Observaciones en el mundo real sobre la efectividad del sistema flash de monitorización de glucosa en la práctica clínica en Chile / Real-world observations of the effectiveness of the flash glucose monitoring in clinical practice in Chile

OBJETIVO: Evaluar el tiempo en rango de glucosa y su asociación con otras medidas del control glicémico establecidas por el consenso internacional del tiempo en rango en usuarios de vida real del sistema flash de monitorización de glucosa FreeStyle LibreTM en Chile. MÉTODOS: Se analizaron los datos provenientes de la base de datos Freestyle Libre™ entre diciembre de 2014 y enero de 2022. Las lecturas se dividieron en 10 grupos (deciles) del mismo tamaño (cada decil contenía aproximadamente 498 usuarios) en función del tiempo en rango. Para cada decil se calculó la media de determinaciones diarias, el promedio de glucosa, la HbA1c, la desviación estándar de glucosa, el coeficiente de variación de la glucosa, el tiempo en rango, el tiempo de glucosa (porcentaje) por encima de 250 mg/dL (TA250), el tiempo de glucosa (porcentaje) por encima de 180 mg/dL (TA180), el tiempo por debajo (porcentaje) de 70 mg/dL (TB70) y el tiempo por debajo (porcentaje) de 54 mg/dL (TB54). RESULTADOS: Desde diciembre de 2014 hasta enero de 2022 hubo 4984 lectores. El grupo con el mayor tiempo en rango mostró significativamente una menor glucosa promedio que el grupo con el tiempo en rango más bajo (decil 1: media 248,3 mg/dL, decil 10: media 113,2 mg/L, diferencia ­135,1 mg/dL, p<0.05). Asimismo, el mayor tiempo en rango se asoció con una menor desviación estándar (decil 1: media 93,7mg/dL, decil 10: media 26,7mg/L, diferencia: -67,0 mg/ dL, p<0,05), menor coeficiente de variación (decil 1: media 37,8%, decil 10: media 23,3%, diferencia: -14,5%, p<0,05), menor TA250 (decil 1: media 46,5%, decil 10: media 0,2%, diferencia: -46,3%, p<0.05), menor TA180 (decil 1: media 73,9%, decil 10: media 3,8%, diferencia: -70,1%, p<0.05), menor TB70 (decil 5: mediana 6,13%, decil 10: mediana 1,70%, diferencia: -4,43%, p<0.05) y menor TB54 (decil 5: mediana 1,79%, decil 10: mediana 0,12%, diferencia: -1,67%, p<0.05). El mayor tiempo en rango se asoció también significativamente con más determinaciones diarias (decil 1: media 11,4, decil 10: media 16,6, diferencia: 5,2, p<0,05). La frecuencia media de las determinaciones entre todos los lectores fue de 14,7 determinaciones diarias. CONCLUSIONES: En los pacientes con diabetes en Chile, el empleo del sistema flash de monitorización demuestra la asociación entre el mayor tiempo en rango, la reducción de la variabilidad de la glucosa y un menor riesgo de hiperglucemias e hipoglicemias y también con un mayor compromiso.

OBJECTIVE: To evaluate glucose time in range and its association with other metrics of glucose control established by the International Consensus on TIR amongst real-life patients using the Flash Glucose Monitoring system FreeStyle LibreTM in Chile. METHODS: Data from the Freestyle Libre™ database between December 2014 and January 2022 were analyzed. Readers were divided into 10 groups (deciles) of the same size (each decile had approximately 498 users) according to time in range. For each decile of time in range, the mean of daily scans, average glucose, estimated HbA1c, glucose standard deviation, glucose coefficient of variation, time in range, glucose time (percentage) above 250 mg/dL (TA250), and glucose time (percentage) above 180 mg/dL (TA180), and the median of glucose time (percentage) below 70 mg/dL (TB70) and glucose time (percentage) below 54 mg/dL (TB54), were calculated. RESULTS: From December 2014 to January 2022, there were 4984 readers. The group with the highest TIR showed significantly lower average glucose than the group with the lowest TIR (decile 1: mean 248.3 mg/dL, decile 10: mean 113.2 mg/L, difference: ­135.1 mg/dL, p<0.05). In addition, more time in range was associated with a lower glucose standard deviation (decile 1: mean 93.7 mg/dL, decile 10: mean 26.7 mg/L, difference: -67.0 mg/dL, p<0.05), lower glucose coefficient of variation (decile 1: mean 37.8%, decile 10: mean 23.3%, difference: -14.5%, p<0.05), lower TA250 (decile 1: mean 46.5%, decile 10: mean 0.2%, difference: -46.3%, p<0.05),lower TA180 (decile 1: mean 73.9%, decile 10: mean 3.8%, difference: -70.1%, p<0.05), lower TB70 (decile 5: median 6.13%, decile 10: median 1.70%, difference: -4.43%, p<0.05) and lower TB54 (decile 5: median 1.79%, decile 10: median 0.12%, difference: -1.67%, p<0.05). Greater TIR was also associated with significantly more daily scans (decile 1: mean 11.4, decile 10: mean 16.6, difference: 5.2, p<0.05). Mean scan frequency amongst all readers was 14.7 daily scans. CONCLUSIONS: In patients with diabetes from Chile, the use of the flash glucose monitoring system demonstrates the association between greater TIR, reduced glucose variability, and reduced risk of hyperglycemia and hypoglycemia, and also its association with greater engagement.

