Distinctive gastrointestinal motor dysfunction in patients with MNGIE.

BACKGROUND: Mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) is a rare mitochondrial disease caused by mutations in TYMP, encoding thymidine phosphorylase. Clinically it is characterized by severe gastrointestinal dysmotility associated with cachexia and a demyelinating sensorimotor polyneuropathy. Even though digestive manifestations are progressive and invariably lead to death, the features of gastrointestinal motor dysfunction have not been systematically evaluated. The objective of this study was to describe gastrointestinal motor dysfunction in MNGIE using state-of-the art techniques and to evaluate the relationship between motor abnormalities and symptoms. METHODS: Prospective study evaluating gastrointestinal motor function and digestive symptoms in all patients with MNGIE attended at a national referral center in Spain between January 2018 and July 2022. KEY RESULTS: In this period, five patients diagnosed of MNGIE (age range 16-46 years, four men) were evaluated. Esophageal motility by high-resolution manometry was abnormal in four patients (two hypoperistalsis, two aperistalsis). Gastric emptying by scintigraphy was mildly delayed in four and indicative of gastroparesis in one. In all patients, small bowel high-resolution manometry exhibited a common, distinctive dysmotility pattern, characterized by repetitive bursts of spasmodic contractions, without traces of normal fasting and postprandial motility patterns. Interestingly, objective motor dysfunctions were detected in the absence of severe digestive symptoms. CONCLUSIONS AND INFERENCES: MNGIE patients exhibit a characteristic motor dysfunction, particularly of the small bowel, even in patients with mild digestive symptoms and in the absence of morphological signs of intestinal failure. Since symptoms are not predictive of objective findings, early investigation is indicated.

Clinical significance of small bowel manometry patterns suggestive of intestinal obstruction.

INTRODUCTION: Minute rhythm and prolonged simultaneous contractions are patterns of postprandial small bowel contractile activity that historically have been considered as suggestive of mechanical intestinal obstruction; however, these patterns have been also encountered in patients with motility-like symptoms in the absence of bowel obstruction. The objective of this study was to determine the current diagnostic outcome of patients with these intestinal manometry patterns. METHODS: Retrospective study of patients with chronic digestive symptoms evaluated by intestinal manometry at our center between 2010 and 2018. RESULTS: The minute rhythm (MRP) or prolonged simultaneous contractions (PSC) postprandial patterns were detected in 61 of 488 patients (55 MRP and 6 PSC). Clinical work-up detected a previously non-diagnosed partial mechanical obstruction of the distal intestine in 10 (16%) and a systemic disorder causing intestinal neuropathy in 32 (53%). In the remaining 19 patients (31%, all with MRP), the origin of the contractile pattern was undetermined, but in 16, substantial fecal retention was detected within 7 days of the manometric procedure by abdominal imaging, and in 6 of them colonic cleansing completely normalized intestinal motility on a second manometry performed within 39 ± 30 days. CONCLUSION AND INFERENCE: Currently, the most frequent origin of MRP and PSC encountered on small bowel manometry is intestinal neuropathy, while a previously undetected mechanical obstruction is rare. Still, in a substantial proportion of patients, no underlying disease can be identified, and in them, colonic fecal retention might play a role, because in a subgroup of these patients, manometry normalized after colonic cleansing. Hence, colonic preparation may be considered prior to intestinal manometry.

Benefit of extending the protocol for high resolution manometry according to the version 4.0 of the Chicago criteria. A multicenter study.

BACKGROUND: The last version of the Chicago Criteria for high resolution esophageal manometry proposes an expanded protocol including complementary maneuvers to improve the diagnostic yield of the exploration. Our aim was to determine the diagnostic gain of the CCv4.0 protocol compared to the CCv3.0 protocol. METHODS: All manometry recordings performed in 4 reference centers during the first 10 months after the implementation of the new protocol were retrospectively reviewed. The time spent to complete the protocol was measured, and the changes in diagnosis resulting from the new CCv4.0 were compared to CCv3.0. KEY RESULTS: From a total of 756 HRM performed, 606 studies could be properly analyzed. The duration of the studies was 18.3 ± 4.3 min. From these, 11.3 ± 3.4 min were spent to complete the CCv3.0 protocol, and 7.4 ± 3.6 min were spent for the remaining maneuvers. A discordant diagnosis between CCv3.0 and CCv4.0 was obtained in 12% of patients: 32% of patients with ineffective esophageal motility turned to normal motility; 24% of patients with esophagogastric junction outlet obstruction (EGJOO) turned to a non-obstructive disorder; and 1% of patients with an apparently normal EGJ relaxation, turned to an obstructive disorder. EGJOO according to CCv4.0 was more prevalent in patients referred for dysphagia (11%) than those referred for GERD (4%; p = 0.003). CONCLUSIONS AND INFERENCES: Prolongation of the time spent to complete the CCv4.0 protocol leads to a change in the diagnosis of 12% of patients. Clinically relevant changes are mainly related to the evaluation of EGJOO.

