Regulatory Effects of N-3 PUFAs on Pancreatic ß-cells and Insulin-sensitive Tissues.

The N-3 polyunsaturated fatty acids (PUFAs) have a wide range of health benefits, including antiinflammatory effects, improvements in lipids metabolism and promoting insulin secretion, as well as reduction of cancer risk. Numerous studies support that N-3 PUFAs have the potentials to improve many metabolic diseases, such as diabetes, nonalcoholic fatty liver disease and obesity, which are attributable to N-3 PUFAs mediated enhancement of insulin secretion by pancreatic ß-cells and improvements in insulin sensitivity and metabolic disorders in peripheral insulin-sensitive tissues such as liver, muscles, and adipose tissue. In this review, we summarized the up-to-date clinical and basic studies on the regulatory effects and molecular mechanisms of N-3 PUFAs mediated benefits on pancreatic ß-cells, adipose tissue, liver, and muscles in the context of glucose and/or lipid metabolic disorders. We also discussed the potential factors involved in the inconsistent results from different clinical researches of N-3 PUFAs.

The Discovery of Endoplasmic Reticulum Storage Disease. The Connection between an H&E Slide and the Brain.

The revolutionary evolution in science and technology over the last few decades has made it possible to face more adequately three main challenges of modern medicine: changes in old diseases, the appearance of new diseases, and diseases that are unknown (mostly genetic), despite research efforts. In this paper we review the road travelled by pathologists in search of a method based upon the use of routine instruments and techniques which once were available for research only. The application to tissue studies of techniques from immunology, molecular biology, and genetics has allowed dynamic interpretations of biological phenomena with special regard to gene regulation and expression. That implies stepwise investigations, including light microscopy, immunohistochemistry, in situ hybridization, electron microscopy, molecular histopathology, protein crystallography, and gene sequencing, in order to progress from suggestive features detectable in routinely stained preparations to more characteristic, specific, and finally, pathognomonic features. Hematoxylin and Eosin (H&E)-stained preparations and appropriate immunohistochemical stains have enabled the recognition of phenotypic changes which may reflect genotypic alterations. That has been the case with hepatocytic inclusions detected in H&E-stained preparations, which appeared to correspond to secretory proteins that, due to genetic mutations, were retained within the rough endoplasmic reticulum (RER) and were deficient in plasma. The identification of this phenomenon affecting the molecules alpha-1-antitrypsin and fibrinogen has led to the discovery of a new field of cell organelle pathology, endoplasmic reticulum storage disease(s) (ERSD). Over fifty years, pathologists have wandered through a dark forest of complicated molecules with strange conformations, and by detailed observations in simple histopathological sections, accompanied by a growing background of molecular techniques and revelations, have been able to recognize and identify arrays of grotesque polypeptide arrangements.

The risks of ubiquinone and ß-carotene deficiency and metabolic disorders in patients with oral cancer.

BACKGROUND: Cancer development is mediated by oxidative stress and inflammation, which may correlate with metabolic disorders. The aim of this study was to evaluate antioxidant vitamins status and metabolic parameters in patients with oral cancer according to tumor-node-metastasis (TNM) stages. METHODS: A total of 194 patients with oral cancer were enrolled in this study. The patients were stratified for four groups according to cancer stages and that the statistics are comparisons across these groups. The levels of antioxidant vitamins (ubiquinone, ß-carotene, vitamin A and E), metabolic parameters, oxidative stress, antioxidant enzymes activity, and inflammatory markers were measured. RESULTS: More than half of the subjects had high blood pressure, central obesity, hyperglycemia, and hyperlipidemia regardless of TNM stage. With regard to antioxidant vitamins status, 46 and 94% of patients had ß-carotene and ubiquinone deficiency, respectively. Patients in T3 and T4 stages had significantly lower antioxidant enzyme (catalase, p = 0.03) activity and higher inflammatory markers levels (high sensitivity C-reactive protein and interleukin-6, p < 0.01) than patients in the other stages. In addition, the level of ß-carotene was negatively associated with waist circumference, and ubiquinone was positively associated with the level of high-density lipoprotein cholesterol (p < 0.05). Higher ß-carotene and ubiquinone levels were negatively associated with hypertriglyceridemia and the risk of metabolic syndrome (p < 0.05). CONCLUSIONS: A high proportion of patients with oral cancer had ubiquinone or ß-carotene deficiency and metabolic disorders. The level of ubiquinone or ß-carotene was negatively associated with the risk of central obesity, hypertriglyceridemia, and metabolic syndrome. Since patients with oral cancer suffer from high oxidative stress and inflammation (particularly in the T3 and T4 stages), supplementation with antioxidant vitamins such as ubiquinone or ß-carotene could be preferentially applied.

