[Cadmium polyneuropathy: a rare, but not less important, cause of peripheral neuropathy]. / Polineuropatía por cadmio: una causa infrecuente, pero no menos importante, de neuropatía periférica.

INTRODUCTION: Cadmium is an important heavy metal in neurobiology, with potential neurotoxic effects, often in the form of polyneuropathy (PNP). CASE REPORT: We present an exceptional case of PNP due to cadmium of toxic-occupational origin, specifically a 47-year-old man, aeronautical mechanic, with a 5-year clinical picture, consisting of a tingling sensation having a 'glove and stocking' distribution of symptoms and bimanual manipulative clumsiness. The neurological examination revealed bilateral achilles hyporeflexia and protopathic-thermal-algesic exteroceptive hypoesthesia in hands and feet. The following complementary rests were requested: toxic-metabolic-infectious-vitamin profile, full craniospinal MRI, electroneurographic-electromyographic study (ENG-EMG) of the upper and lower limbs, PET-CT body and 24-hour video-electroencephalogram. The results were consistent with an axonal, distal, symmetric sensory-motor PNP, of moderate intensity, chronic evolution, with active denervation, of toxic-occupational origin due to cadmium. The patient continued on sick leave to cease exposure to cadmium, initiating intensive multimodal neurorehabilitation program, with serial analytical determinations of toxins and new ENG-EMG studies every 6 months. With normalization of the altered values ??and complete clinical restitution at one-year follow-up. CONCLUSIONS: This case highlights the importance of including the toxicological determination of cadmium in case of suspicion of a PNP of toxic-occupational origin, once ruled out other etiologies, in order to early interrupt occupational exposure, as it is a potentially reversible cause of peripheral neuropathy. Currently there is no specific pharmacological treatment against cadmium tested in humans. Randomized clinical trials carried out in these patients are warranted to develop an anti-cadmium drug in refractory cases despite the end of exposure.

TITLE: Polineuropatía por cadmio: una causa infrecuente, pero no menos importante, de neuropatía periférica.Introducción. El cadmio es un metal pesado importante en neurobiología, con potenciales efectos neurotóxicos, frecuentemente en forma de polineuropatía. Caso clínico. Presentamos un caso excepcional de polineuropatía por cadmio de origen tóxico-ocupacional, en concreto, un varón de 47 años, mecánico aeronáutico, con un cuadro de cinco años de evolución, consistente en sensación de hormigueo 'en guante y calcetín' y torpeza manipulativa bimanual. En la exploración destacaba una hiporreflexia aquílea bilateral, y una hipoestesia exteroceptiva protopático-térmico-algésica en las manos y los pies. Se solicitó analítica general completa con perfil tóxico-metabólico-infeccioso-vitamínico, resonancia magnética craneomedular completa, estudio electroneurográfico-electromiográfico de los miembros superiores e inferiores, tomografía por emisión de positrones-tomografía axial computarizada body y videoelectroencefalograma de 24 horas. Los resultados fueron compatibles con una polineuropatía sensitivomotora axonal, distal, simétrica, de intensidad moderada, de evolución crónica y desnervación activa, de origen tóxico-ocupacional por cadmio. El paciente prosiguió la baja laboral para cesar la exposición al cadmio, iniciando neurorrehabilitación intensiva multimodal, y determinaciones analíticas seriadas de tóxicos y nuevos estudios electroneurográficos-electromiográficos cada seis meses, con normalización de los valores alterados y restitución clínica ad integrum al año. Conclusiones. Este caso enfatiza la importancia de incluir la determinación toxicológica del cadmio ante la sospecha de una polineuropatía de origen tóxico-ocupacional, descartadas otras etiologías, para interrumpir precozmente dicha exposición laboral, al ser una causa potencialmente reversible de neuropatía periférica. Actualmente no existe un tratamiento farmacológico específico frente al cadmio demostrado en seres humanos. Urgen ensayos clínicos aleatorizados en estos pacientes, para desarrollar un fármaco frente al cadmio en casos refractarios pese a finalizar la exposición.

Metabolic correction in the management of diabetic peripheral neuropathy: improving clinical results beyond symptom control.