Evaluation of abdominal gas by plain abdominal radiographs.

BACKGROUND: Our aim was to determine the reliability of plain abdominal radiographs for the evaluation of abdominal gas content in patients with functional digestive symptoms. METHODS: Abdominal CT scan scout views, mimicking a conventional plain abdominal radiograph, were obtained from 30 patients both during episodes of abdominal distension and basal conditions. Physicians (n = 50) were instructed to rate the estimated volume of gas in the 60 images presented in random sequence using a scale graded from 0 to ≥600 ml. KEY RESULTS: The gas volumes estimated in the scout views differed from those measured by CT by a median of 90 (95% CI 70-102) ml, and the misestimation was not related to the absolute volume in the image. The accuracy of the observers, measured by their mean misestimation, was not related to their specialty or the training status (misestimation by 96 (95% CI 85-104) ml in staff vs 78 (70-106) ml in residents; p = 0.297). The accuracy was independent of the order of presentation of the images. Gas volume measured by CT in the images obtained during episodes of abdominal distension differed by a median of 39 (95% CI 29-66) ml from those during basal conditions, and this difference was misestimated by a median of 107 (95% CI 94-119) ml. The accuracy of these estimations was not related to the absolute gas volumes (R = -0.352; p < 0.001) or the magnitude of the differences. CONCLUSIONS & INFERENCES: Plain abdominal radiographs have limited value for the evaluation of abdominal gas volume in patients with functional gut disorders.

Severity of gastrointestinal bleeding is similar between patients receiving direct oral anticoagulants or vitamin K antagonists

Background: gastrointestinal bleeding (GIB) is a commonadverse event related to anticoagulation therapy. However,evidence comparing the severity, etiology and outcome ofGIB in patients taking direct oral anticoagulants (DOAC) vs.vitamin K antagonists (VKA) is scarce.Aim: to evaluate the severity, etiology and outcomes of GIBin patients under DOACs compared to VKA.Methods: patients under oral anticoagulant therapy admitted to the emergency department with acute GIB wereprospectively recruited from July 2016 to January 2018 ata tertiary referral hospital. Demographic and clinical out comes were obtained from medical records. GIB severitywas classified as mild, major, or severe according to theclinical presentation and type of support needed. Etiologyand location of bleeding, number of packed red blood cells(PRBC) transfused, and length of hospital stay were recorded until discharge or in-hospital death.Results: a total of 208 patients with acute GIB under oralanticoagulant treatment were recruited: 119 patients wereon VKA and 89 patients on DOAC, with similar characteristics. Thirty-one patients had severe GIB; 134 had major and43 had mild GIB, with no differences in severity, numberof PRBC, and length of hospital stay between the groups.Peptic disease was the most frequent etiology of GIB inpatients on VKA (20.2 % vs. 13.6 %, p = 0.20). Diverticularbleeding was the most frequent adverse event in patientson DOAC (14.3 % vs. 24.8 %, p = 0.056).Conclusions: severity and clinical outcomes of GIB aresimilar between patients on DOAC and patients on VKA,regardless of GIB etiology. (AU)

Effect of colonic distension on small bowel motility measured by jejunal high-resolution manometry.

