The prevalence of sleep impairments and predictors of sleep quality among patients with asthma.

BACKGROUND: Sleep is a significant dimension of daily life. However, only a few studies have examined the sleep quality of asthmatics in a real-world clinical settings. OBJECTIVE: This study is aimed to estimate the prevalence of sleep impairments among asthmatic patients and examine the relationship between sleep quality, asthma control, rhinitis symptoms, and sociodemographic characteristics. METHODS: The present study adopted the observational cross-sectional research design that has been designed by the Italian Respiratory Society and used valid assessments to measure the study variables. RESULTS: Data from 1150 asthmatic patients (mean age 51.01 years ± 16.03) were subjected to analysis. 58.3% of the patients had impaired sleep quality (Pittsburgh Sleep Quality Index [PSQI] total scores > 5), and their mean PSQI score was 5.68 (SD = 3.4). A significant correlation emerged between sleep quality and asthma control (p = 0.0001) and a significant albeit weak correlation emerged between PSQI total scores and Total 5 Symptoms Score (r = 0.24, p = 0.0001). Sleep quality was significantly associated health-related quality of life [HRQoL]. (r = 0.50, p < 0.001). After exclusion of patients at risk for Obstructive Sleep Apnea Syndrome (OSAS) and Gastro Esophageal Reflux Disease (GERD), the most important determinants of PSQI score were HRQoL, In the entire sample asthma control is the strongest predictor of both sleep quality and HRQoL. CONCLUSIONS: The results of this real-world study highlight the prevalence, impact and predictors of sleep disturbances in asthmatic patients and suggest the need for physicians to detect poor sleep quality.

Association of TCF7L2 gene variants with low GAD autoantibody titre in LADA subjects (NIRAD Study 5).

AIMS: We previously demonstrated the presence of two different populations among adult-onset autoimmune diabetes (latent autoimmume diabetes of adults; LADA) having high or low titre of antibodies to glutamic acid decarboxylase (GADA). The transcription factor 7-like 2 (TCF7L2) gene has been recognized as the major gene associated with Type 2 diabetes. The aim of the present study was to evaluate whether the phenotypic heterogeneity of LADA based on GADA titre is associated with TCF7L2 polymorphisms. METHODS: Two hundred and fifty patients identified as LADA, divided into two subgroups with low (< or = 32 arbitrary units) or high (> 32 units) GADA titre, 620 subjects with Type 2 diabetes [from the Non-Insulin Requiring Autoimmune Diabetes (NIRAD) study cohort of 5330 subjects] in addition to 551 consecutive cases of Type 1 diabetes and 545 normoglycaemic subjects were analysed for the rs12255372 and rs7903146 polymorphisms of the TCF7L2 gene using Taqman. RESULTS: The genotype and allele distributions of the two polymorphisms revealed similar frequencies in subjects with low GADA titre and Type 2 diabetes. High GADA titre, Type 1 diabetes and controls also showed comparable frequencies. A significant increase of GT/TT genotypes of the rs12255372 single-nucleotide polymorphism (SNP) and CT/TT genotypes of the rs7903146 SNP was observed in low GADA titre and Type 2 diabetes compared with high GADA titre, Type 1 diabetes and controls (P < or = 0.04 for both comparisons). The risk alleles of both variants were increased in low GADA titre and Type 2 diabetes compared with high GADA titre, Type 1 diabetes and control subjects (P < 0.02 for all comparisons). CONCLUSIONS: TCF7L2 common genetic variants of susceptibility are associated only with low GADA antibody titre in LADA patients.

Early Results of Mechanochemical Ablation with Flebogrif® in great Saphenous Vein Insufficiency: does Polidocanol Concentration Affect Outcome?

