Predicting the liver histology in chronic hepatitis C: how good is the clinician?

OBJECTIVE: Liver biopsy is believed to be necessary before antiviral treatment in hepatitis C. Studies have found symptoms and biochemistry poorly predictive of grade and stage. In practice, a combination of factors is used to anticipate histology. The aim of this study is to evaluate the ability of global clinical assessment to predict histology in hepatitis C. METHODS: Fifty-four consecutive patients referred to a university center for consideration of antiviral therapy were enrolled. Clinical and laboratory data were recorded as was a prediction of the inflammatory grade (0-3) and fibrotic stage (0-3), with fibrotic stage 3 referring to cirrhosis. Liver biopsies were read by a blinded pathologist. The predictive value of the clinical assessment and individual parameters was assessed. RESULTS: All predictions were < or = 1 point off the actual grade and stage. Thirty-six (66.7%) patients' grades and 41 (75.9%) patients' stages were exactly predicted. All four cirrhotic patients (sensitivity 100%, specificity 94%) and one case of hemochromatosis were correctly predicted. Spider nevi, organomegaly, white blood cell count < or = 4 x 10(9)/L, ALT > 120 U/L, bilirubin > 20 micromol/L, albumin < or = 35 g/L, and ferritin > 200 microg/L predicted grade > or =2. Stage > or =2 was associated with age > 40 yr, previous decompensation, spider nevi, organomegaly, white blood cell count < or = 4 x 10(9)/L, albumin < or = 35 g/L, platelets < or = 150 x 10(9)/L, and international normalized ratio > 1.2. Grade correlated with stage (Spearman coefficient = 0.54, p < 0.001). By multivariate analysis, ferritin plus spider nevi or hypoalbuminemia was independently predictive of inflammation. Spider nevi and thrombocytopenia, with either splenomegaly or hypoalbuminemia, were useful three-variable models for predicting fibrosis. The corresponding scoring systems produced useful likelihood ratios. CONCLUSIONS: Global clinical assessment mirroring clinical practice in a tertiary liver transplant center is moderately accurate in predicting grade and stage in hepatitis C. Liver biopsy is the current gold standard; however, the amount of new information gleaned is less than was perceived. The need for routine biopsy before antiviral treatment in hepatitis C should be reevaluated in a multicenter study.

Graft-versus-host disease after liver transplantation complicated by systemic aspergillosis with pancarditis.

Graft-versus-host disease after liver transplantation complicated by systemic aspergillosis with pancarditis. Can J Gastroenterol 2000;14(7):637-640. Acute graft-versus-host disease (GVHD) is a common complication after bone marrow transplantation, with characteristic rash and diarrhea being the most common features. After liver transplantation, however, this phenomenon is very rare. Most transplant patients are on a variety of medications, including immunosuppressants; therefore, the differential diagnosis of skin rash or diarrhea is broad. A 37-year-old man who underwent liver transplantation for primary biliary cirrhosis, and developed a rash and watery diarrhea, is presented. Skin and colonic biopsies confirmed acute GVHD. A pulse of intravenous steroids was given. The skin rash improved, but he developed pancytopenia. His course was complicated by central line infection, jugular and subclavian vein thrombosis, pseudomembranous colitis, recurrent bacteremia, cholestasis on total parenteral nutrition and cytomegalovirus infection. After the onset of pleuritic chest pain and clinical sepsis, spiral computed tomography scan of his chest and abdomen revealed septic infarcts in multiple organs. Despite empirical treatment with amphotericin B, he died of multiorgan dysfunction syndrome within 72 h. Autopsy revealed systemic aspergillosis with pancarditis, endocardial vegetations, and septic pulmonary, splenic, hepatic and renal infarcts. The pathogenesis and experience with this rare, but often fatal, complication of liver transplantation are reviewed. In contrast to GVHD after bone marrow transplantation, pancytopenia is common and liver dysfunction is rare. One should have a high level of suspicion in the liver transplant recipient presenting with rash and/or diarrhea.

Inhibition of poly(ADP-ribose) polymerase attenuates inflammation in a model of chronic colitis.

