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Biomedical subjects

K Prabhakaran

Publications and source records attributed to K Prabhakaran.

At least 37 records · Page 2Linked to original sources
PubMed2004

Chylous ascites following liver resection--case report.

Chylous ascites is an intraperitoneal collection of fluid that appears milky because of the presence of unusual amounts of fat. It is a result of interference, interruption, or obstruction of lymph flow through chyle-transporting vessels, and remains rare as a complication of surgical intervention. Liver resection has been infrequently reported as a cause of chylous ascites. We report a case of chylous ascites developing after laparotomy and right lobe liver resection, which was diagnosed early and managed conservatively with minimal morbidity. The key lies in awareness of the condition, early diagnosis, and aggressive management with nutritional support.

Chemotherapy, Adjuvant↗
PubMed2004

Urogenital sinus, rectovaginal fistula, and an anterior stenosed anus--another cloacal variant.

The persistent cloaca is one of the most complex and challenging developmental malformations. It is a rare anomaly occurring only in the female newborn and is represented by the association of urogenital sinus with an anorectal malformation (ARM). Each case is probably unique. We report here one such case of cloaca with the VATER association-tracheoesophageal fistula (TOF) with a urogenital sinus, rectovaginal fistula, and an anteposed stenosed anus, along with preaxial syndactyly of the right hand. The spine, renal, and cardiac systems were normal. Interim management was directed towards repair of the TOF and a right transverse defunctioning colostomy. Despite thorough radioendoscopic preoperative investigations, the complexity of the cloacal anomaly was not delineated until surgery. This case is a rather rare combination of an intermediate form of the cloacal-ARM spectrum. Such patients present with many diagnostic and therapeutic problems. Interval surgery should be directed towards decompression of the affected organ systems, and definitive surgery must be carefully planned and, whenever possible, done in a single stage with simultaneous multisystem repair to correct all significant malformations related to the cloacal complex.

Abnormalities, Multiple↗
PubMed2004

Anorectal malformation with congenital absence of vagina: a case report and review of the literature.

Congenital anorectal malformations are relatively common, and associated genitourinary malformations have been reported in up to 40% of patients. Uterovaginal malformations are also not rare in children. They are known to occur with increased frequency in children with anorectal malformations, but the diagnosis may still be difficult. We report herein one such case of anorectal malformation associated with congenital total absence of the vagina in which the uterovaginal malformation was not diagnosed until the operative repair of the anorectal malformation. The operative procedure was thereafter directed, along with the anorectoplasty, towards restoring a functional uterovaginal tract. Review of the literature revealed that such a diagnosis is unsuspected or delayed in more than half of affected patients. Furthermore, these patients present with many diagnostic and therapeutic problems. Our report highlights the need to be aware of this condition to allow for an earlier diagnosis and appropriate operative treatment.

Abnormalities, Multiple↗
PubMed2004

Bronchoplasty for bronchial stenosis in a neonate: a case report.

Bronchial stenosis is an uncommon problem in children. Management can be difficult because of the small luminal diameter and proximity of the lung parenchyma to the bronchial lesion. Bronchoplasty procedures have obvious advantages in children because of their long life expectancy. Long-term functional results are superior compared with pneumonectomy because of preserved lung tissue. A premature neonate weighing only 779 g at birth was born with severe respiratory distress syndrome complicated with hyperbillirubinemia and bronchopulmonary dysplasia. The child underwent bronchoplasty using a costal cartilage graft for a right main bronchus stenosis after 2 failed attempts at bronchoscopic dilatations. In spite of all complications, the child improved sufficiently to be discharged without any oxygen dependency. Our case highlights the successful application of bronchoplasty in a very small baby. Preoperative and intraoperative bronchoscopy was helpful in localization of the endobronchial lesion. Understanding the principle, precise attention to technical detail and meticulous postoperative care contribute toward long-term benefit for pulmonary conservation.

Abnormalities, Multiple↗
PubMed2004

Management of ventral hernia after giant exomphalos with external pressure compression using helmet device.

