Systematic Review and Meta-Analysis of Global Neuroma Incidence in Upper Extremity Amputees.

BACKGROUND: Neuromas substantially decrease a patient's quality of life and obstruct the use of prosthetics. This systematic review and meta-analysis aimed to determine the global incidence of neuroma formation in upper extremity amputees. METHODS: A literature search was performed using 3 databases: Web of Science, MEDLINE, and Cochrane. Inclusion criteria for the systematic review were those studies investigating only upper extremity amputees and reported postamputation neuroma. A random-effects, inverse-variance analysis was conducted to determine the pooled proportion of neuromas within the upper extremity amputation population. Critical appraisal using the JBI Checklist for Studies Reporting Prevalence Data of each individual article were performed for the systematic review. RESULTS: Eleven studies met the inclusion criteria collating a total of 1931 patients across 8 countries. More than three-fourth of patients are young men (77%; age range, 19-54 years) and had an amputation due to trauma. The random-effects analysis found the pooled combined proportion of neuromas to be 13% (95% confidence interval, 8%-18%). The treatment of neuroma is highly variable, with some patients receiving no treatment. CONCLUSIONS: The pooled proportion of neuroma incidence in the 1931 patients was 13%. With the known global prevalence of upper extremity amputees, this translates to nearly 3 million amputees suffering from a neuroma globally. Increasing training in preventative surgical methods could contribute to lowering this incidence and improving the outcomes of this patient population.

Isquemia Mesentérica secundaria a Trombosis Arterial Abdominal Múltiple, Reporte de un Caso

Masculino de 61 años, que acude con cuadro de dolor abdominal generalizado, asociado a distensión y defensa. Refiere que el dolor empezó aproximadamente 6 horas previo a la consulta. Entre los antecedentes clínicos relevantes hay historia de hipertensión arterial y fibrilación auricular. Al llegar a cuarto de urgencias, entre los hallazgos relevantes de laboratorio se identifica un valor de creatinina de 2.31 mg/dL y elevación de los valores de lactato. A pesar del manejo, y sin otros hallazgos relevantes al examen físico, el paciente persistía con dolor abdominal severo. Debido a la sospecha clínica de isquemia mesentérica, se le realizó una angio-tomografía abdominal donde se evidenció trombosis arterial múltiple que comprometía la arteria mesentérica superior, inferior y otras estructuras vasculares. El paciente fue trasladado a un hospital de tercer nivel y llevado al salón de operaciones, pero debido al gran compromiso vascular que presentaba, falleció en el procedimiento. (provisto por Infomedic International)

A 61-year-old male, who presented with generalized abdominal pain, associated with distention and defense. He reports that the pain started approximately 6 hours prior to the consultation. Relevant medical history includes a history of arterial hypertension and atrial fibrillation. Upon arrival to the emergency room, relevant laboratory findings included a creatinine value of 2.31 mg/dL and elevated lactate values. Despite management, and without other relevant findings on physical examination, the patient persisted with severe abdominal pain. Due to clinical suspicion of mesenteric ischemia, an abdominal angio-tomography was performed, showing multiple arterial thrombosis involving the superior and inferior mesenteric artery and other vascular structures. The patient was transferred to a tertiary hospital and taken to the operating room, but due to the great vascular compromise he died during the procedure. (provided by Infomedic International)

Development of improved SRC-3 inhibitors as breast cancer therapeutic agents.

Steroid receptor coactivators (SRCs) possess specific and distinct oncogenic roles in the initiation of cancer and in its progression to a more aggressive disease. These coactivators interact with nuclear receptors and other transcription factors to boost transcription of multiple genes, which potentiate cancer cell proliferation, migration, invasion, tumor angiogenesis and epithelial-mesenchymal transition (EMT). Targeting SRCs using small molecule inhibitors (SMIs) is a promising approach to control cancer progression and metastasis. By high-throughput screening analysis, we recently identified SI-2 as a potent SRC SMI. To develop therapeutic agents, SI-10 and SI-12, the SI-2 analogs are synthesized that incorporate the addition of F atoms to the SI-2 chemical structure. As a result, these analogs exhibit a significantly prolonged plasma half-life, minimal toxicity and improved hERG activity. Biological functional analysis showed that SI-10 and SI-12 treatment (5-50 nM) can significantly inhibit viability, migration and invasion of breast cancer cells in vitro and repress the growth of breast cancer PDX organoids. Treatment of mice with 10 mg/kg/day of either SI-10 or SI-12 was sufficient to repress the growth of xenograft tumors derived from MDA-MB-231 and LM2 cells. Furthermore, in spontaneous and experimental metastasis mouse models developed from MDA-MB-231 and LM2 cells, respectively, SI-10 and SI-12 effectively inhibited the progression of breast cancer lung metastasis. These results demonstrate that SI-10 and SI-12 are promising therapeutic agents and are specifically effective in blocking tumor metastasis, a key point in tumor progression to a more lethal state that results in patient mortality in the majority of cases.

