[Adult-onset of recurrent Coats disease]. / Enfermedad de Coats recidivante diagnosticada en sujeto adulto.

CASE REPORT: A male diagnosed with Coats disease at the age of 30 years, had a relapse of this condition 14 years later. His first symptom of blurred vision occurred in both episodes and similar findings of unilateral retinal exudation and lipid deposition at boundary were seen. Angiography showed the characteristic early hyperfluorescence of the telangiectasias and late leakage of dye. DISCUSSION: Coats disease is relatively uncommon and, as the degree of involvement varies from case to case, a randomized, prospective study of treatment would probably not be feasible. Despite the characteristic features of this disease, the differential diagnoses must be considered in both children and adults.

Enfermedad de Coats recidivante diagnosticada en sujeto adulto / Adult-onset of recurrent coats disease

Caso clínico: Paciente varón que con 30 años tuvo el primer episodio de enfermedad de Coats y recurrencia 14 años más tarde. Clínicamente ambos episodios tienen como síntoma de inicio visión borrosa y exploración típica de exudación masiva retiniana con corona de exudados duros. La angiografía presenta hallazgos característicos de telangiectasia retiniana con dilatación anormal de vasos con hiperfluorescencia precoz y fuga tardía. Discusión: Coats es una entidad clínica poco frecuente y con grado de severidad variable, que hacen difíciles los estudios randomizados prospectivos. Pese a los hallazgos característicos, hay que descartar otros diagnósticos tanto en el niño como en el adulto causantes de esa misma clínica

Case report: A male diagnosed with Coats disease at the age of 30 years, had a relapse of this condition 14 years later. His first symptom of blurred vision occurred in both episodes and similar findings of unilateral retinal exudation and lipid deposition at boundary were seen. Angiography showed the characteristic early hyperfluorescence of the telangiectasias and late leakage of dye. Discussion: Coats disease is relatively uncommon and, as the degree of involvement varies from case to case, a randomized, prospective study of treatment would probably not be feasible. Despite the characteristic features of this disease, the differential diagnoses must be considered in both children and adults

Ruptura prematura de membranas ovulares: incidencia y manejo en el Hospital Dr. Patrocinio Peñuela Ruíz IVSS 2001-2004 / Ovular premature rupture of membranes: incidence and management in the Hospital Dr. Patrocinio Peñuela Ruíz IVSS 2001-2004

Se realizó un estudio retrospectivo, longitudinal, descriptivo en la maternidad del Hospital “Dr. Patrocinio Peñuela Ruíz” durante el período 2001-2004, basado en la revisión de 132 historias clínicas con diagnóstico de RPM. Encontrándose los siguientes resultados: el grupo etáreo predominante fue 25-29 años (36,36 por ciento), la edad gestacional 37-41 semanas (72,72 por ciento), se presentó principalmente en nulíparas (53,03 por ciento), el inicio de trabajo de parto fue predominantemente menos de 24 horas (68,18 por ciento), el apgar del RN al 1° y 5° minuto fue 7-10 pts (89,35 por ciento) el 53,03 por ciento de las madres no presentó enfermedad asociada, ni complicaciones postparto (90,90 por ciento). La conducta tomada en la mayoría de los casos fue inducción del trabajo de parto (56,06 por ciento), sin embargo terminaron en cesárea segmentaría (88,63 por ciento), de las cuales 13,63 por ciento por SFA, 25,75 por ciento DCP y 50 por ciento distocia de dilatación y descenso post-inducción fallida. El uso de cefalosporinas (78,03 por ciento) favoreció la evolución clínica satisfactoria de madres con diagnóstico de PRM y la triple cura en los casos de corioamnioitis (2,27 por ciento). Se concluye que no existe ninguna controversia cuando la RPM se acompaña de sufrimiento fetal o corioamnioitis clínica, en cuyo caso la terminación del embarazo es la conducta indicada. Sin embargo, cuando ésta se produce sin signo alguno de trabajo de parto, corioamnionitis clínica o sufrimiento fetal, el resultado perinatal está sometido a un delicado equilibrio entre prematuridad e infección corioamniótica (sepsis materna o fetal). El tiempo juega entonces un papel preponderante y todos los esfuerzos médicos se derigen a obtener una rápida madurez fetal con un mínimo de riesgo séptico. Con el manejo actual de la ruptura prematura de membranas que se hace en el HPPR se obtuvo en general un resultado aceptable, ya que la frecuencia de infección materna fue muy baja.

