Pentoxifylline (PTX)--an alternative treatment in Graves' ophthalmopathy (inactive phase): assessment by a disease specific quality of life questionnaire and by exophthalmometry in a prospective randomized trial

PURPOSE: To investigate the effect of pentoxifylline (PTX) in subjects with inactive Graves' ophthalmopathy (GO) through a specific quality of life (QOL) questionnaire and exophthalmometry readings. METHODS: Eighteen females were randomly divided in two groups. Group A (n=9) was treated with PTX 1200 mg orally/day for 6 months. Group B (n=9) received placebo during the initial 6 months and then PTX for another 6 months. Proptosis measurements were carried out every 3 months and a questionnaire graded from 0 to 10 according to the severity of the symptoms was performed at baseline and after placebo and PTX administration. RESULTS: At baseline, Group A questionnaire score values were 5.5 (median; range 3.5 to 8.0), and 5.0 after 6 months (3.0 to 6.0; p=0.01). In Group B, baseline values were not significantly different after 6 months of placebo: 6.0 (4.5 to 7.0) and 5.5 (4.5 to 7.0), respectively. However, a significant change was observed 6 months after PTX: 4.0 (2.0 to 5.0; p<0.001). Patients in Group A had a progressive improvement of proptosis during PTX: at baseline, 23 mm (median; range 20 to 32); after 3 months, 23 mm (18 to 30; p=0.02); and after 6 months, 23 mm (18 to 30; p=0.005). In Group B, proptosis remained stable during placebo: at baseline, 23 mm (21 to 25); after 3 months, 23 mm (20 to 25); and after 6 months, 23.5 mm (20 to 25). A significant change was observed after 3 and 6 months of PTX: 22 mm (19 to 24; p=0.0006) and 20.8 mm (17 to 25; p=0.0003), respectively. CONCLUSIONS: Pentoxifylline seems to improve the QOL of patients in the inactive phase of GO. The objective findings of the proptosis readings corroborate to suggest that PTX may be an effective and promising drug in the inactive phase of GO.     

Techniques and complementary techniques. Fiberoptic bronchoscopy in mechanically ventilated children

Fiberoptic bronchoscopy can be performed at the patient's bedside. This technique allows direct visualization of the upper and lower airways up to the segmental and subsegmental bronchi. Its most frequent indications are airway examination ot evaluate damage produced by toxins or the endotracheal tube, patency of the endotracheal tube and extubation failure. It is also used to obtain microbiological samples, facilitate intubation when difficult, aspirate airway sections or mucus plugs, perform bronchoalveolar lavage and administer drugs. With prior preparation, adequate monitoring and sedation, material according to the size of the patient and correct techniques, there are few complications. However, the procedure can produce trauma and obstruction of the airway, bronchial hemorrhage, barotrauma, loss of alveolar recruitment, bronchospasm, hypoxemia, bradycardia, and bronchopulmonary infection.     

Three-wall decompression technique using transpalpebral and endonasal approach in patients with Graves' ophthalmopathy

PURPOSE: To evaluate the effects of the three-wall decompression technique using transpalpebral and endonasal approach in patients suffering from Graves' ophthalmopathy. METHODS: In this prospective study, we present a consecutive series of 15 subjects (17 eyes) who were submitted to orbital decompression by removing the inferior and lateral walls using transpalpebral incision combined with a transnasal endoscopic resection of the medial wall. The surgical technique involved the preservation of the bone structure between the lamina papyracea of the ethmoid and the maxillary orbital floor. MAIN RESULTS: The mean ocular recession based on Hertel measurements was 6.00 mm (range, 4-9 mm). None of the patients presented pre-operation diplopia, and one developed post-operation diplopia. Visual acuity was preserved in all cases. CONCLUSION: It is safe and efficient to perform three-wall decompression, combining transpalpebral and endoscopic transnasal approach, with preservation of the bone structure and the bone lateral to the infraorbital canal with fixation by two titanium plates on the lateral edge and removal of intraorbital fat, which results in significant proptosis reduction and minimal complications.     