BACKGROUND: Flebogrif® (Balton, Poland) is a novel mechanochemical ablation (MOCA) device for saphenous vein insufficiency. It combines endothelial damage performed by radial retractable cutting hooks together with chemical ablation through sclerosant injection of 3% polidocanol foam according to its IFU. The objective of this study is to evaluate Flebogrif's efficacy in terms of recanalization rate and recurrence by varying polidocanol foam concentrations. METHODS: We performed 24 MOCAs on 23 patients with Flebogrif® between January and May 2019. In 12 cases the polidocanol foam was prepared at a 3% concentration, and in another 12 at 1.5%. Great saphenous vein (GSV) recanalization and truncular recurrence were evaluated at 1 and 3 months with a Duplex Ultrasound Anatomy (DUS) examination. RESULTS: At 1- and 3-month follow-ups, none of the 14 patients treated with the polidocanol 3% foam were observed to have had great saphenous vein GSV recanalization and truncular recurrence. Only 2 of the 14 (14.3%) cases treated with polidocanol 1.5% foam showed evidence of recanalization within the first centimetres from the sapheno-femoral junction (p > .05). All patients experienced clinical benefits without recurrence of symptoms. CONCLUSION: MOCA with Flebogrif® is a safe, relatively inexpensive and effective alternative to standard methods in the treatment of saphenous insufficiency with encouraging short-term results. Despite our relatively small patient sample, no statistical significance in evidence of recurrence in the group of patients treated with 3% foam and those treated with 1.5% foam was noted. Longer term analysis of GSV patency and recurrence is necessary to further evaluate Flebogrif's impact and actual indications in the treatment of chronic venous disease.

Standard Carotid Endarterectomy versus Carotid Artery Stenting with Closed-Cell Stent Design and Distal Embolic Protection: does the age matter?

Carotid artery endarterectomy (CEA) is considered the gold standard for treatment of symptomatic and asymptomatic carotid disease. Carotid artery stenting (CAS) is a less invasive approach and therefore could be considered a viable alternative to CEA, especially in high-risk patients or those with relative contraindications to CEA (i.e. actinic stenosis, post-CEA restenosis, previous neck or tracheostomy surgery, contralateral laryngeal nerve paralysis, etc.). METHODS: The aim of this study is to evaluate the short- and medium-term outcomes of CAS performed with a single type of closed-cell stent design and distal filter protection by comparing the procedure with CEA based upon 3 endpoints: overall survival rate, stroke free survival rate and restenosis free survival rate.The same endpoints were also evaluated in 2 different age groups, more and less than 70 years, to show possible age-based differences on outcomes.Among 105 patients (77 males, 28 females), 74 were submitted to CEA and 31 were subject to CAS.In all cases the same self-expanding stent with closed-cell design (XACT Carotid Stent, Abbott Vascular) and the same distal embolic protection device (Emboshield NAV, Abbott Vascular) were employed. RESULTS: At 12 months, no statistically significant difference was observed in overall survival rates (CEA 93.2% vs CAS 93.5%, p=0.967) and restenosis free survival rates (CEA 94.5% vs CAS 96.8%, p=0.662).An increased stroke free survival rate was observed in the CEA group when compared to the CAS group (CEA 100.0% vs CAS 93.5%, p=0.028).The age-based endpoints didn't show any significant difference. CONCLUSION: These results suggest that CEA still remains the gold standard of treatment for carotid stenosis given its greater efficacy in the prevention of stroke CAS. However, CAS could be considered as an alternative treatment to CEA to be used in select cases only.

High-pressure, high-temperature molecular doping of nanodiamond.

The development of color centers in diamond as the basis for emerging quantum technologies has been limited by the need for ion implantation to create the appropriate defects. We present a versatile method to dope diamond without ion implantation by synthesis of a doped amorphous carbon precursor and transformation at high temperatures and high pressures. To explore this bottom-up method for color center generation, we rationally create silicon vacancy defects in nanodiamond and investigate them for optical pressure metrology. In addition, we show that this process can generate noble gas defects within diamond from the typically inactive argon pressure medium, which may explain the hysteresis effects observed in other high-pressure experiments and the presence of noble gases in some meteoritic nanodiamonds. Our results illustrate a general method to produce color centers in diamond and may enable the controlled generation of designer defects.

A new variation in the promoter region, the -604 C>T, and the Leu72Met polymorphism of the ghrelin gene are associated with protection to insulin resistance.