PURPOSE: The aim of this study was to evaluate an alternative technique of reducing a ventral hernia that follows the primary conservative treatment of a giant omphalocoele. METHODS: The patient is a full-term male neonate with a giant exomphalos. Initially triple dye was applied as an eschar-inducing agent. This resulted in a ventral hernia after 1 month. It was decided to achieve expansion of the abdominal cavity based on the principle of external pressure compression using a sphygmomanometer cuff over the hernia. The cuff was worn continuously, and manual pressure was applied daily. Care was taken to avoid intraabdominal hypertension using the reading of the manometer that was attached. The external pressure was corroborated with observations of respiration and circulation. RESULTS: The child did not show any ill effects of raised intraabdominal pressure. Throughout the treatment, the child was on full oral feedings and did not require any ventilator support. Reduction of the ventral hernia was achieved in 9 months. Surgical repair of the residual hernia defect was carried out by double breasting of the fascia. CONCLUSIONS: The application of controlled external pressure using a specially constructed device is a safe, noninvasive, and effective method of achieving reduction of a ventral hernia after primary conservative treatment of a giant omphalocoele.

Bandages↗
PubMed2004

Receptor mechanisms mediating cyanide generation in PC12 cells and rat brain.

Cyanide is generated in neurons and this report examines the two different receptors which mediate cyanide formation in neuronal tissue. An opiate receptor blocked by naloxone increases cyanide production both in rat brain and in rat pheochromocytoma (PC12) cells. A muscarinic receptor in PC12 cells releases cyanide and the effect is blocked by atropine. In rat brain, in vivo, a muscarinic agonist inhibits cyanide generation, possibly by acting on receptor subtypes different from those in PC12 cells. Cyanide generation by a muscarinic agonist in PC12 cells is blocked by pertussis toxin but that caused by an opiate is not. Thus, two different receptors and two different second messenger systems can mediate cyanide generation in PC12 cells. In parallel with the in vivo data, cultured primary rat cortical cells also show decreased cyanide release following muscarinic stimulation. Both blockade of cyanide generation by muscarinic receptor activation and cyanide release by opiate agonists from cortical cells are pertussis toxin insensitive. Similarly, little cyanide generation was seen following cholera toxin treatment. These data indicate that opiate receptors increase and muscarinic receptors decrease cyanide production in rat brain tissue by G-protein independent mechanisms. This work supports the suggestion that the powerful actions of cyanide may be important for neuromodulation in the CNS.

Analysis of Variance↗
PubMed2004

Successful listing of patients for liver transplant was related to participation of referring doctor in the transplant program.

INTRODUCTION: Experience with liver transplantation is limited in many parts of Asia. Therefore, patients from nontransplant centers may not be referred in a timely fashion for transplants. Our aim was to evaluate the pattern of referral for liver transplantation and their outcomes in Singapore. METHODS: Consecutive patients referred from 1990 to 2001 were reviewed. Patients from any hospital in Singapore (or the region) could be referred to the program. They were discussed at the weekly meetings. Appropriate patients were placed on the waiting list. "Pending" indicated that the disease was early or there were unsettled medical or social issues. Unsuitable patients were "rejected" for transplant. RESULTS: There were 385 patients referred over a 12-year period. Hepatitis B cirrhosis and hepatocellular carcinoma (HCC) were the most common indications among adults, whereas biliary atresia was the most common for children. Pediatric patients were more likely than adult patients to be listed for transplant (53/76 vs 106/309, P < .001). Patients referred by regular attendees of the program were more likely to be accepted than nonattendees (38% vs 25%, P = .04). "Disease too early", "advanced HCC", and "refusal by family members" were the most common reasons for rejection. CONCLUSION: Members of the Liver Transplant Program were more likely to refer suitable patients for transplant at the appropriate time. Better interaction between gastroenterologists inside and outside the transplant program would help to improve the timing of referrals for liver transplantation, and hence, patient survival.

Adult↗
PubMed2004

Adefovir dipivoxil as the rescue therapy for lamivudine-resistant hepatitis B post liver transplant.

INTRODUCTION: Complications of hepatitis B virus (HBV) infection are among the most common indications for liver transplant in many parts of Asia. However, none of the current posttransplant hepatitis B prophylaxis strategies, namely, lamivudine, hepatitis B immunoglobulin monotherapy, or combination therapy, is ideal. Our aim was to evaluate the use of adefovir dipivoxil (ADV) as a rescue therapy for posttransplant HBV patients who developed lamivudine resistance. METHODS: Twenty-two consecutive patients with HBV-related liver disease, who underwent first liver transplants from 1995 to 2002, received HBV prophylaxis with indefinite lamivudine with substitution of ADV for patients who developed drug resistance and clinical deterioration, defined as persistent elevation of transaminases or histologic deterioration. RESULTS: Sixteen patients (73%) were alive at their last follow-up and six (38%) had developed hepatitis B recurrence at a median of 46 (range 9 to 74) months posttransplant. Two with persistently normal transaminases and normal liver histology at 3 and 42 months postrecurrence have been continued on lamivudine. Four showed clinical deterioration and received ADV for a median of 24 months; all displayed normalization of transaminases and a 2 to 5 log drop in HBV DNA titers. Three had paired biopsies before and after substitution of ADV with two showing improvement and one stable appearance. The median serum creatinine value increased slightly from 126 to 138 micromol/L (P = 0.72). CONCLUSION: ADV is an effective rescue therapy for patients with lamivudine-resistant hepatitis B post-liver transplant. Further studies are needed to ascertain the optimal posttransplant hepatitis B prophylaxis.

