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OBJECTIVE: To investigate the effect of a multistage ultra-endurance triathlon on body composition in ultra-triathletes. DESIGN: Descriptive field study. SETTING: The "World Challenge Deca Iron Triathlon 2006" in Monterrey, Mexico, in which every day for 10 consecutive days athletes had to perform the distance of one Ironman triathlon. SUBJECTS: Eight male ultra-endurance athletes (mean (SD) age 40.6 (10.7) years, weight 76.4 (8.4) kg, height 175 (4) cm and body mass index (BMI) 24.7 (2.2) kg/m2). INTERVENTIONS: None. MAIN OUTCOME MEASUREMENTS: Determination of body mass, protein mass, body fat, per cent body fat, mineral mass, total body water, intracellular water, extracellular water and lean body mass with a direct segmental multifrequency bioelectrical impedance method before the race and after each stage in order to show changes in body composition. RESULTS: A statistically significant decrease of body mass (-2.4 kg, p = 0.014), body fat (-5 kg, p = 0.0078) and per cent body fat (-6.4%, p = 0.0078) occurred at the end of the first day compared to values taken in the pre-race period. In contrast, at the same time, a statistically significant increase of protein mass (+0.7 kg, p = 0.035), mineral mass (+0.2 kg, p = 0.04), total body water (+1.8 litres, p = 0.042), intracellular water (+1.6 litres, p = 0.034) and lean body mass (+2.6 kg, p = 0.023) was shown. After the first day until the end of the challenge, body fat (-3 kg, p>0.05) and per cent body fat (-3.9%, p>0.05) showed a statistically significant decrease, whereas the other parameters showed no changes. CONCLUSIONS: Athletes taking part in a multistage ultra-endurance triathlon over 10 Ironman triathlon distances in 10 consecutive days lost 3 kg of body fat; skeletal muscle mass, mineral mass and body water were unchanged.

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We report 10 HTLV-I virus seropositive subjects, eight of them with HTLV-I associated myelopathy (HAM), two of them also infected with HIV as well as two asymptomatic HTLV-I+ relatives of two unrelated patients. HTLV-I is endemic in several tropical areas, where it causes different neurological diseases. Only few patients have been reported in our country since 1994. We studied 8 patients, who fulfilled the clinical criteria for chronic spastic paraplegia, and 2 other non-symptomatic HTLV-I seropositive relatives, with electromyography (EMG), motor and sensory conduction velocities (NCV), somatosensory, visual and brainstem auditory evoked potentials (SSEP, VEP and BAEP), Magnetic Resonance Images (MRI) and cerobrospinal fluid (CSF) analysis. The latter was carried out only in seven symptomatic patients. In every case positive ELISA tests for HTLV-I/II were confirmed by Western Blot. The two asymptomatic persons were clinically and electromyographically assessed, one of them was also submitted to SSEPs studies. Three patients were males. Patient's ages ranged from 5 to 65 years old. All symptomatic patients showed muscular weakness, spasticity with pyramidal signs and sphincter disturbances. Five of them had paresthesias and 2 had burning pain on their feet. The EMGs and the NCVs were normal in 7 patients and in the 2 asymptomatic ones. SSEPs, obtained by stimulating the posterior tibial nerves, were impaired in 7 patients and in the asymptomatic person who received the procedure. The 7 symptomatic patients who underwent lumbar puncture had positive tests for HTLV-I in CSF, 3 out of these 7 patients had also high protein levels and 4 had increased number of lymphocytes. In 2 patients intrathecal IgG production could also be demonstrated. MRI were normal in 7 patients and in the 2 asymptomatics, the exception being a female who had bilateral hyperintense lesions in cerebral white matter in T2. In conclusion, tropical spastic paraparesis is apparently a rare disorder in Argentina. However, some cases have been reported recently. Most probably, its prevalence is currently underestimated. Its diagnosis should be considered in every patient with progressive spastic paraplegia.