A multi-omics investigation of the molecular characteristics and classification of six metabolic syndrome relevant diseases.

Metabolic syndrome (MTS) is a cluster of concurrent metabolic abnormal conditions. MTS and its component metabolic diseases are heterogeneous and closely related, making their relationships complicated, thus hindering precision treatment. Methods: We collected seven groups of samples (group a: healthy individuals; group b: obesity; group c: MTS; group d: hyperglycemia, group e: hypertension, group f: hyperlipidemia; group g: type II diabetes, n=7 for each group). We examined the molecular characteristics of each sample by metabolomic, proteomic and peptidomic profiling analysis. The differential molecules (including metabolites, proteins and peptides) between each disease group and the healthy group were recognized by statistical analyses. Furthermore, a two-step clustering workflow which combines multi-omics and clinical information was used to redefine molecularly and clinically differential groups. Meanwhile, molecular, clinical, network and pathway based analyses were used to identify the group-specific biological features. Results: Both shared and disease-specific molecular profiles among the six types of diseases were identified. Meanwhile, the patients were stratified into three distinct groups which were different from original disease definitions but presented significant differences in glucose and lipid metabolism (Group 1: relatively favorable metabolic conditions; Group 2: severe dyslipidemia; Group 3: dysregulated insulin and glucose). Group specific biological signatures were also systematically described. The dyslipidemia group showed higher levels in multiple lipid metabolites like phosphatidylserine and phosphatidylcholine, and showed significant up-regulations in lipid and amino acid metabolism pathways. The glucose dysregulated group showed higher levels in many polypeptides from proteins contributing to immune response. The another group, with better glucose/lipid metabolism ability, showed higher levels in lipid regulating enzymes like the lecithin cholesterol acyltransferase and proteins involved in complement and coagulation cascades. Conclusions: This multi-omics based study provides a general view of the complex relationships and an alternative classification for various metabolic diseases where the cross-talk or compensatory mechanism between the immune and metabolism systems plays a critical role.

The Adipokine Profile and the Cardiometabolic Risk in Non-Obese Young Adults

Background: Young, non-obese adults are considered at low risk for cardiometabolic diseases, although markers of an unhealthy metabolic state are not uncommon findings in this population. Adipose tissue dysfunction, evaluated by the adipokine profile, significantly influences lipid and glucose metabolism and low-grade systemic inflammation. Aims: To determine the relation between adipose tissue dysfunction and the already confirmed cardiometabolic risk indicators, including the atherogenic index of plasma, lipid accumulation product, homeostatic model assessment of insulin resistance, and the low-grade inflammation markers, namely, interleukin 6 and high-sensitivity C-reactive protein. Study Design: Cross-sectional study. Methods: We recruited 93 non-obese, healthy young adults. Anthropometric, lipid profile, inflammatory markers, and adipokines were measured. An abnormal adipokine profile (high leptin-to-adiponectin ratio) was considered as a marker of a dysfunctional adipose tissue. The correlation between the leptin-to-adiponectin ratio and the anthropometric measurements, atherogenic index of plasma, lipid accumulation product, homeostatic model assessment of insulin resistance, interleukin 6, and high-sensitivity C-reactive protein was determined. Results: We found a direct correlation between the abnormal adipokine profile and the cardiometabolic risk indicators mentioned above, except for the low-grade inflammatory markers. In the regression model derived from our data, the leptin-to-adiponectin ratio was best correlated with the unfavorable plasma lipid profile, as estimated by the atherogenic index of plasma (r=0.097, confidence interval=0.015-0.180, p=0.021). A significantly higher leptin-to-adiponectin ratio was found in the insulin-resistant group (p=0.012) and in the highest lipid accumulation product quartile (p=0.032). Conclusion: In a non-obese young population, the high rate of leptin-adiponectin may be a good predictor of cardiovascular and metabolic risk assessment.

