Enhanced insulin secretion and glucose tolerance in rats exhibiting low plasma free fatty acid levels and hypertriglyceridaemia due to congenital albumin deficiency.

Congenitally analbuminaemic individuals and rats (NARs) exhibit several metabolic abnormalities, including hypertriglyceridaemia and plasma free fatty acid deficiency. Our aim was to study glucose homeostasis and insulin secretion in NARs. Plasma concentrations of lipids, glucose and insulin and secretion of insulin from the pancreatic islets were measured in female NARs and control animals (Sprague-Dawley rats; SDRs). Glucose homeostasis tests were also performed. Plasma glucose levels were similar between NARs and SDRs, irrespective of feeding status. However, fed insulinaemia was ∼37% higher (P 0.05) in NARs than in SDRs. The NARs displayed a markedly increased glucose tolerance, i.e. the integrated glycaemic response was one-third that of the control animals. Enhanced glucose tolerance was associated with threefold higher insulinaemia at peak glycaemia after a glucose load than in the control animals. Similar peripheral insulin sensitivity was observed between groups. Isolated pancreatic islets from NARs secreted significantly more insulin than islets from SDRs in response to a wide range of glucose concentrations (2.8-33.3 mm). Despite having similar liver glycogen contents in the fully fed state, NARs had ∼40% (P 0.05) lower glycogen contents than SDRs after 6 h fasting. The injection of a gluconeogenic substrate, pyruvate, elicited a faster rise in glycaemia in NARs compared with SDRs. Overall, NARs displayed enhanced glucose tolerance, insulin secretion and gluconeogenic flux. The higher glucose tolerance in NARs compared with SDRs is attributed to enhanced islet responsiveness to secretagogues, while peripheral insulin sensitivity seems not to be involved in this alteration. We propose that the enhanced glucose metabolism is a chronic compensatory adaptation to decreased free fatty acid availability in NARs.

The higher susceptibility of congenital analbuminemic rats to Ca2+-induced mitochondrial permeability transition is associated with the increased expression of cyclophilin D and nitrosothiol depletion.

Congenital analbuminemia is a rare autosomal recessive disorder characterized by a trace level of albumin in blood plasma and mild clinical symptoms. Analbuminemic patients generally present associated abnormalities, among which dyslipidemia is a hallmark. In this study, we show that mitochondria isolated from different tissues (liver, heart and brain) from 3-month-old analbuminemic rats (NAR) present a higher susceptibility to Ca(2+)-induced mitochondrial permeability transition (MPT), as assessed by either Ca(2+)-induced mitochondrial swelling, dissipation of membrane potential or mitochondrial Ca(2+) release. The Ca(2+) retention capacity of the liver mitochondria isolated from 3-month-old NAR was about 50% that of the control. Interestingly, the assessment of this variable in 21-day-old NAR indicated that the mitochondrial Ca(2+) retention capacity was preserved at this age, as compared to age-matched controls, which indicates that a reduced capacity for mitochondrial Ca(2+) retention is not a constitutive feature. The search for putative mediators of MPT sensitization in NAR revealed a 20% decrease in mitochondrial nitrosothiol content and a 30% increase in cyclophilin D expression. However, the evaluation of other variables related to mitochondrial redox status showed similar results between the controls and NAR, i.e., namely the contents of reduced mitochondrial membrane protein thiol groups and total glutathione, H(2)O(2) release rate, and NAD(P)H reduced state. We conclude that the higher expression of cyclophilin D, a major component of the MPT pore, and decreased nitrosothiol content in NAR mitochondria may underlie MPT sensitization in these animals.

Lack of plasma albumin impairs intravascular lipolysis and explains the associated free fatty acids deficiency and hypertriglyceridemia.