Crohn's disease is a chronic disease characterized by oxidant-induced tissue injury and increased intestinal permeability. A consequence of oxidative damage is the accumulation of DNA strand breaks and activation of poly(ADP-ribose) polymerase (PARP), which subsequently catalyzes ADP-ribosylation of target proteins. In this study, we assessed the role of PARP in the colitis seen in interleukin (IL)-10 gene-deficient mice. IL-10 gene-deficient mice demonstrated significant alterations in colonic cellular energy status in conjunction with increased permeability, proinflammatory cytokine release, and nitrosative stress. After 14 days of treatment with the PARP inhibitor 3-aminobenzamide, IL-10 gene-deficient mice demonstrated normalized colonic permeability; reduced tumor necrosis factor-alpha and interferon-gamma secretion, inducible nitric oxide synthase expression, and nitrotyrosine levels; and significantly attenuated inflammation. Time course studies demonstrated that 3-aminobenzamide rapidly altered cellular metabolic activity and decreased cellular lactate levels. This was associated with normalization of colonic permeability and followed by a downregulation of proinflammatory cytokine release. Our data demonstrate that inhibition of PARP activity results in a marked improvement of colonic inflammatory disease and a normalization of cellular metabolic function and intestinal permeability.

Antibiotic therapy attenuates colitis in interleukin 10 gene-deficient mice.

BACKGROUND & AIMS: Interleukin (IL)-10 gene-deficient mice, raised under germfree conditions, do not develop colitis, implying a role for bacteria. This study mapped the appearance of luminal colonic bacteria and, using antibiotic treatment, determined their association with colitis in IL-10 gene-deficient mice. METHODS: Mice were treated with ciprofloxacin or with neomycin and metronidazole. The intestine was harvested for histological scoring and bacterial assessment. RESULTS: At 2 weeks of age, before the development of colitis, IL-10 gene-deficient mice demonstrated an earlier appearance of Streptococcus and Clostridium sp., and had a greater proportion (P < 0.01) of bacteria adherent to the colonic mucosa. This pattern of increased adherent bacteria persisted for the 12 weeks of study. Treatment of mice before the onset of colonic inflammation, with either antibiotic regime, reduced mucosal adherent bacteria and prevented colitis (P < 0.01). In contrast, treatment of established colitis with neomycin and metronidazole did not reduce adherent bacterial levels, yet was more efficacious (P < 0.05) in treating established colitis than ciprofloxacin, which did reduce adherent colonic bacteria. CONCLUSIONS: In the IL-10 gene-deficient mouse model, the appearance and number of mucosal adherent colonic bacteria are altered before the onset of colitis. Antibiotics both prevent and treat the colitis through correction of this primary bacterial alteration.

Hepatosplenic T-cell lymphoma of alphabeta lineage in a 16-year-old boy presenting with hemolytic anemia and thrombocytopenia.

The authors report an unusual case of peripheral T-cell lymphoma in a 16-year-old boy who presented initially with jaundice, splenomegaly, anemia, and thrombocytopenia. A lymphoma was found subsequently in the spleen, which was infiltrated extensively in the red pulp by medium-sized, blastic-appearing lymphoma cells. Immunologic characterization of these cells revealed positivity for CD3, CD5, CD45RO, CD56, and T-cell intracellular antigen (TIA), and negativity for CD2, CD3, CD4, CD8, CD57, CD34, and terminal deoxynucleotidyl transferase (TdT). Conventional cytogenetic studies revealed the presence of isochromosome 7q. On follow up, this patient deteriorated rapidly, with evidence of liver and bone marrow involvement. Although the overall clinical and pathologic features of this disease were characteristic of hepatosplenic gammadelta T-cell lymphoma, the T-cell receptor of this tumor showed an immunophenotype of alphabeta not gammadelta lineage. Using the Southern blot technique, the authors demonstrated monoclonal gene rearrangement of the T-cell receptor beta-chain. Thus, they confirmed the existence of hepatosplenic alphabeta T-cell lymphoma. In view of its overall similarity to hepatosplenic gammadelta T-cell lymphoma, this unusual entity probably represents a slight biologic variation of the same disease.

Interleukin-10 gene-deficient mice develop a primary intestinal permeability defect in response to enteric microflora.

