[Treatment of testicular hydrocele with aspiration and injection of polidocanol (Ethoxysclerol)].
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Biomedical subjects
Publications and source records attributed to L Lund.
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A case of toxic shock syndrome (TSS) with meningismus as main symptom is presented. The case illustrates that, in cases of rigidity of the neck and back, not directly explainable, TSS should be considered as a possible diagnosis. Toxic syndrome (TSS) is a severe, acute infectious disease with great variations in symptomatology (1,2). Its lethality is approximately 5% (3). The prognosis depends on early diagnosis and treatment.
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Fasting serum lipids, apolipoproteins and glycosylated serum proteins were studied in 20 women before, after three months of treatment and two months after termination of treatment with oral contraceptives containing 30 micrograms ethinyloestradiol (EE) plus 150 micrograms levonorgestrel or desogestrel. Levonorgestrel + EE induced significant increases in total triglycerides (48%), apoB (19%) and the ratio apoB/apoA-I (18%) and no significant changes in HDL-cholesterol (8% decrease), apoA-I, % HDL-cholesterol, total cholesterol and serum glycosylated proteins. Desogestrel + EE induced significant increases in HDL-cholesterol (12%), % HDL-cholesterol (15%), triglycerides (35%) and apoA-I (20%), no changes in total cholesterol, apoB and glycosylated serum proteins and a significant decrease in the ratio apoB/apoA-I (17%). Two months after termination of treatment the values for all parameters for both preparations were similar to those observed before treatment. The differences between the effects of the two preparations on the parameters HDL-cholesterol, % HDL-cholesterol, apoA-I, apoB and the ratio apoB/apoA-I were statistically significant and can be explained by a difference in the intrinsic androgenicity of the two progestagens.
The oral administration of 150 micrograms desogestrel and 30 micrograms ethinyl estradiol (EE2) increases (P less than 0.001) serum concentrations of sex-hormone-binding globulin (SHBG) and corticosteroid-binding globulin (CBG), whereas treatment with 150 micrograms levonorgestrel and 30 micrograms EE2 only increases serum CBG concentrations. No changes in serum albumin concentrations occurred during or after treatment with either preparation, and increases in SHBG and CBG returned to the pretreatment values 1 month after treatment ceased. The serum distribution of levonorgestrel was unchanged during treatment, whereas the increase in serum SHBG concentrations after treatment with the preparation containing desogestrel decreased (P less than 0.001) the percentage of non-protein-bound 3-keto- desogestrel and the percentage of albumin-bound 3-keto- desogestrel but increased (P less than 0.001) the SHBG-bound fraction. Oral contraceptives containing either progestogen decrease the mean serum non-protein-bound testosterone concentrations, especially during treatment with desogestrel (P less than 0.001), and desogestrel may therefore by the more appropriate progestogen for the treatment of women prone to androgenic side effects.
Clinical cases of lactation failure in sows from 6 swine herds in Illinois were investigated for the presence of bacterial endotoxins in blood and the concurrent microbial status of uterus, milk, and intestine. Twenty-five affected sows were compared with 13 contemporary healthy sows (controls) in the same herds. A higher prevalence of bacterial endotoxin in blood of affected sows than in the controls, although not statistically significant, supported earlier theories of endotoxin involvement in the disease. Further, a positive relationship was noticed between prevalence of solely gram-negative bacteria in ileum and milk and development of dysgalactia and endotoxemia. No such relationship was found for bacterial isolates from the uterus, suggesting lack of association between lactation failure and metritis.
The effects of the oral contraceptive combinations of 0.125 mg desogestrel + 0.050 mg ethinylestradiol (EE), and of 0.125 mg levonorgestrel + 0.050 mg EE on serum cortisol and the urinary excretion of 17-oxogenic steroids and free cortisol were studied in 16 healthy females. Adrenal responsiveness was studied by the metyrapone test. Both contraceptive combinations increased (P less than 0.001) serum cortisol concentrations but the rhythmic fluctuation at different times of the day remained unchanged. The urinary excretion of 17-oxogenic steroids was lower (P less than 0.01) during treatment than before or after treatment with both contraceptive combinations. The metyrapone test showed normal adrenal responsiveness during the treatment cycles. The urinary excretion of free cortisol was unchanged when desogestrel + EE was used, but increased (P less than 0.01) during treatment with levonorgestrel + EE. However, even then, the urinary free cortisol was within the normal range of the population. All the test results of hormone determinations normalized soon after finishing the contraceptive treatments. It is suggested that the abnormalities seen were due to an increased serum binding capacity of cortisol induced by EE and not a sign of pathological changes in adrenal function. No major differences in the biological effects of the two combinations tested were seen.
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Carbamazepine and its epoxide in plasma were measured by liquid chromatography in 25 patients treated with a mean dose of carbamazepine of 12.5 +/- 3.3 mg/kg body weight. The mean concentrations of parent drug and metabolite were 5.4 +/- 2.5 mug/ml and 1.10 +/- 0.42 mug/ml, respectively. A singificant correlation was found between the plasma concentrations of the two compounds (r = 0.64; p less than 0.001), but marked interindividual variation existed in the ratio of carbamazepine to carbamazepine to epoxide. Based on simultaneous measurements in plasma and cerebrospinal fluid, the unbound fraction of carbamazepine in plasma was of the order of 20% as compared to 45% for the epoxide. Thirteen ambulant patients suffering from partial epilepsy with complex symptomatology, who were already being treated with phenytoin in optimal doses (plasma level 14-20 mug/ml) were also given carbamazepine. At plasma levels of the latter of about 5 mug/ml there was no further reduction in the frequency of partial or generalized epileptic seizures. In five patients the dose was increased to produce plasma concentrations of 7 - 8 mug/ml. There was still no improvement and side-effects were seen in three patients.
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