Las enfermedades metabólicas del hígado / Metabolic liver diseases / Doenças metabólicas hepáticas

El hígado humano, órgano unitario con múltiples funciones vitales, ocupa una posición anatómica privilegiada y estratégica, que le permite recibir información del resto de los órganos y sistemas de la economía. Es posible estar ante una enfermedad hepática con probables complicaciones sistémicas o frente a trastornos extrahepáticos que pueden afectar el hígado. Tal es el caso de las alteraciones en el metabolismo de determinados sustratos que tienen un impacto directo en este órgano y que ocasionan enfermedades hepáticas diversas. Así, se mencionan entre otras: la deficiencia de alfa 1 antitripsina (glicoproteína) que produce colestasis neonatal y cirrosis hepática en adolescentes y adultos con potencial desarrollo de hepatocarcinoma, y la alteración del metabolismo de ciertos metales como el cobre y el hierro, los que al acumularse en el hígado (sobrecarga hepática), dan por resultado las enfermedades de Wilson y hemocromatosis, respectivamente. Estas enfermedades metabólicas, si bien son de baja frecuencia en Argentina, y algunas de ellas difícilmente diagnosticadas en todo el mundo, pueden derivar en una muerte temprana. Esta breve revisión tiene como objetivo enfatizar que las enfermedades metabólicas que afectan al hígado no son una rareza y que pueden presentarse en diversas formas, y así mimetizarse con otras hepatopatías. Lo importante es tenerlas siempre presente.

Human liver, an extraordinary organ with multiple vital functions, takes up a privileged anatomic position, whose strategic site enables it to receive information from the rest of the organism. It is possible to observe liver disease with probable systemic complications, or extrahepatic manifestations that can affect the liver.They could be overthrow metabolisms because of some substances with a direct impact on the gland leading to different liver diseases. Such is the case of Alpha 1 antitrypsin deficiency (a glycoprotein deficiency) which leads to neonatal colestasis and cirrhosis in young and adults, and potentially develop hepatocellular carcinoma. Copper and ironmetabolisms and their accumulation load the hepatocites as a result give rise to Wilson disease and hemochromatosis, respectively. These metabolic diseases, of less frequency in Argentina, are hard to be diagnosed world wide and can lead to premature death. This short revision is aimed at emphasizing that metabolic diseases are not rare and can mimicry different liver diseases.

O fígado humano, órgão unitário com múltiplas funções vitais, ocupa uma posição anatômica privilegiada e estratégica, o que lhe permite receber informações do resto dos órgãos e sistemas da economia. É possível estar diante de uma doença hepática com prováveis complicações sistêmicas ou perante distúrbios extra hepáticos que podem afetar o fígado. Tal é o caso das alterações no metabolismo de certos substratos que têm um impacto direto neste órgão, causando diversas doenças hepáticas. Deste modo, são mencionadas, dentre outras: a deficiência de alfa 1 antitripsina (glicoproteína) que produz colestase neonatal e cirrose hepática nos adolescentes e adultos com potencial desenvolvimento de hepatocarcinoma e a alteração do metabolismo de certos metais como o cobre e o ferro, os quais ao se acumularem no fígado (sobrecarga hepática), resultam nas doenças de Wilson e Hemocromatose, respectivamente. Estas doenças metabólicas, apesar de serem de baixa frequência na Argentina, e algumas delas dificilmente diagnosticadas em todo o mundo, podem levar à morte precoce. Esta breve revisão visa enfatizar que as doenças metabólicas que afetam o fígado não são uma raridade e podem se apresentar de várias formas, mimetizando-se com outras hepatopatias. O importante é que estejam sempre presentes.

