Glucose alteration and insulin resistance in asymptomatic obese children and adolescents / Alteração de glicose e resistência à insulina em crianças e adolescentes obesos assintomáticos

Abstract Objective Obesity is associated with the abnormal glucose metabolism preceding type 2 diabetes mellitus. Thus, further investigation on the prediction of this lethal outcome must be sought. The objective was the profile glycemic assessment of asymptomatic obese children and adolescents from Salvador, Brazil. Method A fasting venous blood sample was obtained from 90 consecutive obese individuals aged 8-18 years, of both sexes, for laboratory determinations of glycated hemoglobin, basal insulin, and the Homeostasis Model Assessment Insulin Resistance index. The clinical evaluation included weight, height, waist circumference, assessment of pubertal development, and acanthosis nigricans research. The body mass index/age indicator was used for the severity of overweight assessment. Results Glycemic alterations were evidenced clinically and biochemically, although these individuals had no complaints or symptoms related to blood sugar levels. Quantitative and qualitative variables were respectively expressed measures of central tendency/dispersion and simple/relative frequency, using the SPSS, version 20.0. A p-value <0.05 was considered significant. Conclusion Notably, this study found a high prevalence of glucose and insulin disorders in asymptomatic obese children and adolescents.

Resumo Objetivo A obesidade está associada ao metabolismo da glicose anormal que antecede o diabetes mellitus tipo 2. Assim, uma investigação adicional sobre a predição desse resultado letal deve ser antecipada. O objetivo era a avaliação do perfil glicêmico de crianças e adolescentes obesos assintomáticos de Salvador, Brasil. Método Uma amostra de sangue venoso em jejum foi obtida de 90 indivíduos obesos consecutivos entre 8-18 anos, de ambos os sexos, para determinações laboratoriais de hemoglobina glicosilada, insulina basal e Índice do Modelo de Avaliação da Homeostase de Resistência à Insulina (HOMA-IR). A avaliação clínica incluiu peso, estatura, circunferência da cintura, avaliação do desenvolvimento puberal e pesquisa sobre a acantose nigricans. Utilizamos o indicador de índice de massa corporal/idade referente à gravidade da avaliação de sobrepeso. Resultados Alterações glicêmicas foram comprovadas clínica e bioquimicamente, apesar de esses indivíduos não apresentarem queixas ou sintomas relacionados a níveis de açúcar no sangue. Variáveis quantitativas e qualitativas foram, respectivamente, medidas expressas de tendência central/dispersão e amostra/frequência relativa, com o software Pacote Estatístico para as Ciências Sociais, versão 20.0. O valor de p < 0,05 foi considerado significativo. Conclusão Observamos, contudo, alta prevalência de distúrbios de glicose e insulina em crianças e adolescentes obesos assintomáticos.

Hiperinsulinemia y resistencia insulínica en niños de dos escuelas públicas de Oaxaca, México / Hyperinsulinemia and insulin resistance in children

Background: Obesity during childhood is a risk factor for developing cardiovascular diseases during adulthood. Aim: To measure insulin and glucose levels and parameters of insulin resistance in obese, overweight and normal weight Mexican children. Material and Methods: Comparative study of 21 obese children with a body mass index (BMI) over percentile 95, aged 10 ± 1 years (10 males), 14 children aged 10 ± 2 (7 males) with a BMI between percentiles 85 and 94 and 16 children aged 9 ± 2 years (3 males) with a body mass index between percentiles 10 and 84. Body weight, blood pressure and waist circumference were measured and a blood sample was obtained to measure fasting glucose and insulin levels. Homeostasis model of insulin resistance (HOMA) and quantitative insulin sensitivity check index (QUICKI) were calculated. Results: Among obese, overweight and normal weight children, insulin levels were 14.9 (95% CI 10.90-18.99), 7.20 (CI 5.12-9.28) and 4.73 (CI 95% 1.92-7.53) uU/ml, respectively. The figures for HOMA were 3.16 (95% CI 2.20-4.12), 1.49 (95% CI 1.03-1.94) and 0.97 (95% CI 0.35-1.60), respectively. The figures for QUICKI were 0.331 (95% CI 0.319-0.343), 0.371 (95% CI 0.349-0.393) and 0.419 (95% CI 0.391-0.446), respectively. Compared to their normal weight counterparts, the risk of obese children and those with a waist circumference over percentile 90 of having a HOMA over 3.16 was 17 and 10 times higher, respectively. BMI correlated better than waist circumference with insulin levels. Conclusions: Obese children have higher levels of insulin resistance than their normal weight counterparts.