Leserbrief Zum Beitrag von W. Harth und R. Linse: “Botulinophilie” Der Hautarzt (2001) 52:312–316

Ohne Zusammenfassung     

白三烯抑制剂在哮喘治疗中的进展

目的：介绍白三烯抑制剂治疗哮喘的进展。方法：综述近年来国外有关文献,介绍和评价白三烯抑制剂的临床疗效,不良反应和用法用量。结果：白三烯抑制剂有效地治疗哮喘发作,且副作用较少。结论：白三烯抑制剂临床使用安全有效,是一类新的哮喘治疗药物。     

Oleamide activates peroxisome proliferator-activated receptor gamma (PPARγ) in vitro

Background

Lipid metabolism is altered in subjects with liver steatosis. FAS is a key enzyme in de novo lipogenesis and both FAS gene expression and enzymatic activity are primarily regulated by metabolic signals in the liver. Lipoprotein lipase (LPL), the rate-limiting enzyme for the hydrolysis of core triglycerides, plays a pivotal role in lipid metabolism. This study aims to investigate if circulating levels of FAS and LPL could be clinically associated with liver steatosis.

Methods

In this work, we present data obtained from a subsample of 94 subjects with liver steatosis enrolled by NUTRIEPA study, a nutritional trial in subjects with liver steatosis. Serum levels of FAS protein and LPL activity were evaluated by ELISA test and by a fluorescent method, respectively. The diagnosis and the degree of liver steatosis were based on laboratory and ecographic measurements. Statistical methods included Kruskal-Wallis analysis of variance and Wilcoxon signed-rank test, where appropriate. The ?? ² test has been performed to analyse categorical variables.

Results

The subjects with severe steatosis had significantly higher serum levels of FAS protein and LPL activity compared to subjects with mild and moderate liver steatosis. Moreover, a positive trend in serum levels of FAS expression from lower to higher degree of steatosis was also detected.

Conclusions

We describe a relationship between human liver steatosis and elevated levels of circulating lipogenic enzymes. Increased serum levels of FAS expression and LPL activity could be considered a marker of severe liver steatosis.     

Moderate Ingestion of Alcohol Is Associated With Acute Ethanol‐Induced Suppression of Circulating CTX in a PTH‐Independent Fashion

The “J shape” curve linking the risk of poor bone health to alcohol intake is now well recognized from epidemiological studies. Ethanol and nonethanol components of alcoholic beverages could influence bone remodeling. However, in the absence of a solid underlying mechanism, the positive association between moderate alcoholic intake and BMD remains questionable because of confounding associated social factors. The objective of this work was to characterize the short‐term effects of moderate alcohol consumption on circulating bone markers, especially those involved in bone resorption. Two sequential blood‐sampling studies were undertaken in fasted healthy volunteers (age, 20–47 yr) over a 6‐h period using beer of different alcohol levels (<0.05–4.6%), solutions of ethanol or orthosilicic acid (two major components of beer), and water ± calcium chloride (positive and negative controls, respectively). Study 1 (24 subjects) assessed the effects of the different solutions, whereas study 2 (26 subjects) focused on ethanol/beer dose. Using all data in a “mixed effect model,” we identified the contributions of the individual components of beer, namely ethanol, energy, low‐dose calcium, and high‐dose orthosilicic acid, on acute bone resorption. Markers of bone formation were unchanged throughout the study for all solutions investigated. In contrast, the bone resorption marker, serum carboxy terminal telopeptide of type I collagen (CTX), was significantly reduced after ingestion of a 0.6 liters of ethanol solution (>2% ethanol; p ≤ 0.01, RM‐ANOVA), 0.6 liters of beer (<0.05–4.6% ethanol; p < 0.02), or a solution of calcium (180 mg calcium; p < 0.001), but only after calcium ingestion was the reduction in CTX preceded by a significant fall in serum PTH (p < 0.001). Orthosilicic acid had no acute effect. Similar reductions in CTX, from baseline, were measured in urine after ingestion of the test solutions; however, the biological variability in urine CTX was greater compared with serum CTX. Modeling indicated that the major, acute suppressive effects of moderate beer ingestion (0.6 liters) on CTX were caused by energy intake in the early phase (～0–3 h) and a “nonenergy” ethanol component in the later phase (～3 to >6 h). The early effect on bone resorption is well described after the intake of energy, mediated by glucagon‐like peptide‐2, but the late effect of moderate alcohol ingestion is novel, seems to be ethanol specific, and is mediated in a non–calcitonin‐ and a non–PTH‐dependent fashion, thus providing a mechanism for the positive association between moderate alcohol ingestion and BMD.     