Epidemiología del embarazo ectopico en el Hospital "Dr. Patrocinio Peñuela Ruíz": IVSS 2005 / Epidemiology of ectopic pregnancy at the Hospital Dr. Patrocinio Peñuela Ruíz: IVSS 2005

El embarazo ectópico es la implantación del huevo fertilizado fuera de la cavidad uterina. Se presenta en el 2 por ciento de los embarazos en Estados Unidos, en nuestro país en un 0,007 a 4,4 por mil y es la segunda causa de morbimortalidad en el primer trimestre del embarazo. Conocer la relación de algunos factores epidemiológicos, clínicos diagnósticos y terapéuticos en esta entidad. Estudio retrospectivo de 18 pacientes con diagnóstico embarazo ectópico periodo enero-diciembre 2005, en la maternidad del Hospital “Dr. Patrocinio Peñuela Ruíz” IVSS, Estado Táchira. Se utilizó el porcentaje como método estadístico. El grupo etáreo predominante fue 30-34 años (38,88 por ciento), la edad gestacional 5-9 semanas (66,66 por ciento), se presentó principalmente en nulíparas (38,88 por ciento), los antecedentes mayormente relacionados fue el aborto (33,33 por ciento) y la esterilización quirúrgica (27,77 por ciento). La clínica al momento del ingreso fue dolor abdominal más sangrado activo (77,77 por ciento) con fondo de saco de Douglas abombado y doloroso (77,77 por ciento) en los casos de Embarazo ectópico accidentado (72,22 por ciento). El diagnóstico definitivo se obtuvo por medio de la ecografía más cuantificación de HCG (66,66 por ciento). La forma de presentación fue accidentado 72,22 por ciento y no accidentado u organizado en 27,77 por ciento. La localización tubárica 94,44 por ciento fue la mayormente reportada en los hallazgos operatorios y de ellas la ampullar 61,11 por ciento. La conducta tomada en todos los casos fue procedemiento quirúrgico de las cuales se realizó 77,77 por ciento salpingectomia total. Para disminuir la morbilidad y mortalidad que produce el Embarazo Ectópico es preciso diagnósticarlo precozmente. En las últimas décadas ha aumentado la frecuencia de embarazo ectópico, relacionado este incremento principalmente con conductas sexuales no responsables o no protegidas, que llevan entre otros problemas a padecer infecciones de transmisión.

Tema de revisión: ruptura prematura de membranas ovulares / Tema de review: rupture premature of the membranes ovular

Actualmente existe una alta proporción de RPM (2-22 por ciento) y es una de las patologías obstétricas más frecuentes, considerada un problema de salud pública, por ser responsable de la mayoría de partos pretermino (30 por ciento); tiene estrecha relación con la morbi-mortalidad materno-perinatal. Su incidencia es muy variable y depende en gran parte de la situación socioeconómica de la embarazada debido a la menor probabilidad de recibir cuidados médicos prenatales adecuados. Puede presentarse al final del embarazo causada por un debilitamiento natural de las membranas y por la fuerza de las contracciones; también ocurre en etapas tempranas del embarazo y fundamentalmente se asocia a infecciones locales (cervicovaginitis) e infecciones del tracto urinario; mala nutrición y sobredistensión uterina. Otros factores vinculados son los antecedentes de parto pretermino, hemorragia vaginal y tabaquismo. Produce numerosas complicaciones en el binomio materno-fetal como infecciones (corioamnioitis), parto pretermino, compresión del cordón umbilical y prolapso del cordón provocando sufrimiento fetal e incluso muerte fetal. Existen 2 tipos de manejo: activo (culminación del embarazo por cesárea o inducción del trabajo de parto) y expectante (espera del inicio espontáneo del trabajo de parto).

