[Hematemesis revealing chronic volvulus of a wandering spleen]. / Hématémèse révélatrice du volvulus chronique d'une rate baladeuse.

A 23 years old woman was admitted on emergency for an upper digestive tract bleeding and endoscopy found gastric varices. CT scan revealed a splenomegaly, a twisted aspect of the splenic pedicle and varices in the gastrosplenic ligament. Arteriography showed a narrow splenic artery and varices in the gastrosplenic ligament. After a recurrent bleeding, splenectomy was performed. There was a chronic volvulus of a wandering spleen; the splenic venous flow was passing through the left gastroepiploic vein and a gastrosplenic vein. Chronic volvulus of a wandering spleen with gastric varices is an unfrequent pathology, diagnosed by imaging and requiring splenectomy.

Inhibition of nitric oxide synthesis in the forearm arterial bed of patients with advanced cirrhosis.

Increased vascular production of nitric oxide (NO) may contribute to the peripheral vasodilation and hyperdynamic state complicating advanced liver cirrhosis. In this study, we examined the effect on forearm blood flow of local brachial artery infusion of noradrenaline (NA) and NG-monomethyl-L-arginine (L-NMMA), an inhibitor of NO-synthase, in 10 alcoholic ascitic cirrhotic patients (patients with decompensated alcohol-induced liver disease: DALD group) and 10 patients with well-compensated alcohol-induced liver disease (CALD group). Forearm blood flow was measured by venous occlusion plethysmography. As compared with the CALD group, the DALD group had higher cardiac index and forearm blood flow as well as lower systemic blood pressure and vascular resistance. Infusions of NA and L-NMMA produced similar reduction in resting blood flow in the CALD group. However, in the DALD group, NA was significantly less effective than L-NMMA. The forearm vasoconstrictor response to NA was also significantly reduced in the DALD group when compared with the CALD group. In the DALD group, NA decreased forearm blood flow by 21.0 +/- 6.2% and increased vascular resistance by 37.2 +/- 12.3%, whereas respective changes in the CALD group were 41.8 +/- 6.2% (P < .01) and 77.8 +/- 9.9% (P < .02). In contrast, L-NMMA induced greater forearm vasoconstriction in the DALD group than in the CALD group. In decompensated patients, L-NMMA decreased forearm blood flow by 50.4 +/- 2.7% and increased vascular resistance by 115.9 +/- 14.4%, whereas changes in compensated patients were 38.2 +/- 4.9% (P < .05) and 77.4 +/- 16.2% (NS), respectively. These results are consistent with the hypothesis that increased vascular synthesis of NO contributes to the high dynamic state of patients with advanced cirrhosis.

Short-term changes in energy metabolism after 1 month of a regular oral diet in severely malnourished cirrhotic patients.

Malnutrition in patients with liver cirrhosis is currently associated with abnormal fuel metabolism. The aim of this study was to evaluate changes in energy production and substrate oxidation rates in a group of 26 nonanorectic severely malnourished cirrhotic patients in stable clinical condition after 1 month of an oral diet. Child-Pugh score, nutritional status, energy expenditure, rates of nutrient oxidation, and plasma levels of intermediary metabolites in the postabsorptive phase were assessed before and after 1 month of oral nutrition. Upon entry onto the study, caloric and protein intakes were 40.1 +/- 2.0 kcal/kg and 1.44 +/- 0.8 g/kg, respectively. The Child-Pugh score did not change during the study, whereas nutritional status improved as shown by increased muscular midarm circumference, ([MMAC] P < .02), height-creatinine index (P < .05), triceps skinfold thickness ([TST] P < .01), and fat mass (P < .001). Inflammatory state improved during the study, as shown by the decrease of C-reactive protein ([CRP] P < .01) and orosomucoid (P < .001). The ratio of caloric intake to resting energy expenditure (REE) increased (1.53 +/- 0.06 v 1.66 +/- 0.07, P < .05), as well as the rate of glucose oxidation ([Gox] 73.6 +/- 9.9 v 128.1 +/- 10.3 mg/min, P < .001) and urine nitrogen excretion (6.69 +/- 0.47 v 7.96 +/- 0.48 g/d, P < .02). On the other hand, the rate of lipid oxidation (Lox) decreased (67.3 +/- 3.9 v 47.3 +/- 4.9 mg/min, P < .001) and was correlated with the decrease of free fatty acid (FFA) levels (P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Nutritional and metabolic consequences of basal hyperinsulinemia in alcoholic liver cirrhosis: relationship with postprandial changes in erythrocyte insulin-receptor affinity.