Hyperinsulinemia and hyperglycemia: risk factors for recurrence of benign paroxysmal positional vertigo / Hiperinsulinismo e hiperglicemia: fatores de risco para recorrência de vertigem postural paroxística benigna

INTRODUCTION: Changes in carbohydrate metabolism may lead to recurrence of benign paroxysmal positional vertigo.OBJECTIVE: To evaluate the influence of the disturbance of carbohydrate metabolism in the recurrence of idiopathic BPPV.METHODS: A longitudinal prospective study of a cohort, with 41 months follow-up. We analyzed the results of 72 glucose-insulin curves in patients with recurrence of BPPV. The curves were classified into intolerance, hyperinsulinemia, hyperglycemia and normal.RESULTS: The RR for hyperinsulinism was 4.66 and p = 0.0015. Existing hyperglycemia showed an RR = 2.47, with p = 0.0123. Glucose intolerance had a RR of 0.63, with p = 0.096. When the examination was within normal limits, the result was RR = 0.2225 and p = 0.030.DISCUSSION: Metabolic changes can cause dizziness and vertigo and are very common in people who have cochleovestibular disorders. However, few studies discuss the relationship between idiopathic BPPV and alterations in carbohydrate metabolism. In the present study, we found that both hyperglycemia and hyperinsulinemia are risk factors for the recurrence of BPPV, whereas a normal test was considered a protective factor; all these were statistically significant. Glucose intolerance that was already present was not statistically significant in the group evaluated.CONCLUSION: Hyperinsulinemia and hyperglycemia are risk factors for the recurrence of idiopathic BPPV and a normal exam is considered a protective factor.

INTRODUÇÃO: As alterações do metabolismo do carboidrato podem levar a recorrência de vertigem posicional paroxística benigna.OBJETIVO: Avaliar a influência dos distúrbios do carboidrato na recorrência da VPPB idiopática.MÉTODO: Estudo longitudinal, do tipo coorte, prospectivo, com 41 meses de acompanhamento. Analisaram-se 72 resultados de curvas glicoinsulinêmicas em pacientes portadores de recorrência de VPPB. As curvas foram classificadas em intolerância, hiperinsulinemia, hiperglicemia e normal.RESULTADOS: O hiperinsulinismo teve RR = 4,66 e p = 0,0015. A hiperglicemia apresentou um RR = 2,47 e p = 0,0123. Na intolerância a glicose o RR = 0,63 e p = 0,096. No exame normal, o RR = 0,2225 e p = 0,030.DISCUSSÃO: As alterações metabólicas podem causar tontura e vertigem e são muito frequentes na população que apresenta distúrbios cocleovestibulares. Contudo, poucos trabalhos falam sobre a relação entre a VPPB idiopática e as alterações nos carboidratos. No presente estudo, verificou-se que tanto a hiperglicemia, quanto o hiperinsulinismo são fatores de risco para recorrência de VPPB, ao passo que o exame normal foi considerado fator protetor, todos estes estatisticamente significantes. Já a intolerância à glicose não teve significância estatística no grupo avaliado.CONCLUSÃO: O hiperinsulinismo e a hiperglicemia se comportam como fatores de risco para a recorrência de VPPB idiopática, assim como o exame normal como um fator protetor.

Evaluación de la insulinemia post carga oral de glucosa como método diagnóstico de resistencia a la insulina / Evaluation of serum insulin levels after an oral glucose load for the diagnosis of insulin resistance

Background: In our country, the assessment of insulin resistance (IR) measuring serum insulin levels at 60 and 120 minutes after a 75 g oral glucose tolerance test (OGTT), is usual. However, there is no information about the distribution of serum insulin levels in the Chilean population. Aim: To assess the distribution of serum insulin levels at 60 and 120 minutes during OGTTs and suggest a statistical cut-off point to estimate the degree of IR. Material and Methods: Retrospective analysis of 1815 OGTTs performed in non-diabetic subjects aged between 18 and 75 years, at a university medical center. HOMA-IR (Homeostasis Model Assessment), insulin sensitivity index of Matsuda (ISI-Composite), and their correlation with serum insulin levels at 60 and 120 minutes were calculated. Results: The 75th percentiles for serum insulin levels at 60 and 120 minutes were 127 and 81 µU/mL, respectively. There was a high correlation between HOMA-IR and ISI-Composite (r = -089, p < 0.001). There was a weaker although significant correlation between HOMA-IR and ISI-Composite and insulin levels at 60 (r = 0.56 and -0.79 respectively, p < 0,001) and 120 minutes (r = 0.54 and -0.75 respectively, p < 0,001). Conclusions: We propose 60 and 120 min serum insulin levels of 130 and 80 µU/mL respectively, as cut-off values for normality during OGTT in Chilean normoglycemic individuals.