BACKGROUND: Abnormalities in lipid metabolism and transport are hallmarks in analbuminemic Nagase rats (NAR) and humans. Triglyceridemia is nearly 3- to 5-fold higher in female NAR than in control Sprague-Dawley rats (SDR). Also, NAR present with a severe plasma free fatty acid (FFA) deficit. There are conflicting results regarding the mechanisms underlying NAR hypertriglyceridemia. OBJECTIVE: We aimed at investigating whether liver lipogenesis and triglyceride secretion rates into the plasma contribute to the hypertriglyceridemia in NAR. We also studied whether heparin or albumin administration would release the hypothesized lipolysis inhibition in NAR. METHODS: The incorporation of tritiated water into lipids and the linear accumulation rate of plasma triglycerides after Triton WR1339 injection were the measures of liver lipogenesis and triglyceride secretion rates. RESULTS: Lipogenesis (596 ± 40 vs. 929 ± 124 µmol 3H2O/g/h) and triglyceride (4.25 ± 1.00 vs. 7.04 ± 1.68 mg/dL/min) secretion rates were slower (P ≤ 0.05) in fasted NAR than in control SDR. The injection of either heparin or albumin elicited an increase in NAR plasma FFA levels over time. FFA levels reached control levels 90 min after the albumin administration, increasing from 0.36 ± 0.05 to 1.34 ± 0.16 mEq/L (P ≤ 0.05). These results indicate that the lack of plasma albumin inhibits intravascular lipolysis and causes the FFA deficit observed in NAR. CONCLUSION: NAR hepatic triglyceride synthesis and output do not contribute to NAR hypertriglyceridemia. We propose that the lack of albumin diminishes intravascular lipolysis which reduces the plasma triglyceride removal rate and explain both NAR hypertriglyceridemia and FFA deficiency.

Diminished macrophage cholesterol removal rate by the altered HDL metabolism in the Nagase analbuminemic rat.

Dyslipoproteinemia of the Nagase analbuminemic rat (NAR) is characterized by elevated concentrations of VLDL and LDL attributed to increased rates of liver lipoprotein synthesis. Increased lysophosphatidylcholine (LPC) in NAR HDL has been attributed to high plasma LCAT activity. We show here that, as compared with Sprague-Dawley rats (SDR), NAR plasma triacylglycerol (TAG), total cholesterol (TC), HDL TAG, protein, total phospholipids (PL), LPC, and PS are increased. These alterations rendered the NAR HDL particle more susceptible to the activity of the enzyme hepatic lipoprotein lipase (HL), which otherwise was unaltered in our study. Fractional catabolic rates in blood of the autologous 125I-apoHDL (median and lower quartile values), were, respectively, 0.231 and 1.645 (n = 10) in NAR as compared with 0.140 and 0.109 (n = 10) in SDR (P = 0.012), corresponding to synthesis rates of HDL protein of 89.8 +/- 33.7 mg/d in NAR and 17.4 +/- 6.5 mg/d in SDR (P = 0.0122). Furthermore, Swiss mouse macrophage free-cholesterol (FC) efflux rates, measured as the percent [14C]-cholesterol efflux/6 h, were 8.2 +/- 2.3 (n = 9) in NAR HDL and 11.2 +/- 3.2 (n = 10) in SDR HDL (P = 0.03). Therefore, in NAR the modification of the HDL composition slows down the cell FC efflux rate, and together with the increased rate of plasma HDL metabolism influences the reverse cholesterol transport system.

Enhanced glomerular permeability to macromolecules in the Nagase analbuminemic rat.

