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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Liver biopsy specimens were studied in 26 patients in whom liver function abnormalities developed during intravenous hyperalimentation (IVH). The clinical manifestations and duration of IVH were evaluated in relation to the morphological changes seen in the liver. Early hepatic changes consisted of fatty metamorphosis, and progressive intrahepatic cholestasis developed as IVH was continued. Essential fatty acid deficiency, amino acid imbalance, caloric excess, and toxic manifestations of certain amino acids are postulated as causative factors. The hepatic steatosis secondary to IVH may be treated by lowering the dextrose concentration of the infusion or by administering dextrose-free amino acid solutions. The clinical importance of this common complication of IVH is the difficulty in distinguishing it from other causes of cholestasis in seriously ill patients.
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PMID:Hepatic dysfunction during hyperalimentation. 41 12

Cholestasis has been previously described after long-term hyperalimentation in infants. The present case documents the development of cholestasis in an adult after a relatively short period of total parenteral nutrition (TPN), i.e., hyperalimentation. Other causes for cholestasis, such as exogenous or endogenous hepatotoxic agents or allergic type hepatitis, do not offer an adequate explanation for the changes observed in this patient. The changes observed are consistent with the hypothesis that a taurine deficiency would interfere with bile salt conjugation and form a block at the cellular level.
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PMID:Cholestasis in association with short-term parenteral alimentation. 83 73

Cholelithiasis in infants is rare, and has usually been associated with hemolysis, ileal disease, congenital anomalies of the biliary tree, hyperalimentation, and prolonged fasting. With the increased use of abdominal ultrasonography (US), more cases of cholelithiasis are being discovered. We report our experience with 13 infants diagnosed on abdominal US to have gallstones. There were 9 boys and 4 girls with an average age at diagnosis of 2.6 months (range, 0 to 9 months). Predisposing factors could be identified in only 6 of the 13 patients. Two patients with obstructive jaundice underwent cholecystectomy and common bile duct exploration. One patient with choledocolithiasis and common bile duct dilatation was observed. His stone passed spontaneously, with resolution of symptoms. Ten patients without cholestasis remained asymptomatic, with disappearance of lithiasis in five of them. Neonatal cholelithiasis is more common than previously suspected; it seems to affect males more often than females and is usually not associated with known predisposing factors. It appears to be a temporary, self-limiting phenomenon, and an aggressive approach is not warranted in the asymptomatic infant. Surgical or radiological intervention should be reserved for the symptomatic patients or those with underlying lithogenic disorders.
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PMID:Cholelithiasis in newborns and infants. 140 10

Total parenteral nutrition (TPN) has become a mainstay of modern neonatal care for the increasing population of premature infants who survive their initial pulmonary disease. As with other advances in neonatal therapy, hyperalimentation has associated complications and limitations, primary among them its toxicity to the liver. The basic pathologic lesion is bile cholestasis which is probably multifactorial in etiology. Amino acid solutions, excessive calorie-to-nitrogen ratios, and deficient trace elements and antioxidants have all been implicated in this process. Total parenteral nutrition-cholestasis can progress to portal fibrosis and irreversible cirrhosis if long-term hyperalimentation is required. Most at-risk for this iatrogenic condition are those premature infants less than 1500 g birth weight who are exposed to TPN for longer than two weeks. Enteral feedings providing as little as 10 percent of caloric intake are beneficial, and the prognosis for recovery is good once enteral feedings are established.
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PMID:Hyperalimentation associated hepatotoxicity in the newborn. 156 68