Hipoglicemia hiperinsulínica: a propósito de un caso / Hyperinsulinemic hypoglycemia: report of a case

El diagnóstico de hipoglicemia se confirma con la triada de Whipple: síntomas de hipoglicemia, concentración plasmática baja de glucosa, y desaparición de los síntomas con la elevación de los niveles de glucosa. Se presenta el caso de una paciente de 26 años de edad, que consultó a nuestro servicio en julio de 2013 por episodios intermitentes que se iniciaron en octubre del año precedente, consistentes en visión borrosa, cambios conductuales y discurso incoherente, sin relación con la ingesta o el ayuno, que aumentaron en frecuencia los meses previos a la consulta y llegaron a asociarse a pérdida de conocimiento y relajación de esfínteres, requiriendo asistencia médica prehospitalaria. Ocasionalmente hubo registros bajos de glicemia capilar, y hubo mejoría sintomatológica con la administración de glucosa e.v. Durante una prueba de ayuno presentó una hipoglicemia sintomática con glicemia 48 mg/dl, insulinemia 21,1 µU/ml, péptido C 2.257 ng/ml. La ecografía de abdomen identificó una imagen sólida en la unión de cuerpo y cola del páncreas. La lesión fue enucleada quirúrgicamente, y la anatomía patológica confirmó su origen neuroendócrino .

The diagnosis of hypoglycemia is confirmed by Whipple’s triad: symptoms of hypoglycemia, low plasma glucose concentrations, and disappearance of symptoms after glucose administration. The case of a 26-year-old woman is presented. She consulted our Service in July 2013 due to intermittent episodes that had begun in October of the preceding year, characterized by blurred vision, slurred speech, and behavioral changes, unrelated to food ingestion. They increased in frequency, and were associated eventually with loss of consciousness and loss of sphincters control, requiring medical care. Occasionally, low capillary glucose levels were recorded, and there was improvement in symptoms with i.v. glucose administration ev.During a fasting test she had symptomatic hypoglycemia with serum glucose of 48 mg/dl, serum insulin 21.1 µU/ml, and serum C-peptide 2.257 ng/ml. Abdominal ultrasound identified a rounded image in the union of the body and tail of the páncreas; this was confirmed by MRI. The lesion was surgically enucleated, and the pathology report confirmed its neuroendocrine origin .

[Congenital Hyperinsulinism: review of 12 Tunisian cases]

Congenital hyperinsulinism in infancy [CHI] is a heterogeneous disorder with respect to genetics and response to therapy. Data on CHI are sporadic in North African population. To characterize the clinical features and outcome of 12 Tunisian patients with CHI. data of patients diagnosed with CHI during the period 1989-2007 were retrospectively analyzed. Diagnosis was considered whenever hyperinsulinemia 10 UI/ml was concomitant to hypoglycemia<3mmol/l and/or high insulin to glucose ratio>0.3 and/or positif glucagon test. Transient causes of hypoglycemia, adrenal and growth hormone deficiency were excluded. There were nine infants diagnosed at a median age of 17 months and three newborns. Permanent hyperammoniemia, found in one patient, guided to leucine-sensitive hyperinsulinism. Seven patients presented with seizures, two with psychomotor delay and one with recurrent malaises. Among 42 assays of plasmatic insulin, when in hypoglycemia, 40% only were 10 U/ml. Three patients resisted to diazoxide and underwent subtotal pancreatectomy complicated by diabetes mellitus in two cases and persistent hypoglycemia in one patient. Histological examination concluded to diffuse hyperplasia of pancreatic cells. Diazoxide was discontinued in four out the eight responders patients. Four patients died, seven patients developed variable degrees of mental retardation and five suffered from epilepsy. Early onset forms were, as reported in the literature, mostly resistant to medical therapy. The high proportion of neurological sequelae is related to diagnosis delay or to a late surgery. We focus on the importance of a precocious diagnosis and aggressive treatment of hypoglycemia

Insulino resistencia y síndrome metabólico en pacientes con enfermedad coronaria definida por angiografía / Insulin-resistance and metabolic syndrome in patients with coronary heart disease defined by angiography

Se examinó la frecuencia de insulino-resistencia (IR) y síndrome metabólico (SM) en pacientes coronarios empleando diferentes criterios de definición y se analizó cuáles mostraban mejor asociación con la presencia y gravedad de la afección. Fue un estudio casos-controles en 100 pacientes con edades entre 40 y 70 años que concurrieron a un centro hospitalario para realizarse una angiografía. IR fue definido por insulina >15 mU/l, el modelo hemostático de insulino-resistencia (HOMA-IR) >3.1 y la combinación del índice de masa corporal (IMC) >27.5 kg/m² con HOMA-IR >3.6. SM fue definido según International Diabetes Federation y American Heart Association / National Heart, Lung, and Blood. Insulina >15 mU/l y HOMA-IR >3.1 tuvieron la misma sensibilidad, (60.3%), y se asociaron significativamente con la extensión de la enfermedad coronaria, p = 0.001 y p = 0.009 respectivamente. En cambio, IMC >27.5 kg/m² con HOMA-IR >3.6 mostró menor sensibilidad, (43.1%), y menor asociación con la gravedad, (p = 0.028). Los odds ratio (OR) para enfermedad coronaria fueron respectivamente: 3.16 (IC 95% 1.28-7.79), p = 0.012; 2.93 (IC 95% 1.20-7.19) p = 0.019; 2.86 (IC 95% 1.10-7.41), P = 0.031. La frecuencia de SM definida según American Heart Association / National Heart, Lung, and Blood fue mayor en coronarios versus controles (62.1% versus 33.3%, p = 0.003), se asoció con la enfermedad en uno o en múltiples vasos (p = 0.011) y fue su predictor, OR = 4.22 (IC 95% 1.65-10.83) p = 0.003. Sin embargo, SM definido según International Diabetes Federation no se asoció con la presencia ni con la gravedad de la enfermedad.