Caracterización de la función diastólica y sistólica en pacientes con diagnóstico de síndrome metabólico / Characterization of diastolic and systolic function in patients diagnosed with metabolic syndrome

OBJETIVOS: Caracterizar la función diastólica ysistólica de los pacientes con diagnóstico deSíndrome Metabólico que asisten a la clínica defactores de riesgo de la Unidad de Cardiología delHospital General San Juan de Dios, durante junioy julio de 2009. Metodología: Estudio descriptivotransversal,realizado en pacientes con SíndromeMetabólico, diagnosticado por 3 o más criteriossegún NCEP-ATP III, entre las edades de 18 a 75años. La función diastólica y sistólica se obtuvo pormedio de Ecocardiograma. Resultados: Se realizaron141 Ecocardiogramas, que mostraron disfuncióndiastólica en el 83% de los pacientes y la funciónsistólica normal en el 99% de los casos; de lospacientes con disfunción diastólica el 74%disfunción grado I; 85% de la muestra fueron degénero femenino, de ellas el 40% tenía 4 criteriosde Síndrome Metabólico; el 95% de los hombrespresentó disfunción diastólica y el 100% funciónsistólica normal; las mujeres con disfuncióndiastólica correspondían al 81% y la función sistólicase encontró normal en 98% de ellas. Conclusiones:El 83% presentó disfunción diastólica. Hubo 2 casosde disfunción sistólica en pacientes de génerofemenino, correspondiente al 1%, en el 99% lafunción sistólica fue normal. 46% de los casos dedisfunción diastólica se presentó en pacientesmenores de 60 años de edad. 46% de los pacientestenía 4 criterios de síndrome metabólico y de éstos65% tuvo disfunción diastólica grado I...

Bone scintigraphy elucidates different metabolic stages of melorheostosis.

Melorheostosis is a rare benign non-hereditary sclerosing dysplasia involving the bone, often in a sclerotomal distribution. we report the case of a 27 years old lady with painful swelling of the left hand and forearm lasting for almost 15 years. The patient experienced aggravation of symptoms and limitation of motion during the past two months. Radiographic assessment revealed hyperostosis involving the left 3(rd) and 4(th) metacarpal bones and corresponding digits as well as the left ulna and distal humerus, with no soft tissue ossification. Angiographic and blood pool images of bone scintigraphy showed increased activity of mid-metacarpal region, corresponding to the sclerotom C-8. Delayed static views showed increased radiotracer uptake of the left 4(th) metacarpal bone and the corresponding digit as well as the left ulna and humerus, but no abnormal osteoblastic activity of the 3(rd) left metacarpal and digit. Histopathologic assessment confirmed the diagnosis of Melorheostosis. The case confirms that even in the same sclerotomal distribution, the multiple foci of involvement can present in different metabolic stages. In fact, the disease does not progress uniformly and different lesions can be seen in dissimilar stages of activity. Hence, metabolic imaging can be important to unmask which of the radiographically detected bony lesions are metabolically active and have the potential to be the source of current patient's symptoms and which of them are old, metabolically inactive and silent lesions, which are not clinically relevant to the patient's complaints.

From glycosylation disorders to dolichol biosynthesis defects: a new class of metabolic diseases.

