investigations than upon age. In the group which has been studied, slight or frank haemorrhagic complications (0.05/year/patient) were the result of a demonstrable overdosage in only one case in four. They were not responsable for any deaths in this series.--because of the referral patterns, the patients studied consisted of 79 with ischaemic heart disease, 27 with peripheral vascular disease, 9 cerebrovascular accidents, and 6 with thrombo-emoblic problems, not counting the 23 complications during the course of the study. In those patients with ischaemic heart disease, well-regulated anticoagulant treatment was associated with a favourable clinical course, and the correlation was significant.--there is not argument against the administering of a full and prolonged course of ACT to a patient of more than 75 years of age.

Age Factors↗
PubMed1976

The influence of fasting and stress on the response of rats to warfarin.

A study was undertaken to investigate the influence of fasting (24 hours), epinephrine (four 0.25 mg/kg s.c. doses at hourly intervals), adrenocorticotropin (two 40 I.U. s.c. doses at 2-hour intervals) and immobilization stress (4 hours) on the response of rats to some coumarin or indanedione anticoagulants. The anticoagulants were always administered first and were followed immediately or within the next hour by the appropriate challenge. Fasting produced a significant enhancement of the antiprothrombin response to warfarin (0.5 mg/kg i.v. or 0.75-3.0 mg/kg s.c.), bishydroxycoumarin (7.5 mg/kg i.p. or 10 mg/kg s.c.) and phenindione (40 mg/kg p.o). Epinephrine and immobilization stress, but not adrenocorticotropin, similarly prolonged the prothrombin time after warfarin (0.75-3.0 mg/kg s.c.). When used in the absence of anticoagulants, all challenges had no effect on the prothrombin time. In addition, fasting did not affect the response of anticoagulated animals to vitamin K. Plasma free fatty acids were significantly increased by the various challenges. The binding constant of warfarin to undiluted plasma proteins were decreased from the control value by a factor of 1.7 and 2.0 as a result of immobilization stress and fasting, respectively. Fasting per se increased the amount of bound endogenous free fatty acids per mole of protein; the latter parameter was further increased in the presence of warfarin. The present data show that fasting and stress enhance the anticoagulant response to warfarin and suggest that this might be due to an interference of endogenous free fatty acids with binding of warfarin to plasma proteins.

Adrenocorticotropic Hormone↗
PubMed1977

Pulmonary embolism and its prophylaxis following the Charnley total hip replacement.

The incidence of pulmonary emboli after a standardized technique of total hip replacement in a series of 7,959 hip arthroplasties operated on between 1962 and 1973 was 1.04% fatal and 7.89% non-fatal. 1,174 had no prophylaxis against embolism with a fatality rate of 2.3% and non-fatal embolism in 15.2%. Phenindione, intravenous heparin and dextran all reduced the complication rate to about 1% fatal and 8% non-fatal but none was statistically better than another. Statistically, plaquenil (hydroxychloroquine sulphate), was as good as any of the other methods used and had few complications. Analysis of the blood groups, pre and post-operative hemoglobin levels, major and revision surgery showed little relationship to the incidence of embolism. The most frequent time of onset of embolism (75%) occurred in the second and third postoperative weeks with only 10% in the first week.

Blood Transfusion↗