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Mitochondrial disorders are a group of diseases that can affect virtually all organ systems. A 19 year old man was seen in 1993 with neurologic abnormalities consisting of impaired function of muscles, diplopia, progressive loss of vision, impaired phonation and swallowing, during the last 10 years. Physical examination disclosed moderate wasting of the four limb muscles, mild motor weakness of neck muscles, symmetrical hyporeflexia, cerebellar dysfunction, severe external ophtalmoplegia and ptosis. Fundii oculi examination showed retinitis pigmentosa. The electromyogram demonstrated myopathic changes with normal nerve conduction velocities. The cerebrospinal fluid was normal, except for a mild increase in lactic acid. Histochemical study of a muscle biopsy specimen demonstrated ragged red fibers and increase of the subsarcolemal oxidative activity of mitochondriae. The diagnosis of Kearns-Sayre disease was confirmed and he was discharged advising physical therapy. On February 1995, he was again admitted, this time with right cardiac failure and worsening of all his previous symptoms and signs. He complained of myalgias and his muscle weakness was more striking on clinical examination. Echocardiography showed biventricular dilatation and left ventricular hypertrophy with preserved systolic function. A new muscle biopsy revealed an heteroplasmic deletion of 5 Kb with 80% of mutant mitochondrial DNA. In brief, we report a patient with the clinical phenotype of Kearns-Sayre syndrome who presented an acute congestive cardiac failure due to cardiomyopathy, an association which has seldom been, reported in the literature.

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Amidarone (AMD) is an antiarrhythmic drug with side effects on the nervous system. Cerebellum is seldom involved: We describe the case of a 56 years old male patient with a history of 4 month of cerebellar involvement characterized by gait unsteadiness, ataxia, nistagmus and vertigo. He was on treatment with AMD because of ventricular arrythmia. The cerebellar syndrome progressively disappeared after drug withdrawal and he was symptoms-free 4 months later. Similar symptoms appeared after another one month of automedication with the same drug. Structural lesions, metabolic, nutritional deficiencies or toxics were excluded. Mechanisms of cerebellar toxicity of AMD are yet unknown. The knowledge of the toxic effects of this drug, widely used in our country, would allow its early recognition.

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We reviewed 538 charts of patients hospitalized with acute ischemic strokes between 1983 and 1991. The inclusion criteria for cardioembolism were: 1) sudden onset and maximal neurological focal deficit from the beginning, 2) brain CT showing an ischemic infarct, hemorrhagic infarct, or multiple infarcts, 3) cardioembolic sources demonstrated by echocardiography or heart catheterization, and 4) absence of stenotic-occlusive cerebrovascular disease. Sixty-nine patients (12.8%) filled the criteria for cardiogenic brain embolism. Cardiac sources were: 1) nonvalvular atrial fibrillation in 20 patients (29.0%), 2) rheumatic heart disease in 14 (20.3%), 3) nonischemic dilated cardiomyopathy in 13 (18.8%). Nine of these (69%) had cardiac involvement due to Chagas' disease, 4) ischemic heart disease in 11 (15.9%), and 5) other less common conditions such as bacterial endocarditis, mitral valve, and congenital heart malformation in 11 (15.9). Transient ischemic attacks preceding stroke occurred in 11 patients (15.9%), six patients had previous strokes, and 14 patients (20.3%) had silent infarcts. Early recurrence of embolism (three initial weeks) occurred in 5 patients (7.2%), and 28.6% of the patients had hemorrhagic transformation within this period. Taken together, our figures show that, although they are well in line with the current literature, nonischemic dilated cardiomyopathy is one of the main causes of cerebral embolism in our community. This reflects the presence of a regional factor, namely Chagas' disease.

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We reviewed 538 charts of patients hospitalized with acute ischemic strokes between 1983 and 1991. The inclusion criteria for cardioembolism were: 1) sudden onset and maximal neurological focal deficit from the beginning, 2) brain CT showing an ischemic infarct, hemorrhagic infarct, or multiple infarcts, 3) cardioembolic sources demonstrated by echocardiography or heart catheterization, and 4) absence of stenotic-occlusive cerebrovascular disease. Sixty-nine patients (12.8

) filled the criteria for cardiogenic brain embolism. Cardiac sources were: 1) nonvalvular atrial fibrillation in 20 patients (29.0