The effect of normal, metaplastic, and neoplastic esophageal extracellular matrix upon macrophage activation.

INTRODUCTION: Macrophages are capable of extreme plasticity and their activation state has been strongly associated with solid tumor growth progression and regression. Although the macrophage response to extracellular matrix (ECM) isolated from normal tissue is reasonably well understood, there is a relative dearth of information regarding their response to ECM isolated from chronically inflamed tissues, pre-neoplastic tissues, and neoplastic tissues. Esophageal adenocarcinoma (EAC) is a type of neoplasia driven by chronic inflammation in the distal esophagus, and the length of the esophagus provides the opportunity to investigate macrophage behavior in the presence of ECM isolated from a range of disease states within the same organ. METHODS: Normal, metaplastic, and neoplastic ECM hydrogels were prepared from decellularized EAC tissue. The hydrogels were evaluated for their nanofibrous structure (SEM), biochemical profile (targeted and global proteomics), and direct effect upon macrophage (THP-1 cell) activation state (qPCR, ELISA, immunolabeling) and indirect effect upon epithelial cell (Het-1A) migration (Boyden chamber). RESULTS: Nanofibrous ECM hydrogels from the three tissue types could be formed, and normal and neoplastic ECM showed distinctive protein profiles by targeted and global mass spectroscopy. ECM proteins functionally related to cancer and tumorigenesis were identified in the neoplastic esophageal ECM including collagen alpha-1(VIII) chain (COL8A1), lumican, and elastin. Metaplastic and neoplastic esophageal ECM induce distinctive effects upon THP-1 macrophage signaling compared to normal esophageal ECM. These effects include activation of pro-inflammatory IFNγ and TNFα gene expression and anti-inflammatory IL1RN gene expression. Most notably, neoplastic ECM robustly increased macrophage TNFα protein expression. The secretome of macrophages pre-treated with metaplastic and neoplastic ECM increases the migration of normal esophageal epithelial cells, similar behavior to that shown by tumor cells. Metaplastic ECM shows similar but less pronounced effects than neoplastic ECM suggesting the abnormal signals also exist within the pre-cancerous state. CONCLUSION: A progressively diseased ECM, as exists within the esophagus exposed to chronic gastric reflux, can provide insights into novel biomarkers of early disease and identify potential therapeutic targets.

Steroid receptor coactivator 3 (SRC-3/AIB1) is enriched and functional in mouse and human Tregs.

A subset of CD4 + lymphocytes, regulatory T cells (Tregs), are necessary for central tolerance and function as suppressors of autoimmunity against self-antigens. The SRC-3 coactivator is an oncogene in multiple cancers and is capable of potentiating numerous transcription factors in a wide variety of cell types. Src-3 knockout mice display broad lymphoproliferation and hypersensitivity to systemic inflammation. Using publicly available bioinformatics data and directed cellular approaches, we show that SRC-3 also is highly enriched in Tregs in mice and humans. Human Tregs lose phenotypic characteristics when SRC-3 is depleted or pharmacologically inhibited, including failure of induction from resting T cells and loss of the ability to suppress proliferation of stimulated T cells. These data support a model for SRC-3 as a coactivator that actively participates in protection from autoimmunity and may support immune evasion of cancers by contributing to the biology of Tregs.

Intra-abdominal cystic lymphangioma of the mesocolon sigmoids: a rare entity in adult patient woman.

The lymphangioma is a benign neoplasm, mostly connate, it occurs more often in children. It is more frequently located in the head-neck region, as well as in the armpit, and less frequently in the abdomen. The diagnosis, as well as their appearance is variant, they can be asymptomatic depending on the size. The signs on the physical exam are usually nonspecific and can look like an acute abdomen. Imaging tests used are the ultrasound and tomography, which determine the therapeutic behavior. The differential diagnosis should be made with other intra-abdominal injuries, such as cavernous hemangioma, mesotheliomas, pancreatic and ovarian tumors and even peritoneal hydatid cyst. The definitive treatment is surgical in most cases, with complete excision of the mass. The definitive diagnosis is obtained with the histopathological study of the surgical piece.