Current Clinical Management Guidelines of Diabetic Peripheral Neuropathy (DPN) are based on adequate glucose control and symptomatic pain relief. However, meticulous glycemic control could delay the onset or slow the progression of diabetic neuropathy in patients with DM type 2, but it does not completely prevent the progression of the disease. Complications of DPN as it continues its natural course, produce increasing pain and discomfort, loss of sensation, ulcers, infections, amputations and even death. In addition to the increased suffering, disability and loss of productivity, there is a very significant economic impact related to the treatment of DPN and its complications. In USA alone, it has been estimated that there are more than 5,000,000 patients suffering from DPN and the total annual cost of treating the disease and its complications is over $10,000 million dollars. In order to be able to reduce complications of DPN, it is crucial to improve or correct the metabolic conditions that lead to the pathology present in this condition. Pathophysiologic mechanisms implicated in diabetic neuropathy include: increased polyol pathway with accumulation of sorbitol and reduced Na+/K+-ATPase activity, microvascular damage and hypoxia due to nitric oxide deficit and increased oxygen free radical activity. Moreover, there is a decrease in glutathione and increase in homocysteine. Clinical trials in the last two decades have demonstrated that the use of specific nutrients can correct some of these metabolic derangements, improving symptom control and providing further benefits such as improved sensorium, blood flow and nerve regeneration. We will discuss the evidence on lipoic acid, acetyl-L-carnitine, benfotiamine and the combination of active B vitamins L-methylfolate, methylcobalamin and piridoxal-6-phosphate. In addition, we discuss the role of metformin, an important drug in the management of diabetes, and the presence of specific polymorphic genes, in the risk of developing DPN and how metabolic correction can reduce these risks.

Recomendaciones para el soporte nutricional y metabólico especializado del paciente crítico. Actualización. Consenso SEMICYUC-SENPE: Paciente cardíaco / Guidelines for specialized nutritional and metabolic support in the critically-ill patient. Update. Consensus of the Spanish Society of Intensive Care Medicine and Coronary Units-Spanish Society of Parenteral and Enteral Nutrition

El paciente con patología cardíaca puede presentar 2 tipos de desnutrición: la caquexia cardíaca, que aparece en situaciones de insuficiencia cardíaca congestiva crónica, y una malnutrición secundaria a complicaciones de la cirugía cardíaca o de cualquier cirugía mayor realizada en pacientes con cardiopatía. Se debe intentar una nutrición enteral precoz si no se puede utilizar la vía oral. Cuando la función cardíaca esté profundamente comprometida la nutrición enteral es posible, pero a veces precisará suplementación con nutrición parenteral. La hiperglucemia aguda sostenida en las primeras 24 h en pacientes ingresados por síndrome coronario agudo, sean o no diabéticos, es un factor de mal pronóstico en términos de mortalidad a los 30 días. En el paciente crítico cardíaco con fallo hemodinámico en situación estable, un soporte nutricional de 20-25 kcal/kg/día es eficaz para mantener un estado nutricional adecuado. El aporte proteico debe ser de 1,2-1,5 g/kg/día. Se administrarán fórmulas poliméricas o hiperproteicas habituales, según la situación nutricional previa del paciente, con restricción de sodio y volumen según su situación clínica. La glutamina es la mayor fuente de energía para el miocito, vía conversión a glutamato, protegiendo además a la célula miocárdica de la isquemia en situaciones críticas. La administración de 1 g/ día de w-3 (EPA+DHA), en forma de aceite de pescado, puede prevenir la muerte súbita en el tratamiento del síndrome coronario agudo y también puede contribuir a una disminución de los ingresos hospitalarios, por eventos cardiovasculares, en la insuficiencia cardíaca crónica (AU)

Patients with cardiac disease can develop two types of malnutrition: cardiac cachexia, which appears in chronic congestive heart failure, and malnutrition due to the complications of cardiac surgery or any other type of surgery in patients with heart disease. Early enteral nutrition should be attempted if the oral route cannot be used. When cardiac function is severely compromised, enteral nutrition is feasible, but supplementation with parenteral nutrition is sometimes required. Sustained hyperglycemia in the first 24 hours in patients admitted for acute coronary syndrome, whether diabetic or not, is a poor prognostic factor for 30-day mortality. In critically- ill cardiac patients with stable hemodynamic failure, nutritional support of 20-25 kcal/ kg/ day is effective in maintaining adequate nutritional status. Protein intake should be 1.2-1.5 g/ kg/ day. Routine polymeric or high protein formulae should be used, according to the patient’s prior nutritional status, with sodium and volume restriction according to the patient’s clinical situation. The major energy source for myocytes is glutamine, through conversion to glutamate, which also protects the myocardial cell from ischemia in critical situations. Administration of 1 g/ day of omega-3 (EPA+DHA) in the form of fish oil can prevent sudden death in the treatment of acute coronary syndrome and can also help to reduce hospital admission for cardiovascular events in patients with chronic heart failure (AU)

Guidelines for specialized nutritional and metabolic support in the critically-ill patient: update. Consensus SEMICYUC-SENPE: cardiac patient.