Adenine↗
PubMed2004

Renal impairment and diabetes mellitus after liver transplant.

INTRODUCTION: One of the major concerns in liver transplant patients who survive past 1 year posttransplant is the development of chronic diseases. AIM: We studied two important clinical conditions that can have a chronic course-renal impairment and diabetes mellitus-among long-term liver transplant survivors. METHODS: All adult patients transplanted and followed for at least 1 year were evaluated for clinical status, blood tests, and imaging studies. The occurrence and development of renal impairment, defined as a serum creatinine above 125 micromol/L or creatinine clearance less than 75 mL/min, or diabetes mellitus were evaluated for contributing factors. RESULTS: The 35 evaluated patients of mean age at transplant of 50 years had a mean follow-up duration of 45 months. The incidence of posttransplant renal impairment was 22.8% at 1 year and 47.6% at 3 years. This disorder was associated with pretransplant renal impairment and with a diagnosis of diabetes. Posttransplant diabetes mellitus was observed in 48.6% with 41.1% resolving over time. CONCLUSION: Posttransplant renal impairment appears to be a potential long-term problem. Although this relates to pretransplant conditions, longer follow-up is required to examine whether posttransplant factors contribute to its progression.

Adolescent↗
PubMed2004

Persistent thrombocytopenia in liver transplant patients.

INTRODUCTION: The occurrence of thrombocytopenia in the perioperative period after a liver transplant is not uncommon. However, there are few studies on persistent thrombocytopenia during the longer follow up period of patients after liver transplantation. We examined the prevalence of and contributing factors to persistent thrombocytopenia beyond 1 year post-liver transplantation. METHODS: We analyzed adult patients followed for at least 1 year posttransplant with full blood counts and abdominal scans, as well as clinical notes. RESULTS: The 35 patients of mean age at transplant of 50 years and showed a mean follow-up of about 4 years showed a prevalence of persistent thrombocytopenia at 12 months of 54% and at 3 years of 25%. Factors that were associated with persistent thrombocytopenia were pretransplant variceal bleeding, splenomegaly, and thrombocytopenia at 3 and 6 months posttransplant. After multivariate analysis only the latter represented independent factors for persistent thrombocytopenia at 1 and 3 years posttransplant, respectively. CONCLUSION: Persistent thrombocytopenia improved over time posttransplant; no bleeding problem was observed among the affected cases.

Adolescent↗
PubMed2004

The MELD score may help to determine optimum time for liver transplantation.

BACKGROUND: The model for end-stage liver disease (MELD) score is a good predictor of mortality on the waiting list and short-term survival post liver transplantation. AIM: Our aim was to determine if there is a pretransplant MELD score beyond which liver transplantation is prohibitive. PATIENTS AND METHODS: Forty-six adult patients underwent primary liver transplantation from January 1996 to December 2002. Patients followed to the most recent visit or death underwent survival analysis using Cox regression and Kaplan Meier methods. RESULTS: There was a significant correlation between the pretransplant MELD score and survival at 6 months posttransplant (P=.037 95% CI: 1.004-1.13). Patients with pretransplant MELD score greater than or equal to 32 showed significantly greater mortality compared with those less than 32 (HR 9.18, 95%CI=1.16-72.44). CONCLUSION: Pretransplant MELD may help to determine the optimum time for liver transplantation.

Adult↗
PubMed2003

p38 Mitogen-activated protein kinase regulates Bax translocation in cyanide-induced apoptosis.