Serum levels of alpha-tocopherol (vitamin E) in Parkinson's disease.

To elucidate the possible role of vitamin E in the pathogenesis of Parkinson's disease (PD), we compared serum levels of alpha-tocopherol (vitamin E), measured by high-performance liquid chromatography, and the vitamin E/cholesterol ratio of 42 Parkinson's disease (PD) patients using their spouses as the control group. The serum levels of vitamin E did not differ significantly between the groups (13.84 +/- 0.56 micrograms/ml for PD and 14.80 +/- 0.57 micrograms/ml for controls), nor did the vitamin E/cholesterol ratio (0.64 +/- 0.03 for both groups). There was no influence of antiparkinsonian therapy on vitamin E or the vitamin E/cholesterol ratio. Serum levels of the vitamin E and vitamin E/cholesterol ratio did not correlate with age, age at onset, scores of the Unified Parkinson's Disease Rating Scale or the Hoehn and Yahr staging in the PD group. These results suggest that serum vitamin E concentrations do not play a role in the pathogenesis of PD.

Postprandial glucose-dependent insulinotropic polypeptide and insulin responses in patients with chronic pancreatitis with and without secondary diabetes.

OBJECTIVE: To study GIP and insulin release after a test meal in patients with chronic pancreatitis with and without secondary diabetes mellitus. METHODS: 28 patients with chronic pancreatitis were classified in groups I and II according to the presence or absence of secondary diabetes mellitus. Twelve healthy subjects were included as controls. After a test meal plasma GIP levels and serum insulin levels were determined at 0, 30, 60, 120 and 180 min. RESULTS: A significant diminished GIP response was found in the groups of patients with respect to the control group. No association could be detected with severity of pancreatic insufficiency. Higher values of GIP were demonstrated at 60 and 120 min in patients without diabetes than in patients with it. CONCLUSIONS: An abnormal GIP response is present in cases of chronic pancreatitis irrespective of the presence or severity of pancreatic insufficiency. This response is further affected if secondary diabetes mellitus is present.

Relationship of basal and postprandial intraduodenal bile acid concentrations and plasma cholecystokinin levels with abdominal pain in patients with chronic pancreatitis.

Abdominal pain in patients with chronic pancreatitis has been related to an increase in plasma cholecystokinin (CCK) levels. The aim of the study was to disclose the relation of the altered response with the low intraduodenal bile acids levels found in these patients. Twenty patients with chronic pancreatitis were classified into groups I (n = 11) and II (n = 9) according to the presence or absence of pain. Intraduodenal trypsin and bile acids concentrations and plasma CCK levels were measured before and 30, 60, and 90 min after a test meal. Comparisons between values in both groups were carried out. Correlation of intraduodenal trypsin and bile acids with plasma CCK was analyzed. Patients with pain exhibited significantly lower intraduodenal trypsin levels at 30 and 90 min and lower basal and postprandial intraduodenal bile acids levels than patients without pain. In patients with pain, basal and postprandial plasma CCK levels were significantly higher than in patients without pain. A negative correlation was demonstrated between intraduodenal bile acids and plasma CCK. In patients with chronic pancreatitis and pain, a reduction in intraduodenal postprandial trypsin and basal and postprandial bile acids concentrations, as well as an increase in basal and postprandial plasma CCK levels, was encountered. A negative correlation between intraduodenal bile acids and plasma CCK concentrations was detected that may be implicated in the pathogenesis of pain.