Plasma albumin restricts capillary water filtration. Accordingly, the glomerular ultrafiltration coefficient is higher in Nagase analbuminemic rats (NAR) than in Sprague-Dawley controls. We investigated whether the glomerular permeability to macromolecules is also enhanced in NAR. SDS-PAGE fractionation of urine proteins showed several bands with molecular masses between 60 and 90 kDa in NAR only. Acute administration of BSA to NAR led to nearly complete disappearance of these proteins from urine, an effect partially reversed when most of the exogenous albumin was cleared from circulation. The fractional clearance of 70-kDa dextran was increased in NAR, indicating a size defect. Binding of cationized ferritin to the glomerular basement membrane was decreased in NAR, suggesting associated depletion of fixed anions. The magnitude of cationic ferritin binding correlated negatively with the fractional clearance of 70-kDa dextran, suggesting that the two abnormalities may share a common pathogenic mechanism. Collectively, these results suggest enhanced glomerular permeability to macromolecules in NAR. Albumin may be necessary to maintain the normal glomerular permselectivity properties.

[Hypoalbuminemia in dialysis. Is it a marker for malnutrition or inflammation?]. / Hipoalbuminemia en diálisis. Es marcador de desnutrición o de inflamación?

Hypoalbuminemia in dialysis is a highly prevalent condition associated with morbidity and mortality. Hypoalbuminemia, although not synonymous of malnutrition, is highly related to it. Poor nutrient intake, frequently observed in uremia, may cause malnutrition and subsequently hypoalbuminemia. In addition, it has been recently reported that a systemic inflammatory response may participate in developing hypoalbuminemia in chronic renal failure. Uremia per se, or through mechanisms stimulated by the use of current dialysis membranes and/or solutions, seems to trigger the inflammatory process, remarkably associated with hypoalbuminemia. Infections, to which patients on dialysis are particularly predisposed, stimulate production of the inflammatory response as well. Other conditions non-associated to inflammatory response, such as the protein losses through dialysis, may cause and increase malnutrition. Overhydration, frequently present in patients with renal failure, on the one hand causes dilution of serum albumin concentrations, and on the other hand, is cause of onset and/or enhancement of congestive cardiac failure, which in turn may be associate with malnutrition. Patients with chronic renal failure develop hypoalbuminemia due to a complex setting of conditions, with systemic inflammatory response as a major cause; notwithstanding, other factors such as malnutrition and overhydration can also play a relevant role. Therefore, diagnostic and therapeutic approaches should be individualized.

Serum electrolytes in hospitalized pellagra alcoholics.

BACKGROUND: Owing to high diarrhoea and protein malnutrition frequencies in pellagra, we hypothesised that pellagra patients would have higher electrolyte disturbances than non-pellagra alcoholics. OBJECTIVE: To compare serum electrolytes of hospitalised alcoholics with or without pellagra. DESIGN: Retrospective and descriptive case-control study. SETTING: Internal Medicine wards at a University Hospital, Medical School of Uberaba, Brazil. SUBJECTS: Medical records were reviewed to obtain relevant clinical details, main diagnosis and laboratory data, including serum electrolytes on hospital admission of pellagra patients (n=33) and a randomly chosen control group of alcoholics (n=37), matched in age, gender and socio-economic status. Anaemia was ascertained by haemoglobin <12.5 g/dl (men) and 1.5 g/dl (women), and hypoalbuminemia by serum albumin <3.3 g/dl. RESULTS: Pellagra and controls showed similar age (39.4+/-13.1 vs 45.0+/-11.4 years) and a male predominance of gender (69.7 vs 78.4%), and similar associated diagnoses, including high blood pressure (21.2 vs 16.2%), peripheral neuropathy (12.1 vs 13. 5%), and pneumonia (9.1 vs 13.5%). Despite displaying similar serum sodium (136.6+/-6.1 vs 137.8+/-5.7 mEq/I), magnesium (1.72+/-0.74 vs 1.62+/-0.34 mg/dl), phosphorus (3.79+/-0.87 vs 3.87+/-0.78 mEq/1) than controls,in addition to higher hypoalbuminemia (76.2 vs 33%) and anaemia (60.6 vs 35.1%) frequencies. CONCLUSIONS: Higher anaemia and hypoalbuminemia frequencies associated with lower serum potassium levels suggest increased protein malnutrition prevalence among pellagrins.