Patients with cardiac disease can develop two types of malnutrition: cardiac cachexia, which appears in chronic congestive heart failure, and malnutrition due to the complications of cardiac surgery or any other type of surgery in patients with heart disease. Early enteral nutrition should be attempted if the oral route cannot be used. When cardiac function is severely compromised, enteral nutrition is feasible, but supplementation with parenteral nutrition is sometimes required. Sustained hyperglycemia in the first 24 hours in patients admitted for acute coronary syndrome, whether diabetic or not, is a poor prognostic factor for 30-day mortality. In critically-ill cardiac patients with stable hemodynamic failure, nutritional support of 20-25 kcal/kg/day is effective in maintaining adequate nutritional status. Protein intake should be 1.2-1.5 g/kg/day. Routine polymeric or high protein formulae should be used, according to the patient's prior nutritional status, with sodium and volume restriction according to the patient's clinical situation. The major energy source for myocytes is glutamine, through conversion to glutamate, which also protects the myocardial cell from ischemia in critical situations. Administration of 1 g/day of omega-3 (EPA+DHA) in the form of fish oil can prevent sudden death in the treatment of acute coronary syndrome and can also help to reduce hospital admission for cardiovascular events in patients with chronic heart failure.

[Guidelines for specialized nutritional and metabolic support in the critically-ill patient. Update. Consensus of the Spanish Society of Intensive Care Medicine and Coronary Units-Spanish Society of Parenteral and Enteral Nutrition (SEMICYUC-SENPE): cardiac patient]. / Recomendaciones para el soporte nutricional y metabólico especializado del paciente crítico. Actualización. Consenso SEMICYUC-SENPE: paciente cardíaco.

Patients with cardiac disease can develop two types of malnutrition: cardiac cachexia, which appears in chronic congestive heart failure, and malnutrition due to the complications of cardiac surgery or any other type of surgery in patients with heart disease. Early enteral nutrition should be attempted if the oral route cannot be used. When cardiac function is severely compromised, enteral nutrition is feasible, but supplementation with parenteral nutrition is sometimes required. Sustained hyperglycemia in the first 24 hours in patients admitted for acute coronary syndrome, whether diabetic or not, is a poor prognostic factor for 30-day mortality. In critically-ill cardiac patients with stable hemodynamic failure, nutritional support of 20-25 kcal/kg/day is effective in maintaining adequate nutritional status. Protein intake should be 1.2*-1.5 g/kg/day. Routine polymeric or high protein formulae should be used, according to the patient's prior nutritional status, with sodium and volume restriction according to the patient's clinical situation. The major energy source for myocytes is glutamine, through conversion to glutamate, which also protects the myocardial cell from ischemia in critical situations. Administration of 1 g/ day of omega-3 (EPA+DHA) in the form of fish oil can prevent sudden death in the treatment of acute coronary syndrome and can also help to reduce hospital admission for cardiovascular events in patients with chronic heart failure.

Cerebrospinal fluid levels of selenium in patients with Alzheimer's disease.

We compared CSF and serum selenium levels, measured by atomic absorption spectrophotometry, in 27 patients with Alzheimer's disease (AD) (13 females, 14 males, mean +/- SD age 73.6 +/- 7.4 years) without major clinical signs of undernutrition, and 34 matched controls (18 females, 16 males, mean +/- SD age 70.7 +/- 7.8 years). CSF and serum selenium levels did not differ significantly between AD-patient (11.4 +/- 7.8 ng/ml and 28.5 +/- 13.0 ng/ml, respectively) and control groups (13.3 +/- 7.0 ng/ml and 22.5 +/- 17.5 ng/ml). These values were not correlated with age, age at onset, duration of the disease, and scores of the MiniMental State Examination in the AD group. Weight and body mass index were significantly lower in AD patients than in controls. These results suggest that CSF selenium concentrations are apparently unrelated with the reported oxidative stress processes in patients with AD.