Fecal chymotrypsin levels in children with pancreatic insufficiency.

The fecal chymotrypsin (FC) levels in samples collected over 24 h were determined by a new commercial colorimetric method from Boehringer Mannheim in 82 children suffering from various pancreatic disorders. The patients were divided into 4 groups, in accordance with the following etiologies: cystic fibrosis of the pancreas (CFP), chronic severe hepatic disorders (CSH), primary malabsorption syndrome (PMS) and malnutrition due to nondigestive causes (M). The control group comprised 48 children of similar ages. The 24th FC levels as U/g (mean +/- SD) were: 34 +/- 6 in the control group, 2 +/- 2 in the CFP group, 15 +/- 6 in the M group, 19 +/- 9 in the CSH group and 43 +/- 13 in the PMS group. The differences between the CFP patients and all the other groups were statistically significant. These results indicate that the FC levels may be suitable as a diagnostic indication of CFP and capable of differentiating between this disorder and other causes of pancreatic insufficiency.

Serum levels of beta-carotene and other carotenoids in Parkinson's disease.

To elucidate the possible role of carotenoids in the risk for developing Parkinson's disease (PD), we compared serum levels of beta-carotene, alpha-carotene and lycopene, measured by high performance liquid chromatography, of 61 PD patients using their spouses as the control group. The serum levels of these 3 carotenoids did not differ significantly between PD patients and control groups. There was no influence of antiparkinsonian therapy on serum carotenoids levels, and these did not correlate with age, age at onset, scores of the Unified Parkinson Disease Rating Scale or the Hoehn and Yahr staging in the PD group. These results show that serum carotenoids concentrations are apparently unrelated to the risk for developing PD.

Serum lipid peroxides in patients with Parkinson's disease.

To elucidate whether high serum lipid peroxidation rates may increase the risk of developing Parkinson's disease (PD), we assessed serum levels of malondialdehyde (MDA), an intermediate in lipid peroxidation processes, in 37 PD patients, with their spouses as the control group. Serum MDA levels did not differ significantly between these two groups (8.7 +/- 0.51 and 8.8 +/- 0.48 nmol/ml, resp.), and were not influenced by antiparkinsonian therapy in the PD patients. Serum MDA levels were inversely correlated with age and age at onset (P less than 0.01) in the PD group, but they were not correlated with disease duration, Unified Parkinson's Disease Rating Scale scores or Hoehn and Yahr staging. In the control group there was no correlation between serum MDA and age. These results suggest that, although serum levels of lipid peroxides were similar in both the PD and control groups, high serum lipid peroxidation rates might constitute a risk factor for younger onset of PD in predisposed individuals.

Serum levels of zinc and copper in patients with Parkinson's disease.

Several recent studies have shown decreased copper and increased zinc concentrations in the substantia nigra and increased copper concentrations in the cerebrospinal fluid of Parkinson's disease patients. To elucidate whether changes in serum levels of these trace elements may increase the risk of developing Parkinson's disease (PD), we assessed serum levels of zinc and copper by flame atomic absorption spectrophotometry, and albumin and ceruloplasmin, in 32 (Zn) and 39 PD patients (Cu), respectively, with their spouses as the control group. Serum zinc, albumin, copper and ceruloplasmin levels and the zinc/albumin and copper/ceruloplasmin ratios, did not differ significantly between the two groups and were not influenced by antiparkinsonian therapy in the PD patients. Serum zinc/albumin ratio (r = 0.43), ceruloplasmin (r = -0.36) and copper/ceruloplasmin ratio (r = 0.36) correlated significantly with age, but not with age of onset, duration of the disease, scores of the Unified Parkinson's Disease Rating Scale and Hoehn and Yahr staging in PD patients. These values did not correlate with age in the control group. These results suggest that serum levels of zinc and copper do not play any role as risk factors for PD.

Serum levels of ascorbic acid (vitamin C) in patients with Parkinson's disease.