Elevated serum levels of bone sialoprotein (BSP) predict long-term mortality in patients with pancreatic adenocarcinoma.

Patients with pancreatic adenocarcinoma (PDAC) still face a very limited prognosis. At early stage, surgical tumor resection might offer long-term survival but disease recurrence is common and the existing stratification algorithms are often unsuitable to identify patients who particularly benefit from surgery. Here, we investigated the potential role of bone sialoprotein (BSP) as a circulating marker in patients undergoing resection of PDAC. We used ELISA to determine serum concentrations of BSP in a cohort of 132 PDAC patients as well as 39 healthy controls. Circulating BSP levels were significantly higher in PDAC patients compared to healthy controls. Notably, elevated preoperative BSP levels above the ideal cut-off value of 4743 pg/ml turned out as a significant predictor for an impaired postoperative survival. The potential of preoperative BSP levels as a prognostic marker was further underlined by uni- and multivariate Cox-regression analyses including various tumour- and patient-specific. Finally, high tumoral BSP expression was also associated with a significantly impaired long-term survival. In conclusion, we identified a novel role of circulating BSP as a biomarker in PDAC patients undergoing tumor resection. Such data might help to establish new preoperative stratification strategies to better identify patients who particularly benefit from tumor resection.

Serum levels of kisspeptin are elevated in critically ill patients.

INTRODUCTION: Members of the adipokine family such as resistin, adiponectin and omentin have recently been described as novel biomarkers with a diagnostic and prognostic role in the context of critically ill patients during intensive care unit (ICU) treatment. Kisspeptin represent another member of this family and has been shown to be closely correlated to different members of the adipokine family in manifold diseases. However, its role in critical illness and sepsis is currently unknown. MATERIALS AND METHODS: Kisspeptin serum concentrations were measured in 133 ICU patients admitted to the medical ICU. Results were compared with 36 healthy controls. RESULTS: Kisspeptin serum levels were elevated in the serum of critically ill patients at admission to the ICU, when compared to healthy controls, and remained increased after 72 hours of ICU treatment. Notably, kisspeptin levels were independent of the presence of sepsis and etiology of critical illness. In line, serum concentrations of kisspeptin were not correlated to concentrations of inflammatory cytokines or established sepsis markers. Serum kisspeptin correlated inversely with the glomerular filtration rate. In contrast to the reported role of other members of the adipokine family, serum levels of kisspeptin were neither predictive for short term survival during ICU treatment nor for patients' overall survival. Kisspeptin levels did not correlate with other adipokines measured in serum, including leptin, resistin, ghrelin, or adiponectin. CONCLUSIONS: Although circulating kisspeptin levels were strongly elevated in ICU-patients, elevated kisspeptin levels were not predictive for an impaired patients' survival.

microRNA 193a-5p Regulates Levels of Nucleolar- and Spindle-Associated Protein 1 to Suppress Hepatocarcinogenesis.

BACKGROUND & AIMS: We performed an integrated analysis to identify microRNAs (miRNAs) and messenger RNAs (mRNAs) with altered expression in liver tumors from 3 mouse models of hepatocellular carcinoma (HCC) and human tumor tissues. METHODS: We analyzed miRNA and mRNA expression profiles of liver tissues from mice with diethylnitrosamine-induced hepatocarcinogenesis, conditional expression of lymphotoxin alpha and lymphotoxin beta, or inducible expression of a Myc transgene (Tet-O-Myc mice), as well as male C57BL/6 mice (controls). miRNA mimics were expressed and miRNAs and mRNAs were knocked down in human (Huh7, Hep3B, JHH2) hepatoma cell lines; cells were analyzed for viability, proliferation, apoptosis, migration, and invasion. Cells were grown as xenograft tumors in nude mice and analyzed. We combined in silico target gene prediction with mRNA profiles from all 3 mouse models. We quantified miRNA levels in 146 fresh-frozen tissues from patients (125 HCCs, 17 matched nontumor tissues, and 4 liver samples from patients without cancer) and published human data sets and tested correlations with patient survival times using Kaplan-Meier curves and the log-rank test. Levels of NUSAP1 mRNA were quantified in 237 HCCs and 5 nontumor liver samples using the TaqMan assay. RESULTS: Levels of the miRNA 193a-5p (MIR193A-5p) were reduced in liver tumors from all 3 mouse tumor models and in human HCC samples, compared with nontumor liver tissues. Expression of a MIR193A-5p mimic in hepatoma cells reduced proliferation, survival, migration, and invasion and their growth as xenograft tumors in nude mice. We found nucleolar and spindle-associated protein 1 (NUSAP1) to be a target of MIR193A-5p; HCC cells and tissues with low levels of MIR193A-5p had increased expression of NUSAP1. Increased levels of NUSAP1 in HCC samples correlated with shorter survival times of patients. Knockdown of NUSAP1 in Huh7 cells reduced proliferation, survival, migration, and growth as xenograft tumors in nude mice. Hydrodynamic tail-vein injections of a small hairpin RNA against NUSAP1 reduced growth of Akt1-Myc-induced tumors in mice. CONCLUSIONS: MIR193A-5p appears to prevent liver tumorigenesis by reducing levels of NUSAP1. Levels of MIR193A-5p are reduced in mouse and human HCC cells and tissues, leading to increased levels of NUSAP1, associated with shorter survival times of patients. Integrated analyses of miRNAs and mRNAs in tumors from mouse models can lead to identification of therapeutic targets in humans. The currently reported miRNA and mRNA profiling data have been submitted to the Gene Expression Omnibus (super-series accession number GSE102418).