The frequency of insulin-resistance (IR) and metabolic syndrome (MS) were examined in coronary patients using different criteria of definition. It was also analyzed which of them indicated a strong association with the presence and severity of the disease. This was a case-control study on 100 patients between 40 and 70 years old, assisted in a hospital center and there examined by angiography. IR was defined by insulin >15 mU/l, Homeostatic Model Assessment for insulin-resistance (HOMA-IR) >3.1 and the combination body mass index (BMI) >27.5 kg/m² with HOMA-IR >3.6. MS was defined according to International Diabetes Federation and American Heart Association/National Heart, Lung and Blood Institute. Insulin >15 mU/l and HOMA-IR >3.1 had similar sensibility, 60.3%, and were significantly associated with the extension of coronary heart disease, p = 0.001 and p = 0.009 respectively. Whereas, BMI>27.5 kg/m² with HOMA-IR>3.6 showed a lower sensibility, 43.1% and less association with severity, p = 0.028. The odds ratio (OR) for coronary heart disease were respectively: 3.16 (CI 95 1.28-7.79), p = 0.012; 2.93 (CI 95% 1.20-7.19) p = 0.019; 2.86 (CI 95% 1.10- 7.41), p = 0.031. The frequency of SM defined according to American Heart Association/National Heart, Lung and Blood Institute was higher in coronary patients vs. controls (62.1% vs. 33.3%, p = 0.003). It was associated with disease in one or more vases (p = 0.011) and was its predictor, OR = 4.22 (CI 95% 1.65-10.83) p = 0.003. However, SM defined according to International Diabetes Federation was not associated with the presence or severity of coronary heart disease.

Hiperinsulinismo na infância: quando apenas uma dosagem de insulina não é suficiente / Hyperinsulinism in infancy and childhood: when an insulin level is not always enough

INTRODUÇÃO: A hipoglicemia em bebês e crianças pode causar convulsões, atraso de desenvolvimento e dano cerebral permanente. O hiperinsulinismo (HI) é a causa mais comum de hipoglicemia, seja transitória ou permanente. A HI é caracterizada pela secreção inadequada de insulina, o que resulta em hipoglicemia persistente, de leve a grave. As diferentes formas de HI representam um grupo de doenças clínica, genética e morfologicamente heterogêneo. CONTEÚDO: Hiperinsulinismo congênito está associado às mutações de SUR-1 e Kir6.2, glucoquinase, glutamato desidrogenase, 3-hidroxiacil-CoA desidrogenase de cadeia curta e expressão ectópica de SLC16A1 na membrana plasmática das células beta. O HI pode estar associado ao estresse perinatal, como asfixia do nascimento, toxemia materna, prematuridade ou retardo do crescimento intra-uterino, resultando em hipoglicemia neonatal prolongada. Mimetismo de HI neonatal inclui pan-hipopituitarismo, hipoglicemia induzida por fármaco, insulinoma, anticorpos antiinsulina e estimuladores do receptor de insulina, síndrome de Beckwith-Wiedemann e distúrbios congênitos de glicosilação. Exames laboratoriais para HI podem incluir quantificação de glicose, insulina, β-hidroxibutirato, ácidos graxos, amônia e perfil de acilcarnitinas plasmáticos, além de ácidos orgânicos urinários. Os exames genéticos estão disponíveis em laboratórios comerciais para os genes sabidamente associados à hiperinsulinemia. Testes de resposta insulínica aguda (RIA) são úteis na caracterização fenotípica. Exames de imagem e histológicos também estão disponíveis para diagnosticar e classificar o HI. O objetivo do tratamento de crianças com HI é prevenir os danos cerebrais da hipoglicemia, mantendo níveis de glicose plasmática acima de 70mg/dl por terapia farmacológica ou cirúrgica. CONCLUSÃO:A terapêutica do HI requer abordagem multidisciplinar que inclui endocrinologistas pediátricos, radiologistas, cirurgiões e patologistas, os quais são treinados para diagnosticar..