To elucidate the possible role of vitamin C in the risk for developing Parkinson's disease (PD), we compared serum levels of ascorbic acid (vitamin C), measured by a fluorometric method, of 63 PD patients using their spouses as the control group. The serum levels of vitamin C did not differ significantly between the groups (47.13 +/- 0.89 micrograms/ml for PD and 47.60 +/- 0.60 micrograms/ml for controls). There was no influence of antiparkinsonian therapy on vitamin C. Serum levels of vitamin C did not correlate with age, age at onset and duration of the disease, scores of the Unified PD Rating Scale or the Hoehn and Yahr staging in the PD group. These results suggest that serum vitamin C concentrations are apparently unrelated to the risk of developing PD.

Serum levels of vitamin A in Parkinson's disease.

To elucidate a possible role of vitamin A in the pathogenesis of Parkinson's disease (PD) we compared serum levels of retinol (vitamin A), measured by HPLC, and the vitamin A/retinol binding protein (RBP) ratio of 42 PD patients (22 males and 20 females, mean age 67.3 +/- 1.34 years) and their respective spouses as control group (20 males and 22 females, mean age 66.2 +/- 1.42). The serum levels of vitamin A did not differ significantly between the 2 groups (0.59 +/- 0.03 microgram/dl for PD patients and 0.57 +/- 0.03 microgram/dl for controls), nor did the vitamin A/RBP ratio (0.87 +/- 0.04 and 0.82 +/- 0.03, respectively). There was no influence of antiparkinsonian therapy on vitamin A or vitamin A/RBP ratio. Serum levels of vitamin A, and vitamin A/RBP ratio did not correlate with age, age at onset, scores of the Unified Parkinson's Disease Rating Scale or the Hoehn and Yahr staging in the PD group. These results suggest that serum concentrations of vitamin A, do not play a role in the pathogenesis of PD.

Peripheral iron metabolism in patients with Parkinson's disease.

To elucidate the possible role of peripheral metabolism of iron in the risk for developing Parkinson's disease (PD), we compared serum levels of iron, transferrin and ferritin, and 24-h iron excretion in urine after a single intramuscular dose of 1 mg/kg desferrioxamine, in 68 PD patients and their spouses as the control group. All these values did not differ significantly between the groups, they were not influenced by antiparkinsonian therapy, and they did not correlate with age, age at onset and duration of the disease, scores of the Unified PD Rating Scale or the Hoehn and Yahr staging in the PD group, with the exception of the 24-h urinary iron excretion with the duration of the disease (r = 0.32, p < 0.05). These results suggest that peripheral metabolism of iron is apparently unrelated to the risk of developing PD.

Unusual serum bile acid pattern in children with the syndrome of hepatic ductular hypoplasia.

Fasting bile acids in serum of eight children with the syndrome of hepatic ductular hypoplasia were analyzed by gas chromatography. The children did not receive any kind of treatment during the month before the analysis. Serum concentrations of total bile acids ranged from 110.8-303.7 mumol/1. The predominant bile acids were chenodeoxycholic and cholic acids accounting for 62.8-86.5% of the total. The ratio of cholic acid to chenodeoxycholic acid ranged between 0.43 and 1.11. Monohydroxylated bile acids were found in increased amounts in all patients (5.1-23.9%), 3 beta-hydroxy-5-cholenoic acid being the major monohydroxylated bile acid (3.1-17.1%). Other unusual bile acids such as ursodeoxycholic acid and 12-oxo-3 alpha, 7 alpha-dihydroxy-5 beta-cholanoic acid (7.3-14.9%) were also detected. Neither 3 beta-hydroxy-5-cholenoic nor lithocholic acid levels were statistically correlated to cholic or chenodeoxycholic acids. However, a statistically significant correlation between total bile acid levels and 12-oxo-3 alpha, 7 alpha-dihydroxy-5 beta-cholanoic acid levels was found. These findings are interesting as far as the origin of the unusual bile acids found in this cholestatic syndrome is concerned. The large amounts of 3 beta-hydroxy-5-cholenoic acid measured in children with the syndrome of hepatic ductular hypoplasia could indicate the existence of an alternative fetal pathway of bile acid synthesis.

Anorexia in end-stage renal disease: pathophysiology and treatment.