The nutritional and metabolic consequences of basal hyperinsulinemia were investigated in a group of 13 alcoholic cirrhotic patients; 7 healthy subjects were studied as a control group. Two groups of patients were defined on the basis of fasting insulin level: group 1 (n = 7) displayed acute hyperinsulinemia (> mean of control group + 2SD), and group 2 (n = 6) had lower insulin levels. Nutrition status was assessed by means of anthropometric parameters; the rates of nutrient oxidation were measured after an overnight fast and 2 h after a standard meal intake. Group 1 had better nutrition status in terms of fat mass than group 2 (p < 0.05). Although the basal rates of nutrient oxidation were in the same range in the three groups, postprandially, the rate of lipid oxidation was significantly different (p < 0.01). Moreover, group 1 showed greater inhibition of postprandial lipid oxidation than the control group (p < 0.05), whereas there was no difference between group 2 and the control group. In the postprandial phase, erythrocyte insulin-receptor binding and affinity increased paradoxically in group 1, whereas they decreased in group 2 and healthy subjects (changes in binding, p < 0.025; changes in affinity, p < 0.01). In conclusion, basal hyperinsulinemia in alcoholic liver cirrhosis is related to more marked inhibition of postprandial lipid oxidation and better-preserved nutrition status and may lead to a paradoxical postprandial increase in insulin-receptor affinity.

Rapid emergence of quinolone resistance in cirrhotic patients treated with norfloxacin to prevent spontaneous bacterial peritonitis.

We carried out quantitative culturing of stools from 31 hospitalized alcoholic patients with cirrhosis and ascites, before treatment with 400 mg of norfloxacin per day, weekly for the first month, and then every 2 weeks thereafter for 15 to 229 days (median, 54 days). Members of the family Enterobacteriaceae virtually disappeared from the stools (< 10(2)/g), but treatment had little effect on enterococci. No selection of resistant organisms occurred in 15 patients, but the remaining 16 patients developed fecal organisms resistant to fluoroquinolones between days 14 and 43 of treatment (median, 25 days). Staphylococcus aureus was isolated four times, coagulase-negative Staphylococcus spp. were isolated six times, Citrobacter freundii was isolated four times, Enterobacter cloacae was isolated three times, Klebsiella oxytoca was isolated twice, Proteus rettgeri was isolated once, and untypeable streptococci were isolated six times. Some isolates persisted, while others were transient (one to seven consecutively positive cultures). The MICs of four quinolones (nalidixic acid, norfloxacin, ofloxacin, and ciprofloxacin) were determined by use of experimental microwell strips (ATB CMI; Biomerieux S.A.). All the strains isolated before treatment were susceptible to the four quinolones, with low MICs, whereas those isolated during norfloxacin treatment were highly resistant. Long-term norfloxacin administration thus carries a risk of disturbing the bacterial ecology in these patients, suggesting that digestive decontamination should no longer be prescribed routinely to cirrhotic patients with ascites.

Postprandial de novo lipogenesis in alcoholic liver cirrhosis: relationship with fuel homeostasis and nutritional status.

The prevalence and nutritional consequences of postprandial de novo lipogenesis were evaluated in 24 stable alcoholic cirrhotic patients. Energy expenditure and the rates of nutrient oxidation were assessed by indirect calorimetry after an overnight fast and 2 h after a standard meal supplying 15 kcal/kg (63 kJ/kg) of body weight. Postprandially, net lipogenesis occurred in 16 patients (group L+) as shown by a respiratory quotient clearly above 1.00 (P < 0.01). The rate of lipid oxidation remained positive in 8 patients (group L-). The main mechanism involved in this metabolic pathway appeared to be a sharp postprandial hyperinsulinaemia. When compared to group L+, patient group L- showed an impaired thermic effect of food (P < 0.05), a lower rate of glucose oxidation (P < 0.05) and a mild hyperketonaemia (P < 0.05) at fasting levels. Muscular and fat masses were lower (respectively P < 0.05 and P = 0.05) and the severity of the disease as assessed by the Child-Pugh classification was more pronounced in this group (P < 0.02). The occurrence of postprandial lipogenesis in stable cirrhotic patients is related to better nutritional status. Such a metabolic pathway may explain the nutritional heterogeneity of cirrhotics and is likely to have an effect on the benefits of refeeding.

The thermogenic and metabolic effects of food in liver cirrhosis: consequences on the storage of nutrients and the hormonal counterregulatory response.