BACKGROUND: Abnormal motility patterns in the jejunum can be detected in patients with prominent colonic content, and these abnormalities may be due to either a primary jejunal dysfunction or a reflex distortion. The objective of the present study was to determine the effect of colonic distension on small bowel postprandial motility using high-resolution manometry. METHODS: Single center, controlled, parallel, randomized, single blind study in healthy subjects testing the effect of colonic filling vs sham infusion on the responses to a meal in 16 healthy subjects. Nutrients were continuously infused in the proximal jejunum (2 Kcal/min) during the 2-h study period to induce a steady-state postprandial motor pattern. Jejunal motility was measured by water-perfused, high-resolution manometry. After 1 h postprandial recording (basal period), gas was infused during 7.5 min via a rectal tube (720 mL or sham infusion), and jejunal motility was recorded for another hour. KEY RESULTS: Jejunal postprandial motility during the basal period was characterized by two overlapping components: a) continuous segmental activity (non-propagated or shortly propagated) and b) intercurrent propagated fronts (3.8 ± 1.1 fronts of 2-5 clustered contractions/h >10 cm propagation). As compared to sham infusion, colonic gas filling: a) inhibited continuous segmental contractile activity (by 17 ± 4%; p = 0.044 vs control group) and b) stimulated intermittent propagated fronts (up to 9.0 ± 2.2 fronts/h; p = 0.017 vs control group). CONCLUSIONS AND INFERENCES: Long retrograde reflexes induced by colonic distension distort the balance between segmental and propagated activity, and may affect the normal response of the jejunum to food ingestion. Jejunal manometry in patients may be artifacted by colonic overload.

Severity of gastrointestinal bleeding is similar between patients receiving direct oral anticoagulants or vitamin K antagonists.

BACKGROUND: Gastrointestinal bleeding (GIB) is a common adverse event related to anticoagulation therapy. However, evidence comparing the severity, etiology and outcome of GIB in patients taking direct oral anticoagulants (DOAC) vs. vitamin K antagonists (VKA) is scarce. AIMS: To evaluate the severity, etiology and outcomes of GIB in patients under DOACs compared to VKA. METHODS: Patients under oral anticoagulant therapy admitted to the emergency department with acute GIB were prospectively recruited from July 2016 to January 2018 at a tertiary referral hospital. Demographic and clinical outcome were obtained from medical records. Severity of the GIB event was classified as mild, major or severe according to clinical presentation and the type of support needed. Etiology and location of bleeding, number of packed red blood cells transfused (PRBC) and length of hospital stay were recorded until discharge or in-hospital death. RESULTS: A total of 208 patients with acute GIB under oral anticoagulant treatment were recruited: 119 patients were on VKA and 89 patients on DOAC with similar characteristics. Thirty-one patients had severe GIB; 134 major and 43 mild, with no differences in severity, number of PRBC and length of hospital stay between the groups. Peptic disease was the most frequent etiology of GIB in patients on VKA (20.2 % vs. 13.6%, p=0.20). Diverticular bleeding was the most frequent adverse event in patients on DOAC (14.3% vs. 24.8%, p= 0.056). CONCLUSIONS: Severity and clinical outcomes of GIB are similar between patients on DOAC and patients on VKA, regardless of etiology of GIB.

Normative reference values for esophageal high-resolution manometry in healthy adults: A systematic review.

BACKGROUND AND PURPOSE: Establishing normative values of high-resolution esophageal manometry is necessary for accurate interpretation and comparison of measurements. In this systematic review, we aimed to summarize normal values for different esophageal high-resolution manometry systems. Moreover, we assessed the effect of body position, bolus consistency, and provocative maneuvers on these normative thresholds. We searched Medline, Embase, and the Cochrane Library from January 1st, 2006, to January 20th, 2020, for studies that reported normative data of high-resolution manometry in healthy volunteers. We assessed methodological quality of the included studies and planned a descriptive analysis. We analyzed data from 54 articles describing normative thresholds in high-resolution manometry using solid-state or water-perfused systems. Forty-six studies performed the manometry study in the supine position with liquid swallows, whereas sixteen studies described normative values in the upright position. Twelve studies assessed normative values for different bolus consistencies, and nine studies evaluated different provocative maneuvers. There is a considerable variety of normative values for esophageal high-resolution manometry depending on the equipment used and the protocols performed to obtain measurements. This should be taken into account when evaluating measurements in clinical practice and when comparing results of published research studies.

Distinguishing subgroups among µ-opioid receptor agonists using Na(+),K(+)-ATPase as an effector mechanism.