Anorexia is a frequent complication of uraemic syndrome, which contributes to malnutrition in dialysis patients. Uraemic anorexia has been associated with many factors. This paper reviews the current knowledge about mechanisms responsible for uraemic anorexia, the treatments and new drugs used to control the loss of appetite. Traditionally, anorexia in dialysis patients has been considered as a sign of uraemic toxicity, therefore, two hypotheses have been proposed, the 'middle molecule' and 'peak-concentration' hypotheses, both of which are still unproved. Recently, our group proposed the tryptophan-serotonin hypothesis, which is based on a disorder in the amino acid profile acquired in the uraemic status. This is characterised by low concentrations of large neutral and branched chain amino acids (LNAA/BCAA) in the cerebrospinal fluid. This situation permits a high level of tryptophan transport across the blood-brain barrier, causing an increase in the synthesis of serotonin (responsible for appetite inhibition). There are two main treatment targets for anorexia in dialysis patients. The first is to decrease the free plasma tryptophan concentration and transport across the blood brain barrier to the cerebrospinal fluid, thus decreasing the intracerebral serotonin levels. Nutritional formulae enriched with LNAA and BCAA have this effect. Secondly, plasma levels of cytokines with cachectin effect (TNF-alpha), should be decreased. This also induces a decrease in LNAA and BCAA levels. In this group are megestrol acetate, anti-TNF-alpha antibodies, thalidomide, pentoxifyilline, n-3 fatty acids and possibly nandrolone decanoate. Additionally, other targets should be explored including antagonists of cholecystokinin (a potent anorexigen retained by renal failure), analogues of neuropeptide Y (the most potent orexigen), cannabinoids, cyproheptadine, hydrazine sulfate. In conclusion, uraemic anorexia is a complex complication associated with malnutrition, high morbidity and mortality. The pharmacological treatment should address key points in the pathogenesis of uraemic anorexia, reducing intra-cerebral concentration of serotonin with LNAA/BCAA oral diet formulae and the plasma levels of pro-inflammatory molecules. Others forms of treatment should also be explored.

Uremic anorexia: a consequence of persistently high brain serotonin levels? The tryptophan/serotonin disorder hypothesis.

Anorexia is a frequent part of uremic syndrome, contributing to malnutrition in dialysis patients. Many factors have been suggested as responsible for uremic anorexia. In this paper we formulate a new hypothesis to explain the appetite disorders in dialysis patients: "the tryptophan/serotonin disorder hypothesis." We review current knowledge of normal hunger-satiety cycle control and the disorders described in uremic patients. There are four phases in food intake regulation: (1) the gastric phase, during which food induces satiety through gastric distention and satiety peptide release; (2) the post absorptive phase, during which circulating compounds, including glucose and amino acids, cause satiety by hepatic receptors via the vagus nerve; (3) the hepatic phase, during which adenosine triphosphate (ATP) concentration is the main stimulus inducing hunger or satiety, with cytokines inhibiting ATP production; and (4) the central phase, during which appetite is regulated through peripheral (circulating plasma substances and neurotransmitters) and brain stimuli. Brain serotonin is the final target for peripheral mechanisms controlling appetite. High brain serotonin levels and a lower serotonin/dopamine ratio cause anorexia. Plasma and brain amino acid concentrations are recognized factors involved in neurotransmitter synthesis and appetite control. Tryptophan is the substrate of serotonin synthesis. High plasma levels of anorectics such as tryptophan (plasma and brain), cholecystokinin, tumor necrosis factor alpha, interleukin-1, and leptin, and deficiencies of nitric oxide and neuropeptide Y have been described in uremia; all increase intracerebral serotonin. We suggest that brain serotonin hyperproduction due to a uremic-dependent excess of tryptophan may be the final common pathway involved in the genesis of uremic anorexia. Various methods of ameliorating anorexia by decreasing the central effects of serotonin are proposed.

Maternal serum interleukin 1, 2, 6, 8 and interleukin-2 receptor levels in preterm labor and delivery.