Sodium serum levels in hypoalbuminemic adults at general medical wards.

Hypoalbuminemia may cause interstitial edema and hemodilution, which we hypothesized may influence serum sodium levels. Our purpose was to compare serum sodium levels of hospitalized adults with or without hypoalbuminemia. All sodium and albumin serum levels of 142 adults hospitalized at general medical wards over a six-month period were searched at a University Hospital mainframe computer. Relevant laboratory data and clinical details were also registered. Hypoalbuminemia was defined by serum albumin concentration < 3.3 g/dl Fisher, Mann-Whitney, and Student's t tests were applied to compare groups with or without hypoalbuminemia. Ninety-nine patients, classified as hypoalbuminemic, had lower blood hemoglobin (10.68 +/- 2.62 vs. 13.54 +/- 2.41), and sodium (135.1 +/- 6.44 vs. 139.9 +/- 4.76 mEq/l) and albumin (2.74 +/- 0.35 vs. 3.58 +/- 0.28 g/dl) serum levels than non-hypoalbuminemic (n = 43). Pearson's coefficient showed a significant direct correlation between albumin and sodium serum levels (r = 0.40) and between serum albumin and blood hemoglobin concentration (r = 0.46). Our results suggest that hypoalbuminemic adults have lower serum sodium levels than those without hypoalbuminemia, a phenomenon that may be at least partially attributed to body water retention associated with acute phase response syndrome.

Estudios controlados de los efectos clínicos de la administración de albúmina en pacientes pediátricos en estado crítico con hipoalbuminemia / Controlled trial about the effects of albumin administration to pediatric patients in critical condition who have hipoalbuminemia

La albúmina es una proteína plasmática sintetizada por el hígado con múltiples funciones. La hipoalbuminemia es un dato de laboratorio frecuente en pacientes graves con diferentes patologías. La administración de albúmina exógena humana es una práctica clínica generalizada a pesar de no tener evidencia científica concluyente de su eficacia. Se estudiaron 14 pacientes pediátricos enfermos graves en la unidad de terapia intensiva (TTIP) del Hospital Central Militar (HCM) con hipoalbuminemia (< 3 g/dL). Se excluyeron aquellos pacientes con enfermedad renal, hepática o cáncer. Estudio prospectivo, abierto y aleatorio de la administración de albúmina humana exógena (1 g/kg/dosis), contra placebo (solución salina) hasta tener niveles normales de albúmina, monitorizando cada 4 días el nivel de albúmina. Se siguieron hasta su salida del hospital o su defunción, se determinaron PRISM y SNAP a su ingreso. Las variables clínicas estudiadas fueron los días de hospitalización, días de ventilación mecánica, días de estancia en la UTIP, total de días de ayuno y mortalidad. No se encontraron efectos clínicos benéficos en la tolerancia a la nutrición enteral, tiempo para cubrir requerimientos nutricionales totales, días de ventilación mecánica y día de nutrición parenteral total al administrar albúmina en el grupo de estudio vs. el control. No se encontró disminución de la morbilidad y mortalidad en los pacientes tratados con albúmina. El uso de la administración de albúmina exógena humana es una práctica cara

Increase in skeletal muscle protein content by the beta-2 selective adrenergic agonist clenbuterol exacerbates hypoalbuminemia in rats fed a low-protein diet.