OBJECTIVE: Previous studies suggested that polymorphisms in the coding region of the preproghrelin were involved in the etiology of obesity and might modulate glucose-induced insulin secretion. We evaluated the association of a new variation, -604C>T, in the promoter region of the ghrelin gene, of Leu72Met (247C>A) and of Gln90Leu (265A>T), all haplotype-tagging single nucleotide polymorphisms (SNPs), with measures of insulin sensitivity in 1420 adult individuals. RESEARCH METHODS: The three SNPs were genotyped using ABI PRISM 7900 HT Sequence Detection System. We used multiple linear regression analysis for quantitative traits and THESIAS software for haplotype analysis. RESULTS: We observed a protective effect exerted by Met72 variant of Leu72Met SNP on insulin resistance parameters; a significant decreasing trend from Leu/Leu to Leu/Met and to Met/Met homozygous subjects in triglycerides, fasting insulin levels and HOMA-IR index (P=0.02, 0.01 and 0.003, respectively), and, consistently, an increase in ghrelin levels (P=0.003) was found. A significant decrease from CC to TC and to TT genotypes in insulin levels and HOMA-IR index was also detected (P=0.00l for both), but only in subjects homozygous for Leu72, where the protective effect of Met72 was not present. The haplotype analysis results supported the data obtained by the evaluation of each single SNP, showing the highest value of insulin levels and HOMA-IR index in the -604(c)247(c) haplotype intermediate value in -604(T)247(C) and lowest value in -604(C)247(A). CONCLUSION: Our observations suggest a protective role of the Met72 variant and of -604 T allele in modulating insulin resistance. These SNPs or an unknown functional variant in linkage disequilibrium could increase ghrelin levels and probably insulin sensitivity.

A 10-year (1996-2005) prospective study of the incidence of Type 1 diabetes in Moscow in the age group 0-14 years.

AIMS: To provide data on the incidence of Type 1 diabetes (T1D) in Moscow, determined prospectively from 1996 to 2005 for a total of > 10 million subjects aged < 15 years. METHODS: Data on T1D incidence in patients with newly discovered T1D resident in Moscow diagnosed between 1 January 1996 and 31 December 2005 were analysed. Primary ascertainment was based in endocrinology departments of children's hospitals in Moscow. A secondary source were the archives of Moscow Region where patients are registered to obtain exemption from paying for medication. RESULTS: We identified 2031 new cases of T1D patients with a degree of ascertainment through primary and secondary sources of 94%. Overall the incidence rate of the disease was 12.9 per 100,000 per year (95% confidence interval 12.3- 13.4). The cumulative risk of the disease was 0.28 per 1000 in the age group 0-4 years, 0.84 in the age group 5-9 years and 1.8 in the age group 10-14 years. The incidence rate in girls increased by a mean of 6% per year in all age groups (P < 0.05 for all comparisons), whereas in boys it increased by a mean of 7% in the age group 10-14 years. Thirty percent of cases presented with diabetic ketoacidosis and coma at diagnosis, whereas hyperglycaemia without ketonuria was present in 20% of patients. CONCLUSIONS: This is the first study to report on validated incidence data for T1D in Moscow. We conclude that the incidence of T1D in Moscow is comparable to that of those European countries having intermediate incidence rates, and that the incidence is increasing.

Kinesins in neurological inherited diseases: a novel motor-domain mutation in KIF5A gene in a patient from Southern Italy affected by hereditary spastic paraplegia.

Kinesins are a family of proteins for anterograde transport of the molecules from the neuronal cell body and their impairment has been widely associated with neurodegeneration of the motor neurons. KIF5A gene causes autosomal dominant spastic paraplegia 10, a neurological disorder characterized by spasticity and weakness of the lower limbs (SPG10). We carried out a screening of KIF5A gene in 50 subjects affected by HSP negative to diagnostic test for SPG4, ATL1 and REEP1. We identified a novel variation p.Ile255Met in a 58-year-old man who developed progressive gait disturbance due to spastic paraparesis complicated by axonal neuropathy.

Differential roles of splanchnic and peripheral tissues in the pathogenesis of impaired glucose tolerance.