Sugar absorption by the biliary ductular epithelium under steady-state conditions was examined using isolated perfused rat liver. The test sugar and mannitol (as a putative marker of paracellular entry) were added to the glucose-free recirculating perfusate each at a concentration of 5 mmol/L, and apparent active biliary ductular absorption equated with the change in concentration of the test sugar relative to that of mannitol. A metabolizable hexose (D-glucose), pentose (D-xylose), and three nonmetabolizable hexoses (alpha-methyl-glucoside, 3-o-methyl-glucose, and L-glucose) were used. All five monosaccharides were well absorbed at constant rates for 2 hours with apparent rates of absorption (mumol.kg body weight-1.min-1, mean +/- SE) of D-glucose, 0.24 +/- 0.01; L-glucose, 0.20 +/- 0.02; 3-o-methyl-glucose, 0.19 +/- 0.02; alpha-methyl-glucoside, 0.16 +/- 0.03; and D-xylose, 0.10 +/- 0.04. The addition of phloridzin to the perfusate inhibited D-glucose absorption in part but did not inhibit L-glucose absorption. When perfusate Na+ was replaced by N-methylglucamine, the bile-plasma ratio of mannitol remained unchanged, as did the apparent absorption rate of D-glucose and 3-o-methyl-glucose. In contrast, absorption of L-glucose and alpha-methyl-D-glucoside gradually ceased. The addition of 15 mmol/L glucose to the perfusate caused decreased bile flow and increased taurocholate concentration in bile, suggesting that glucose absorption by the biliary ductules induced water reabsorption. It is concluded that sugars are absorbed by the biliary ductular system by Na(+)-dependent and Na(+)-independent transport systems, the substrate affinities of which differ from those reported for apical membrane hexose transport systems in renal tubular and intestinal epithelia. Ductular absorption of solutes such as glucose that enter bile passively may have biological use, because ductular absorption decreases the concentration of substrates for bacterial growth in gallbladder bile. On the other hand, ductular absorption of solutes induces reabsorption of biliary water, resulting in decreased bile flow; this might contribute to cholestasis during prolonged hyperalimentation with solutions containing glucose.
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PMID:Sugar absorption by the biliary ductular epithelium of the rat: evidence for two transport systems. 158 53

The risk of developmental of total parenteral nutrition (TPN)-associated cholestatic jaundice in neonates receiving intravenous hyperalimentation is high. Numerous factors have been cited as contributing to TPN cholestasis; however, the exact etiology remains obscure. This retrospective study was undertaken in order to identify any factors which might contribute to this syndrome. The hospital records of 172 neonates requiring TPN for a minimum of 1 week were reviewed. In addition, a subgroup of 32 infants requiring TPN for a minimum of 7 weeks was also examined. Cholestasis was defined as a direct serum bilirubin greater than 2.0 mg/dl during the course of TPN therapy. Significant factors for the development of cholestasis in both groups (n = 172, n = 32) included: number of operations (2.56 vs. 1.08, p = 0.0000), the number of days the patients received antibiotics (40.3 vs 12.9, p = 0.0000), and delayed start of enteral feedings (33.8 vs 14.1, p = 0.0000). Fifteen of the 32 patients who received TPN for at least 7 weeks did not develop cholestasis. In this subgroup (n = 32), there were no differences in birth weight, gestational age, days from birth to the start of TPN, or respiratory distress between those who developed cholestasis and those who remained anicteric. In contrast, there were significant differences between the cholestasis and noncholestasis groups in number of operations (13 vs 6, p = 0.0407), and days until enteral feedings were started (33.1 vs 18.9, p = 0.0289). This study suggests that the factor(s) contributing to the development of TPN-associated cholestasis are likely multifactorial. There appears to be a direct correlation between increasing severity of cholestatic jaundice and duration of TPN. This review does add a new parameter to the various causative factors suggested, namely the number of operative procedures. This new variable could be related to the stress of surgery itself or to the repeated administration of anesthetic agents.
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PMID:An analysis of factors contributing to the development of total parenteral nutrition-induced cholestasis. 251 4

Bile acid metabolism was examined in two children with bile acid malabsorption, who were being treated with intravenous hyperalimentation. Fecal bile acid excretion was 1,261 mumol/m2/day in a child with bile acid malabsorption of unknown origin, and 1,877 mumol/m2/day in a child with secondary bile acid malabsorption after an operation for long-segment aganglionosis. These values were approximately 10 times higher than those in diarrheal or nondiarrheal children without apparent abnormalities in bile acid metabolism. Fecal bile acids in these patients with bile acid malabsorption were almost completely conjugated, with little unconjugated bile acid present. It is possible that the disturbed bile acid deconjugation in the intestine might be caused by a rapid intestinal transit time, which was found in our patients with bile acid malabsorption. In the analysis of biliary lipid composition, children with bile acid malabsorption were shown to have a chenodeoxycholate-dominant pattern, an increased glycine- to taurine-conjugated bile acid ratio, and markedly supersaturated cholesterol. Such profiles may be related not only to bile acid malabsorption but also to cholestasis, presumably due to intravenous hyperalimentation.
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PMID:Fecal and biliary bile acid patterns in children with bile acid malabsorption. 673 82