miR-30c and miR-193 are a part of the TGF-ß-dependent regulatory network controlling extracellular matrix genes in liver fibrosis.

OBJECTIVE: MicroRNAs (miRNAs) have recently emerged as novel regulators in liver fibrosis. miR-30c and miR-193 are involved in fibrotic remodeling processes and cancer development, respectively. This study aimed to explore the role of miR-30c and miR-193 in liver fibrosis. METHODS: The regulation of miRNAs in carbon tetrachloride-induced liver fibrosis was analyzed by microarray. Expression patterns of miR-193 and miR-30c were further confirmed in fibrotic liver samples obtained from two murine models of hepatic fibrosis and human tissues. On a functional level, miRNA levels were analyzed in the context of transforming growth factor (TGF-ß) mediated activation of hepatic stellate cells (HSCs). Finally, predicted targets were assessed for their roles in fibrosis by transfecting murine HSCs with miRNA mimics. RESULTS: Microarray analysis in murine fibrotic livers revealed a panel of 44 dysregulated miRNAs. In addition to previously established miRNAs known to be regulated in liver fibrosis in a TGF-ß-dependent manner (e.g., miR-29, miR-133), miR-193 and miR-30c were observed to be specifically downregulated not only in experimental hepatofibrogenesis but also in human liver fibrosis, while they showed a reciprocal expression pattern after recovery from liver fibrosis. Functional experiments confirmed the TGF-ß-dependent downregulation of these respective new miRNAs in HSCs. Finally, we identified TGF-ß2 and SNAIL1, important regulators of extracellular matrix, as potential target genes of miR-193 and miR-30 in liver fibrosis. CONCLUSION: These results suggest that miR-30 and miR-193 are members of a network of miRNAs modifying the TGF-ß-dependent regulation of extracellular matrix-related genes in HSCs in the manifestation and resolution of liver fibrosis.

A positive feedback loop between RIP3 and JNK controls non-alcoholic steatohepatitis.

Non-alcoholic fatty liver disease (NAFLD) represents the most common liver disease in Western countries and often progresses to non-alcoholic steatohepatitis (NASH) leading ultimately to liver fibrosis and liver cancer. The occurrence of hepatocyte cell death-so far characterized as hepatocyte apoptosis-represents a fundamental step from benign steatosis toward progressive steatohepatitis. In contrast, the function of RIP3-dependent "necroptosis" in NASH and NASH-induced fibrosis is currently unknown. We show that RIP3 is upregulated in human NASH and in a dietary mouse model of steatohepatitis. RIP3 mediates liver injury, inflammation, induction of hepatic progenitor cells/activated cholangiocytes, and liver fibrosis through a pathway suppressed by Caspase-8. This function of RIP3 is mediated by a positive feedback loop involving activation of Jun-(N)-terminal Kinase (JNK). Furthermore, RIP3-dependent JNK activation promotes the release of pro-inflammatory mediators like MCP-1, thereby attracting macrophages to the injured liver and further augmenting RIP3-dependent signaling, cell death, and liver fibrosis. Thus, RIP3-dependent necroptosis controls NASH-induced liver fibrosis. This pathway might represent a novel and specific target for pharmacological strategies in patients with NASH.

U6 is unsuitable for normalization of serum miRNA levels in patients with sepsis or liver fibrosis.