To identify the mechanism(s) of the altered glucoregulatory response to a glucose load in subjects with impaired glucose tolerance, we selectively quantitated the components of net splanchnic glucose balance, i.e., splanchnic glucose uptake and hepatic glucose output, as well as peripheral glucose uptake, by combining [3-3H]glucose infusion with hepatic vein catheterization. After intravenous glucose infusion (6 mg X kg-1 X min-1 for 90 min), blood glucose rose to 172 +/- 7 mg/dl in controls and 232 +/- 13 mg/dl in subjects with impaired glucose tolerance (P less than 0.01). The response of plasma insulin did not differ significantly between the two groups (29 +/- 4 vs. 40 +/- 10 microU/ml at 90 min in control and in glucose intolerant subjects, respectively; P = NS). In both groups, glucose infusion caused the net splanchnic glucose balance to switch from the net output of the basal state to a net glucose uptake. However, this effect was more marked in subjects with impaired glucose tolerance than in control subjects (at 90 min: 2.83 +/- 0.53 vs. 1.60 +/- 0.18 mg X kg-1 X min-1, respectively: P less than 0.05). The different pattern of splanchnic glucose balance was entirely accounted for by a greater rise in splanchnic glucose uptake in the group of glucose intolerants , as the suppression of endogenous glucose output by the glucose load was practically complete in both groups. In contrast, glucose uptake by peripheral tissues increased considerably less in subjects with impaired glucose tolerance than in controls (2.2-2.6 vs 3.6-4.1 mg X kg-1 X min-1, respectively, between 60 and 90 min; P less than 0.01-0.001). Furthermore, a net splanchnic lactate uptake was present in the basal state, which was inhibited by the glucose load and switched to a comparable net lactate output in both groups. These results indicate that the mechanism responsible for the altered glucoregulation in subjects with impaired glucose tolerance resides entirely in the peripheral tissues whose ability to dispose of a glucose load is drastically reduced. On the other hand, no defect is detectable in any of the explored mechanisms regulating splanchnic glucose metabolism during the disposal of an exogenous glucose load.

Adenotonsillectomy for obstructive sleep apnea in children with Prader-Willi syndrome.

The aim of our study was to evaluate the efficacy of adenotonsillectomy for the treatment of obstructive sleep apnea syndrome (OSA) in pediatric patients with Prader-Willi syndrome (PWS), and to describe the postoperative complications. Five patients (4 males; median age, 4.4 years; range, 1.6-14.2 years) were studied. All patients underwent an overnight cardiorespiratory sleep study. All patients had adenotonsillar hypertrophy (ATH), and two were also obese. The preoperative obstructive apnea/hypopnea index (AHI; median and range) was 12.2 (9.0-19.9) events/hr; the mean oxygen saturation was 95 (79-96)%; the nadir oxygen saturation was 71 (58-78)%; and the oxygen desaturation index (ODI) was 15.8 (11.4-35.9) events/hr. Preoperatively, patients were classified as having moderate to severe OSA. A second sleep study, performed 16 (3-43) months after adenotonsillectomy, showed a significant decrease in AHI (P = 0.009) and ODI (P = 0.009). Mean and nadir oxygen saturation did not differ significantly postsurgery (P = 0.188, P = 0.073, respectively). Four out of five children showed at least one postoperative complication. Difficult awakening from anesthesia, hemorrhages, and respiratory complications requiring reintubation and/or supplemental oxygen administration were observed. In conclusion, patients with PWS and OSA who underwent adenotonsillectomy showed a significant decrease in AHI and number of oxygen desaturations.

Oral complications of head and neck radiotherapy: prevalence and management.

