[Andean children with aneurysmal bone cyst treated with polidocanol (use off-label)]. / Niños andinos con quiste óseo aneurismático tratados con polidocanol (uso fuera de etiqueta).

INTRODUCTION: The aneurysmal bone cyst is a rare benign but aggressive osteolytic tumor for which there is still no ideal treatment, the reports on treatment by sclerotherapy in the pediatric population are scarce and in our region even less. The objective is to communicate the experience of the treatment of aneurysmal bone cyst with polydocanol 3%. MATERIAL Y METHODS: Retrospective, descriptive and cross-sectional study. Period: June/2017 to June/2021. Inclusion: patients with histological diagnosis of aneurysmal bone cyst; Under general anesthesia and fluoroscopic guidance, intralesional puncture with 16G needle was performed through which 3% polydocanol was slowly administered. Data: medical history. Quantitative variables shall be expressed in measures of central tendency and dispersion; qualitative variables shall be expressed as frequencies or percentages. RESULTS: Nine consecutive patients were included, all of whom had pain and tumor in one of the extremities. Gender: 3 female and 6 male. Age: median 10.5 years (range: 2-15.1). Weight: median 32.8 kg (range: 11-44.5). Total procedures: 44; procedures per patient: mean 4.9 (SD: ± 2.0). Procedure time: mean 33.9 minutes (SD: ± 18.3); radiation: mean 1.34 mGy (SD: ± 1.55). Hospitalization: one day, except one patient. Complications: skin damage in one case, no recurrences follow-up: 12 to 50 months. CONCLUSION: In this pediatric series, polydocanol 3% was useful and effective for the treatment of aneurysmal bone cyst, with few complications. One disadvantage is that it requires several sessions and in addition, no significant difference has been demonstrated between other forms of treatment in terms of the recurrence rate.

INTRODUCCIÓN: El quiste óseo aneurismático es un raro tumor osteolítico benigno, pero agresivo para el que aún no existe tratamiento ideal. Los comunicados sobre tratamiento mediante escleroterapia en población pediátrica son escasos y en nuestra región más aún. El objetivo es comunicar la experiencia del tratamiento del quiste óseo aneurismático con polidocanol 3%. MATERIAL Y MÉTODOS: Estudio retrospectivo, descriptivo y transversal. Período: Junio de 2017 a Junio de 2021. Inclusión: pacientes con diagnóstico histológico de quiste óseo aneurismático. Bajo anestesia general y guía fluoroscópica se realizó punción intralesional con aguja 16G a través de la cual se administró lentamente el polidocanol 3%. Datos: historia clínica. Las variables cuantitativas se expresarán en medidas de tendencia central y de dispersión; las variables cualitativas se expresarán como frecuencias o porcentajes. RESULTADOS: Se incluyeron nueve pacientes consecutivos, todos presentaban dolor y tumoración en alguna de las extremidades. Género: tres femeninos y seis masculinos. Edad: mediana 10.5 años (rango: 2-15.1). Peso: mediana 32.8 kg (rango: 11-44.5). Total de procedimientos: 44, procedimientos por paciente: promedio 4.9 (DE: ± 2.0). Tiempo de procedimiento: promedio 33.9 minutos (DE: ± 18.3); radiación: promedio 1.34 mGy (DE: ± 1.55). Hospitalización: un día, excepto un paciente. Complicaciones: Daño de piel en un caso, no recidivas. Seguimiento: de 12 a 50 meses. CONCLUSIÓN: En esta serie pediátrica el polidocanol 3% fue útil y efectivo para el tratamiento del quiste óseo aneurismático con escasas complicaciones. Una desventaja es que requiere varias sesiones y además, no se ha demostrado una diferencia significativa entre otras formas de tratamiento en términos de la tasa de recurrencia.

Characterization of a gastric tumor cell line defective in MHC class I inducibility by both alpha- and gamma-interferon.