), 2) rheumatic heart disease in 14 (20.3

), 3) nonischemic dilated cardiomyopathy in 13 (18.8

). Nine of these (69

) had cardiac involvement due to Chagas disease, 4) ischemic heart disease in 11 (15.9

), and 5) other less common conditions such as bacterial endocarditis, mitral valve, and congenital heart malformation in 11 (15.9). Transient ischemic attacks preceding stroke occurred in 11 patients (15.9

), six patients had previous strokes, and 14 patients (20.3

) had silent infarcts. Early recurrence of embolism (three initial weeks) occurred in 5 patients (7.2

), and 28.6

of the patients had hemorrhagic transformation within this period. Taken together, our figures show that, although they are well in line with the current literature, nonischemic dilated cardiomyopathy is one of the main causes of cerebral embolism in our community. This reflects the presence of a regional factor, namely Chagas disease.

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We reviewed 538 charts of patients hospitalized with acute ischemic strokes between 1983 and 1991. The inclusion criteria for cardioembolism were: 1) sudden onset and maximal neurological focal deficit from the beginning, 2) brain CT showing an ischemic infarct, hemorrhagic infarct, or multiple infarcts, 3) cardioembolic sources demonstrated by echocardiography or heart catheterization, and 4) absence of stenotic-occlusive cerebrovascular disease. Sixty-nine patients (12.8

) filled the criteria for cardiogenic brain embolism. Cardiac sources were: 1) nonvalvular atrial fibrillation in 20 patients (29.0

), 2) rheumatic heart disease in 14 (20.3

), 3) nonischemic dilated cardiomyopathy in 13 (18.8

). Nine of these (69

) had cardiac involvement due to Chagas disease, 4) ischemic heart disease in 11 (15.9

), and 5) other less common conditions such as bacterial endocarditis, mitral valve, and congenital heart malformation in 11 (15.9). Transient ischemic attacks preceding stroke occurred in 11 patients (15.9

), six patients had previous strokes, and 14 patients (20.3

) had silent infarcts. Early recurrence of embolism (three initial weeks) occurred in 5 patients (7.2

), and 28.6

of the patients had hemorrhagic transformation within this period. Taken together, our figures show that, although they are well in line with the current literature, nonischemic dilated cardiomyopathy is one of the main causes of cerebral embolism in our community. This reflects the presence of a regional factor, namely Chagas disease.

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Em um ensaio clínico realizado em 12 voluntários sadios determinou-se a perda total de sangue gastrintestinal através de eritrócitos marcados pelo Cr51. O ensaio duplo-cego cruzado revelou uma diferença altamente significativa (p < 0,001) entre a indometacina e acemetacina após administraçäo oral durante sete dias de ácido 1-(p-clorobenzoil) - 5-metoxi- 2-metilindol- 3-acetoxi-acético (acemetacina, TV 1322, Mostanol) 200mg/dia, indometacina 200mg/dia e placebo. A perda total média de sangue, em um período de sete dias, foi de 12,4ml com indometacina, 4,5ml com acemetacina e 5,0ml com placebo. Em um ensaio clínico com 16 pacientes reumáticos em uso prolongado de medicamentos antiinflamatórios näo-hormonais encontrados habitualmente no mercado, determinou-se de igual modo a perda total gastrintestinal de sangue. Em um ensaio duplo-cego cruzado com período de wash-out foram comparadas as quantidades de sangue eliminadas durante um tratamento de sete dias com acemetacina (240mg/d) com as quantidades eliminadas durante o mesmo período com indometacina (200mg/d). Também chamou atençäo uma diferença altamente significativa (p < 0,001) entre os dois preparados. Com indometacina a eliminaçäo total de sangue por semana foi de 13,8ml, com acemetacina 6,5ml. Durante o período de wash-out foram eliminados em média 6,0ml de sangue por semana. Näo houve diferença entre os resultados de ambos os ensaios. As investigaçöes realizadas em 23 pacientes e 12 voluntários näo revelaram nenhum indício de que a nova droga antiinflamatória acemetacina provoque lesöes da mucosa do trato gastrintestinal evidenciadas por perda de sangue

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