Omega-3 fatty acids in adipose tissue and risk of myocardial infarction: the EURAMIC study.

Omega-3 fatty acids have potential antiatherogenic, antithrombotic, and antiarrhythmic properties, but their role in coronary heart disease remains controversial. To evaluate the association of omega-3 fatty acids in adipose tissue with the risk of myocardial infarction in men, a case-control study was conducted in eight European countries and Israel. Cases (n=639) included patients with a first myocardial infarction admitted to coronary care units within 24 hours from the onset of symptoms. Controls (n=700) were selected to represent the populations originating the cases. Adipose tissue levels of fatty acids were determined by capillary gas chromatography. The mean (+/-SD) proportion of alpha-linolenic acid was 0.77% (+/-0.19) of fatty acids in cases and 0.80% (+/-0.19) of fatty acids in controls (P=0.01). The relative risk for the highest quintile of alpha-linolenic acid compared with the lowest was 0.42 (95% confidence interval [CI] 0.22 to 0.81, P-trend=0.02). After adjusting for classical risk factors, the relative risk for the highest quintile was 0.68 (95% CI 0.31 to 1.49, P-trend=0.38). The mean proportion of docosahexaenoic acid was 0.24% (+/-0.13) of fatty acids in cases and 0.25% (+/-0.13) of fatty acids in controls (P=0. 14), with no evidence of association with risk of myocardial infarction. In this large case-control study we could not detect a protective effect of docosahexaenoic acid on the risk of myocardial infarction. The protective effect of alpha-linolenic acid was attenuated after adjusting for classical risk factors (mainly smoking), but it deserves further research.

Cerebrospinal fluid selenium and chromium levels in patients with Parkinson's disease.

We compared CSF and serum levels of selenium and chromium, measured by atomic absorption spectrophotometry, in 28 patients with Parkinson's disease (PD) and 43 matched controls. The CSF and serum levels of these trace metals did not differ significantly between PD patients and controls. CSF selenium and chromium levels were not correlated with age, age at onset, duration of the disease, scores of the Unified Parkinson Disease Rating Scale of the Hoehn and Yahr staging in the PD group. Although antiparkinsonian therapy did not influence significantly the CSF levels of selenium, PD patients not treated with levodopa had significantly higher CSF selenium levels than controls (p < 0.01). It is possible that increased CSF selenium levels could indicate an attempt of protection against oxidative stress. The normality of CSF and serum chromium levels suggest that these values are not related with the risk for PD.

[Neuroprotective and neurorestorative therapy in Parkinson's disease]. / Tratamiento neuroprotector y neurorrestaurador en la enfermedad de Parkinson.

It has been suggested a possible role of oxidative stress, neuromelanin, mitochondrial dysfunction, calcium-binding protein deficiency, nitric oxide, trophic factors deficiency, and cytokines, in the pathogenesis of Parkinson's disease. Based on these mechanisms it might be established neuroprotective therapies but, up to date, the results reported are inconsistent. Many experimental data suggest the usefulness of some restorative therapy, such as neural grafts, genic therapies, etc. This article reviews the current knowledge on the possible neuroprotective and restorative treatments in Parkinson's disease.

Premorbid smoking, alcohol consumption, and coffee drinking habits in Parkinson's disease: a case-control study.

A number of studies have reported lower cigarette consumption in patients with Parkinson's disease (PD) previous to onset of the disease. In an attempt to determine whether there existed a "premorbid attitude" by patients against the use of socially accepted "drugs," the premorbid tobacco, alcohol, and coffee consumption habits were compared in 128 PD patients and 256 controls. Patients and controls were selected by case control method and were recruited from the same health area and socioeconomic stratum. In males, the habits of smoking more than 10 cigarettes/day (p < 0.001) and drinking more than 50 g/day of alcohol (p < 0.001) were significantly less frequent in the PD patients than in the controls, but the differences in coffee consumption were nonsignificant. In females behavior did not differ significantly between the PD group and the controls for any of the three habits. There was no correlation between the amount of smoking and alcohol drinking and age at onset of PD or current Hoehn and Yahr's staging. Our results suggest the existence of a premorbid personality in males with PD, possibly conditioning a restrictive attitude toward the consumption of such toxic substances as tobacco and alcohol, yet a more tolerant attitude toward habits more widely accepted socially, like coffee consumption.