This investigation examined how the nutritional status of rats fed a low-protein diet was affected when the animals were treated with the beta-2 selective agonist clenbuterol (CL). Males (4 weeks old) from an inbred, specific-pathogen-free strain of hooded rats maintained at the Dunn Nutritional Laboratory were used in the experiments (N = 6 rats per group). CL treatment (Ventipulmin, Boehringer-Ingelheim Ltd., 3.2 mg/kg diet for 2 weeks) caused an exacerbation of the symptoms associated with protein deficiency in rats. Plasma albumin concentrations, already low in rats fed a low-protein diet (group A), were further reduced in CL rats (A = 25.05 +/- 0.31 vs CL = 23.64 +/- 0.30 g/l, P < 0.05). Total liver protein decreased below the level seen in either pair-fed animals (group P) or animals with free access to the low-protein diet (A = 736.56 +/- 26 vs CL = 535.41 +/- 54 mg, P < 0.05), whereas gastrocnemius muscle protein was higher than the values normally described for control (C) animals (C = 210.88 +/- 3.2 vs CL = 227.14 +/- 1.7 mg/g, P < 0.05). Clenbuterol-treated rats also showed a reduction in growth when compared to P rats (P = 3.2 +/- 1.1 vs CL = -10.2 +/- 1.9 g, P < 0.05). This was associated with a marked decrease in fat stores (P = 5.35 +/- 0.81 vs CL = 2.02 +/- 0.16 g, P < 0.05). Brown adipose tissue (BAT) cytochrome oxidase activity, although slightly lower than in P rats (P = 469.96 +/- 16.20 vs CL = 414.48 +/- 11.32 U/BAT x kg body weight, P < 0.05), was still much higher than in control rats (C = 159.55 +/- 11.54 vs CL = 414.48 +/- 11.32 U/BAT x kg body weight, P < 0.05). The present findings support the hypothesis that an increased muscle protein content due to clenbuterol stimulation worsened amino acid availability to the liver and further reduced albumin synthesis causing exacerbation of hypoalbuminemia in rats fed a low-protein diet.

Increase in skeletal muscle protein content by the ß-2 selective adrenergic agonist clenbuterol exacerbates hypoalbuminemia in rats fed a low-protein diet

This investigation examined how the nutritional status of rats fed a low-protein diet was affected when the animals were treated with the ß-2 selective agonist clenbuterol (CL). Males (4 weeks old) from an inbred, specific-pathogen-free strain of hooded rats maintained at the Dunn Nutritional Laboratory were used in the experiments (N = 6 rats per group). CL treatment (Ventipulmin, Boehringer-Ingelheim Ltd., 3.2 mg/kg diet for 2 weeks) caused an exacerbation of the symptoms associated with protein deficiency in rats. Plasma albumin concentrations, already low in rats fed a low-protein diet (group A), were further reduced in CL rats (A = 25.05 ñ 0.31 vs CL = 23.64 ñ 0.30 g/l, P<0.05). Total liver protein decreased below the level seen in either pair-fed animals (group P) or animals with free access to the low-protein diet (A = 736.56 ñ 26 vs CL = 535.41 ñ 54 mg, P<0.05), whereas gastrocnemius muscle protein was higher than the values normally described for control (C) animals (C = 210.88 ñ 3.2 vs CL = 227.14 ñ 1.7 mg/g, P<0.05). Clenbuterol-treated rats also showed a reduction in growth when compared to P rats (P = 3.2 ñ 1.1 vs CL = -10.2 ñ 1.9 g, P<0.05). This was associated with a marked decrease in fat stores (P = 5.35 ñ 0.81 vs CL = 2.02 ñ 0.16 g, P<0.05). Brown adipose tissue (BAT) cytochrome oxidase activity, although slightly lower than in P rats (P = 469.96 ñ 16.20 vs CL = 414.48 ñ 11.32 U/BAT x kg body weight, P<0.05), was still much higher than in control rats (C = 159.55 ñ 11.54 vs CL = 414.48 ñ 11.32 U/BAT x kg body weight, P<0.05). The present findings support the hypothesis that an increased muscle protein content due to clenbuterol stimulation worsened amino acid availability to the liver and further reduced albumin synthesis causing exacerbation of hypoalbuminemia in rats fed a low-protein diet

Avaliaçäo de Hipoalbuminemia como fator de risco para diarréia associada à nutriçäo enteral / Hipoalbuminemia assessment as a risk factor for enteral nutrition relatet diarrhea