We evaluated the effects of intracerebroventricular administration of ouabain on the antinociception induced by five µ-opioid receptor agonists in a tail flick test on female CD-1 mice and the effects of these µ-opioid receptor agonists on mice forebrain synaptosomal ouabain-sensitive Na(+),K(+)-ATPase activity. The subcutaneous administration of the µ-opioid receptor agonists tested produced a dose-dependent antinociceptive effect. The antinociception induced by morphine (1-32 mg/kg), levorphanol (0.4-6.4 mg/kg), and buprenorphine (0.02-0.64 mg/kg) was antagonised in a dose-dependent manner by ouabain (0.001-10 ng, i.c.v.), whilst the antinociception produced by fentanyl (0.02-0.16 mg/kg) and methadone (2-10 mg/kg) was not influenced significantly by ouabain (1-100 ng, i.c.v.). Incubation in vitro of forebrain synaptosomes with morphine (10(-9)-10(-4) M), levorphanol (10(-10)-10(-4) M), buprenorphine (10(-10)-10(-5) M), or fentanyl (10(-10)-10(-5) M) stimulated significantly ouabain-sensitive Na(+),K(+)-ATPase activity in a concentration-dependent way. The order of efficacy (using the Emax as a measure of intrinsic efficacy) was: morphine (29.83±0.56%)>levorphanol (18.61±1.26%)>buprenorphine (14.91±0.74%)>fentanyl (10.10±1.73%). On the other hand, methadone (10(-10)-10(-5) M) did not significantly modify the ouabain-sensitive Na(+),K(+)-ATPase activity (Emax=5.11±0.92%). These results suggest that Na(+),K(+)-ATPase activity is involved in the antinociceptive effects of morphine, levorphanol and buprenorphine, but not in that produced by fentanyl and methadone. Thus, we can conclude that at least two subgroups can be distinguished among the µ-opioid receptor agonists taking into consideration the role of Na(+),K(+)-ATPase in their antinociceptive effects.

Changes in morphine-induced activation of cerebral Na(+),K(+)-ATPase during morphine tolerance: biochemical and behavioral consequences.

There is ample evidence of the biological changes produced by the sustained activation of opioid receptors. We evaluated the adaptive changes of cerebral Na(+),K(+)-ATPase in response to the sustained administration of morphine (minipumps, 45mg/kg/day, 6 days) in CD-1 mice and the functional role of these changes in opioid antinociception. The antinociceptive effect of morphine as determined with tail-flick tests was reduced in morphine-tolerant mice. There were no significant changes in the density of high-affinity Na(+),K(+)-ATPase α subunits labeled with [(3)H]ouabain in forebrain membranes from morphine-tolerant compared to those of morphine-naive animals. Western blot analysis showed that there were no significant differences between groups in the changes in relative abundance of α(1) and α(3) subunits of Na(+),K(+)-ATPase in the spinal cord or forebrain. However, the morphine-induced stimulation of Na(+),K(+)-ATPase activity was significantly lower in brain synaptosomes from morphine-tolerant mice (EC(50)=1.79±0.10µM) than in synaptosomes from morphine-naive mice (EC(50)=0.69±0.12µM). Furthermore, adaptive alterations in the time-course of basal Na(+),K(+)-ATPase activity were observed after sustained morphine treatment, with a change from a bi-exponential decay model (morphine-naive mice) to a mono-exponential model (morphine-tolerant mice). In behavioral studies the antinociceptive effects of morphine (s.c.) in the tail-flick test were dose-dependently antagonized by ouabain (1 and 10ng/mouse, i.c.v.) in morphine-naive mice, but not in morphine-tolerant mice. These findings suggest that during morphine tolerance, adaptive cellular changes take place in cerebral Na(+),K(+)-ATPase activity which are of functional relevance for morphine-induced antinociception.

Sigma-1 receptors do not regulate calcium influx through voltage-dependent calcium channels in mouse brain synaptosomes.