BACKGROUND: Hypoglycemia in infants and children can lead to seizures, developmental delay, and permanent brain damage. Hyperinsulinism (HI) is the most common cause of both transient and permanent disorders of hypoglycemia. HI is characterized by dysregulated insulin secretion, which results in persistent mild to severe hypoglycemia. The various forms of HI represent a group of clinically, genetically, and morphologically heterogeneous disorders. CONTENT: Congenital hyperinsulinism is associated with mutations of SUR-1 and Kir6.2, glucokinase, glutamate dehydrogenase, short-chain 3-hydroxyacyl-CoA dehydrogenase, and ectopic expression of SLC16A1 on β-cell plasma membrane. Hyperinsulinism may be associated with perinatal stress such as birth asphyxia, maternal toxemia, prematurity or intrauterine growth retardation, resulting in prolonged neonatal hypoglycemia. Mimickers of hyperinsulinism include neonatal panhypopituitarism, drug-induced hypoglycemia, insulinoma, antiinsulin and insulin-receptor stimulating antibodies, Beckwith-Wiedemann Syndrome, and congenital glycosylation disorders. Laboratory testing for hyperinsulinism may include quantification of blood glucose, plasma insulin, plasma β-hydroxybutyrate, plasma fatty acids, plasma ammonia, plasma acylcarnitine profile and urine organic acids. Genetic testing is available at commercial laboratories for genes known to be associated with hyperinsulinism. Acute insulin response (AIR) tests are useful in phenotypic characterization. Imaging and histological tools are also available to diagnose and classify hyperinsulinism. The goal of treatment in infants with hyperinsulinism is to prevent brain damage from hypoglycemia by maintaining plasma glucose levels above 700 mg/l (70 mg/dl) through pharmacologic or surgical therapy. SUMMARY: The treatment of hyperinsulinism requires a multidisciplinary approach that includes pediatric endocrinologists, radiologists, surgeons, and pathologists who trained to diagnose...

Hiperinsulinismo congénito: revisión de aspectos diagnósticos y terapéuticos a propósito de un caso clínico / Congenital hyperinsulinism: review of diagnostic and therapeutic

El hiperinsulinismo congénito (HC) es la causa más común de hipoglicemia persistente en el primer año de vida. Se acompaña de riesgo elevado de daño neurológico irreversible. En los últimos años se ha profundizado en el conocimiento sobre su patogenia, destacándose la heterogenicidad clínica, histológica y genética, con claras implicancias en el diagnóstico y tratamiento. Se describe el caso de un lactante portador de HC que debuta con hipoglicemias sintomáticas a los 5 meses de vida. El objetivo de esta comunicación es, a la luz de los conocimientos actuales, analizar los criterios diagnósticos y terapéuticos de esta patología. Se destaca la importancia de aplicar un algoritmo para guiar el estudio paraclínico y descartar las etiologías más frecuentes asociadas con la hipoglicemia.

Congenital hyperinsulinism (HC) is the most common etiology of persistent hypoglycemia in infants. It is associated with a high risk of irreversible neurological damage. Knowledge about its pathogenesis has improved in the past few years. It is characterized by a heterogeneous clinical presentation, histology and genetic which leads to special diagnosis and treatment features. This is a case report of a 5 month old with HC who had symptomatic hypoglycemia. The objective of this communication is to analyze the diagnosis and treatment criteria of HC. The need to follow a clinical and laboratory guideline for diagnosis will help exclude other causes of hypoglycemia.

Hipoglicemia na infância: resultados de um protocolo de avaliação prospectiva em crianças com até 1 ano de idade / Childhood hypoglycemia: results of prospective evaluation protocols in children with up to 1 year of age

O objetivo deste trabalho é relatar a experiência na aplicação de um protocolo de avaliação de hipoglicemia. Realizamos um estudo prospectivo com treze crianças com sintomas de hipoglicemia atendidas no Hospital de Clínicas de Porto Alegre, com idade média de 5,3 ± 4,5 meses, das quais oito pacientes eram do sexo feminino. Os pacientes foram submetidos ao teste de jejum, estímulo com glucagon e dosagens de glicemia, lactato, pH, ácidos graxos, insulina, peptídeo C, TSH, GH e cortisol, além de urina para avaliação de cetonúria. Dos treze pacientes avaliados, oito apresentaram hipoglicemia persistente e cinco apresentaram hipoglicemia transitória. O diagnóstico mais freqüente foi hiperinsulinismo persistente. Sugerimos a utilização de um protocolo simples de avaliação para hipoglicemia, que contempla as principais etiologias em crianças e que facilita o manejo desses pacientes.