METHYLATION STATUS OF BCL6 DISTINGUISHES DNA SAMPLES FROM BENIGN AND MALIGNANT LYMPHOPROLIFERATIVE DISORDERS

INTRODUCTION: Core biopsy of the breast has become the method of choice for tissue diagnosis of screen detected microcalcifications and some mass lesions in many breast assessment centres. Biopsy results are not available until the following day. Imprint cytology of fresh breast core samples allows same-day reporting and patient counselling.
AIM: To determine the accuracy of core imprint cytology when compared with core biopsy diagnosis when used in a breast assessment centre setting.
METHODS: Core imprints (CI) were prepared and reported on all fresh core biopsies (CB) performed at the Sir Charles Gairdner Hospital Breast Centre from May to December 2000. Fresh core samples were placed on a glass microscope slide. Core radiographs were taken for microcalcification lesions (MC). A laboratory technician gently and quickly rolled the cores on the slide with fine forceps. The cores were fixed in formalin, processed and reported next day. The imprint slide was air dried and stained with DiffQuik. CI were reported using four categories: Insufficient, Benign, Indeterminate and Malignant. Counselling and planning for management were possible on the same day in women with malignant diagnoses. Clinicians were advised not to discuss negative or indeterminate CI results with women and to defer to the final CB report.
RESULTS: Cores were performed on 381 lesions. There were 83 carcinomas (38 in MC and 45 in masses) and 56 were called malignant on CI (absolute sensitivity 67.5%; 78.9% for MC and 57.8% for masses). 3 malignancies on CB were negative on CI giving a false negative rate of 3.6%. There were no false positive diagnoses. The predictive value of a benign diagnosis was 95.3%. There were no adverse effects in the histology of CB.
CONCLUSION: CI was an accurate method of providing an immediate diagnosis of malignancy in two thirds of malignancies confirmed on CB.     

High glucose enhances inducible nitric oxide synthase expression. Role of protein kinase C-betaII

The aim was to determine whether high glucose levels interfere with nitric oxide (NO) production and inducible NO synthase (iNOS) protein expression in interleukin-1beta-stimulated vascular smooth muscle cells from normotensive Wistar Kyoto and spontaneously hypertensive rats. Cells were incubated with either normal (5.5 mM) or high (22 mM) d-glucose for 72 h and with interleukin-1beta (10 ng/ml) for the last 24 h. High glucose increased nitrite levels, iNOS expression and protein kinase C activity in cells from normotensive rats and had no effect in cells from hypertensive rats. High glucose effects on nitrite production and iNOS expression was abolished by the selective inhibitor for the protein kinase C-betaII, 5,21:12,17-dimetheno-18H-dibenzo[i,o]pyrrolo[3,4-1] [1,8]diacyclohexadecine-18,20 (19H)-dione, 8-[(dimethylamino) methyl]-6,7,8,9,10,11-hexahydro-monomethanesulfonate (LY379196, 30 nM). Calphostin C (1 microM) and LY379196 (10 microM) reduced nitrite levels and iNOS expression only in cells from normotensive rats treated with both media. These results suggest that high glucose increases inducible nitric oxide synthase induction and subsequent NO production by activating the protein kinase C-betaII; this mechanism seems to be altered in hypertension.