Nesse estudo de coorte retrospectivo foram avaliados 202 pacientes que receberam nutriçäo enteral no Hospital das Clínicas da UFMG entre janeiro de 1987 e dezembro de 1995. O objetivo principal do trabalho foi estudar o papel da hipoalbuminemia como fator de risco para o desenvolvimento de diarréia associada à nutriçäo enteral. Os objetivos secundários foram a avaliaçäo das indicaçöes e da incidência de complicaçöes da nutriçäo enteral e da presença de outros fatores de risco para diarréia, como o uso de medicamentos e a localizaçäo da sonda de nutriçäo enteral. As principais indicaçöes de nutrriçäo enteral foram as doenças neurológicas (62 pacientes, 30,7 porcento), seguidas por câncer de cabeça e pescoço (23 pacientes, 11,4 porcento) e doenças benignas do esôfago (23 pacientes, 11,4 porcento). Diarréia foi a complicaçäo de maior incidência (58 pacientes, 28,7 porcento), seguida por estase (14 pacientes, 6,9 porcento) e constipaçäo intestinal (13 pacientes, 6,4 porcento). Hipoalbuminemia, avaliada nos pontos-de-corte para a albumina sérica de 3,0 , 2,5 e 2,0 g/dl, näo se comportou como fator de risco para diarréia, embora tenha havido uma tendência à maior incidência da complicaçäo nos pacientes hipoalbuminêmicos, e a albumina sérica média nos pacientes com diarréia tenha se mostrado significativamente menor que nos pacientes sem diarréia . Na avaliaçäo de outros fatires de risco para diarréia , os agentes antisecretores mostraram tendência a associaçäo com essa complicaçäo. A administraçäo da dieta no intestino delgado foi a variável que mais claramente se correlacionou com diarréia. Näo houve correlaçä estatística entre uso de antibióticos e diarréia. Esses resultados sugerem que: a) o uso de antisecretores e a administraçäo intermitente da dieta diretamente no intestino delgado podem ser fatores de risco para diarréia em pacientes em nutriçäo enteral; b) o uso de antimicrobianos pode näo se correlacionar com diarréia nesses pacientes; c) hipoalbuminemia näo se comporta como fator de risco para diarréia em nutriçäo enteral.(au)

Nagase analbuminemic rats have faster plasma triacylglycerol and VLDL synthesis rates.

Serum triacylglycerol (TG) concentration is markedly elevated in Nagase analbuminemic rats (NAR) as compared to Sprague-Dawley rats (SDR) and reflects a high level of mainly VLDL. Hepatic production of triacylglycerol, as measured by the Triton-WR1339 infusion technique of impairing TG removal from blood, and plasma metabolic rate of pulse-infused [125I]apo VLDL, were higher in NAR. However, contrary to previous reports, this elevated TG production could not be controlled by previous treatment of NAR with (i) bovine albumin infused intra-arterially or into the peritoneal cavity, or with (ii) dextran (Mol.wt. 73,500) injected intraperitoneally. Albumin administration expanded the plasma volume and could explain the apparent reduction of blood lipids found by others. Nonetheless, intraperitoneal dextran, as compared to saline, reduced the plasma cholesterol concentration regardless of the variation in the hematocrit level and thus, by raising the osmotic pressure of blood might regulate the metabolism of cholesterol-rich lipoproteins such as LDL and HDL in NAR.

Low serum albumin and the increased risk of amikacin nephrotoxicity.

