A Case of Lichenoid Drug Eruption Caused by Allopurinol / 대한피부과학회지

Lichenoid drug eruption is a lichenoid skin eruption caused by certain drugs and compounds, and can be similar to lichen planus. A 51-year-old man who had taken antihypertensive drugs (enalapril, dilazep dihydrochloride) and cholesterol lowering drug (atorvastatin) for 4 years had received allopurinol for asymptomatic hyperuricemia for 4 months. He developed pruritic erythematous papules and plaques with silvery scales on the face, trunk and extremities after taking allopurinol for 3 months. He had no fever, no eosinophilia and no systemic abnormalities. Histopathologic findings showed hyperkeratosis, parakeratosis, hypergranulosis, band-like lymphohistiocytic infiltration and perivascular lymphohistiocytic infiltration in the dermis, which were compatible with lichenoid drug eruption. The skin rashes disappeared after he stopped taking allopurinol and was treated with steroids.

Cross over placebo control trial of dilazep in beta-thalassemia/hemoglobin E patients.

An attempt was made to find better symptomatic treatment for beta-thalassemia/hemoglobin E (beta-thal/Hb E) patients in order to reduce their blood demand. Oral administration of dilazep was prescribed for these patients and a clinical trial was conducted over a 2-year period as a cross over placebo control study. Seventeen beta-thal/Hb E patients were enrolled in the study. All of them received dilazep and placebo for 10 months at different periods of time and were taken care of by the same doctor throughout the study. The blood demand of the same patients during the period of receiving dilazep with the period of receiving placebo, was 1.5 +/- 1.8 U/10 months versus 2.2 +/- 2.6 U/10 months, respectively. Thus dilazep showed a benefit in decreasing the blood demand by about 50% although the results did not reach statistical significance (p = 0.1). There was a statistical difference in hemoglobin concentration of the patients receiving dilazep compared with placebo (p = 0.038). While receiving dilazep the mean +/- SD hemoglobin level was 5.82 +/- 0.8 g/dl, significantly higher than while receiving placebo (5.66 +/- 0.9 g/dl) (p = 0.038). The liver, and renal function tests, and cardiac enzyme levels of the patients showed no significant changes throughout the study. However, one case had a problem with bleeding following tooth extraction whilst receiving dilazep and needed 1 unit of blood transfusion. In conclusion, administration of dilazep to patients with beta-thal/Hb E increased the patients' hemoglobin and reduced their blood demand with few side effects.

A double-blind placebo control trial of dilazep in beta-thalassemia/hemoglobin E patients.

Since the obtained results from the pilot study indicated that dilazep which was a membrane stabilizer would be benefit to treatment and prevention of anemia and chronic leg ulcer in beta-thalassemia/hemoglobin E (beta-thal/HbE) patients, the authors had continued the study in a second phase, ie a double blind placebo control trial. Twenty-seven beta-thal/HbE patients were recruited in the study. Eight patients who suffered from chronic leg ulcer were given dilazep. The rest of patients were given dilazep or placebo according to a randomized table. Hence, 16 patients received dilazep and 11 received placebo. When we compared the number of unit of blood transfusion, hemoglobin level, 2-3 DPG and P50 value between the dilazep and placebo groups using unpaired t-test, we found that there were no statistical differences in any of the parameters. However, when we compared the data within the group using paired t-test, there was statistical decrease in blood requirement after treatment in the dilazep group (p < 0.05). Concerning with the treatment of chronic leg ulcer, 3 in 8 patients were completely healed within 3 months, 4 in 8 patients were improved and 1 in 8 patients was not improved. There were complaints of skin itching and mild epigastric pain in placebo group but the liver function tests, kidney function tests and cardiac enzyme did not significantly change during the medication.

Cytoprotective effect of dilazep on hydrogen peroxide-perturbed vascular endothelial cells.

The effect of dilazep and dimethyl thiourea (DMTU) on the hydrogen peroxide-derived injury of culture pulmonary artery epithelial cells (CPAEC) was assessed by colorimetric assay of MTT formazan (MTT formazan assay). When CPAEC were treated with hydrogen peroxide, neither cell lysis nor detachment of the cells from surface of the well was observed. However, the MTT formazan formation was decreased in a time and dose dependent manner. The decrease in the formation was significantly suppressed in the presence of dilazep (0.1 to 10 microM) or DMTU (0.01 to 0.3 microM). CPAEC treated with hydrogen peroxide in the same way enhanced an activation of prothrombin, and this enhancement was significantly inhibited in the presence of dilazep (1 to 3 microM). These data indicate that dilazep exerts a cytoprotective effect against challenges of intracellular oxidant produced by hydrogen peroxide and suppresses augmented procoagulant activity of injured cells.

Increase in spontaneous platelet aggregation in beta-thalassemia/hemoglobin E disease: a consequence of splenectomy.

Clinical symptoms related with disturbances of the circulatory system are often observed in beta-thalassemia/hemoglobin E (beta-thal/HbE) patients after splenectomy. Pulmonary thrombosis is one of the important contributing factors. However, the pathogenesis of this phenomenon was not known. Previous studies on platelet functions were controversial as platelet-rich plasma (PRP) was employed for all of the studies. By centrifugation, most of the hyperactive platelets were excluded before platelet aggregation tests were performed. Besides, the role of red cells related to platelet aggregation was not investigated. In this study, a platelet function test was designed to avoid these two handicaps of previous work as mentioned, by using whole blood from 15 normal and 40 beta-thal/HbE patients (15 nonsplenectomized and 25 splenectomized) to study spontaneous platelet aggregation. The principle of the test was to evaluate platelet number in whole blood by electronic platelet counter at time 0 (45 minutes after blood collection) and this number was used as 100% of free unaggregated platelets. Then the same specimen of whole blood was incubated at 37 degrees C with continuous stirring by magnetic stirrer in an aggregometer for 8 minutes; at 1 minute intervals free unaggregated platelets were evaluated and calculated as a percentage of the initial control value. The results indicated increased spontaneous platelet aggregation in whole blood of post-splenectomized beta-thal/HbE patients. The residual free platelet number were 24% at 8 minutes after incubation. Effects of red blood cells on spontaneous platelet aggregation were studied by mixing autologous beta-thal/HbE red cells obtained from splenectomized and non-splenectomized patients with platelet rich plasma.(ABSTRACT TRUNCATED AT 250 WORDS)