AIM: The aim of the study was to evaluate the short-term and long-term toxicity caused by radiation treatment in the head and neck with the technique of intensity-modulated radiotherapy (IMRT). METHODS: We selected 20 patients, 18 men and 2 women aged between 21 and 71 years, undergoing radiation therapy (IMRT) in head and neck. Patients were visited during radiotherapy and followed for six months after the end of the therapy. We assessed the presence of: mucositis, xerostomia, dysgeusia, dysphagia, pain, trismus and, in the case of late-onset complications, radiation cavities. RESULTS: Acute toxicity: in 20 patients, 18 reported mucositis, 19 xerostomia, 17, dysgeusia, 15 dysphagia, 18 had pain and 3 patients had trismus. Tardive toxicity: in 14 patients, 5 reported mucositis, 11 xerostomia, 6 dysgeusia, 2 dysphagia, 3 had pain, 4 trismus and in 4 patients were found radiation cavities. CONCLUSION: Acute complications with higher prevalence were xerostomia (19 of 20 patients), dysgeusia of 2nd grade (11 patients of 20), mucositis of 1st grade and pain of 1st grade (10 patients of 20). Among the late complications it was noted a maintenance of the high prevalence of xerostomia (11 patients of 14) and an increase in prevalence of trismus (4 patients of 14) against a reduction of all other complications. The presence of radiation cavities in 4 patients of 14 was also recorded.

Disordered eating behavior and mental health correlates among treatment seeking obese women.

BACKGROUND AND OBJECTIVES: Previous research has suggest that obesity is associated with increased risk for psychopathological disorders, however, little is known about which obese patients are most vulnerable to psychopathological disorders. We therefore investigated 126 treatment-seeking obese women to describe eating disorder pathology and mental health correlates, and to identify disordered eating behaviors that may place obese at increased risk for psychopathological disorders. MATERIALS AND METHODS: The Structured Clinical Interview for DSM-IV (SCID) was used to identify Eating Disorders (ED). A battery of psychological tests, including the Anxiety Scale Questionnaire (ASQ,) Clinical Depression Questionnaire (CDQ), Eating Disorder Inventory-2 (EDI-2) Eating Attitudes Test-26 (EAT-26) scales and structured clinical interview were administered to all the patients. We analyzed the link between psychopathological disorders and eating attitudes by using both multiple regression analysis and non-parametric correlation. RESULTS: Disordered eating behaviors and emotional behavioral aspects related to Anorexia Nervosa, such as ineffectiveness, are strongly linked to the depression and anxiety in obese subjects. No correlation was found between psychopathological disorders and age or anthropometric measurements. CONCLUSIONS: Findings corroborate earlier work indicating that psychological distress is elevated in obese treatment seeking, bolstering the need for mental health assessment of such individuals. The feeling of ineffectiveness constitutes the major predictor of psychopathological aspects. This is an important result which may inform the development of effective interventions for obese patients and prevention of psychopathological disorders.

Direct assessment of splanchnic uptake and metabolic effects of human and porcine insulin.

The hepatic vein catheterization technique was used to quantitate the splanchnic uptake and the metabolic effects of biosynthetic human insulin (BHI) and porcine insulin (PI) in normal man. BHI and PI were infused into a peripheral vein (0.9-1.3 mU kg-1 min-1) for 60 min together with SRIH (0.6 mg/h) to inhibit endogenous insulin secretion and glucose to induce moderate hyperglycemia (9-10 mmol/liter). During the infusion period, arterial-hepatic venous difference of plasma C-peptide as well as splanchnic C-peptide output fell by more than 98% indicating virtually complete cessation of endogenous insulin release. Under these conditions, the arterial-hepatic venous differences in plasma insulin concentrations represent a valid and direct measurement of splanchnic insulin uptake. During BHI infusion, arterial insulin levels rose to 82 +/- 11 (SE) microU/ml (range: 33-105 microU/ml). Splanchnic insulin uptake paralleled the rise of arterial insulin, reaching 430 +/- 72 microU kg-1 min-1 at 60 min. No appreciable difference between BHI and PI was demonstrable. A highly significant correlation between arterial insulin concentrations and splanchnic insulin uptake was found (r = 0.816; P less than 0.001). Accordingly, both fractional splanchnic insulin extraction and splanchnic insulin clearance remained unchanged throughout insulin infusion and averaged 70 +/- 4% and 5.3 +/- 2 ml kg-1 min-1, respectively. With BHI infusion, splanchnic glucose balance (-8.5 +/- 0.9 mumol kg-1 min-1, basal) became positive (7.3 +/- 1 mumol kg-1 min-1). In contrast, basal splanchnic lactate uptake was inhibited by BHI and there was lactate production (from 3.4 +/- 0.9 to -1.7 +/- 1.4 mumol kg-1 min-1). Similar changes in splanchnic glucose and lactate metabolism occurred during PI infusion. These studies indicate that: 1) A considerable amount of insulin (70 +/- 4%) is extracted by the splanchnic bed on a single passage, after exogenous administration of either human insulin or PI; 2) over a physiological range of insulin concentrations (33-105 microU/ml) a linear relationship exists between arterial insulin concentrations and splanchnic insulin removal; and 3) BHI and PI do not differ appreciably with respect to their uptake and metabolic effects at the splanchnic level.