OBJECTIVE: To determine the concentrations of maternal serum interleukins (ILs) 1, 2, 6, 8 and IL-2 receptors (IL-2R) in patients in their second and third trimesters of pregnancy and in preterm labor and delivery without evidence of chorioamnionitis. STUDY DESIGN: The study was conducted in La Paz Maternal Hospital, Madrid. Maternal serum IL concentrations were measured in 103 gravidas during preterm labor and delivery. The Mann-Whitney U test was used for analysis. RESULTS: Women in preterm labor and delivery had significantly higher median IL-2R concentration. Women who responded to tocolysis had significantly lower serum concentrations of IL-6. IL-2R and IL-6 serum concentrations predict delivery in 48 h and before 34 weeks gestation. CONCLUSIONS: Compared with non-laboring gravidas, those in idiopathic preterm labor or delivery had significantly higher concentrations of maternal serum IL-2R. Both IL-6 and IL-2R may predict failure of tocolysis. IL-2 does not seem to play an important role in pregnancy.

Protein-losing enteropathy is associated with peritoneal functional abnormalities in peritoneal dialysis patients.

OBJECTIVE: To evaluate the relationship between acquired peritoneal transport disorders and the presence of protein-losing enteropathy (PLE), and their contribution to the protein malnutrition in peritoneal dialysis (PD) patients. PATIENTS AND METHODS: We studied 31 clinically stable PD patients that received a fat overload diet for 3 days. We measured intestinal absorption of fecal fat (normal < 6 g/24-hour stool) and nitrogen (normal < 2 g/24-hr stool), intestinal protein permeability [fecal clearance of alpha1-antitrypsin (Calpha1AT) (normal < 12 mL/24-hr stool)], and nutritional markers [normalized protein nitrogen appearance (nPNA), half-life medium-term proteins, and body mass index]. Peritoneal solute transport was measured by mass transfer coefficient (MTC), and water transport by peritoneal ultrafiltration (UF) capacity. To define protein maldigestion it was necessary to find high fecal nitrogen values with normal Calpha1AT; PLE was defined when both values were elevated. RESULTS: High fecal nitrogen (mean 2.1+/-1 g/24-hr stool) and fat (mean 5.8+/-3.6 g/24-hr stool) were found in 15 patients; 6 patients had high Calpha1AT levels (PLE). These 6 patients showed a worse nutritional status: lower albumin (3.57+/-0.57 g/dL vs 3.98+/-0.38 g/dL, p < 0.05) and transferrin (243+/-70 mg/dL vs 272+/-44.3 mg/dL, p < 0.05), as well as lower triglycerides (131.3+/-31.7 mg/dL vs 187+/-116 mg/dL, p< 0.05). Higher urea MTCs were found in 10 patients, normal in 7, and lower in 14. Higher creatinine MTCs were found in 8 patients, normal in 15, and lower in 8. Normal peritoneal UF capacity was found in 25 and lower in 6 patients. These 6 patients showed higher urea and creatinine MTCs and Calpha1AT. A positive linear correlation between Calpha1AT, urea MTC (r = 0.56, p < 0.01), and creatinine MTC (r = 0.46, p < 0.01) was found. A similar situation occurred between Calpha1AT, fecal fat (r = 0.45, p < 0.05), and fecal nitrogen (r = 0.43, p < 0.05). Thirteen patients with previous history of peritonitis showed higher Calpha1AT than those without peritonitis (10.2+/-8 mL/24-hr stool vs 5.2+/-4.4 mL/24-hr stool, p < 0.05). CONCLUSIONS: We confirm that protein and fat malabsorption, maldigestion, and PLE are present in some PD patients. Higher fecal Calpha1AT is associated with malnutrition and poorer showings of the viability markers of peritoneal membrane function.

Diverticular disease and treatment with gastric acid inhibitors do not predispose to peritonitis of enteric origin in peritoneal dialysis patients.