Polyisoprenoid alcohols are membrane lipids that are present in every cell, conserved from archaea to higher eukaryotes. The most common form, alpha-saturated polyprenol or dolichol is present in all tissues and most organelle membranes of eukaryotic cells. Dolichol has a well defined role as a lipid carrier for the glycan precursor in the early stages of N-linked protein glycosylation, which is assembled in the endoplasmic reticulum of all eukaryotic cells. Other glycosylation processes including C- and O-mannosylation, GPI-anchor biosynthesis and O-glucosylation also depend on dolichol biosynthesis via the availability of dolichol-P-mannose and dolichol-P-glucose in the ER. The ubiquity of dolichol in cellular compartments that are not involved in glycosylation raises the possibility of additional functions independent of these protein post-translational modifications. The molecular basis of several steps involved in the synthesis and the recycling of dolichol and its derivatives is still unknown, which hampers further research into this direction. In this review, we summarize the current knowledge on structural and functional aspects of dolichol metabolites. We will describe the metabolic disorders with a defect in known steps of dolichol biosynthesis and recycling in human and discuss their pathogenic mechanisms. Exploration of the developmental, cellular and biochemical defects associated with these disorders will provide a better understanding of the functions of this lipid class in human.

Lifestyle interventions for the treatment of class III obesity: a primary target for nutrition medicine in the obesity epidemic.

Although rates of obesity have increased universally in the United States over the past 30 y, it is clear that certain individuals are more susceptible to weight gain than others. Extreme obesity [body mass index (in kg/m(2)) > 40] is increasing at rates greater than any other class of obesity in the United States. Severely obese patients often suffer from a wide variety of comorbidities. Although weight-loss surgery is the most effective treatment, it offers little in the way of large-scale containment due to its costly and invasive nature. Lifestyle interventions that induce modest weight loss and improve fitness can significantly lower disease risk. As medical professionals in the field of nutrition, we must focus first on the patient cohort that suffers most from the modern obesogenic environment. Lifestyle interventions specifically targeted toward the class III obese cohort should be a high priority in nutrition medicine.

Hepatic cirrhosis, dystonia, polycythaemia and hypermanganesaemia--a new metabolic disorder.

We report a new constellation of clinical features consisting of hypermanganesaemia, liver cirrhosis, an extrapyramidal motor disorder and polycythaemia in a 12 year-old girl born to consanguineous parents. Blood manganese levels were >3000 nmol/L (normal range <320 nmol/L) and MRI revealed signal abnormalities of the basal ganglia consistent with manganese deposition. An older brother with the same phenotype died at 18 years, suggesting a potentially lethal, autosomal recessive disease. This disorder is probably caused by a defect of manganese metabolism with the accumulation of manganese in the liver and the basal ganglia similar to the copper accumulation in Wilson disease. In order to assess the genetic basis of this syndrome we investigated two candidate genes: ATP2C2 and ATP2A3 encoding the manganese-transporting calcium-ATPases, SPCA2 and SERCA3, respectively. Genotyping of the patient and the family for microsatellite markers surrounding ATP2C2 and ATP2A3 excluded these genes. The patient was found to be heterozygous for both gene loci. Despite the unknown pathophysiology, we were able to develop a successful treatment regime. Chelation therapy with disodium calcium edetate combined with iron supplementation is the treatment of choice, lowering blood manganese levels significantly and improving clinical symptoms.

Towards ontology-driven navigation of the lipid bibliosphere.

BACKGROUND: The indexing of scientific literature and content is a relevant and contemporary requirement within life science information systems. Navigating information available in legacy formats continues to be a challenge both in enterprise and academic domains. The emergence of semantic web technologies and their fusion with artificial intelligence techniques has provided a new toolkit with which to address these data integration challenges. In the emerging field of lipidomics such navigation challenges are barriers to the translation of scientific results into actionable knowledge, critical to the treatment of diseases such as Alzheimer's syndrome, Mycobacterium infections and cancer. RESULTS: We present a literature-driven workflow involving document delivery and natural language processing steps generating tagged sentences containing lipid, protein and disease names, which are instantiated to custom designed lipid ontology. We describe the design challenges in capturing lipid nomenclature, the mandate of the ontology and its role as query model in the navigation of the lipid bibliosphere. We illustrate the extent of the description logic-based A-box query capability provided by the instantiated ontology using a graphical query composer to query sentences describing lipid-protein and lipid-disease correlations. CONCLUSION: As scientists accept the need to readjust the manner in which we search for information and derive knowledge we illustrate a system that can constrain the literature explosion and knowledge navigation problems. Specifically we have focussed on solving this challenge for lipidomics researchers who have to deal with the lack of standardized vocabulary, differing classification schemes, and a wide array of synonyms before being able to derive scientific insights. The use of the OWL-DL variant of the Web Ontology Language (OWL) and description logic reasoning is pivotal in this regard, providing the lipid scientist with advanced query access to the results of text mining algorithms instantiated into the ontology. The visual query paradigm assists in the adoption of this technology.