Several lines of evidence suggest that σ(1) receptors regulate intracellular calcium concentration [Ca(2+)](i). However, no previous studies have demonstrated a consistent role for these receptors in the modulation of extracellular calcium entry through plasmalemmal voltage-dependent calcium channels (VDCCs). To search for evidence of such a role we compared [Ca(2+)](i) under basal conditions and after depolarization with KCl in fura-2-loaded synaptosomes from wild-type and σ(1) receptor knockout (σ(1)R-KO) mice. We also tested the effects of the selective σ(1) receptor agonists PRE-084 and (+)-pentazocine and antagonists BD-1047 and NE-100 on the increase in [Ca(2+)](i) induced by depolarization with 60mM KCl. Mibefradil, a nonselective blocker of VDCCs, was used as a positive control. Basal [Ca(2+)](i) and the increase in [Ca(2+)](i) caused by KCl-induced depolarization were similar in brain synaptosomes from both wild-type and σ(1)R-KO mice. Mibefradil (1-30 µM) and all σ(1) receptor ligands studied (3-100 µM) inhibited the KCl-induced increase in [Ca(2+)](i) in a concentration-dependent way. The order of maximum inhibition for the ligands compared here was NE-100>BD-1047=PRE 084>(+)-pentazocine. There were no appreciable differences in their effects between wild-type and σ(1)R-KO mice. These findings indicate that σ(1) receptors are not involved in calcium influx through VDCCs or in the inhibitory effects of these σ(1) ligands on Ca(2+) channels.

Novel potent and selective σ ligands: evaluation of their agonist and antagonist properties.

Novel enantiomers and diastereoisomers structurally related to σ ligand (+)-MR200 were synthesized to improve σ(1)/σ(2) subtype selectivity. The selective σ(1) ligand (-)-8 showed an antagonist profile determined by phenytoin differential modulation of binding affinity in vitro, confirmed in vivo by an increase of κ opioid analgesia. The σ(2) ligand (-)-9 displayed agonist properties in an in vitro isolated organ bath assay and antiproliferative effects on LNCaP and PC3 prostate cancer cell lines.

Role of cannabinoid CB1 receptors and Gi/o protein activation in the modulation of synaptosomal Na+,K+-ATPase activity by WIN55,212-2 and delta(9)-THC.

In the present study, we evaluated the effects of the synthetic cannabinoid receptor agonist (R)-(+)-[2,3-Dihydro-5-methyl-3-(4-morpholinylmethyl)pyrrolo[1,2,3-de]-1,4-benzoxazin-6-yl]-1-naphthalenylmethanone mesylate (WIN55,212-2) and the active component of Cannabis delta-9-tetrahydrocannabinol (triangle up(9)-THC) on Na(+),K(+)-ATPase activity in synaptosomal mice brain preparation. Additionally, the potential exogenous cannabinoids and endogenous opioid peptides interaction as well as the role of G(i/o) proteins in mediating Na(+),K(+)-ATPase activation were also explored. The ouabain-sensitive Na(+),K(+)-ATPase activity was measured in whole-brain pure intact synaptosomes (obtained by Percoll gradient method) of female CF-1 mice and was calculated as the difference between the total and the ouabain (1 mM)-insensitive Na(+),K(+)-ATPase activities. Incubation in vitro of the synaptosomes with WIN55,212-2 (0.1 pM-10 microM) or triangle up(9)-THC (0.1 pM-0.1 microM), in a concentration-dependent manner, stimulated ouabain-sensitive Na(+),K(+)-ATPase activity. WIN55,212-2 was less potent but more efficacious than triangle up(9)-THC. N-(Piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide (AM-251) (10 nM), a CB(1) cannabinoid receptor selective antagonist, had not effect per se but antagonized the enhancement of Na(+),K(+)-ATPase activity induced by both, WIN55,212-2 and triangle up(9)-THC. AM-251 produced a significant reduction in the E(max) of cannabinoid-induced increase in Na(+),K(+)-ATPase activity, but did not significantly modify their EC(50). On the other hand, co-incubation with naloxone (1 microM), an opioid receptor antagonist, did not significantly modify the effect of WIN55,212-2 and completely failed to modify the effect of triangle up(9)-THC on synaptosomal Na(+),K(+)-ATPase. Finally, pre-incubation with 0.5 microg of pertussis toxin (G(i/o) protein blocker) completely abolished the enhancement of ouabain-sensitive Na(+),K(+)-ATPase activity induced by WIN55,212-2. A lower dose, 0.25 microg, decreased the E(max) of WIN55,212-2 by 70% but did not significantly affect its EC(50). These results suggest that WIN55212-2 and triangle up(9)-THC indirectly enhance Na(+),K(+)-ATPase activity in the brain by activating cannabinoid CB(1) receptors in a naloxone-insensitive manner. In addition, the effect of WIN55,212-2 on neuronal Na(+),K(+)-ATPase is apparently due to activation of G(i/o) proteins.