The aim of this study is to present the experience of applying hypoglycemia evaluation protocol. We performed a prospective study with 13 children with hypoglycemia symptoms at the Hospital of Clinicas of Porto Alegre, with range age 5.3 ± 4.5 months and eight patients are female. The patients had been submitted to glucagon fasting test and blood glucose, lactate, pH, C peptide, insulin, fatty acids, TSH, GH, cortisol, and urine ketones were measured. Eight patients presented persistent hypoglycemia and five presented transitory hypoglycemia. The most frequent diagnosis was persistent hyperinsulinism. We suggest the use of a simple protocol for the evaluation of hypoglycemia, which contemplates the identifications of the main etiologies in children and facilitates the handling of these patients.

Hiperinsulinemia y cambios en el espesor intima media de la pared arterial / Hyperinsulinemia and changes in the half intima thickness of the arterial wall

Existen evidencias que relacionan hiperinsulinemia con aterosclerosis, pero no hay consenso sobre la fisiopatogenia de esta asociación. Está reconocido que el aumento del espesor intima media arterial ocurre en las etapas iniciales de la aterosclerosis. Objetivo: 1) Relacionar el nivel de insulina en sangre con el espesor intima media (EIM) de la pared arterial en dos grupos de sujetos jóvenes no diabéticos, Hiperinsulinémicos y Normoinsulinémicos. 2) Analizar la asociación entre el Homeostasis Model Assessmen (HOMA) y el EIM de la pared arterial en ambos grupos. 3) Comparar el colesterol total (col-total), colesterol-HDL (col-HDL), colesterol-LDL (col-LDL), triglicéridos (TG), índice cintura cadera (ICC), presión arterial (PA), índice de masa corporal (IMC) y ácido úrico, entre ambos grupos investigados y su asociación con el EIM de la pared arterial. Se estudiaron 98 sujetos de ambos sexos con edades entre 18 y 35 años, 59 Hiperinsulinémicos y 39 Normoinsulinémicos, grupo control (GC). Se determinó en ayunas: Insulinemia, glucemia, col-total, col-HDL, col-LDL, TG, ácido úrico y HOMA. Luego del suministro por vía oral de 75 grs. de glucosa, se controló glucemia e insulinemia a los 30, 60, y 120 minutos. Se valoró la PA, el ICC y el IMC. Se midió el EIM en el segmento de la arteria carótida común (ACC), sobre la pared ecográficamente lejana, utilizando ultrasonido de superficie con un transductor de 7.5 MHZ El grupo hiperinsulinémico presentó diferencias significativas con respecto al normoinsulinémico (GC) en todas las variables muestreadas.

Pancreatectomía proximal en nesidioblastosis / Proximal pancreatectomy in case of nesidioblastosis

En 1938 Laidiaw acuñó el término de nesidioblastosis refiriéndose a una neodiferenciación de los islotes de Langerhans, originada del epitelio de los conductos pancreáticos. Se presenta un caso clínico de un niño de 19 meses de edad, con convulsiones secundarias a hipoglucemia intratable. Se diagnosticó hiperinsulinismo con base en criterios clínicos y bioquímicos. Los hallazgos histopatológicos del páncreas mostraron la presencia de racimos de islotes de células P por todo el tejido acinar localizados en cabeza y un tercio proximal del cuerpo. Se realizó el diagnóstico de nesidioblastosis y para su tratamiento se practicó pancreatectomía proximal (60%), con una pancreático yeyunostomía distal (Y en Roux). Después del tratamiento, el paciente tuvo normalización de los niveles séricos de glucosa y de insulina. Se concluye que este procedimiento resultó efectivo al revertir la hipoglucemia, por lo que constituye el primer tratamiento alternativo al método convencional.

A 19 month old child who presented seizures secondary to intractable hypoglycemia, fulfilling the clinical and biochemical criteria for hyperinsulinism was studied. Histopathological findings of the pancreas showed the presence of small clusters of b cell islets throughout acinar tissue near ducts, in both the head and the proximal third of the body. Proximal pancreatectomy (60%) and distal pancreatic jejunostomy (Roux in Y) were performed. This procedure was effective in reverting hypoglycemia and constitutes the first successful alternative treatment.

Polycystic ovarian syndrome and hyperinsulinaemia

To determine the occurrence of hyperinsulinaemia in women with polycystic ovarian syndrome [PCOS]. A descriptive study. Isra University Hospital, Hyderabad from January 2002 to December 2003. Total 64 subjects were recruited from gynaecological outpatients department, between the ages of 15 and 40 years with clinical diagnosis of polycystic ovarian syndrome, presenting with weight gain, oligomenorrhoea, secondary amenorrhoea, hirsuitism or infertility and either ultrasound evidence of PCOS or raised Leutinizing Hormone [LH]/ Follicular Stimulating Hormone [FSH] ratio. Patient's venous blood was checked for fasting serum insulin. Out of total 64 women selected, 37[57.81%] were between 21 - 30 years of age. Weight gain was the commonest presenting complain [84.37%] followed by oligomenorrhoea [79.68%]. Infertility was found in 46 women [71.87%] and hyperandrogenism was observed in 43 women [62.49%]. Thirty-nine women [60.93%] had ultrasound evidence of PCOS and 43 [67.18%] had LH / FSH ratio greater than 2:1. Hyperinsulinaemia was seen in 27 [42.19%] women. In this study, 27 women [42.19%] had hyperinsulinaemia which indicates significant insulin resistance. Thus, all the patients presenting with clinical or biochemical evidence of PCOS must undergo checking of fasting serum insulin levels