Execution of cyanide-induced apoptosis is mediated by release of cytochrome c from mitochondria. To determine how cyanide initiates cytochrome c release, Bax translocation was investigated in primary cultures of cortical neurons. Under nonapoptotic (control) conditions, Bax resided predominantly in the cytoplasm. After 300-microM cyanide treatment for 1 h, Bax translocated to the mitochondria, as shown by immunocytochemical staining and subcellular fractionation; Western blot analysis confirmed "cytosol-to-mitochondria" translocation of Bax. Temporal analysis showed that Bax translocation preceded cytochrome c release from the mitochondria, which was initiated 3 h after cyanide treatment. In double-immunofluorescence labeling for both Bax and cytochrome c, it was observed that cytochrome c was released only in cells showing Bax in mitochondria. The role of p38 mitogen-activated protein (MAP) kinase in Bax translocation was studied. The p38 MAP kinase was activated 30 min after cyanide, and its phosphorylation level of activity began to decrease 3 h later. SB203580, a p38 MAP kinase inhibitor, blocked translocation of Bax to mitochondria, whereas SB202474, a control peptide, had no effect on translocation. Inhibition of p38 MAP kinase by SB203580 blocked all downstream effects of Bax translocation, including cytochrome c release, caspase activation, and internucleosomal DNA fragmentation. These results demonstrated that Bax translocation is critical for cyanide-induced cytochrome c release and that p38 MAP kinase regulates Bax translocation from cytosol to mitochondria.

Animals↗
PubMed2002

Oxidative stress and cyclooxygenase-2 induction mediate cyanide-induced apoptosis of cortical cells.

Cyanide (KCN)-induced generation of reactive oxygen species (ROS) involves cyclooxygenase-2 (COX-2)-mediated reactions in some neurons. The present study examines the extent to which COX isoforms are involved in KCN-induced apoptotic cell death processes of cultured cortical cells. After treatment with KCN (10-300 microM), COX-2 was expressed in a time- and concentration-dependent manner increasing markedly over a 4-h period. However, no significant changes were observed in COX-1 levels at any cyanide concentration. Correlated with COX-2 up-regulation, KCN induced a time-dependent apoptotic death. TUNEL staining showed that the COX-2 inhibitor NS-398 (30 microM) blocked KCN-induced apoptosis, whereas the selective COX-1 inhibitor valeryl salicylate did not affect the level of apoptotic cell death. Exposure of cells to KCN (300 microM) for 24 h resulted in DNA fragmentation, which was also reduced by NS-398. Prostaglandin E(2) (PGE(2)) accumulation in cell culture supernatants was increased by KCN and NS-398 blocked PGE(2) generation. PCR studies further confirmed that COX-2 expression was increased by KCN. Antioxidants phenyl-N-test-butylnitrone, superoxide dismutase, and catalase significantly inhibited KCN-induced COX-2 up-regulation and subsequent apoptosis. N(G)-nitro-L-arginine methylester an inhibitor of nitric oxide synthase, blocked KCN-induced PGE(2) production and apoptosis, but not COX-2 expression. Increased nitric oxide levels caused by cyanide may directly activate the COX-2 enzyme. These data show that cyanide treatment of cortical cells involves increased COX-2 expression, PGE(2) accumulation, and ROS generation, resulting in apoptotic cell death.

Animals↗
PubMed2002

Cyanide induces different modes of death in cortical and mesencephalon cells.

A comparative study was conducted in rat primary cortical (CX) and mesencephalic (MC) neurons to investigate intracellular cascades activated during cyanide-induced injury and to determine the point at which the cascades diverge to produce either apoptosis or necrosis. Cyanide treatment (400 microM) for 24 h produced primarily apoptosis in CX cells, whereas the same concentration of cyanide induced predominantly necrosis in MC cells as indicated by increased propidium iodide staining and cellular lactate dehydrogenase efflux. Cyanide increased generation of cellular reactive oxygen species (ROS) in both CX and MC cells, but the rate of formation and nature of the oxidative species varied with cell type. Catalase decreased cyanide-induced ROS generation in CX but not in MC cells. Nitric oxide generation was more prominent after cyanide treatment of MC compared with CX cells. N-Methyl-D-aspartate receptors were more involved in CX apoptosis than in MC necrosis. Mitochondrial membrane potential decreased moderately in CX cells on exposure to cyanide, whereas MC cells responded with a more pronounced reduction in potential. In CX cells cyanide produced a concentration-dependent release of cytochrome c from mitochondria and increased caspase activity, whereas little change was seen in MC neurons. Thus, cyanide-induced necrosis of MC cells involved generation of excessive amounts of nitric oxide and superoxide accompanied by mitochondrial depolarization. In contrast cyanide causes a lower level of oxidative stress in CX cells, involving mainly hydrogen peroxide and superoxide, and a moderate change in mitochondrial membrane potential that lead to cytochrome c release, caspase activation, and apoptosis.

