ABSTRACT
BACKGROUND: Although there has been success in reducing lead exposure with the phase-out of leaded gasoline, exposure to lead in Mexico continues to threaten the health of millions, much of which is from lead-based glazes used in pottery that leaches into food. OBJECTIVES: An extensive historical review and analysis of available data on blood lead levels in Mexican populations was conducted. We used a calculated geometric mean to evaluate the effect of lead on the pediatric burden of disease. METHODS: An extensive bibliographic search identified 83 published articles from 1978 to 2010 with blood lead level (BLL) data in Mexican populations representing 150 data points from more than 50,000 study participants. Values from these publications were categorized into various groupings. We then calculated the incidence of disease and disability-adjusted life-years resulting from these BLLs using the World Health Organization's burden of disease spreadsheets for mild mental retardation. RESULTS: Reviewing all relevant studies, the geometric means of Mexican BLLs in urban and rural areas were found to be 8.85 and 22.24 ug/dL, respectively. Since the phase-out of leaded gasoline, the mean in urban areas was found to be 5.36 ug/dL and the average in rural areas is expected to be much higher. The U.S. Centers for Disease Control and Prevention's (CDC) upper limit of blood lead in children under the age of 6 years is 5 ug/dL and the current U.S. average is 1.2 ug/dL. Our results indicate that more than 15% of the population will experience a decrement of more than 5 IQ points from lead exposure. The analysis also leads us to believe that lead is responsible for 820,000 disability-adjusted life-years for lead-induced mild mental retardation for children aged 0 to 4 years. CONCLUSION: Lead continues to threaten the health of millions and remains a significant cause of disability in Mexico. Additional interventions in reducing or managing lead-based ceramic glazes are necessary to protect the public health.
Subject(s)
Environmental Exposure/adverse effects , Intellectual Disability/epidemiology , Lead/blood , Lead/toxicity , Child, Preschool , Humans , Incidence , Infant , Infant, Newborn , Intellectual Disability/chemically induced , Mexico/epidemiology , Rural Population , Urban PopulationABSTRACT
INTRODUCTION: Lennox Gastaut syndrome (LGS) is an epileptic encephalopathy characterized by tonic, atonic, and atypical absence seizures usually refractory to pharmacological treatment. Patients generally continue with seizures despite treatment with the commercially available antiepileptic drugs (AEDs). Lacosamide (LCM) is a new AED recently approved for treatment of partial onset seizures with or without secondary generalization. Lacosamide has a novel mechanism of action that seems to be different in relation to other conventional AEDs. OBJECTIVE: To report LCM-caused worsening of tonic seizures and electroencephalographic pattern in a patient with Lennox-Gastaut syndrome. CASE REPORT: We report the evolution of a patient with LGS resistant to several AEDs with a cryptogenic hepatopathy in whom LCM caused worsening of tonic seizures and electroencephalographic pattern. Once LCM was discontinued, the patient returned to his clinical and electrical baseline. CONCLUSION: Lennox Gastaut syndrome may exacerbate tonic seizures and electrical pattern of patients with LGS.
Subject(s)
Acetamides/adverse effects , Intellectual Disability/chemically induced , Intellectual Disability/diagnosis , Spasms, Infantile/chemically induced , Spasms, Infantile/diagnosis , Electroencephalography/drug effects , Humans , Intellectual Disability/physiopathology , Lacosamide , Lennox Gastaut Syndrome , Male , Spasms, Infantile/physiopathology , Young AdultABSTRACT
We have studied fifty cases of thallium intoxication during the past nine years. Twenty-eight occurred in women and twenty-two in men. One of the patients was a new born whose mother had this type of intoxication during her third trimester of pregnancy. The ages varied from one day to 84 years and in all cases the source of thallium was ingestion of rat poison, except for the baby who received it across the placenta and an other patient whose source was transdermal. Twenty-three of the cases of intoxication were accidental, twenty-one were suicidal attempts and five were homicidal. One case did not know the source of intoxication. Thallium levels were measured in the urine of all the patients, some were measured in blood, as well as cerebrospinal fluid. The main clinical manifestation was a mixed type of severe peripheral neuropathy, with abdominal pain, nausea, vomiting and alopecia and some cases had psychiatric manifestations. Electrophysiological studies and nerve biopsy examined with electron microscopy in three patients. Magnetic nuclear resonance, computerized axial tomography of the abdomen and cranium were performed in two patients. There was only one death and the rest of the patients recovered almost completely. Pathophysiology and pharmacological management of this type of neurointoxication are revised.