Hypermetabolism in clinically stable patients with liver cirrhosis.

BACKGROUND: Hypermetabolism has a negative effect on prognosis in patients with liver cirrhosis. Its exact prevalence and associations with clinical data, the nutritional state, and beta-adrenergic activity are unclear. OBJECTIVE: We investigated resting energy expenditure (REE) in 473 patients with biopsy-proven liver cirrhosis. DESIGN: This was a cross-sectional study with a controlled intervention (beta-blockade) in a subgroup of patients. RESULTS: Mean REE was 7.12 +/- 1.34 MJ/d and correlated closely with predicted values (r = 0.70, P < 0.0001). Hypermetabolism was seen in 160 patients with cirrhosis (33.8% of the study population). REE was > 30% above the predicted value in 41% of the hypermetabolic patients with cirrhosis. Hypermetabolism had no association with clinical or biochemical data on liver function. REE correlated with total body potassium content (TBP; r = 0.49, P < 0.0001). Hypermetabolic patients had lower than normal body weight and TBP (P < 0.05). About 47% of the variance in REE could be explained by body composition whereas clinical state could maximally explain 3%. Plasma epinephrine and norepinephrine concentrations were elevated in hypermetabolic cirrhotic patients (by 56% and 41%, respectively; P < 0.001 and 0.01). Differences in REE from predicted values were positively correlated with epinephrine concentration (r = 0.462, P < 0.001). Propranolol infusion resulted in a decrease in energy expenditure (by 5 +/- 3%; P < 0.05), heart rate (by 13 +/- 4%; P < 0.01), and plasma lactate concentrations (by 32 +/- 12%; P < 0.01); these effects were more pronounced in hypermetabolic patients (by 50%, 33%, and 68%, respectively; each P < 0.05). CONCLUSIONS: Hypermetabolism has no association with clinical data and thus is an extrahepatic manifestation of liver disease. Increased beta-adrenergic activity may explain approximately 25% of hypermetabolism.

Syndrome X and mortality: a population-based study. Risk Factor and Life Expectancy Research Group.

The present report analyzes the prevalence of the cluster of metabolic abnormalities defined as syndrome X (high blood glucose, high blood pressure, low high density lipoprotein (HDL) cholesterol, and high triglycerides) and its impact on cardiovascular disease mortality in a large cohort of men and women (22,561 men and 18,495 women). These individuals were participants in a series of epidemiologic investigations of cardiovascular disease conducted in Italy between 1978 and 1987. They were followed for an average of 7 years, during which time a total of 1,218 deaths occurred (1,003 in men and 215 in women). Deaths were coded according to the International Classification of Diseases, 9th Revision (ICD-9). The prevalence of the full cluster of metabolic abnormalities (syndrome X) was low in the population as a whole, with only 3.0 percent of men and 3.4 percent of women exhibiting the full cluster of abnormalities that comprise syndrome X. The risk of death from all causes and cardiovascular disease increased with increased numbers of metabolic abnormalities in both men and women. Mortality from cancer was significantly increased in women (but not in men) with syndrome X, compared with women with no metabolic abnormalities. Population attributable risks for all cause mortality and cardiovascular disease mortality were 0.06 and 0.09 in men and 0.04 and 0.48 in women when assessed by population cutpoints. These data from a large population-based epidemiologic investigation indicate that the presence of a full cluster of metabolic abnormalities from syndrome X is an important risk factor for cardiovascular disease and all-cause mortality in both men and women, but that the low prevalence of such a cluster in the population reduces the public health impact of syndrome X. The majority of individuals who die from cardiovascular disease present elevations in any one, two, or three of the metabolic abnormalities. The notion of the cluster of metabolic abnormalities (syndrome X) should not distract our attention from established individual risk factors that have been proven to be major causes of cardiovascular disease death and disability in our society.

