Isolated aberrant right cysticohepatic duct injury during laparoscopic cholecystectomy: Evaluation and treatment challenges of a severe postoperative complication associated with an extremely rare anatomical variant.

A typical bile duct branching patterns represent one of the major causes of bile duct injury (BDI) during laparoscopic cholecystectomy (LC). The most common classified variations of bile duct branching, involve the right posterior sectoral duct (RPSD) and its joining with the right anterior or left hepatic duct. Variant bile duct anatomy can rarely be extremely complex and unclassified. This report describes an extremely rare case of an isolated injury to an aberrant right hepatic duct formed by the joining of ducts from segments V, VII, and VIII draining into the cystic duct (cysticohepatic duct) during LC, associated with an inferior RPSD opening to left hepatic duct. Detailed evaluation of both endoscopic and magnetic cholangiograms established the diagnosis. Bile duct injury was subsequently managed surgically by a demanding Roux-en-Y hepaticojejunostomy. This extremely rare case aims to serve as a useful reminder of the consistent inconsistency of biliary anatomy, alerting surgeons to beware of variant bile duct branching patterns during open or LC that constitute a dreadful pitfall for severe and life-threatening bile duct injuries.

Effect of sodium valproate monotherapy on serum uric acid concentrations in ambulatory epileptic children: a prospective long-term study.

PURPOSE: Hyperuricemia has been shown to be related to cardiovascular morbidity and mortality. There is controversial data about the effect of sodium valproate (VPA) monotherapy on serum uric acid concentrations. The purpose of this study was to investigate by a long-term, prospective method, whether treatment with VPA monotherapy may alter serum uric acid concentrations and liver function tests in ambulatory epileptic children. MATERIAL AND METHODS: Serum uric acid concentrations were determined in 28 ambulatory epileptic children before and at 6, 12 and 24 months of VPA monotherapy. Serum concentrations of biochemical markers of liver and renal function, such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), gamma-glutamyltransferase (gamma-GT) and creatinine (Cr) were also measured before and at 6, 12 and 24 months of VPA monotherapy. Serum VPA concentrations remained within the therapeutic range (50-100 mg/L) during the period of study. RESULTS: No statistically significant changes in serum uric acid concentrations were found at 6, 12 or 24 months of treatment. Serum ALT concentrations were significantly increased at 6 and 12 months of treatment, AST concentrations at 6 and 12 months of treatment and LDH concentrations at 12 months of treatment. CONCLUSIONS: VPA monotherapy does not have a significant effect on serum uric acid concentrations in ambulatory epileptic children. Further studies are needed to definitively address whether it would be useful for physicians to routinely check for elevated serum uric acid levels in children treated with VPA.

Early and persistent increase in serum lipoprotein (a) concentrations in epileptic children treated with carbamazepine and sodium valproate monotherapy.

PURPOSE: The aim of this study was to investigate by a prospective, self-controlled method, whether treatment with carbamazepine (CBZ) and sodium valproate (VPA) monotherapy may alter serum lipoprotein (a) [Lp(a)] concentrations in epileptic children. METHODS: Serum Lp(a) concentrations have been determined in 18 epileptic children before and at 6, 12 and 24 months of treatment with CBZ monotherapy and in 30 epileptic children before and at 6, 12 and 24 months of treatment with VPA monotherapy. Serum total cholesterol, triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, apolipoproteins A-I and B concentrations and serum concentrations of biochemical markers of liver and renal function were also measured in the study participants. RESULTS: Serum Lp(a) concentrations were significantly increased at 6, 12 and 24 months of CBZ and VPA monotherapy. There were no significant correlations between serum Lp(a) and serum lipids, lipoproteins, apolipoproteins, concentrations of biochemical markers of liver and renal function or antiepileptic-drugs concentrations. CONCLUSIONS: Children who receive CBZ or VPA monotherapy may have significant and persistent increase in serum lipoprotein (a) concentrations, occuring early in the course of therapy. It may be useful to measure serum Lp(a) concentrations routinely in epileptic children taking these antiepileptic drugs, especially in those that are already at higher atherosclerotic risk.

Serum total amylase, pancreatic amylase and lipase activities in epileptic children treated with sodium valproate monotherapy.

To investigate by a prospective, self-controlled method, whether early treatment with sodium valproate (VPA) monotherapy has some effect on serum total amylase and particularly on its pancreatic isoenzyme and lipase activities in epileptic children. Serum total amylase, pancreatic amylase and lipase activities have been evaluated in 23 epileptic children, before and at 6 and 12 months of VPA monotherapy. All children remained without clinical symptoms of pancreatitis during the period of study. Serum pancreatic amylase activities were significantly decreased at 6 and 12 months of treatment with VPA, whereas serum total amylase and lipase activities did not show any significant changes at 6 or 12 months of treatment. Non-pancreatic isoenzyme activities of amylase were significantly higher at 6 and 12 months of treatment. Three patients (13%) had slightly elevated serum total amylase levels at 6 and 12 months of treatment. There was no significant correlation of serum pancreatic amylase levels or non-pancreatic isoenzyme levels of amylase with serum VPA levels at 6 and 12 months of treatment. Non-pancreatic amylase activities, probably derived from salivary glands, may be increased in children treated with VPA monotherapy. Measurement of serum pancreatic amylase and/or serum lipase activities is indicated in patients with increased serum total amylase levels but without clinical symptoms of pancreatitis and, furthermore, in patients with symptoms suggesting dysfunction of pancreas, in order to avoid unnecessary discontinuing of VPA.

Early alteration in bone metabolism in epileptic children receiving carbamazepine monotherapy owing to the induction of hepatic drug-metabolizing enzymes.