The thermogenic effect of food and the rates of oxidation and storage of nutrients were evaluated by indirect calorimetry in 10 cirrhotic patients and seven normal controls for a 6-hour period, after they had consumed a standard meal supplying 15 kcal/kg body weight with 15%, 30%, and 55% protein, fat, and carbohydrate calories, respectively. Although the thermogenic response to food was not significantly lower in patients than in controls (51.6 +/- 13.5 v 72.2 +/- 8.8 kcal/6 h), patients exhibited a delayed and blunted increment of energy expenditure after the meal intake (P less than .025). The greater part of the glucose load was oxidized in patients (70.2 +/- 3.9% v 50.4 +/- 3.9% in controls; P less than .01), suggesting a defective glucose storage as glycogen. This result could be related to insulin resistance, which was evidenced by a large increase in glucose and insulin levels after the meal intake in patients (P +/- .001). Conversely, lipid oxidation was sharply reduced and de novo lipogenesis occurred in patients, so that the rate of lipid storage was increased. The profiles of circulating levels of catecholamines, thyroid hormones (free thyroxine [FT4] and triiodothyronine [T3]), and glucagon were assayed during the test. Norepinephrine and glucagon levels remained higher in patients throughout the test (P less than .001), whereas thyroid hormones stayed in the same range in the two groups. After an initial increase, glucose levels decreased sharply, inducing an activation of counterregulatory hormones, glucagon, and notably, epinephrine, for which the increment was correlated with the decrease of glucose (r = -.917; P less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Aging, energy expenditure and nutritional status: evidence for denutrition-related hypermetabolism.

Resting energy expenditure (REE) and nutritional status have been evaluated in 39 elderly inpatients (mean age 84.0 +/- 6.9 years). The nutritional status declined with aging as shown by significant negative correlations between age and, respectively, weight (p < 0.001), fat free mass (FFM) (p < 0.01) and body mass index (BMI) (p < 0.01). The best prediction for REE when considering the whole population was given by FFM (p < 0.001). Increased REE was observed in patients after recent surgery, related to an inflammatory state, as shown by increased plasma levels of C-reactive protein and orosomucoid. Irrespectively of the inflammatory state, REE was also found to be related to the nutritional status: patients who showed a BMI < 20 had higher REE than patients with a BMI > 20 (28.4 +/- 1.3 vs. 22.1 +/- 0.7 kcal/kg of body weight; p < 0.001; 35.7 +/- 1.6 vs. 30.9 +/- 1.0 kcal/kg of FFM; p < 0.02). These results increasingly suggest that elderly patients may suffer from denutrition relevant to hypermetabolism.

Submaximal oxygen consumption in liver cirrhosis. Evidence of severe functional aerobic impairment.

We studied maximal aerobic work capacity in 24 cirrhotic patients whose clinical condition was well compensated. Nineteen of our patients had no heart or lung disease, and five had mild mechanical ventilatory impairment. The patients performed incremental exercise on a treadmill until subjective exhaustion. The maximal exercise levels reached by all were relatively low and led to a lower observed maximal oxygen uptake (VO2 max), than predicted uptake (19.6 +/- 0.5 vs. 37.9 +/- 0.6 ml/kg; p less than 0.001). Observed VO2 max values correlated strongly with the Pugh score, which reflects the degree of liver failure (r = -0.571; p less than 0.01). Since there were no clear cardiac or pulmonary causes to explain the decrease in work capacity, these observations suggest that liver cirrhosis might induce or be accompanied by muscular impairment. VO2 max, which seems to decline with the functional severity of the disease, may be a useful index for evaluating the capacity of patients for physical rehabilitation.

[Thermic and metabolic effects of meals in liver cirrhosis assessment of oxidation and storage rates of nutrients]. / Effets thermogénique et métabolique du repas chez le cirrhotique: étude des capacités d'oxydation et de stockage des nutriments.

The thermic effect of food was evaluated in 10 cirrhotic patients and 7 normal controls by indirect calorimetry during 6 hours following intake of a mixed meal supplying 15 kcal/kg of body weight and containing 30, 15 and 55 percent as lipid, protein and carbohydrate calories respectively. The rates of storage and oxidation of nutriments, as well as variations of blood glucose, insulin, plasma lactates, free fatty acids, glycerol, and ketonic corps were also evaluated. The thermogenic response to food was lower (p less than 0.025) and delayed in cirrhotic patients. In cirrhotic patients the rate of glucose oxidation was significantly increased (70.2 +/- 3.9 vs 50.4 +/- 3.9 percent of the glucose load; p less than 0.01) suggesting a defect in glycogen storage. These results can be related to insulin resistance as attested by a larger increase of glucose and insulin levels in cirrhotics than in controls (p less than 0.001 and p less than 0.001, respectively). Compared with controls, lipolysis in cirrhotic patients was more suppressed as shown by a sharper decrease of free fatty acids and glycerol levels (p less than 0.001 and p less than 0.02, respectively). Furthermore, the rate of lipid oxidation decreased more in cirrhotic as compared with controls (p less than 0.001) before becoming completely suppressed. De novo lipogenesis appeared between the 2nd and 4th hours. Consequently, the rate of lipid oxidation was significantly reduced in cirrhotic vs controls (14.3 +/- 5.0 vs 30.5 +/- 3.7 percent of the lipid load; p less than 0.02) showing an increased rate of lipid storage.(ABSTRACT TRUNCATED AT 250 WORDS)

Hormonal and metabolic changes during exercise in cirrhotic patients.