MicroRNA (miRNA) levels in serum have recently emerged as potential novel biomarkers for various diseases. miRNAs are routinely measured by standard quantitative real-time PCR (qPCR); however, the high sensitivity of qPCR demands appropriate normalization to correct for nonbiological variation. Presently, RNU6B (U6) is used for data normalization of circulating miRNAs in many studies. However, it was suggested that serum levels of U6 themselves might differ between individuals. Therefore, no consensus has been reached on the best normalization strategy in 'circulating miRNA'. We analyzed U6 levels as well as levels of spiked-in SV40-RNA in sera of 44 healthy volunteers, 203 intensive care unit patients and 64 patients with liver fibrosis. Levels of U6 demonstrated a high variability in sera of healthy donors, patients with critical illness and liver fibrosis. This high variability could also be confirmed in sera of mice after the cecal ligation and puncture procedure. Most importantly, levels of circulating U6 were significantly upregulated in sera of patients with critical illness and sepsis compared with controls and correlated with established markers of inflammation. In patients with liver fibrosis, U6 levels were significantly downregulated. In contrast, levels of spiked-in SV40 displayed a significantly higher stability both in human cohorts (healthy, critical illness, liver fibrosis) and in mice. Thus, we conclude that U6 levels in the serum are dysregulated in a disease-specific manner. Therefore, U6 should not be used for data normalization of circulating miRNAs in inflammatory diseases and previous studies using this approach should be interpreted with caution. Further studies are warranted to identify specific regulatory processes of U6 levels in sepsis and liver fibrosis.

RIP3 inhibits inflammatory hepatocarcinogenesis but promotes cholestasis by controlling caspase-8- and JNK-dependent compensatory cell proliferation.

For years, the term "apoptosis" was used synonymously with programmed cell death. However, it was recently discovered that receptor interacting protein 3 (RIP3)-dependent "necroptosis" represents an alternative programmed cell death pathway activated in many inflamed tissues. Here, we show in a genetic model of chronic hepatic inflammation that activation of RIP3 limits immune responses and compensatory proliferation of liver parenchymal cells (LPC) by inhibiting Caspase-8-dependent activation of Jun-(N)-terminal kinase in LPC and nonparenchymal liver cells. In this way, RIP3 inhibits intrahepatic tumor growth and impedes the Caspase-8-dependent establishment of specific chromosomal aberrations that mediate resistance to tumor-necrosis-factor-induced apoptosis and underlie hepatocarcinogenesis. Moreover, RIP3 promotes the development of jaundice and cholestasis, because its activation suppresses compensatory proliferation of cholangiocytes and hepatic stem cells. These findings demonstrate a function of RIP3 in regulating carcinogenesis and cholestasis. Controlling RIP3 or Caspase-8 might represent a chemopreventive or therapeutic strategy against hepatocellular carcinoma and biliary disease.

Serum concentrations of A Proliferation-Inducing Ligand (APRIL) are elevated in sepsis and predict mortality in critically ill patients.

INTRODUCTION: Inflammatory and autoimmune diseases have been associated with the tumor necrosis factor superfamily member "A PRoliferation Inducing Ligand" (APRIL). However, up to now, APRIL has not been investigated in critical illness or sepsis. We therefore analyzed APRIL serum concentrations in a large cohort of well-characterized intensive care unit patients. METHODS: Serum concentrations of APRIL were measured in 246 critically ill patients, of which 157 fulfilled sepsis criteria in comparison with 81 healthy controls. Clinical data were recorded and correlated with APRIL serum levels. RESULTS: We detected strongly elevated serum levels of APRIL in critically ill patients compared with healthy controls. Levels of APRIL were further elevated in sepsis and significantly correlated with classical markers of inflammation, bacterial infection, or multiorgan failure. Consequently, high APRIL levels were associated with an unfavorable prognosis and predicted mortality with higher diagnostic accuracy than established prognostic scoring systems such as the Acute Physiology and Chronic Health Evaluation II score. CONCLUSION: Serum levels of APRIL were significantly elevated in intensive care unit patients, with the highest concentrations in septic patients, and associated with unfavorable outcome. Besides being used as a single marker, APRIL may be implemented into established scoring systems to further improve their sensitivity and specificity in predicting patient's prognosis.

Micro-RNA profiling in human serum reveals compartment-specific roles of miR-571 and miR-652 in liver cirrhosis.