[Merkel cell carcinoma of the eyelid: a case report]. / Carcinoma de células Merkel palpebral: a propósito de un caso.

PURPOSE/METHODS: We report the case of a 73-year-old white female suffering from Merkel cell carcinoma (MCC) of the eyelid with an evolution of two and half months. MCC is a cutaneous neuroendocrine malignant tumor arising from Merkel cells. These cells are common along the eyelid margin in between the eyelashes. It is infrequent but highly aggressive and with potential metastases. Immunohistochemical and ultrastructural studies may be necessary for an histopathological diagnosis. RESULTS/CONCLUSIONS: Tumor resection with wide security margins must be undertaken as soon as possible. In addition, the patient may require postoperative radiotherapy.

Carcinoma de células merkel palpebral: a propósito de un caso / Merkel cell carcinoma of the eyelid: a case report

Objetivo/Método: El carcinoma de células Merkel (CCM) es un tumor maligno cutáneo neuroendocrino primario que procede de las células Merkel; estas células se encuentran en los párpados a lo largo del margen palpebral entre las pestañas. Es un tumor infrecuente pero altamente agresivo y metastatizante. Para su diagnóstico histopatológico puede ser necesario un estudio inmunohistoquímico y ultraestructural. Presentamos el caso de una paciente de 73 años afecta de CCM palpebral de dos meses y medio de evolución. Resultados/Conclusión: Debe realizarse la resección del tumor con amplios márgenes de seguridad de forma precoz y puede ser necesaria la radioterapia postoperatoria (AU)

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Stimulation of glucose transport by thyroid hormone in 3T3-L1 adipocytes: increased abundance of GLUT1 and GLUT4 glucose transporter proteins.

In 3T3-L1 adipocytes we have examined the effect of tri-iodothyronine (T(3)) on glucose transport, total protein content and subcellular distribution of GLUT1 and GLUT4 glucose transporters. Cells incubated in T(3)-depleted serum were used as controls. Cells treated with T(3) (50 nM) for three days had a 3.6-fold increase in glucose uptake (P<0.05), and also presented a higher insulin sensitivity, without changes in insulin binding. The two glucose carriers, GLUT1 and GLUT4, increased by 87% (P<0.05) and 90% (P<0. 05), respectively, in cells treated with T(3). Under non-insulin-stimulated conditions, plasma membrane fractions obtained from cells exposed to T(3) were enriched with both GLUT1 (3. 29+/-0.69 vs 1.20+/-0.29 arbitrary units (A.U.)/5 microg protein, P<0.05) and GLUT4 (3.50+/-1.16 vs 0.82+/-0.28 A.U./5 microg protein, P<0.03). The incubation of cells with insulin produced the translocation of both glucose transporters to plasma membranes, and again cells treated with T(3) presented a higher amount of GLUT1 and GLUT4 in the plasma membrane fractions (P<0.05 and P<0.03 respectively). These data indicate that T(3) has a direct stimulatory effect on glucose transport in 3T3-L1 adipocytes due to an increase in GLUT1 and GLUT4, and by favouring their partitioning to plasma membranes. The effect of T(3) on glucose uptake induced by insulin can also be explained by the high expression of both glucose transporters.

[Body mass index influence in the insulin action mechanisms]. / Influencia del índice de masa corporal sobre los mecanismos de acción de la insulina.

OBJECTIVE: Improve the knowledge of the "in vitro" insulin action in healthy subjects with different body mass index (BMI), in order to know the role of obesity in the diabetes mellitus. MATERIAL: In 12 healthy subjects with different BMI and normal oral glucose test we made a gluteal biopsy to obtain adipose tissue. In the isolated adipocytes we studied the interaction of insulin with its receptor and the glucose transport. RESULTS: BMI was not correlated with the maximal specific 125I-insulin binding but was negative when correlated with the glucose transport in basal situation (r = -0.63, p < 0.05) as well as when stimulated with insulin (r = -0.67, p < 0.05), when the results were expressed as number of cells. When the data were expressed as surface, BMI was negative correlated with the percentage of maximal specific 125I-insulin binding (r = -0.81, p < 0.05), and also with the basal glucose transport (r = -0.69, p < 0.05) and stimulated with insulin (r = -0.77, p < 0.01). CONCLUSION: The increase of BMI is an important diabetogenic agent, acting at receptor as well as at postreceptor level, and the data should be expressed according to the cellular diameter rather than to the number of cells in subjects with different BMI. A cutting point was established at the 30 BMI level after which the described alterations could be observed.