[Vein of Galen arteriovenous malformations and neonatal convulsions]. / Malformacion arteriovenosa de la vena de Galeno y convulsiones neonatales.

INTRODUCTION: Vein of Galen arteriovenous malformation (VGAM) appears during the embryonic period and gives rise to a complex network of arterial and venous vessels that generates a blood shift, from the brain parenchyma towards the malformation, with haemodynamic repercussions. Heart failure is the most frequent presenting symptom during the neonatal period, yet, convulsions or other neurological signs have occasionally been reported in this stage of life. CASE REPORT: A term infant with symptoms of heart failure and convulsions that began during the first 12 hours of life. CAT and magnetic resonance angiography scans revealed a vascular malformation and areas of cerebral ischaemia. CONCLUSIONS: In the case of our patient, detecting areas of ischaemia in the cerebral hemispheres suggested that the damage could be caused by a "steal" syndrome leading the blood flow away from these areas towards the malformation. This situation can occur either before or after birth and the self-limiting nature of the seizures in cerebral infarcts could lead to them going noticed because they take place inside the uterus or when the patient is not being observed directly by his or her health care providers. We suspect that the convulsions in newborn infants with this malformation may well be more frequent than is currently believed.

Malformación arteriovenosa de la vena de Galeno y convulsiones neonatales / Vein of galen arteriovenous malformations and neonatal covulsions

Introduction. Vein of Galen arteriovenous malformation (VGAM) appears during the embryonic period and gives rise to a complex network of arterial and venous vessels that generates a blood shift, from the brain parenchyma towards the malformation, with haemodynamic repercussions. Heart failure is the most frequent presenting symptom during the neonatal period, yet, convulsions or other neurological signs have occasionally been reported in this stage of life. Case report. A term infant with symptoms of heart failure and convulsions that began during the first 12 hours of life. CAT and magnetic resonance angiography scans revealed a vascular malformation and areas of cerebral ischaemia. Conclusions. In the case of our patient, detecting areas of ischaemia in the cerebral hemispheres suggested that the damage could be caused by a ‘steal’ syndrome leading the blood flow away from these areas towards the malformation. This situation can occur either before or after birth and the self-limiting nature of the seizures in cerebral infarcts could lead to them going noticed because they take place inside the uterus or when the patient is not being observed directly by his or her health care providers. We suspect that the convulsions in newborn infants with this malformation may well be more frequent than is currently believed (AU)

Introducción. La malformación arteriovenosa de la vena de Galeno (MAVG) aparece durante el período embrionario y da lugar a una compleja red de vasos arteriales y venosos que generan una derivación de sangre desde el parénquima cerebral hacia la malformación, con repercusiones hemodinámicas. La insuficiencia cardíaca es la forma de presentación más frecuente durante el período neonatal; sin embargo, las convulsiones u otros signos neurológicos se han referido raramente en esta etapa de la vida. Caso clínico. Se trata de un recién nacido a término que comenzó en las primeras 12 horas de vida con un cuadro de insuficiencia cardíaca y convulsiones. La TAC y la angiorresonancia magnética evidenciaron la malformación vascular y zonas de isquemia cerebral. Conclusiones. En nuestro paciente, la detección de áreas de isquemia en los hemisferios cerebrales sugiere que el daño podría estar ocasionado por un fenómeno de ‘robo’ del flujo sanguíneo desde dichas áreas hacia la malformación. Esta situación puede acontecer antes o después del nacimiento, y el carácter autolimitado de las crisis en los infartos cerebrales podría hacer que éstas pasaran desapercibidas porque acontezcan intraútero o cuando el paciente no está siendo observado directamente por sus cuidadores. Nosotros sospechamos que las convulsiones en los neonatos con esta malformación podrían ser más frecuentes de lo que se considera en la actualidad (AU)