Establishment of T cell lines to bovine beta-casein and beta-casein-derived epitopes in patients with type 1 diabetes.

Enhanced cellular immune response to bovine beta-casein has been reported in patients with type 1 diabetes. In this study we aimed to establish beta-casein-specific T cell lines from newly diagnosed type 1 diabetic patients and to characterise these cell lines in terms of phenotype and epitope specificity. Furthermore, since sequence homologies exist between beta-casein and putative beta-cell autoantigens, reactivity to the latter was also investigated. T cell lines were generated from the peripheral blood of nine recent onset type 1 diabetic patients with different HLA-DQ and -DR genotypes, after stimulation with antigen pulsed autologous irradiated antigen presenting cells (APCs) and recombinant human interleukin-2 (rhIL-2). T cell line reactivity was evaluated in response to bovine beta-casein, to 18 overlapping peptides encompassing the whole sequence of beta-casein and to beta-cell antigens, including the human insulinoma cell line, CM, and a peptide from the beta-cell glucose transporter, GLUT-2. T cell lines specific to beta-casein could not be isolated from HLA-matched and -unmatched control subjects. beta-Casein T cell lines reacted to different sequences of the protein, however a higher frequency of T cell reactivity was observed towards the C-terminal portion (peptides B05-14, and B05-17 in 5/9 and 4/9 T cell lines respectively). Furthermore, we found that 1 out of 9 beta-casein-specific T cell lines reacted also to the homologous peptide from GLUT-2, and that 3 out of 4 of tested cell lines reacted also to extracts of the human insulinoma cell line, CM. We conclude that T cell lines specific to bovine beta-casein can be isolated from the peripheral blood of patients with type 1 diabetes; these cell lines react with multiple and different sequences of the protein particularly towards the C-terminal portion. In addition, reactivity of beta-casein T cell lines to human insulinoma extracts and GLUT-2 peptide was detected, suggesting that the potential cross-reactivity with beta-cell antigens deserves further investigation.

Finasteride in the treatment of hirsutism: new therapeutic perspectives.

OBJECTIVE: To determine of the clinical and hormonal effects of finasteride (Proscar; Merck, Sharp, and Dohme, Rahway, NJ) in the treatment of idiopathic hirsutism and hirsutism in patients with polycystic ovary syndrome (PCOS). DESIGN: Controlled clinical study. SETTING: Istitute of Obstetrics and Gynecology, University of Naples "Federico II." PATIENTS: Ten women affected by idiopathic hirsutism and 15 women with PCOS. INTERVENTIONS: Finasteride was administered orally at a daily dose of 5 mg for a period of 6 months. MAIN OUTCOME MEASURES: Rating of hirsutism with the Ferriman-Gallwey method; serum androgen assays. RESULTS: Finasteride produced a reduction in the average hirsutism scores ( > 50% in all patients), whereas no change was observed in serum T, androstenedione, and DHEAS levels. A significant reduction was measured in serum dihydrotestosterone and 3 alpha, 17 beta-androstenediol glucuronide levels. CONCLUSIONS: This study demonstrates that symptomatic hirsutism has to be considered as a skin disease associated with the increased activity of the 5 alpha-reductase. It also indicates that the selective 5 alpha-reductase inhibitor, finasteride, is very effective and well tolerated in the treatment of both idiopathic hirsutism and of hirsutism in patients with PCOS.