Clinical manifestation of myeloperoxidase deficiency.

Myeloperoxidase (MPO), an iron-containing heme protein localized in the azurophilic granules of neutrophil granulocytes and in the lysosomes of monocytes, is involved in the killing of several micro-organisms and foreign cells, including bacteria, fungi, viruses, red cells, and malignant and nonmalignant nucleated cells. Despite the primary role of the oxygen-dependent MPO system in the destruction of certain phagocytosed microbes, subjects with total or partial MPO deficiency generally do not have an increased frequency of infections, probably because other MPO-independent mechanism(s) for microbicidal activity compensate for the lack of MPO. Infectious diseases, especially with species of Candida, have been observed predominantly in MPO-deficient patients who also have diabetes mellitus, but the frequency of such cases is very low, less than 5% of reported MPO-deficient subjects. Evidence from a number of investigators indicates that individuals with total MPO deficiency show a high incidence of malignant tumors. Since MPO-deficient PMNs exhibit in vitro a depressed lytic action against malignant human cells, it can be speculated that the neutrophil MPO system plays a central role in the tumor surveillance of the host. However, any definitive conclusion on the association between MPO deficiency and the occurrence of cancers needs to be confirmed in further clinical studies. Clinical manifestations of this disorder depend on the nature of the defect; an acquired abnormality associated with other hematological or nonhematological diseases has been occasionally described, but the primary deficiency is the form more commonly reported. Another area of interest pertinent to MPO expression is related to the use of anti-MPO monoclonal antibodies for the lineage assignment of acute leukemic cells, the definition of FAB MO acute myeloid leukemia, the identification of biphenotypic acute leukemias, and their distinction from acute leukemia with minimal phenotypic deviation. The advantage of MPO monoclonal antibodies over the MPO cytochemical assay relies in the ability of the former method to recognize the enzymatically inactive precursor forms of MPO.

La evaluación gasométrica en el Hospital Central Militar análisis cualitativo de 5, 169 gasometrías / The gasometric assessment of patients in the Military Central Hospital. A quantitative analysis of 5, 169 gasometric procedures

Se analizaron 5,169 gasometrías arteriales mediante el cálculo de concordancia, brecha aniónica, cálculo de respuesta compensatoria esperada y de gradiente alvéolo-arterial de oxígeno. Se revisaron además 400 expedientes clínicos para establecer si la información obtenida se incluyó en los mismos. Se encontró que 424 (8 por ciento) gasometrías no fueron interpretadas por carecer de concordancia entre sus valores. Los servicios que más solicitaron el estudio fueron terapia intensiva, pediatría y urgencias de adultos. Las indicaciones más comunes fueron problemas metabólicos asociados a diabetes mellitus, insuficiencia renal y cirrosis. El trastorno ácido-básico más frecuente fue la alcalemia por acidosis metabólica y alcalosis respiratoria asociada a diabetes mellitus e insuficiencia crónica. Los demás trastornos ácido-básicos simples y complejos son poco frecuentes. Se encontraron 661 (13.9 por ciento) gasometrías normales, lo que sugiere que el médico indica adecuadamente el estudio. De los 400 expedientes clínicos revisados sólo en 10 (2.5 por ciento) se realizó una adecuada interpretación, lo que muestra que la gasometría arterial es un recurso subutilizado. La causa más frecuente de hipoxemia con gradiente alvéolo-arterial de oxígeno amplio fue la enfermedad broncopulmonar obstructiva crónica. Hipoxemia con gradiente alvéolo-arterial de oxígeno normal se asoció con enfermedad cerebrovascular. Se concluye que la gasometría arterial es un estudio confiable, generalmente bien indicado pero pobremente evaluado y esto hace que información valiosa se pierda