High glucose uptake by adipocytes in a type 1 diabetic patient with a partial 'honeymoon' period.

Hypoglycaemic episodes and low insulin requirements are frequently seen in the early phase of treatment of Type 1 diabetes mellitus but the mechanism is not clear. We present a diabetic patient with recurrent hypoglycaemia in the early phase of insulin treatment. A very high glucose transport in adipocytes (basal: 176 and insulin stimulated glucose transport 10(-7) mol l(-1): 335 fl cell(-1) s(-1)) was found when compared with reference laboratory diabetic patients (basal: 59 +/- 10 and insulin 10(-7) mol l(-1): 106 +/- 7 fl cell(-1) s(-1), mean +/- SE) and with reference laboratory of non-diabetic subjects (basal: 106 +/- 6 and insulin 10(-7) mol l(-1): 188 +/- 15 fl cell(-1) s(-1)). Insulin binding to adipocytes was in the normal range. The patient was studied again 1 year later when the partial clinical remission had disappeared, and the glucose transport in adipocytes had decreased. In conclusion, an increase in glucose uptake by peripheral tissues may be among the mechanisms of the partial 'honeymoon' period of diabetic patients.

Gliclazide treatment of streptozotocin diabetic rats restores GLUT4 protein content and basal glucose uptake in skeletal muscle.

This study examined whether the treatment of streptozotocin (STZ)-diabetic rats with gliclazide (5 mg/kg body weight twice daily orally) increases muscle glucose uptake. Rats were treated (group G, n = 10) or untreated (group D, n = 11) for 12 days. Normal rats served as controls (group C, n = 11). At the end of the treatment, both basal and insulin-stimulated glucose uptake by the perfused hindquarters were measured. In gastrocnemious muscles, the protein content of GLUT4 and the insulin binding and tyrosine kinase activity of partially purified solubilized insulin receptors were measured. Group G had a lower mean glycemic value during the treatment period than group D (mean +/- SEM, 17 +/- 0.6 v 19.7 +/- 0.5 mmol/L, P < .05), without differences in serum insulin levels. Basal glucose uptake by the hindquarters was significantly higher in group G versus group D (2.8 +/- 0.3 v 1.3 +/- 0.2 mumol/g/h, P < .05), and was not different versus group C (3.6 +/- 0.2 mumol/g/h). Insulin-stimulated glucose uptake was higher (P < .05) in group C compared with the two groups of diabetic rats. Glucose uptake at 10(-7) mol/L insulin was higher in group G than in group D (9.2 +/- 0.6 v 7.0 +/- 0.6 mumol/g/h, P < .05). Both insulin binding and tyrosine kinase activity were similar in muscle insulin receptors from both groups of diabetic rats. The GLUT4 protein content was higher in group G than in group D (95 +/- 10 v 57 +/- 7 arbitrary units [AU]/microgram protein, P < .05) and similar to that of group C (113 +/- 13 AU/microgram protein). In conclusion, gliclazide has a glucose-lowering effect in STZ-diabetic rats that could be attributed to an increase in muscle glucose clearance by a post-insulin receptor mechanism, probably related to a normalization of GLUT4 content.

Sulfonylureas stimulate glucose uptake through GLUT4 transporter translocation in rat skeletal muscle.