Association of DRB1*04-DQB1*0301 haplotype and lack of association of two polymorphic sites at CTLA-4 gene with Hashimoto's thyroiditis in an Italian population.

Hashimoto's thyroiditis (HT) is an autoimmune disease resulting from a complex interaction between genetic and environmental factors. The genetic loci conferring susceptibility need to be still defined. The aim of the present study was to determine whether Cytotoxic T-Lymphocyte-Associated Antigen-4 (CTLA-4), HLA DRB1, and DQB1 genes were associated to HT in an Italian population. We evaluated the allele distribution of the following loci: CTLA-4 exon 1 A49G dimorphism, which resulted in an amino acidic exchange (Thr/Ala) in the leader peptide, CTLA-4 3' microsatellite, HLA DRB1 and DQB1 in 126 patients with HT and in 301 control subjects from an Italian population (Lazio region). CTLA-4 exon 1 A49G dimorphism was typed by Polymerase Chain Reaction and Restriction Fragment Length Polymorphism (PCR-RFLP); CTLA-4 3' microsatellite alleles were defined using a fluorescence-based method. HLA DRB1 and DQB1 alleles were typed using a SSO reverse line blot method and a probeless procedure based on allele group-specific amplification followed by DNA heteroduplex analysis, respectively. Data were initially analyzed by chi2 test or Fisher's exact test. Multiple logistic regression analysis was then applied on factors with significant crude odds ratios and on CTLA-4 exon 1 A49G dimorphism to investigate their independent effects. The two polymorphic sites at CTLA-4 gene did not increase the risk for HT. The distribution of HLA DRB1 and DQB1 alleles did not show any significant difference between patients and controls, however, the DRB1*04-DQB1*0301 haplotype was significantly increased in patients. Other factors that increase the risk of disease were gender and age. Females showed approximately 18 times more risk than males; subjects older than 50 years had an odds ratio of 6.6. These data suggest that these two polymorphic sites at CTLA-4 do not play a major role in the susceptibility of the disease in an Italian population while female gender, age over 50 years, HLA DRB1*04-DQB1*0301 haplotype increase the risk of developing HT.

[The antioxidants (coenzyme Q10) in materno-fetal physiopathology]. / Gli antiossidanti (coenzima Q10) nella fisiopatologia materno-fetale.

BACKGROUND: Coenzyme Q10 (ubidecarenone) is a torpeniod molecule mainly located in bacterial and mitochondrial membranes. It is a part of a specific enzyme system and acts primarily on the transport of electrons in the mitochondrial respiratory chain. It performs an antioxidant action. We studied both fetal and maternal coenzyme Q10 plasma levels in physiological conditions and also in the presence of some pathologies. METHODS: As regards the maternal side, we selected 483 pregnancies, performing 615 blood samples, and divided them into four groups: A: physiological pregnancies; B: spontaneous abortions; C: threatened abortions; D: threatened late abortions and threatened pre-term deliveries. We then selected 61 pregnancies which differed from the previous ones and determined Q10 levels in fetal samples obtained by cordocentesis. We divided a control group from pathological groups: intra-uterine growth retardation (IUGR); Rh-isoimmunization (with intra-uterine transfusion), non immune fetal hydrops, fetal malformations. Coenzyme Q10 levels were determined in only one laboratory by high-performance liquid chromatography (HPLC). Coenzyme Q10 concentrations were expressed as mg/ml, the data as the mean + SD. Statistical analysis was performed employing a linear regression model and the student "t"-test. RESULTS: After working out a normality curve of CoQ10 levels in maternal blood, we noticed that the levels of Coenzyme Q10 were low in spontaneous abortions, in threatened late abortions and in threatened pre-term deliveries. We determined the value of 0.3 mg/ml as a cutoff to differentiate the fetal from the adult values. Moreover, CoQ10 values turned out to be increased only in fetuses affected by non-immune fetal hydrops. CONCLUSIONS: Accordingly, we can say that maternal CoQ10 plasma levels can be considered as a marker of pathological uterine contractile activity. There is a substantial increase in CoQ10 fetal plasma levels in fetuses affected by hypoxic hypoxia and also in those affected by non-immune fetal hydrops.