Alpha/beta and gamma type interferons (IFN), act through distinct cell surface receptors and induce transcription of an overlapping sets of genes. MHC class I genes are inducible by both type of interferons. We have analyzed a gastric tumor cell line, AGS, which was completely defective in MHC class I response to interferon-alpha and gamma. Northern blot analysis demonstrated that the lack of IFN response was related with the absence of up-regulation of specific HLA class I mRNA. Electrophoretic mobility shift assays in various tumor cell lines after IFN-alpha and IFN-gamma treatment showed differential binding of the transcriptional factors to MHC class I regulatory elements. Comparison of kappa-B binding activity showed that IFN-alpha and IFN-gamma induced opposite changes in NF-kappa B binding activity in AGS cells, indicating that the absence of MHC class I response in AGS appears to be independent of kappa-B activity. In contrast, there were remarkable differences in the level of transcriptional factor binding to an interferon-responsive sequence element (IRSE), between AGS and other interferon-responsive tumor cell lines. This result suggests that the low level of transcriptional factor binding to IRSE in AGS cells was responsible of the lack of induction of MHC class I antigens. In this context, overlapping factors in the signal transduction pathway of both type I and II interferons may be involved in the non-responsiveness of this gastric carcinoma tumor cell line.

[Diurnal variations in circulating leukocytes and subsets: relation to plasma cortisol and ACTH]. / Variaciones diarias en leucocitos y subpoblaciones circulantes: relación con el cortisol y la ACTH plasmáticos.

Surface cellular antigens of leukocytes, lymphocytes and corresponding subpopulations have been analysed by using monoclonal antibodies marked with fluorescein (PITC), parallel to those marked with phycoerythrin (PE). Cortisol and ACTH plasmatics have also been determined through RIA, on two samples at 8am. and 8pm. During this twelve hour evolution, a highly significant dependence of the leukocytes, T, T4 and T8 lymphocytes on the circulating ACTH has also been found. In general during the experiment time leukocytes, lymphocytes and subpopulations, have experimented an increase which is significantly related to the pituitary hormone secretion. The existence of this significant correlation establishes the presence of a possible mechanism that connects the cellular immunity to determined hypothalamus hormones.

Effects of dopamine-receptor antagonists and renal denervation on amino acid-induced hyperfiltration.

The mechanism whereby an infusion of amino acids (AA) leads to increments in glomerular filtration rate (GFR) and renal plasma flow (RPF) is incompletely understood. Dopamine (DA) is a catecholamine in which known actions at low doses include the ability to increase both GFR and RPF. Furthermore, urinary DA excretion has been shown to be augmented after an oral protein load. We therefore studied the renal hemodynamic response to intravenous infusion of a 10% mixed AA solution in anesthetized euvolemic Wistar-Furth rats in the presence or absence of specific DA1 [Sch 23390 (SCH)] and DA2 [S-sulpiride (S-SP)] receptor antagonists. Infusion of AA in vehicle-pretreated rats resulted in a 28 +/- 8% increase in GFR and a 29 +/- 6% increase in effective ERPF over baseline values. Administration of AA in the presence of SCH also resulted in elevations in both GFR and ERPF by 23 +/- 3% and 26 +/- 6%, respectively. In contrast, when AA were given in the presence of S-SP, the rise in both GFR and ERPF was completely prevented. To examine whether the AA-induced hyperfiltration was due to DA release from renal nerves or enhanced renal tubule DA synthesis, we administered AA to rats in which the left kidney had been chronically denervated while the right kidney remained intact. Infusion of AA led to significant increments in GFR (33 +/- 4%) and ERPF (34 +/- 7%) only in the intact control kidney, whereas GFR and ERPF remained unaltered in the denervated kidney.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial natriuretic peptide and furosemide effects on hydraulic pressure in the renal papilla.

Atrial peptides (ANP) have been shown to preferentially increase blood flow to juxtamedullary nephrons and to augment vasa recta blood flow. To determine the effect of this alteration in intrarenal blood flow distribution on pressure relationships in inner medullary structures and their significance as a determinant of ANP-induced natriuresis, we measured hydraulic pressures in vascular and tubule elements of the renal papilla exposed in Munich-Wistar rats in vivo during an euvolemic baseline period and again during an experimental period. Rats in Group 1 received intravenous infusion of rANP administered as a 4 micrograms/kg prime and 0.5 microgram/kg/min continuous infusion, and were maintained euvolemic by plasma replacement. Infusion of ANP resulted in significant natriuresis, diuresis and increase in inulin clearance. Within 90 seconds of initiation of this systemic infusion, vasa recta hydraulic pressures were markedly increased and exceeded the small pressure increment occurring in loops of Henle and collecting ducts. Infusion of furosemide in Group 2 rats at a dosage which reproduced the increase in urine flow in Group 1 was associated with small and equivalent increases in both vascular and tubule elements, indicating that the differential pressure response observed in Group 1 was not due to increased tubule fluid flow rates, but was rather a specific ANP-induced vascular effect. Group 3 rats received an infusion of ANP in a setting where its whole kidney hemodynamic effects were prevented. This resulted in a marked blunting of natriuresis and diuresis, and obliteration of the pressure differential between vasa recta and tubules observed in Group 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial natriuretic peptide transcription, storage, and release in rats with myocardial infarction.