We studied the effect of gliclazide on glucose uptake and GLUT4 translocation in skeletal muscle. Rat hindquarters were perfused in the absence or presence of gliclazide (300 micrograms/ml), insulin or both drugs. The basal glucose uptake was increased 2.7-fold by gliclazide (p < 0.05). Gastrocnemius muscles perfused with gliclazide had a significant increase (2.4-fold) in the GLUT4 content in plasma membranes compared to basal conditions (p < 0.05). The stimulations produced by 1 nM insulin on muscle glucose uptake (2.8-fold) and on GLUT4 level in plasma membranes (2.5-fold) were similar to those produced by gliclazide. The effect of insulin on the glucose uptake and on the GLUT 4 translocation was significantly enhanced by gliclazide (3.4-fold and 3.7-fold vs basal, respectively). These data show that sulfonylureas stimulate glucose uptake in skeletal muscle by promoting the movement of GLUT4 to the plasma membrane.

Sulphonylurea stimulates glucose uptake in rats through an ATP-sensitive K+ channel dependent mechanism.

We studied the effect of gliclazide, a second-generation sulphonylurea, on rat skeletal muscle glucose uptake using perfused hindquarter muscle preparations. Gliclazide at concentrations of 10 to 1000 microgram/ml increased (p < 0.05) the basal glucose uptake. The effect of gliclazide on glucose uptake was immediate and dose-dependent, reaching a plateau at a concentration of 300 micrograms/ml; the half-maximal effect was obtained between 25 and 50 micrograms/ml. The glucose uptake stimulated by gliclazide (300-1000 micrograms/ml) did not differ from that achieved by 10(-9) mol/l insulin, and was lower (p < 0.05) than that obtained with 10(-7) mol/l insulin. The combination of gliclazide (300 micrograms/ml) and 10(-9) mol/l insulin produced an increase in glucose uptake (7.7 +/- 0.6 mumol.g-1.h-1, n = 8, mean +/- SEM) which was higher (p < 0.05) than that achieved with 10(-9) mol/l insulin (5.6 +/- 0.7 mumol.g-1.h-1, n = 11) and not different from that obtained with 10(-7) mol/l insulin (9.8 +/- 1.0 mumol.g-1.h-1, n = 11). Diazoxide (100 mumol/l), an ATP-sensitive K+ channel opener, reversed the stimulatory effect of gliclazide (100 microgram/ml) on muscle glucose uptake from 3.1 +/- 0.4 to 0.5 +/- 0.2 mumol.g-1.h-1, (n = 7, p < 0.001). The addition of diazoxide prior to gliclazide into the perfusion medium blocked the gliclazide-induced glucose uptake by the hindquarter muscle preparations. In conclusion, gliclazide alone has an immediate stimulatory effect on glucose uptake by skeletal muscle and together with insulin has an additive effect on muscle glucose uptake. The effect of gliclazide on muscle glucose uptake seems to be due to the inhibition of ATP-sensitive K+ channels.

Impaired tyrosine-kinase activity of muscle insulin receptors from hypomagnesaemic rats.

The effect of magnesium deficiency on glucose disposal, glucose-stimulated insulin secretion and insulin action on skeletal muscle was investigated in rats which were fed a low magnesium-containing diet for 4 days. Control rats were fed a standard diet. Compared to the control rats, the rats fed with low magnesium diet presented: 1) lower serum magnesium levels (0.45 +/- 0.02 vs 0.78 +/- 0.01 mmol/l, p < 0.001), 2) higher basal serum glucose (6.8 +/- 0.02 vs 5.5 +/- 0.2 mmol/l, p < 0.05) and similar basal serum insulin, 3) 40% reduction (p < 0.001) in the glucose disappearance rate after its i.v. administration, and 4) 45% reduction (p < 0.05) in the glucose-stimulated insulin secretion. The insulin action upon the glucose uptake by skeletal muscle was determined by means of hindquarter perfusions. Compared with control rats, magnesium-deficient rats presented: 1) normal basal glucose uptake, 2) lower stimulatory effect on the glucose uptake by insulin at the concentrations of 5 x 10(-10) mol/l (3.0 +/- 0.9 vs 5.4 +/- 0.6, p < 0.05) and 5 x 10(-9) mol/l (6.3 +/- 0.5 vs 8.0 +/- 0.5, p < 0.05), 3) normal glucose uptake at a maximal insulin concentration of 1 x 10(-7) mol/l, and 4) 50% reduction in the insulin sensitivity (ED50: 1.3 +/- 0.3 vs 0.55 +/- 0.1 mol/l, p < 0.05). In partially purified insulin receptors prepared from gastrocnemius muscle, 125I-insulin binding was similar in both groups of rats. However, the autophosphorylation of the beta-subunit of the insulin receptor was significantly reduced by 50% in magnesium-deficient rats and the tyrosine kinase activity of insulin receptors toward the exogenous substrate Poly Glu4; Tyr 1 was also reduced (p < 0.05) by hypomagnesaemia. The abundance of the insulin-sensitive glucose transporter protein (muscle/fat GLUT4), measured by Western blot analysis using polyclonal antisera, was similar in muscles of control and hypomagnesaemic rats. These findings indicate that hypomagnesaemia has a deleterious effect on glucose metabolism due to an impairment of both insulin secretion and action. The insulin resistance observed in skeletal muscle of magnesium-deficient rats may be attributed, at least in part, to a defective tyrosine kinase activity of insulin receptors.