Treatment of acute idiopathic thrombocytopenic purpura in children. A retrospective evaluation of 120 cases.

Acute idiopathic thrombocytopenic purpura (AITP) in children is generally a benign disease with a high frequency of spontaneous remission. Nevertheless the debate over treating or not is still open, because of the high risk of hemorrhage as long as the platelet count remains below 20 x 10(9)/l. We have retrospectively evaluated 120 pediatric cases from our center, receiving different treatments at diagnosis: no treatment (76); IVIG: 400 mg/kg/d for 5 days (28); continuous oral PDN: 1-1.5 mg/kg/d for at least two weeks (16). No patients had been previously treated for AITP. Follow-up is up to fifty months. We found no significant differences as to the percentage of responses among the three groups. We conclude that waiting without treatment is safe and appropriate in most cases; whether the hemorrhagic risk suggests treatment, standard dose continuous oral PDN and IVIG may be equally effective, but IVIG may achieve a significantly faster rise in the platelet count. The timing of treatment and the cost/benefit ratio are discussed.

Usefulness of a 12-month treatment with finasteride in idiophathic and polycystic ovary syndrome-associated hirsutism.

OBJECTIVE: Hirsutism is considered as a skin disease due to increased 5 alpha-reductase activity in the pilosebaceous unit and finasteride is a drug that inhibits this enzymatic activity. This study showed the effectiveness of a chronic treatment with a selective 5 alpha-reductase inhibitor, finasteride, in idiopathic and PCOS-associated hirsutism. METHODS: Finasteride was administered orally at a daily dose of 5 mg for a period of 12 months to 20 women with IH and 20 women with PCOS. MAIN OUTCOME MEASURES: Each group was submitted to clinical (with Ferriman-Gallwey method) and serum hormonal (FSH, LH, 17 beta-estradiol, total and free T, delta 4-androstenedione, DHEAS; dihydrotestosterone, 3 alpha-androstanediol glucuronide) studies at baseline and after 3, 6 and 12 months of treatment. RESULTS: After 3 months of finasteride treatment, a significant decrease in the average hirsutism scores was recorded both in IH (p < 0.0001) and PCOS patients (p < 0.0001). A progressive significant decrease of hirsutism score was observed in IH patients after 6 and 12 months (p < 0.002) and in PCOS patients after 6 but not 12 months. In fact, the maximal therapeutic effect on the hirsutism was obtained after 12 months in the IH and 6 months in PCOS group.

Fertility rate evaluation by laparoscopic approach in the experimental animal.

PURPOSE OF INVESTIGATION: The aim of the present study was to evaluate the effect of laparoscopic insemination (LAP) and natural mating (NM) on fertility rate in experimental animal (Ovis Aries Comisana) during the month of June. METHODS: For the experiment, 97 ewes were used. Laparoscopic insemination was performed with the frozen semen of three different Romanov rams: Laparoscopic insemination I (n = 24); Laparoscopic insemination 2 (n = 26); and laparoscopic insemination 3 (n = 28), and natural mating was performed with two different Ovis Aries Comisana rams with proven fertility: Natural mating I (n = 10); Natural mating 2 (n = 9). Estrus was synchronized with fluorogestone acetate impregnated intravaginal sponges (40 mg, 14 days). Pregnant mare serum gonadotrophin (Folligon, Intervet International) at a dose of 400 UI was given intramuscularly at sponge removal. Artificial insemination was carried out 60 hours after the removal of the sponges in the laparoscopic insemination groups. RESULTS: The mean pregnancy rate at ecographic diagnosis performed at about 36 days from sponge removal for the laparoscopic insemination and natural mating groups were respectively, 62.8% and 78.9% with no significant difference. CONCLUSION: The mean fertility rates for the LAP and NM groups were 56.0 and 73.4, respectively, with no significant difference.