Hiperinsulinismo neonatal persistente: Caso clínico y tratamiento médico con octreotide / Persistent neonatal hypoglycaemia: a clinical case treated with octreotide

El hiperinsulinismo neonatal constituye la causa más común de hipoglicemia persistente en el menor de 1 año. Existe una secreción inapropiada de insulina en condiciones de hipoglicemia debido a una alteración en el receptor de sulfonilurea en la célula beta pancreática. Se describe el caso de un recién nacido prematuro, pequeño para la edad gestacional, que presentó precozmente hipoglicemias de difícil manejo, requiriendo cargas de glucosa de hasta 26 mg/kg/min. Tras confirmar el diagnóstico se inició tratamiento médico con octreotide. Luego de 72 horas de iniciado el tratamiento se logró disminuir el aporte de glucosa endovenosa, suspendiéndolo a las 6 semanas. En el seguimiento no se han presentado complicaciones derivadas del tratamiento, su situación nutricional es adecuada y su desarrollo psicomotor es normal. El uso de octreotide debe ser considerado como alternativa terapéutica en niños con hiperinsulinismo persistente, evitando la cirugía que presenta alta morbimortalidad, especialmente en este grupo etario.

Persistent hyperinsulinemic hypoglycemia of infancy in 38 children

To describe the clinical, biochemical, radiological and electrophysiological features of 38 Saudi children with persistent hyperinsulinemic hypoglycemia of infancy that have been followed since 1983. Data from 38 patients followed at King Faisal Specialist Hospital and Research Centre, Riyadh, Kingdom of Saudi Arabia from 1983 through to 2002 was retrospectively analyzed. Persistent hyperinsulinemic hypoglycemia of infancy was diagnosed on the basis of high intravenous glucose requirement, high insulin to glucose ratio, negative urinary ketones and normal tandem mass spectrometry. The patients were assessed radiologically by brain magnetic resonance imaging, computed tomography, or both and electrophysiologically by brain stem auditory evoked potential, visual evoked response and electroencephalogram. The patients who failed medical therapy had subtotal pancreatectomy. The patients were severely hypoglycemic and intolerant to fast. Hypoglycemic convulsion was the most commonly presenting complaint. Eighteen patients were developmentally delayed and 14 of them had brain atrophy. All patients, except nine, did not respond to medical treatment and had surgery. Four pancreatectomized patients developed diabetes and 2 had malabsorption. One patient was treated medically during childhood and developed diabetes and weight gain during adolescence. Persistent hyperinsulinemic hypoglycemia of infancy is a relatively common and serious disease among Saudi children. Early medical intervention is necessary to avoid neurological damage in our patients who are severely hypoglycemic and medical therapy unresponsive. Surgically and probably medically treated patients are at high risk of developing diabetes that could be the natural outcome of this disease

Insulinorresistencia en bulimia nerviosa / Insulin resistance in nervous bulimia

La bulimia nerviosa es un trastorno de la conducta alimentaria de etiología multicausal que se caracteriza por la presencia de atracones recurrentes y conductas compensatorias inapropiadas de manera repetida con el fin de no ganar peso. Las dietas con alto contenido graso han sido implicadas en la etiología de la insulinorresistencia postulándose que el aumento del depósito de tejido graso aumentaría la adaptación a una elevada oxidación grasa presente en dietas de estas características. La respuesta metabólica a ingestas de alto valor calórico e hipergrasas en un corto período de tiempo seguida de purga y/o ayuno compensador se considera precipitante de hiperinsulinemia

Estudo de 100 pacientes com clínica sugestiva de hipoglicemia e manifestaçöes de vertigem, surdez e zumbido / Study of 100 patients with suggestive clinics of hypoglycemia and manifestations of vertigo, deafness and tinnitus

O estudo avaliou a sensibilidade da história clínica para detectar alterações metabólicas em pacientes com hipoacusia e/ou zumbido e/ou vertigem associados à clínica sugestiva de hipoglicemia. Para tanto, 100 pacientes com este quadro foram submetidos a teste de tolerância à glicose de 5h com dosagem simultânea de insulina (hipoglicemia = glicose < ou = 55 mg/dL em qualquer momento da curva glicêmica). Curvas glicêmicas alteradas foram observadas em 59 pacientes (44 hipoglicêmicas). A hipoglicemia foi detectada apenas após a terceira hora do exame em 38 pacientes. As curvas insulinêmicas foram compatíveis com hiperinsulinismo em 73 pacientes. Apenas quatro pacientes apresentaram ambas as curvas dentro da normalidade. O valor preditivo positivo para detecção de anormalidades no metabolismo glicídico pela história clínica foi de 96 por cento. Este fato sugere a implantação de um teste terapêutico, com dieta específica, como parte da avaliação de pacientes com clínica sugestiva de hipoglicemia e manifestações de vertigem, surdez e zumbido.