OBJECTIVE: Enteric peritonitis (EP) is an infrequent complication of peritoneal dialysis (PD), with severe consequences for peritoneal membrane viability and patient outcome. Factors such as diverticular disease and gastric acid inhibitors have been implicated in its appearance. We investigated several risk factors, including those mentioned below, that can influence the development of EP. DESIGN: Retrospective cross-sectional study. SETTING: Tertiary-care public university hospital. PATIENTS: Fifty-seven PD patients treated in our PD unit during August 1998. MAIN OUTCOME MEASURES: A barium enema was performed on 50 of the 57 patients (the remaining 7 patients refused it) in order to exclude the presence of diverticulosis. All episodes of peritonitis occurring in those patients, including EP, were registered. Enteric peritonitis was defined as that caused by gram-positive, gram-negative, or fungus micro-organisms that colonized the intestinal tract, excluding episodes secondary to genitourinary tract or peritoneal catheter exit-site infections. RESULTS: Twenty-four patients showed diverticular disease in the barium enema, but only 5 of them (21%) had any EP episode. Five of the 26 patients with no diverticula (19%) had EP. Fifty-five episodes of peritonitis were reported in 21 patients; 15 episodes of EP (27.3% of all) developed in 11 patients. Seven of the 11 patients (64%) required peritoneal catheter removal and 3 of them (27%) finally were transferred to hemodialysis due to consequences of the EP episode. Logistic regression analysis did not find any of the independent variables analyzed (age, sex, time on PD, type of PD, peritoneal transport parameters, presence of polycystic kidney disease, constipation or diverticulosis, or treatment with gastric acid inhibitors, or phosphate-binding agents) to be risk factors for developing EP. CONCLUSIONS: Neither diverticulosis nor treatment with gastric acid inhibitors seem to be risk factors for developing peritonitis of enteric origin in PD patients. This type of peritonitis has to be promptly identified and treated in order to diminish the high frequency of peritoneal catheter removal and PD dropout due to such episodes.

Helicobacter pylori infection: a new cause of anorexia in peritoneal dialysis patients.

OBJECTIVE: Helicobacter pylori (HP) infection has frequently been found in dialysis patients. Chronic infections induce overproduction of pro-inflammatory substances. Inflammation has been associated with cachexia and anorexia. We explored the relationship between HP infection, anorexia, and malnutrition in peritoneal dialysis (PD) patients. PATIENTS AND METHODS: The study included 48 clinically stable PD patients divided into four groups: HP+ with anorexia (group I, n = 12); HP+ without anorexia (group II, n = 4); HP- with anorexia (group III, n = 5); and HP- without anorexia (group IV, n = 27). Infection with HP was diagnosed by breath test. Anorexia was evaluated using a personal interview and an eating motivation scale (VAS). The VAS included five questions that are answered before and after eating. The questions concern desire to eat, hunger, feeling of fullness, prospective consumption, and palatability. Biochemical markers of nutrition and inflammation were also determined. RESULTS: At baseline, group I showed lower scores for desire to eat, hunger sensation, prospective consumption, and palatability. They also showed lower lymphocyte counts, prealbumin, transferrin, serum albumin, normalized equivalent of protein-nitrogen appearance (nPNA), and residual renal function (RRF). In addition, the same group showed higher levels of C-reactive protein (CRP) and more sensation of fullness than the remaining groups. In the entire series, we found significant linear correlations between the following markers of nutrition and certain questions on the VAS: albumin with before-lunch desire to eat (r = 0.38, p < 0.05), and prealbumin with before-lunch hunger (r = 0.41, p < 0.05) and after-lunch hunger (r = -0.35, p < 0.05). Negative linear correlations were found between albumin and fullness before lunch (r = -0.45, p < 0.01), and between prealbumin and before-lunch desire to eat (r = -0.39, p < 0.05). Negative linear correlations were also seen between CRP and albumin (r = -0.35, p < 0.05) and between CRP and prealbumin (r = -0.36, p < 0.05). Similarly, CRP showed a negative correlation with before-lunch desire to eat (r = -0.38, p < 0.05) and afterlunch desire to eat (r = -0.45, p < 0.01). After HP eradication, group I showed a significant increase in markers of nutrition and in VAS scores for almost all questions. Simultaneously, they showed a decrease in CRP level. Significant differences were also found in lymphocyte count (1105 +/- 259.4 cells/mm3 vs 1330.8 +/- 316 cells/mm3, p < 0.05), nPNA (0.9 +/- 0.16 g/kg/day vs 1.07 +/- 0.3 g/kg/day, p < 0.05), prealbumin (26.7 +/- 6.5 mg/dL vs 33.9 +/- 56.6 mg/dL, p < 0.01), albumin (3.48 +/- 0.3 g/dL vs 3.67 +/- 0.35 g/dL, p < 0.05), CRP (1.16 +/- 1.14 mg/dL vs 0.88 +/- 1.2 mg/dL, p < 0.054), before-lunch desire to eat (56.6 +/- 6.8 vs 72.2 +/- 4, p < 0.001), after-lunch desire to eat (5.4 +/- 2.6 vs 12.3 +/- 2, p < 0.01), hunger before lunch (55.4 +/- 5.4 vs 73.1 +/- 4.6, p < 0.001), hunger after lunch (5.8 +/- 2.9 vs 11 +/- 4, p < 0.01), fullness before lunch (36.6 +/- 10.3 vs 18.7 +/- 8.8, p < 0.001), consumption after lunch (5 +/- 4.7 vs 17.5 +/- 18, p < 0.05), and palatability (61 +/- 5.3 vs 74.1 +/- 4.1, p < 0.001). CONCLUSION: Infection with HP is associated with anorexia, inflammation, and malnutrition in PD patients. Eradication of HP significantly improves this syndrome. Residual renal function seem to have a protective effect on appetite preservation. The present study supports the hypothesis of the involvement of inflammation in the pathogenesis of malnutrition in PD patients.