The metabolic response to exercise was compared in 10 cirrhotic patients (P) in a stable clinical condition and in 6 sedentary, age-matched, normal subjects (C) performing 32 minutes of treadmill exercise with the same constant workload corresponding to three to four times their resting oxygen uptake. Taking indirect calorimetry as reference, respiratory exchanges indicated that cirrhotic patients consumed carbohydrates almost exclusively, unlike the normal controls, who consumed lipids and glucids in about the same proportions (RQ: 0.98 +/- 0.04 v 0.87 +/- 0.04, P less than .0001). In the patients, this carbohydrate path of exercise metabolism lowered glycemia from the resting value of 5.23 +/- 0.16 mmol/L to 4.03 +/- 0.37 mmol/L (P less than .0001) and raised the plasma lactate concentration from 2.08 +/- 0.24 mmol/L at rest to 3.48 +/- 0.32 mmol/L at the eighth minute of exercise (P less than .001), thus suggesting defective liver glyconeogenesis. Fatty free acids and glycerol remained almost constant during exercise, whereas catecholamines increased. Insulin levels were high in patients at rest (67.1 +/- 14.5 U/mL v 15.1 +/- 3.5 U/mL); they declined sharply at the onset of exercise but nevertheless remained high compared to those observed in the controls (P less than .0001). Glucagon increased in exercising patients from 88.3 +/- 21.3 pg/mL to 127.4 +/- 30.6 pg/mL (NS). Esterified plasma carnitine declined in the patients from 13.0 +/- 2.2 mumol/L to 8.6 +/- 1.5 mumol/L (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

[Energy expenditure and the use of nutriments in cirrhotic patients fasting and at rest. Influence of alcoholic hepatitis and the severity score of the disease]. / Dépenses énergétique et utilisation des nutriments chez le cirrhotique à jeun et au repos. Influence de l'hépatite alcoolique et du score de gravité de la maladie.

Resting energy expenditure and nature of fuels consumed after an overnight fast have been evaluated in 30 cirrhotic patients and 10 normal subjects by indirect calorimetry. Basal metabolic requirements in patients were slightly increased although most of them had as poor nutritional condition assessed by a decreased muscular mass (17.3 +/- 0.8 vs 22.5 +/- 1.2 kg, p less than 0.001). Resting energy expenditure was significantly elevated in 16.7 p. 100 of patients. This hypermetabolic state was related to alcoholic hepatitis. Surface area and the Harris-Benedict equation did not accurately predict the resting energy expenditure. Compared to normal subjects, all patients had higher levels of free fatty acids (0.408 +/- 0.05 vs 0.182 +/- 0.03 mmol/l, p less than 0.001), glycerol (0.109 +/- 0.009 vs 0.035 +/- 0.003 mmol/l, p less than 10(-9)) and ketone bodies (0.137 +/- 0.012 vs 0.099 +/- 0.012 mmol/l, p less than 0.03). The respiratory quotient was lower in cirrhotic patients (0.740 +/- 0.01 vs 0.832 +/- 0.02, p less than 10(-5)). These results show increased lipolysis and a preferential use of fat as fuel substrates in cirrhotic patients: 70 p. 100 of the total calorie expenditure was derived from fat. Fat mobilization was influenced by nutritional status: a positive correlation has been found between fat mass and free fatty acids (p less than 0.02) and between fat mass and glycerol (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

[Non-cardiogenic pulmonary edema associated with severe diabetic ketoacidosis]. / Oedema pulmonaire non cardiogénique associé à une acidocétose diabétique sévère.

Non cardiogenic pulmonary oedema occurs rarely in patients with diabetic ketoacidosis, except in conjunction with an infection. A case is reported of non cardiogenic pulmonary oedema in a patient with severe diabetic ketoacidosis, which resolved within 72 h with oxygen supply only. There were no objective facts which could explain its pathogenesis, despite the important pulmonary asymmetry due to a unilateral diaphragmatic paralysis.