To study the role of atrial natriuretic peptide (ANP) in chronic heart failure, ANP synthesis, storage, and release were examined by measuring atrial ANP messenger ribonucleic acid (mRNA) levels and atrial and plasma ANP concentrations in rats with myocardial infarction produced by coronary artery ligation. Three groups were defined as the following: 1) controls, sham-operated, or operated, but noninfarcted; 2) moderate infarcts, involving 5-30% of the left ventricular circumference; and 3) large infarcts (greater than or equal to 30%). In addition, to determine a possible modulation by dietary Na intake on ANP levels in heart failure, plasma immunoreactive ANP (iANP) levels were measured in rats with and without infarcts given low, regular, or high Na intake for 2 wk, by which time all groups were in neutral balance. Plasma iANP levels varied directly with increasing infarct and atrial sizes, irrespective of Na intake. In contrast, atrial ANP concentration varied inversely with increasing infarct size. The ANP mRNA content index, a measure of total atrial ANP mRNA, was significantly increased in rats with large infarcts compared with control rats. These results indicate that in rats with myocardial infarction, the severity of left ventricular dysfunction, as inferred from infarct size, but not chronic Na intake, is the primary determinant of the extent of activation of the ANP system. Elevated circulating ANP levels are maintained through enhanced atrial synthesis and release. ANP may thus play an important role in the hemodynamic and renal adaptations to chronic heart failure.

Elevated plasma atrial natriuretic peptide levels in diabetic rats. Potential mediator of hyperfiltration.

Infusion of atrial natriuretic peptide (ANP) increases the glomerular filtration rate (GFR), and ANP is released from cardiac myocytes in response to extracellular fluid volume expansion. Since diabetes mellitus is associated with glomerular hyperfiltration and volume expansion, we investigated the relationship between ANP and GFR in diabetic rats given insulin to achieve stable moderate hyperglycemia or normoglycemia. At 2 wk after induction of diabetes, moderately hyperglycemic diabetic rats exhibited elevations of plasma ANP levels averaging 281 +/- 28 pg/ml vs. 158 +/- 15 pg/ml in normoglycemic diabetic rats. In hyperglycemic rats, the GFR was also elevated on average to 2.24 +/- 0.28 ml/min as compared with 1.71 +/- 0.13 ml/min in normoglycemic diabetic rats. To test further the relationship between ANP and GFR in diabetes, moderately hyperglycemic diabetic rats were infused either with a specific ANP antiserum or with nonimmune serum. The infusion of specific ANP antiserum uniformly reduced the GFR on average from 2.38 +/- 0.1 ml/min to 1.60 +/- 0.1 ml/min, whereas the infusion of nonimmune serum was without effect. It is concluded that elevated endogenous ANP levels contribute to the hyperfiltration observed in early diabetes in the rat.

Modulation of the natriuretic response to atrial natriuretic peptide by alterations in peritubular Starling forces in the rat.

The mechanisms underlying the natriuretic response to infusions of atrial natriuretic peptide (ANP) remain incompletely defined. By acting as renal vasodilators, atrial peptides may serve to alter peritubular capillary physical forces and favor a decrease in tubule solute reabsorption. Therefore, we studied the effects of known modifiers of intrarenal Starling forces on the natriuresis induced by infusion of intravenous hANP [4-28] (0.5 microgram/kg/min) in anesthetized, euvolemic Munich-Wistar rats. In the first series of studies, infusion of ANP resulted in a significant natriuresis, diuresis, and increase in inulin clearance and in a slight fall in systemic arterial pressure, as compared to vehicle infusion. Subsequent elevation of renal perfusion pressure by superimposition of angiotensin II infusion (0.1-0.2 microgram/kg/min i.v.) on continued ANP infusion resulted in marked further enhancement of natriuresis, independent of changes in glomerular filtration rate (GFR). In the second set of experiments, in which oncotic pressure in the postglomerular capillaries was elevated by hyperoncotic exchange transfusion, administration of ANP did not result in natriuresis, even though GFR increased by the same magnitude as that seen in isooncotic animals given ANP. These observations are consistent with the view that peritubular capillary hydraulic and oncotic pressures modulate the natriuretic and diuretic effects of ANP.