Proposal for revision of the European Laryngological Society classification of endoscopic cordectomies

A classification of laryngeal endoscopic cordectomies, which included eight different types, was first proposed by the European Laryngological Society in 2000. The purpose of this proposal of classification was an attempt to reach better consensus amongst clinicians and agree on uniformity in reporting the extent and depth of resection of cordectomy procedures, to allow relevant comparisons within the literature when presenting/publishing the results of surgery, and to recommend the use of guidelines to allow for reproducibility amongst practicing laryngologists. A total of 24 article citations of this classification have been found through the science citation index, as well as 3 book chapters on larynx cancer surgery, confirming its acceptance. However, on reflection, and with the passage of time, lesions originating at the anterior commissure have not been clearly described and, for that reason, a new endoscopic cordectomy (type VI) for cancers of the anterior commissure, which have extended or not to one or both of the vocal folds, without infiltration of the thyroid cartilage is now being proposed by the European Laryngological Society Committee on Nomenclature to revise and complete the initially reported classification.     

Declining hepatitis A seroprevalence in adults in Catalonia (Spain): a population-based study

Background  

One of the main uses of seroprevalence studies it to evaluate vaccination programmes. In 1998, a programme of universal vaccination of preadolescents in schools with the hepatitis A vaccine was begun in Catalonia. The objective of this study was to investigate the prevalence and risk factors of hepatitis A virus infection (HAV) in a sample of the adult population of Catalonia in 2002 and to evaluate the changes with respect to a survey carried out in 1996.     

Trends in pancreatic cancer mortality in Europe, 1955–1989

Trends in death certification rates from pancreatic cancer over the period 1955–1989 were analyzed for 25 European countries (excluding the former Soviet Union and a few smaller countries). In 1985–1989, rates for males ranged between 5.3/100,000 (age-standardized world population) in Spain and 10.3/100,000 in Hungary and Czechoslovakia. Other high-mortality areas were located in Northern Europe (Finland, Iceland, Ireland, Denmark) and Central Europe (Austria, Poland, Germany), whilst mortality was lower in Southern Europe (Portugal, Greece). Between 1955 and 1989, mortality rates increased in all the countries considered, the change ranging between 6% in Scotland and 279% in Spain; the rises were higher in the Mediterranean and Eastern European countries than in Northern Europe. Among females, Nordic countries such as Iceland, Sweden and Denmark had the highest mortality rates in 1985–1989 (over 6/100,000) and, as for males, Southern Europe (Spain, Portugal, Greece) appeared as a low-mortality area (around 3/100,000). During the 1955–1989 period, upward trends were observed in all the countries studied, with the highest increase in Greece, Italy, Bulgaria, Poland and Spain. A negative correlation was observed between the percent change in mortality rates between 1955–1959 and 1985–1989 and the rate in 1955–1959 among both males (r = ?0.95, p <0.001) and females (r = ?0.81, p <0.001). Thus, a systematic levelling of rates was observed in most countries, with the exception of the UK and some Nordic countries, whose rates were already high in the late 1950s. Tobacco smoking and dietary factors could account for some of the generalized upward trends. Improved diagnostic and death certification of the disease might also partially explain the observed figures. © 1994 Wiley-Liss, Inc.     

Pathogenic role of glial cells in Parkinson's disease.

Parkinson's disease (PD) is a common neurodegenerative disorder characterized by the progressive loss of the dopaminergic neurons in the substantia nigra pars compacta (SNpc). The loss of these neurons is associated with a glial response composed mainly of activated microglial cells and, to a lesser extent, of reactive astrocytes. This glial response may be the source of trophic factors and can protect against reactive oxygen species and glutamate. Alternatively, this glial response can also mediate a variety of deleterious events related to the production of pro-oxidant reactive species, and pro-inflammatory prostaglandin and cytokines. We discuss the potential protective and deleterious effects of glial cells in the SNpc of PD and examine how those factors may contribute to the pathogenesis of this disease.     

The effects of ticlopidine administration at low doses on the incidence of restenosis following percutaneous transluminal coronary angioplasty

The incidence of restenosis remains the same as initially reported (30%) and no therapeutic approach has reduced its appearance. Platelets-induced smooth muscle cell proliferation probably play a preponderant role in the pathogenesis of restenosis. The aim of this study was to evaluate the effects of ticlopidine (250 mg/day) on restenosis rate after single lesion coronary angioplasty. One hundred seventy nine consecutive patients were prospectively included in this study and were assigned to ticlopidine (group T, n = 91) or to a control group (n = 88) in an alternative fashion. Age (60 +/- 10 vs 58 +/- 9 years), gender (87% vs 87% male), treatment, coronary risk factors, lesion morphology, stenosis severity pre- and postangioplasty, type of vessel, collateral circulation, and left ventricular ejection fraction, were similar in the T and control groups, respectively. Unstable angina was more frequently found in group T patients (81% vs 65%, p less than 0.01). A late angiographic follow-up (7 +/- 2 months after angioplasty) revealed restenosis (greater than 50% luminal narrowing) in 26 patients (28%) in group T and in 21 patients (24%) in the control group (NS). At that time, 88% and 98% of patients without restenosis vs 35% and 48% of patients with restenosis were asymptomatic in the T and control groups, respectively. An exercise test prior to the late control angiogram was abnormal (angina and/or ST segment depression) in 77% and 73% of patients with restenosis in T and control groups, respectively. Thus, in our experience, ticlopidine at a dosage of 250 mg/day was unable to reduce restenosis rate after single lesion coronary angioplasty.     

Skeletal muscle studies in patients with HIV-related wasting syndrome

Previous reports have suggested that HIV-related wasting syndrome may be considered as a form of myopathy. The aim of the present study was to investigate histopathological muscle changes in HIV-related wasting syndrome in order to know if there is a common substrate and whether muscle plays a primary or secondary role in its development. Patients with wasting syndrome diagnosed by Centers for Disease Control (CDC) criteria were prospectively evaluated. Clinical, analytical, nutritional, anthropometrical and muscular data were recorded. The patients were subdivided into two groups: group A was constituted by patients in whom wasting syndrome was the AIDS-defining illness, and group B by patients in whom AIDS diagnosis was previously made. In all cases muscle biopsy was performed and processed for conventional stainings and histochemical reactions. Thirty patients were included (group A, 12; group B, 18). Clinical, analytical, nutritional and anthropometrical data did not essentially differ between the two groups. All patients were malnourished with respect to controls. Histopathological findings in muscle biopsy were heterogeneous and similar in both groups, except for HIV-related myopathies, which were more frequently seen in the patients from group A (P=0.05). In five cases (17%) an unsuspected and potentially treatable myopathy was diagnosed. Patients with polyarteritis nodosa (two) or polymyositis (one) were treated with prednisone, which improved their wasting syndrome. By contrast, patients with AZT-myopathy (two) did not improve when the drug was discontinued. We conclude that in most cases the wasting syndrome cannot be considered as a true myopathy, and probably metabolic and/or nutritional factors may account for wasting development. However, in a subset of patients muscle biopsy allows the diagnosis of a treatable myopathy leading to the improvement of wasting syndrome.