Tumor necrosis factor alpha as a uremic toxin: correlation with neuropathy, left ventricular hypertrophy, anemia, and hypertriglyceridemia in peritoneal dialysis patients.

Tumor necrosis factor alpha (TNF alpha) is usually excreted by the kidney. In dialysis patients, it accumulates. TNF alpha has been implicated in the pathogenesis of malnutrition, diabetic neuropathy, and erythropoietin resistance. We studied TNF alpha plasma levels in 49 stable peritoneal dialysis (PD) patients, with the aim of correlating those levels with the presence and severity of peripheral neuropathy, hypertrophic cardiomyopathy, and anemia. Kt/Vurea' residual renal creatinine clearance (CrC), nutritional markers, and general biochemistry were also determined. The average plasma level of TNF alpha was 67 +/- 32 pg/mL (range: 18.1-156.3 pg/mL; normal value 3-20 pg/mL). No correlation was observed between TNF alpha and KT/Vurea' but a negative correlation with CrC was seen (r: -0.37, p < 0.05). TNF alpha levels were higher in patients with neuropathy as compared to patients with normal results (72.5 +/- 32 pg/mL vs 44 +/- 22 pg/mL, p < 0.05). Patients with neuropathy also showed a lower CrC value (1.5 +/- 1.7 mL/min vs 3.9 +/- 2.6 mL/min, p < 0.01). TNF alpha levels were higher in patients with left ventricular hypertrophy (LVH) with respect to normal individuals (70.4 +/- 32 pg/mL vs 38.5 +/- 20.8 pg/mL, p < 0.05). Patients with severe LVH showed the lowest CrC value. A direct, significant relationship was found between TNF alpha levels and weekly erythropoietin dose (r: 0.41, p < 0.05). Patients with hypertriglyceridemia or taking lipid-lowering agents showed a positive linear correlation between TNF alpha and triglycerides (r = 0.7, n = 14, p < 0.05). These data suggest that accumulation of TNF alpha may contribute to the development or maintenance of some neurologic, hematologic, and cardiac complications of uremic syndrome. Loss of residual renal function conditions an increment in TNF alpha levels. These data continue to add support to the idea that TNF alpha may be considered a uremic toxin.

[Changes in plasma levels of intestinal regulatory peptides following colonic resection in the rat]. / Evolución de los niveles plasmáticos de péptidos reguladores intestinales tras resección de colon en la rata.

The colon is considered as an endocrine organ producing regulatory peptides. Colon resection exerts an influence on remnant bowel including proliferative adaptive phenomena. The aim of this work was to determine the modifications of several regulatory peptides after colectomy and its relation with the gastrointestinal proliferative changes. 75% proximal colectomy was performed in Wistar rats. Seven groups were used according to sacrifice times: 24 h, 48 h, 72 h, 7 days, 14 days, 21 days and control group without resection. Results show significant decreases in somatostatin, neurotensin and cholecystokinin plasma levels maintained up to 21 days postsurgery. Gastrin is elevated with a highest peak at 72 h achieving basal levels at 21 day. Peptide YY show significant high levels between 72 h and 7 days. Secretin plasma levels are increased 24 h post-surgery, decreasing significantly at day 14. It is suggested that maintained low plasmatic levels of somatostatin, a known mucosal growth inhibitor, after colectomy may help the proliferative adaptation.