Hepatobiliary scintigraphy with technetium 99m-labeled p-isopropylacetanilido iminodiacetic acid (99mTc-PIPIDA) was used to evaluate 22 neonates with mixed jaundice. Ten patients were proved to have biliary atresia; ten others were diagnosed as having neonatal hepatitis. In the remaining two, jaundice was secondary to prolonged hyperalimentation. Initial studies in all ten patients with biliary atresia showed no evidence of excretion of the tracer into the intestinal tract. Following three to seven days of oral administration of phenobarbital, repeat studies were performed in six of the ten patients. None showed evidence of excretion. Initial studies of the 12 patients with intrahepatic cholestasis showed definite excretion in five, questionable evidence of excretion in two, and no demonstrable excretion in five. Studies after phenobarbital therapy in five of the seven patients with questionable or no excretion on the initial studies showed definite excretion in four. Only in one patient who had poor hepatic extraction did the phenobarbital therapy not change the scintigraphic pattern. The authors conclude that hepatobiliary scintigraphy with 99mTc-PIPIDA after three to seven days of phenobarbital therapy is a highly accurate test for differentiating biliary atresia from other causes of neonatal jaundice.
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PMID:Hepatobiliary scintigraphy with 99mTc-PIPIDA in the evaluation of neonatal jaundice. 678 55

The ultimate prognosis for patients with short bowel syndrome (SBS) has become progressively more favorable over the past decade. Advances in long-term total parenteral nutrition (TPN) have allowed this group of patients to meet nutritional needs while the process of intestinal adaptation occurs. Unfortunately, a subgroup of patients with SBS have hepatic failure (HF), most often secondary to TPN-induced cholestasis. Combined small bowel and liver transplantation (LT) offers a sound anatomic solution for cases of HF with SGS, but it remains experimental at this time. We propose that an isolated LT is a viable alternative mode of therapy for the patient with HF and SBS. The following characteristics were reviewed for five patients with SBS and HF who underwent LT: age at transplantation, weight, liver function, survival, intestinal length, volume of feeding before surgery, and current feeding tolerance and liver function. Four boys and one girl, aged 5.5 to 15 months (average, 11.9), had LT. The total bilirubin level at the time of transplantation was 14.4 to 37 mg/dL (average, 24.7). The patients weighed between 3.8 and 12 kg (average, 8.0), and feeding tolerance ranged from no enteric to complete enteric feeding (average, < 33% of calories by enteric feeding). Bowel loss was attributed to necrotizing enterocolitis in two cases, volvulus in two, and birth hypoxia in one. Bowel length ranged from 60 to 120 cm (average, 88.6). Four children (80%) survived LT, and the average follow-up period was 9.3 months. Three (75%) are home; one is on combined hyperalimentation and enteral feeding, and two are on full enteric feeding. One remains in a chronic care facility, on combined enteral and intravenous feeding. The average daily enteral feeding now comprises more than 70% of caloric requirements. The total bilirubin level is .6 to .8 mg/dL (average, .71). Isolated LT for HF in the patient with SBS effectively restores liver function, allowing time for further intestinal adaptation.
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PMID:Isolated liver transplantation for liver failure in patients with short bowel syndrome. 807 12

Cholestatic jaundice is the major complication of total parenteral nutrition (TPN). Both the intravenous (IV) route of nutrition and the enteral fast have been implicated as causes of TPN-associated cholestasis (TPN-AC). The purpose of this study was to determine whether TPN-AC is caused by the TPN solution itself or the IV route of administration and enteral fast. Prepubescent rabbits (n = 24) were divided into four groups: CONTROL, fed standard lab chow; TPN, received a standard hyperalimentation solution of dextrose, Aminosyn, and lipids via the jugular vein; ENT, received the same hyperalimentation solution via a duodenostomy tube; and OSM, received a polymeric formula (Osmolite) via a duodenostomy tube. After 14 days on these diets, we measured bile flow, bile acid excretion, sulfobromophthalein (BSP) excretion, plasma amino acid profile, serum liver enzymes, and liver histology. Statistical analysis was by analysis of variance. Hyperalimentation solution significantly depressed hepatobiliary function, whether it was given IV or by gut. Bile flow in both the TPN (36.4 microL/kg/min) and ENT (46.2) groups was significantly less than CONTROL (84.5) or OSM (62.9). Hepatic secretory function, measured by excretion of the cholephilic dye BSP, was depressed in both TPN and ENT (57% and 55% of IV dose excreted in bile over 60 minutes, respectively) compared with CONTROL (84%) or OSM (71%). Serum liver enzymes were normal in all groups. Histological injury similar to TPN-AC in humans (portal inflammation and hepatocyte degeneration) was seen in both groups receiving the hyperalimentation solution.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hepatobiliary dysfunction during total parenteral nutrition is caused by infusate, not the route of administration. 846 53


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