AIM: The purpose of the present study was to know the incidence and risk factors associated with amikacin nephrotoxicity in a cohort of patients form a general medial center. STUDY DESIGN: Prospective follow-up of a cohort of 104 patients treated with intravenous amikacin for at least 36 hours. We assessed serum creatinine every other day and amikacin plasma levels at 48 and 96 hours after treatment was begun. Patients with other risk factors to develop acute renal failure were excluded. The study was conducted at the Hospital de Especialidades, Centro Médico de Occidente, Instituto Mexicano del Seguro Social. RESULTS: Ten patients developed nephrotoxicity (9.6%). According to the logistic regression model, the most powerful predictor of high nephrotoxicity probability was the serum albumin concentration. The lower the serum albumin concentration, the higher the risk of toxicity. The mean serum albumin in the group of patients with nephrotoxicity was 2.6 +/- 0.55 g/dL, while in the group of patients without toxicity it was 3.5 +/- 0.55 g/dL. No differences were observed in the age, sex, diagnosis, renal function and amikacin doses between both groups. Furthermore, low serum albumin concentration was also associated with amikacin accumulation in plasma. The group of patients with hypoalbuminemia (< or = 3.0 g/dL) had a significantly higher trough amikacin plasma level (assessed at 48 and 96 hours of the initiation of treatment) than those with normal serum albumin, with no differences among the age, sex, baseline renal function and received amikacin doses. CONCLUSIONS: We conclude that serum albumin concentration is the most powerful predictor of amikacin nephrotoxicity. The risk factors observed in the present study are similar to those previously observed by us at the Instituto Nacional de la Nutrición Salvador Zubirán.

Hipoalbuminemia grave e diarréia em suporte nutricional enteral / Grave hypoalbuminemia and diarrhea in enteral nutritional support

Em 530 pacientes submetidos a nutriçäo enteral por sonda no período de janeiro de 1985 a julho de 1987, verificou-se que a freqüência de diarréia (três evacuaçöes líquidas por dia) foi de 13,8%, tendo se constituido a complicaçäo digestiva mais freqüente em suporte nutricional enteral. A literatura aponta diversas causas para a ocorrência dessa complicaçäo, entre os quais uso de medicamentos, hipoalbuminemia, osmolalidade, temperatura e velocidade de infusäo. Com o intuito de analisar em nosso meio os fatores associados à ocorrência de diarréia, realizou-se estudo retrospectivo näo consecutivo com 108 pacientes subdivididos em 54 portadores de diarréia e 54 que näo apresentaram diarréia. Os doentes foram pareados de acordo com a moléstia de base e idade. Todos os doentes receberam a mesma dieta enteral polimérica por sonda nasoenteral. Estudaram-se as variáveis posicionamento da sonda, concentraçäo da dieta, velocidade de infusäo, estado febril, nível de albumina sérica, uso de radioterapia, antiácidos e antibióticos. A análise estatística foi feita pelo teste do x**2. Observou-se que houve associaçäo estatística significante (p < 0,05) entre albuminemia inferior a 2,8g/100ml e ocorrência de diarréia. As demais variáveis näo apresentaram associaçöes significativas com a diarréia. Conclui-se que hipoalbuminemia intensa está associada à ocorrência de diarréia durante o uso de dieta enteral

Protein-losing enteropathy in systemic lupus erythematosus

Enteropatia perdedora de proteina no lupus eritematoso sistemico. O caso de uma jovem de 23 anos com lupus eritematoso sistemico e enteropatia perdedora de proteina e descrito. A biopsia de delgado revelou linfangiectasia. O quadro regrediu com o uso de prednisona. A enteropatia perdedora de proteina deve ser suspeitada nos casos de lupus eritematoso sistemico com hipoalbuminemia e funcoes hepatica e renal preservadas. A revisao da literatura e apresentada salientando-se os aspectos fisiopatologicos envolvidos.

Protein-losing enteropathy in systemic lupus erythematosus.

We describe a 23-year old Brazilian woman with systemic lupus erythematosus and protein-losing enteropathy. Small intestinal biopsy revealed lymphangiectasia. Protein-losing enteropathy responded to corticosteroid therapy and should be suspected in cases of systemic lupus erythematosus with hypoalbuminemia without proteinuria and liver failure. A review of the English literature is presented with comments on pathogenesis.