Intracranial pressure dynamics in clinical practice: online PC-based ICP monitoring system.

Correct patient management involves determining the exact point on the intracranial pressure/volume (P/V) curve that corresponds to the patient; this requires calculating intracranial elastance (IE). Intracranial pressure (ICP) monitoring systems should provide the necessary information for this purpose. An ICP monitoring unit is presented that acquires ICP, systemic arterial pressure (SAP) and airway pressure (AWP). The cerebral perfusion pressure (CPP) and the mean values and the peak-to-peak values of the two of them (ICPmean, SAPmean, ICPp-p, SAPp-p,) are calculated. Graphs display the temporal evolution (TE) of the ICP and SAP, as well as histograms of the ICP (%) and intracranial pulse amplitude (ICPAmP) with respect to the ICP or CPP during the preceding 3, 6, 12 or 24 h of monitoring. By digital filtering the ICP respiratory and cardiac components (RCICP, CCICP) are calculated. Finally, the pulse amplitudes (AmP) of the ICP, CCICP and RCICP are computed, as well as the average pulses per minute of SAP, CCICP, AWP and RCICP. Two off-line pulse-amplitude and pulse-morphology oriented toolkits display the afore-mentioned curves, histograms and average pulses per minute, and other additional ones, in order to achieve a deeper patient monitoring study.

An ODA-based coder/decoder for multimedia medical documents.

This paper describes the prototype of a coder/decoder based on the Open Document Architecture (ODA) standard for management of medical documents, as well as the working environment in which it has been developed. The prototype has been assessed in an X-Windows-equipped workstation with a relational database containing patient folders (text and still images) from the departmental information system of the liver transplantation unit.

Valvuloplastia pulmonar percutánea con balón / Percutaneous pulmonary valvuloplasty with balloon

Se efectuó valvuloplastia pulmonar percutánea en 16 pacientes con estenosis pulmonar valvular congénita entre los meses de junio y noviembre de 1987, con edad promedio de 6.5 años. Por vía percutánea se realizó el cateterismo y angiocardiografía confirmatorios. Preferentemente se practicó la valvuloplastia con balón de mayor diámetro (20%) que el anillo valvular pulmonar. En 12 de 16 pacientes sometidos a esta técnica, se obtuvo un dramático descenso de la gradiente transvalvular pulmonar, hasta cifras consideradas no quirúrgicas (gradiente menor a 50 mmHg). En 2 niños, la gradiente no se modificó y en otros 2 esta descendió a cifras aún quirúrgicas, pensamos que podría haber un descenso futuro espontáneo al ceder la estenosis pulmonar infundibular reactiva de éstos pacientes. Hubo un fracaso en que no se logró franquear la válvula pulmonar por la presencia de banda muscular en el infundíbulo, y debió ser intervenido quirúrgicamente. No hubo complicaciones importantes, solo bradicardia e hipotensión arterial pasajera durante la dilatación del balón. El promedio de hospitalización fue de 48 horas. Se concluye que éste procedimiento es una alternativa efectivo, seguro y económico en el tratamiento de la estenosis pulmonar valvular congénita