BACKGROUND AND AIMS: Micro-RNAs (miRNAs) have recently emerged as crucial modulators of molecular processes involved in chronic liver diseases. The few miRNAs with previously proposed roles in liver cirrhosis were identified in screening approaches on liver parenchyma, mostly in rodent models. Therefore, in the present study we performed a systematic screening approach in order to identify miRNAs with altered levels in the serum of patients with chronic liver disease and liver cirrhosis. METHODS: We performed a systematic, array-based miRNA expression analysis on serum samples from patients with liver cirrhosis. In functional experiments we evaluated the relationship between alterations of miRNA serum levels and their role in distinct cellular compartments involved in hepatic cirrhosis. RESULTS: The array analysis and the subsequent confirmation by qPCR in a larger patient cohort identified significant alterations in serum levels of miR-513-3p, miR-571 and miR-652, three previously uncharacterized miRNAs, in patients with alcoholic or hepatitis C induced liver cirrhosis. Of these, miR-571 serum levels closely correlated with disease stages, thus revealing potential as a novel biomarker for hepatic cirrhosis. Further analysis revealed that up-regulation of miR-571 in serum reflected a concordant regulation in cirrhotic liver tissue. In isolated primary human liver cells, miR-571 was up-regulated in human hepatocytes and hepatic stellate cells in response to the pro-fibrogenic cytokine TGF-ß. In contrast, alterations in serum levels of miR-652 were stage-independent, reflecting a concordant down-regulation of this miRNA in circulating monocytes of patients with liver cirrhosis, which was inducible by proinflammatory stimuli like bacterial lipopolysaccharide. CONCLUSION: Alterations of miR571 and miR-652 serum levels in patients with chronic liver disease reflect their putative roles in the mediation of fibrogenic and inflammatory processes in distinct cellular compartments involved in the pathogenesis of liver cirrhosis.

Different roles of P1 and P2 Saccharomyces cerevisiae ribosomal stalk proteins revealed by cross-linking.

The stalk is an essential domain of the large ribosomal subunit formed by a complex of a set of very acidic proteins bound to a core rRNA binding component. While in prokaryotes there is only one type acidic protein, L7/12, two protein families are found in eukaryotes, phosphoproteins P1 and P2, which presumably have different roles. To search for differences zero-length cross-linking by S-S bridge formation was applied using Saccharomyces cerevisiae mutant P1 and P2 proteins carrying single cysteine residues at various positions. The results show a more exposed location of the N-terminal domain of the P2 proteins, which in contrast to P1, can be found as dimers when the Cys is introduced in this domain. Similarly, the Cys containing C-terminal domain of mutant P2 proteins shows a notable capacity to form cross-links with other proteins, which is considerably lower in the P1 type. On the other hand, mutation at the conserved C-domain of protein P0, the eukaryotic stalk rRNA binding component, results in removal of about 14 terminal amino acids. Protein P2, but not P1, protects mutant P0 from this truncation. These results support a eukaryotic stalk structure in which P1 proteins are internally located with their C-terminals having a restricted reactivity while P2 proteins are more external and accessible to interact with other cellular components.

Características cardiotocográficas del producto de madres con hipertensión inducida por el embarazo / Cardiotocographic features of fetus from mothers with pregnancy induced hypertension

Objetivo: Comparar los trazados cardiotocográficos de los productos de madres con y sin Hipertensión Inducida por el Embarazo (HIE) y contrastarlo con el estado del recién nacido. Material y Métodos: Estudio de cohortes de 6 meses en el Instituto Materno Perinatal, revisando un total de 287 registros cardiotocográficos, de los cuales se descartaron 116. Noventa y seis trazados correspondieron a madres con HIE y 75 a madres sin HIE. Se evaluó los siguientes parámetros: Línea de base (LB), Variabilidad, Aceleraciones, Desaceleraciones, Movimientos Fetales, Reactividad al estímulo Vibroacústico. Resultados: La LB se encontró dentro de los valores normales en el 95,83 por ciento de las hipertensas y en el 100 por ciento de las gestantes control. EI RR de presentar Variabilidad < 5 latidos/min en hipertensas fue 1,43 (IC 95 por ciento). Se encontró riesgo elevado de hacer < 5 aceleraciones en 30 min en productos de madres con HIE. No se evidenció desaceleraciones tipo II en productos de madres sin HIE. Conclusiones: Las características cardiotocográficas de productos de madres con HIE son: LB entre 120-160 latidos/min, variabilidad < 5 latidos/min, menos de 5 aceleraciones en 30 min e hipoactividad.