Multimedia article. Laparoscopic Ladd's procedure in two adults: malrotation and the minimally invasive approach.

Malrotation is an intestinal rotation anomaly rarely diagnosed in adults. In the adult patient, obstructing peritoneal bands may lead to nausea and abdominal distention. Familiarity with this presentation as well as the aberrant anatomy associated with the unusual problem facilitates surgical treatment. While the minimally invasive approach requires meticulous dissection due to this abnormal anatomy, laparoscopic treatment does provide the advantages of short convalescence and low morbidity. This video briefly reviews embryologic intestinal development, rotational anomalies and two laparoscopic Ladd's procedures.

Ethanol elimination by rats as a function of reproductive state, gender and nutritional status

Alcohol elimination was studied in rats of different ages, reproductive states and nutritional deprivation, with the following results: 1) blood levels of ethanol 180 min after a single dose of 1.5 g/kg, ip were significantly higher in adult male (74 days old, N=5) than in young male rats (34 days old, N = 5): 92.4 ñ 8.4 vs 6.8 + 3.4 mg/lOO ml, means ñ SD, respectively; 2) when male rats were given a low protein diet for 48 h, blood ethanol levels after a single dose were significantly increased in young males (38.6 ñ 14.6 mg/l00 ml) but no effect after a single dose was found in the same animals at an older age (93.2 ñ 5.0 mg/l00 ml); 3) blood levels in female rats were higher than in young males both in the virgin and pregnant states, but during lactation a significant drop in blood levels of ethanol was observed. Blood levels of ethanol (mg/l00 ml) 180 min after a single dose of 1.5 g/kg, ip, in females, were: virgin (N=6): 44.9 ñ 16. 1, pregnant (N = 5): 40.0 ñ 10.4, lactant (N = 5): 8.8 5.8. This difference between virgin and pregnant and lactant rats was not related to changes in ADH activity which did not differ between groups. The present study indicates that in male rats the effect of a short-term protein deprivation on ethanol elimination is dependent on the age of the animal. In females, reproductive state is an important factor in determining ethanol elimination.

Induction of 5-oxoprolinuria in the rat following chronic feeding with N-acetyl 4-aminophenol (paracetamol).

The urine of rats fed on 1% paracetamol in the diet for up to 10 weeks was analysed using 500 MHz 1H NMR spectroscopy. After 3 weeks, paracetamol-dosed rats were found to excrete massive quantities of an unknown metabolite in the urine. Using a range of 1 and 2 dimensional 1H NMR spectroscopic techniques, solid phase extraction and mass spectrometry, the metabolite was identified at 5-oxoproline (5OXP, pyroglutamic acid). Rats fed paracetamol plus methionine, which prevents the depletion of sulphur-containing amino acids, did not develop 5OXP-uria during the study period. Quantitative 1H NMR spectroscopy of whole urine showed that no 5OXP appeared in the urine in the first 2 weeks of feeding paracetamol to the animals, but urinary concentrations then rose rapidly up to 1 M in some animals. This unusually high concentration of 5OXP in the urine and its prevention by methionine indicates that chronic high level paracetamol dosing leads to severe depletion of sulphur-containing amino acids including cysteine with consequent disruption of the glutathione cycle.

Effect of D- or L-methionine and cysteine on the growth inhibitory effects of feeding 1% paracetamol to rats.

Rats fed 1% paracetamol in the diet failed to grow and a dose-dependent inhibition of growth was observed and found to be independent of hepatoxicity. Addition of 0.5% D- or L-methionine, or L-cysteine to a diet containing 1% paracetamol restored growth. Addition of L-methionine to the drinking water was equally effective. Feeding D-cysteine or sodium sulphate were ineffective. Acute paracetamol toxicity was also prevented by D- as well as by L-methionine. It is concluded that the inhibition of growth was due to depletion of sulphur amino acids in the course of paracetamol metabolism. This was sometimes followed by episodes of liver cell injury. Since the normal human dosage of paracetamol is up to 4 g/day, which is equivalent to 1% of the diet, the possibility of induction of amino acid deficiency by chronic use of paracetamol in normal dosage is raised.

Mechanism and specificity of increased amylase/creatinine clearance ratio in pancreatitis.

The amylase/creatinine clearance ratio (Cam/Ccr ratio) was determined in 239 subjects. In 87 hospitalised patients without pancreatic disease (controls) the Cam/Ccr ratio was 3.02 +/- 0.69 (mean +/- ISD). The ratio was above the normal range in all patients with acute pancreatitis but was normal in those with chronic pancreatitis and carcinoma of the pancreas. In 18 patients with choledocholithiasis a raised ratio distinguished those with pancreatitis as assessed independently by the surgeon at laparotomy from those with a macroscopically normal pancreas. Raised Cam/Ccr ratios were also found in diabetics with ketoacidosis and in three patients with fulminant alcoholic liver disease. Though a positive correlation was found between the Cam/Ccr ratio and serum creatinine concentration, abnormally high ratios did not occur in 30 patients with chronic renal failure. A significant increase in Cam/Ccr ratios was produced in six healthy volunteers by intravenous injection of glucagon. However, it is unlikely that hyperglucagonaemia alone accounts for the increased Cam/Ccr ratio seen in acute pancreatitis, as no correlation was found between the clearance ratio and the plasma glucagon concentration in a series of patients. In two other patients in whom excess circulating pancreatic polypeptide was detected the Cam/Ccr ratio was normal. It is concluded that, in view of the sensitivity and relative specificity of finding an increased Cam/Ccr ratio in acute pancreatitis, its determination should be valuable clinically, especially in those cases of hyperamylasaemia where the cause is in doubt. The mechanism whereby the ratio is increased is unknown, and it is unlikely that either glucagon or pancreatic polypeptide is a major factor in its production.