[L-tryptophan and the eosinophilic myalgia syndrome].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to B H Stricker.
Explore the source record for details and available documents.
A 50-year-old healthy woman started daily treatment with six iodine-containing kelp tablets (Kelpasan), containing 200 mg of kelp each, to lose weight; she took no other medication. Within two months she developed clinical and laboratory evidence of hyperthyroidism, which resolved spontaneously following discontinuation of the tablets. A causal relationship between the intake of the kelp preparation and the thyrotoxic episode could not be established beyond all possible doubt, but the clinical picture and clear temporal relationship strongly pointed in this direction.
The case history is presented of a woman who developed an anaphylactic reaction after intake of floctafenine (Idalon). Thirty minutes after the ingestion of one tablet an urticarial rash appeared and shortly thereafter the patient became unconscious. Since 1976 12 similar cases have been reported to the Netherlands Centre for Monitoring of Adverse Reactions to Drugs. The chemical structure of floctafenine strongly resembles that of glafenine (a well-known cause of anaphylaxis) and the adverse reaction profile is probably similar. It is uncertain, however, whether anaphylactic reactions develop as frequently to floctafenine as to glafenine.
Three female patients had serious anaphylactic reactions to sclerotherapy with polidocanol (Aethoxysklerol) within 15 minutes after administration for varicose veins in the legs. Two of them received the drug for the first time. The first patient developed cardiac arrest which was successfully treated. The second patient showed signs of an adult respiratory distress syndrome, while in the third the ECG was compatible with cardiac ischaemia. Recovery was complete and uneventful in all patients. The incidence of allergic reactions to polidocanol has been estimated at 1:10,000. In view of the considerable underreporting of adverse reactions we feel that the frequency of severe anaphylactic reactions to this drug may be underestimated.
We describe two patients who developed acute renal failure during therapy with fumaric acid-esters. Histologic findings after renal biopsy in one patient were compatible with the diagnosis of acute tubular necrosis (ATN), and renal function was restored after cessation of the medication. The histologic diagnosis in the other patient was tubulo-interstitial nephritis (TIN), possibly reactive to ATN. The recovery of renal function was incomplete after 9 months. Two other patients had deterioration of renal function and proteinuria during therapy with fumaric acid-esters. The symptoms were completely reversible in one patient after discontinuation of the medication, and incompletely reversible in the other. The literature is reviewed and a comparison is drawn with the maleic acid model in the rat.
Four patients developed apnoea after epidural administration of 50 micrograms of sufentanil. In three of these patients apnoea occurred within two minutes after administration. In all cases catheter position was verified to be in the epidural space. It is possible that accumulation plays a causative role in some of those cases in which the drug is given on demand. Because sufentanil-induced apnoea may occur fast and unexpected it is advised that patients should be kept under close supervision for at least two hours following administration.
Explore the source record for details and available documents.
Five case histories are presented of patients developing cholestatic hepatitis associated with the intake of the antibiotic combination agent amoxicillin and clavulanic acid (Augmentin). In two of these cases, signs of hepatic injury recurred after readministration of this combination but not after the intake of amoxicillin alone. In none of the patients was another cause for cholestatic hepatitis found and extrahepatic causes were excluded by ultrasonography, CT scanning, or ERCP. Most viral causes of hepatic injury were excluded in these patients. With the exception of one patient, who developed a transient rash, no immunoallergic signs were present. Biopsy in two patients showed extensive cholestasis without significant necrosis. Clavulanic acid seems to be responsible for this adverse effect.
To test the hypothesis that allopurinol-associated granulomatous hepatitis may present itself with fibrin-ring granulomas, we requested details of such cases, as reported to the World Health Organization, from 13 national adverse reaction monitoring centers, and as reported in the literature. Details and histology of 6 cases were obtained and reviewed. All consisted of acute hypersensitivity signs with fever, rash, arthralgia, or eosinophilia as hallmarks, starting within 6 wk of commencing treatment with allopurinol. In all cases there were either epithelioid granulomas or granulomalike lesions, but none of these contained fibrin rings. It is concluded that, if fibrin-ring granulomas are a manifestation of allopurinol-induced granulomatous hepatitis, this feature is probably uncommon.
We report a patient with Crohn's disease in whom repeated liver biopsies taken at surgery for the bowel disease showed progressive hepatic fibrosis of an unusual type. Dense collagen was deposited in the perisinusoidal space often surrounding individual hepatocytes. The aetiology and pathogenesis of this abnormality remain speculative.
The case history is presented of a patient who developed a maculopapular rash following treatment with 3 different coumarin derivatives. Apparently cross-sensitivity between coumarin derivatives may occur.
During 1981 to mid-1988 three cases of anaphylactic shock after treatment with the quinolone derivative cinoxacin were reviewed by the Netherlands Centre for Monitoring of Adverse Reactions to Drugs and 17 cases of an anaphylactic type of reaction notified to the World Health Organisation Collaborating Centre for International Drug Monitoring. In five out of six patients for whom data were available the reaction began shortly after taking a single capsule of a second or next course of treatment. Cinoxacin is related to nalidixic acid, and one patient previously treated with that agent subsequently had an anaphylactoid reaction to cinoxacin and later developed a skin reaction to nalidixic acid. There were no deaths, and patients treated as an emergency with plasma expanders or with adrenaline and corticosteroids generally recovered promptly and uneventfully. In view of the potentially fatal consequences of anaphylactic reactions to cinoxacin and other quinolones doctors should take care when prescribing these drugs.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.