Paragangliomas del cuerpo carotideo / Carotid body paragangliomas

Los paragangliomas son neoplasias derivadas de la cresta neural, benignas en un alto porcentaje y poco comunes. En la cabeza y cuello, los del cuerpo carotídeo, son los de mayor incidencia. Por lo general, se presentan como una masa asintomática y ocurren en personas entre la cuarta y quinta década de la vida. Su aparición se ha relacionado con la vida en las grandes alturas o con enfermedad pulmonar obstructiva crónica (hipoxia crónica), y existe un grupo con tendencia familiar. Las técnicas de imágenes diagnósticas no invasivas (resonancia magnética, tomografía computarizada, gammagrafía) son los instrumentos ideales para confirmar el diagnóstico. La cirugía se considera la única manera de tratamiento para lograr su curación. En grandes tumores, todavía existe morbilidad de tipo neurovascular durante la extirpación quirúrgica. Para reducir la misma, se ha preconizado la embolización arterial preoperatoria

[Neonatal morbidity and mortality in very low birth weight infants according to exposure to chorioamnionitis]. / Patología neonatal en los menores de 1.500 gramos con relación al antecedente de corioamnionitis.

OBJECTIVES: To study differences in the incidence of neonatal morbidity and mortality among newborns weighing less than 1,500 g according to exposure to chorioamnionitis (CA). PATIENTS AND METHODS: A case-control study of 135 newborns weighing less than 1,500 g at birth and born between 1988 and 1998 was performed. The case group was composed of 45 newborns exposed to clinical or subclinical levels of maternal CA. Each newborn in the case group was matched with two controls, both weighing less than 1,500 g, one of them born immediately before and the other one immediately after. Perinatal records, neonatal morbidity and mortality were analyzed. RESULTS: The mean gestational age was 28.5 weeks (range: 24-38 weeks) with a mean weight of 1,131 g (range: 520-1,500 g). The time of membrane rupture was significantly greater in the case group (176 h vs 57 h; p < 0.001). Forty percent of the cases presented sepsis in the first 72 h of life compared with 10 % of the controls (p < 0.0001). No significant differences in morbidity or mortality were found between the groups, although chronic lung disease (20 % vs 13 %) and intraventricular hemorrhage (24 % vs 17 %) were more frequent in infants exposed to CA. Resuscitation (77.8 % vs 45.6 %; p 0.001) and mechanical ventilation (73 % vs 50 %; p 0.016) were required by a great number of cases than controls. CONCLUSIONS: The presence of CA was associated with a higher risk of early onset infection and the need for neonatal resuscitation and mechanical ventilation. No significant differences were found in morbidity or mortality.

Patología neonatal en los menores de 1.500 gramos con relación al antecedente de corioamnionitis / Neonatal morbidity and mortality in very low birth weight infants according to exposure to chorioamnionitis

Objetivos: Estudiar las diferencias en la incidencia de patología neonatal y mortalidad, en los recién nacidos de menos de 1.500 g, con relación a la presencia de corioamnionitis. Pacientes y métodos: Estudio caso-control de 135 recién nacidos de menos de 1.500 g de peso, nacidos entre 1988-1998. El grupo de "casos" está constituido por 45 recién nacidos con antecedentes de corioamnionitis materna según criterios clínicos o subclínicos. A cada neonato se le asignaron dos controles, el nacido inmediato anterior y posterior de menos de 1.500 g. Se analizaron los siguientes datos: aspectos perinatales, complicaciones neonatales y mortalidad. Resultados: La edad gestacional media fue de 28,5 semanas (límites, 24-38 semanas) con un peso medio de 1.131 g (límites, 520-1.500). Entre los casos hubo un período de rotura de membranas significativamente mayor (176 h frente a 57 h; p < 0,001). Presentaron infección en las primeras 72 h de vida el 40% de los casos frente al 10% de los controles (p < 0,0001). No se encontraron diferencias significativas en la patología ni en la mortalidad entre ambos grupos, aunque la enfermedad pulmonar crónica (20% frente a 13%) y la hemorragia intraventricular (24% frente a 17%) fueron más frecuentes en los expuestos a corioamnionitis. Necesitaron ventilación asistida un mayor número de niños de los casos (73% frente a 50%; p 0,016) al igual que reanimación (77,8% frente a 45,6%; p 0,001). Conclusiones: La presencia de corioamnionitis se asocia con un riesgo mayor de infección precoz y de precisar reanimación neonatal y ventiloterapia. No existen diferencias significativas respecto a la mortalidad u otras patologías de las analizadas en este estudio (AU)