Secreción de insulina y sensibilidad a la insulina durante la prueba de tolerancia a la glucosa oral, en sujetos con tolerancia normal / Secretion of insulin and sensitivity to insulin during the oral glucose tolerance test in individuals with normal tolerance

Se realizó un estudio para seleccionar una serie de indicadores que permitan una estimación confiable del estado de la sensibilidad a la insulina mediante recursos diagnósticos accesibles en nuestro medio. Se calcularon los criterios de interpretación para 6 índices de hiperinsulinismo o resistencia a la insulina (insulinemia en ayunas, IO; área de insulina durante la prueba, ATI; índice insulinogénico inicial, II(0-30); índice insulinogénico total, II(0-180) y los parámetros de resistencia a la insulina, RI y actividad de la célula beta, estos últimos, derivados del modelo homeostático de regulación de la glucemia en ayunas) a partir de los resultados de las determinaciones de glucosa e insulina plasmática durante una prueba de tolerancia a la glucosa por vía oral realizada en 60 sujetos sanos, de ambos sexos sin antecedentes personales o familiares de diabetes mellitus o de trastornos de la tolerancia a la glucosa. Con estos resultados se estudió la frecuencia de trastornos de la sensibilidad a la insulina en otros sujetos con sobrepeso u obesidad. Hubo variaciones entre el número de casos detectados según los distintos criterios, por lo que se evaluó la correlación y la frecuencia de coincidencias en el diagnóstico entre ellos. Se concluyó que con el empleo de sólo 2 de los índices (RI e II0-30) se puede caracterizar el hiperinsulinismo o resistencia a la insulina. Así se pudieron caracterizar 2 poblaciones dentro del grupo de obesos, una con parámetros de tolerancia a la glucosa y de respuesta insulínica idénticos a los del grupo de referencia y otro con resistencia a la insulina (con baja o alta respuesta insulínica inicial). Se consideró que estos resultados preliminares debían ser verificados en una población de sujetos con trastornos de la tolerancia a la glucosa(AU)

Sindrome dos ovarios policisticos: contribuicao para o estudo da resistencia a insulina / Polycystic ovary syndrome: contribution for the study of insulin resistance

Apos uma avaliacao inicial, 25 pacientes com sindrome dos ovarios policisticos (SOP) foram submetidas a teste de tolerancia a glicose oral com dosagens de glicose e insulina. Treze pacientes foram tratadas com espironolactona, 200 mg/dia por 6 meses e reavaliadas aos 3 e 6 meses. Concluimos que : 1- a SOP esta associada com a resistencia a insulina; 2- insulinemia de jejum nao e suficiente para o diagnostico; 3- mulheres obesas com acanthosis nigricans sao mais resistentes a insulina e 4- o uso de um antiandrogenio melhora a...

Cambios en los factores de riesgo metabólicos en pacientes obesos en tratamiento / The effect of treatment on metabolic risk factors in obese patients

Background: Obesity is a threaten to health due to its association with cardiovascular risk factors. Aim: To assess the change in metabolic risk factors after weight reduction in obese patients. Patients and methods: A retrospective analysis of 277 obese patients (198 female) aged 39.5ñ12 years old, that completed a six month treatment period, consisting in a calori restricted diet (800-1200 Kcal/day), physical activity, education and group psychological counseling. At the beginning and at the end of the program, weight, waist circumference, resting energy expenditure (REE), serum lipid profile, plasma glucose and plasma insulin levels were measured. Results: During the treatment period, body mass index decreased from 38ñ7 to 33.2ñ6.4 kg/m2 with a weight loss of 11.7 kg, waist circumference decreased from 106.6ñ14.6 to 93.9ñ13.5 cm, REE decreased from 1774ñ383 to 1585ñ267 Kcal/day, blood glucose fell by 5.8 percent, plasma insulin fell by 40.4 percent, total cholesterol fell by 7.5 percent, LDL cholesterol fell by 8.7 percent, triglycerides fell by 26.6 percent, and total cholesterol/HDL ratio fell by 12.2 percent. Conclusions: Weight loss was associated with improvement in metabolic cardiovascular risk factors in obese patients