Animals↗
PubMed2001

Management of a floating sternum after repair of pectus excavatum.

PURPOSE: The aim of this study was to examine the authors' experience with patients who have floating sternum after correction of pectus excavatum via the classical Ravitch procedure. A floating sternum is defined as a sternum in which the only attachment to the chest wall is its superior (cranial) border, and in which the body is secured only by the manubrium and whatever lateral and inferior fibrous bands are present. Typically, a floating sternum is caused by either extensive resection of the costal cartilages and perichondrium during correction of pectus excavatum or failure of proper regrowth of these cartilages. METHODS: The authors retrospectively assessed the charts of all patients diagnosed with a floating sternum noting age at original correction of pectus excavatum, time from original correction of pectus excavatum to diagnosis of floating sternum, age at correction of floating sternum, complaints before stabilization of the sternum, methods of repair, and postoperative complications. RESULTS: Between July 1993 and June 1999, floating sternum was diagnosed in 7 patients. The mean age of patients who underwent operative correction of a floating sternum was 28.9 years (range, 16 to 42 years). The mean time interval between original correction of pectus excavatum, or "redo," and diagnosis of a floating sternum was 9.9 years (range, 2 to 20 years). Complaints before correction of the floating sternum included sternal pain and instability, exercise intolerance, and difficulty breathing. Operative repair consisted of mobilizing the lateral and inferior edges of the sternum, detaching the fibrous perichondrium, performing anterior sternal osteotomies, and finally supporting the sternum with substernal Adkins struts. All 7 patients had successful stabilization of the sternum. Two of 7 patients underwent 2 procedures to successfully stabilize the sternum. One patient has Adkins struts still in place because of hematopoetic malignancy. Six of 7 patients are now without symptoms. CONCLUSIONS: A floating sternum is a morbid phenomenon that may manifest many years after the original procedure. It can cause significant sternal pain, chest wall instability, and respiratory dysfunction, which are the hallmark indications for correction. Repair of a floating sternum can be accomplished successfully.

Adolescent↗
PubMed2001

Mechanisms of the apoptotic and necrotic actions of trimethyltin in cerebellar granule cells.

In evaluating mechanisms of trimethyltin (TMT)-initiated neuronal damage, the present study focused on involvement of reactive oxygen species, protein kinase C (PKC), and glutamate receptors. Exposure of cerebellar granule cells to TMT (0.01-0.1 microM) produced primarily apoptosis, but higher concentrations were associated with cellular lactate dehydrogenase efflux and necrosis. TMT increased generation of cellular reactive oxygen species, which was inhibited by either L-NAME (inhibitor of nitric oxide synthase, NOS) or catalase, indicating that both NO and H(2)O(2) are formed on TMT exposure. Since chelerythrine (selective PKC inhibitor) also inhibited oxidative species generation, PKC appears to play a significant role in TMT-induced oxidative stress. The metabotropic glutamate receptor antagonist, MCPG, (but not MK-801) prevented oxidative species generation, indicating significant involvement of metabotropic receptors (but not NMDA receptors) in TMT-induced oxidative stress. NOS involvement in the action of TMT was confirmed through measurement of nitrite, which increased concentration dependently. Nitrite accumulation was blocked by L-NAME, chelerythrine, or MCPG, showing that NO is generated by TMT and that associated changes in NOS are regulated by a PKC-mediated mechanism. Oxidative damage by TMT was demonstrated by detection of elevated malondialdehyde levels. It was concluded that low concentrations of TMT (0.01-0.1 microM) cause apoptotic cell death in which oxidative signaling is an important event. Higher concentrations of TMT initiate necrotic death, which involves both an oxidative and a non-oxidative component. TMT-induced necrosis but not apoptosis in granule cells is mediated by glutamate receptors.

Alkaloids↗
PubMed2001

Liver transplantation in a child with severe hypercholesterolaemia in Alagille syndrome.

INTRODUCTION: Liver transplantation is a curative treatment modality in children with end stage liver disease in Alagille syndrome. CLINICAL PICTURE: We report a 3-year-old child with this condition who had severe hypercholesterolaemia, pruritus and extensive xanthomatosis. TREATMENT: Liver transplantation was performed in this patient. OUTCOME: He recovered well with normalisation of his lipid profile. This procedure also resulted in resolution of the disfiguring xanthomatosis.

Alagille Syndrome↗