The purpose of this study was to investigate, by a prospective, self-controlled method, whether early treatment with carbamazepine monotherapy can alter bone metabolism in ambulatory epileptic children with adequate sun exposure, based on the determination of total serum alkaline phosphatase and its bone isoenzyme activities. Serum total alkaline phosphatase and its bone, liver, and intestinal isoenzyme activities were evaluated in 22 epileptic ambulatory children (13 males and 9 females, aged from 5 to 12 years) before and at 3, 6, and 12 months of carbamazepine monotherapy. Serum concentrations of other biochemical markers of bone and liver metabolism, such as calcium, phosphorus, magnesium, gamma-glutamyltransferase, alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase, were also measured in the study participants before and at 6 and 12 months of treatment. Carbamazepine was prescribed at normal dosages (16.4-20 mg/kg/day). Serum total alkaline phosphatase activities were significantly increased at 3 (P = .000), 6 (P = .024), and 12 (P = .037) months of treatment; serum bone alkaline phosphatase activities at 3 (P = .000), 6 (P = .008), and 12 (P = .017) months of treatment; and serum liver alkaline phosphatase activities at 3 (P = .000), 6 (P = .049), and 12 (P = .008) months of treatment, whereas serum intestinal alkaline phosphatase isoenzyme activity was significantly increased only at 3 months of treatment (P = .035). Serum gamma-glutamyltransferase activities were also significantly increased at 6 (P = .000) and 12 (P = .000) months of treatment. No significant changes in the concentrations of serum calcium, phosphorus, magnesium, alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase were noted at 6 and 12 months of treatment. There was a significant correlation between serum gamma-glutamyltransferase activities and serum total alkaline phosphatase activities (r = .689, P = .000 at 6 months; r = .493, P = .020 at 12 months), bone alkaline phosphatase activities (r = .700, P = .000 at 6 months; r = .466, P = .029 at 12 months), and liver alkaline phosphatase activities (r = .427, P = .047 at 6 months; r = .425, P = .048 at 12 months). These findings indicate that ambulatory children who receive carbamazepine monotherapy, even when residing in a country with adequate sunlight, can have their bone metabolism altered early in the course of treatment, as indicated by the elevated activities of serum bone alkaline phosphatase isoenzyme. This early alteration in bone metabolism is probably due to the hepatic enzyme-inducing character of carbamazepine.

Serum amylase, pancreatic amylase and lipase concentrations in epileptic children treated with carbamazepine monotherapy.

BACKGROUND: Serum total amylase and lipase activities have been determined in epileptic patients treated with polytherapy using enzyme-inducing anticonvulsant drugs; however, to our knowledge, serum total amylase, pancreatic amylase and lipase activities have not previously been determined in patients receiving carbamazepine monotherapy. The purpose of this study was to investigate by a prospective, self-controlled method, whether early treatment with carbamazepine monotherapy may alter serum total amylase, pancreatic amylase and lipase concentrations of epileptic children. METHODS: Serum total amylase, pancreatic amylase and lipase activities have been determined in 18 epileptic children before and at 6 and 12 months of treatment with carbamazepine monotherapy. Serum gamma-glutamyltransferase activities were also determined. RESULTS: Serum total amylase concentrations were significantly increased at 6 months of treatment (p=0.034), and serum nonpancreatic amylase concentrations were significantly increased at 6 (p=0.016) and 12 months of treatment (p=0.039), whereas serum pancreatic amylase and lipase concentrations did not significantly change at 6 or 12 months of treatment with carbamazepine monotherapy. Furthermore, serum gamma-glutamyltransferase concentrations were significantly increased at 6 (p=0.000) and 12 months of treatment (p=0.000) with carbamazepine monotherapy. There was no significant correlation between serum nonpancreatic amylase concentrations and serum gamma-glutamyltransferase or carbamazepine concentrations at 6 and 12 months of treatment with carbamazepine monotherapy. CONCLUSIONS: These findings indicate that nonpancreatic amylase concentrations may be increased in patients treated with carbamazepine monotherapy. Therefore, measurement of serum pancreatic amylase and lipase concentrations is suggested in epileptic patients receiving carbamazepine monotherapy with symptoms suggesting pancreatic dysfunction, so that unnecessary discontinuing of treatment with carbamazepine should be avoided.

Alkaline phosphatase and its isoenzyme activity for the evaluation of bone metabolism in children receiving anticonvulsant monotherapy.

This study aimed to investigate whether carbamazepine, sodium valproate or phenobarbital as monotherapy in ambulatory epileptic children with adequate sun exposure have some effect on their bone metabolism based on the determination of total serum alkaline phosphatase (AP) levels and its bone isoenzyme activity. Blood samples were obtained from 118 epileptic children (37 on carbamazepine, 47 on sodium valproate and 34 on phenobarbital) and from corresponding healthy controls matched for age, gender and anthropometric parameters. AP and its liver, bone and intestinal isoenzyme levels, other common biochemical markers of bone and liver metabolism and drug levels were measured in the study participants. Patients on carbamazepine or phenobarbital had significantly elevated AP levels accompanied by increased bone and liver isoenzyme activity compared to controls. An increase of bone AP isoenzyme values, correlated with the duration of treatment ( r= 0.49, P= 0.002), was found in children on sodium valproate without, however, a concomitant significant elevation of total AP values. We conclude that children who receive antiepileptic drugs as monotherapy, even when residing in a Mediterranean country with adequate sunlight, may have their bone metabolism affected as indicated by the elevated levels of bone AP isoenzyme. This isoenzyme, but not total AP values, could therefore be used as a marker for the selection of patients who would be benefited by a thorough evaluation of their bone metabolism profile.