The normal intestinal epithelium provides a barrier relatively impermeable to luminal constituents. However, patients with inflammatory bowel disease experience enhanced intestinal permeability that correlates with the degree of injury. IL-10 gene-deficient mice were studied to determine whether increased intestinal permeability occurs as a primary defect before the onset of mucosal inflammation or is secondary to mucosal injury. At 2 weeks of age, IL-10 gene-deficient mice show an increase in ileal and colonic permeability in the absence of any histological injury. This primary permeability defect is associated with increased mucosal secretion of interferon-gamma and tumor necrosis factor-alpha, and does not involve an increase in nitric oxide synthase activity. Colonic permeability remains elevated as inflammation progresses, while ileal permeability normalizes by 6 weeks of age. IL-10 gene-deficient mice raised under germ-free conditions have no inflammation, and demonstrate normal permeability and cytokine levels. This data suggests that the intestinal permeability defect in IL-10 gene-deficient mice occurs due to a dysregulated immune response to normal enteric microflora and, furthermore, this permeability defect exists prior to the development of mucosal inflammation.

Lactobacillus species prevents colitis in interleukin 10 gene-deficient mice.

BACKGROUND & AIMS: Intestinal luminal microflora, or their products, are likely an important initiating factor in the pathogenesis of inflammatory bowel disease. The aim of this study was to determine the role of colonic aerobic luminal bacteria and Lactobacillus species in the development of colitis in interleukin (IL)-10 gene-deficient mice. METHODS: Intestine from 2-16-week-old mice was scored histologically and cultured for bacteria. Lactobacillus sp. repopulation of the colonic lumen was achieved via daily rectal delivery of Lactobacillus reuteri or oral lactulose therapy. RESULTS: At 2 weeks of age, IL-10 gene-deficient mice showed no colonic injury but did display abnormal colonic bacterial colonization with increased colonic mucosal aerobic adherent and translocated bacteria in conjunction with reduced Lactobacillus sp. levels. In association with the abnormal colonic bacterial colonization, colitis developed by 4 weeks of age. Restoring Lactobacillus sp. to normal levels reduced levels of colonic mucosal adherent and translocated bacteria and attenuated the development of the colitis. CONCLUSIONS: In the neonatal period, IL-10 gene-deficient mice have decreased levels of colonic Lactobacillus sp. and an increase in colonic mucosal adherent and translocated bacteria. Normalizing Lactobacillus sp. levels reduced colonic mucosal adherent and translocated bacteria and prevented colitis.

Lack of correlation between Lewis antigen expression by Helicobacter pylori and gastric epithelial cells in infected patients.

BACKGROUND & AIMS: Lewis antigens are expressed by both human gastric epithelial tissue and Helicobacter pylori. We examined Lewis antigens expressed by gastric epithelium and by H. pylori isolated from the corresponding biopsy tissue. METHODS: H. pylori Lewis expression was determined by enzyme immunoassays, and immunoelectron microscopy was used to confirm the Lewis antigens on some H. pylori cells and in some biopsy specimens. Histopathology using identical monoclonal antibodies specific for Lewis A, B, X, and Y antigens was used to detect these antigens in 24 gastric biopsy specimens. RESULTS: We identified Lewis Y in 100%, Lewis X and Lewis B in 95.8%, and Lewis A in 87.5% of biopsy specimens. In H. pylori, 87.5% expressed Lewis Y, 79.2% Lewis X, and 4.2% (one strain) Lewis B. No Lewis A was detected. Antibody specific for Lewis X labeled the bacteria and associated adhesion pedestal. The cagA gene was present in 92% of strains. CONCLUSIONS: There was no direct relationship between Lewis antigen expression by H. pylori and gastric epithelial cells in infected patients. Expression of Lewis X and Lewis Y by H. pylori suggests the possibility of their requirement for establishment and/or maintenance of infection. An immunoelectron micrograph of H. pylori interaction with the gastric epithelial adhesion pedestal suggests a tentative role for Lewis X in the adhesion process.

Hemorrhagic intestinal Henoch-Schonlein purpura complicated by cytomegalovirus infection.

A 54-year-old man on hemodialysis for acute chronic renal failure and on corticosteroids for Henoch-Schonlein purpura developed massive hematochezia. After extensive clinical investigation, an ileal bleeding site was identified and surgically removed. Pathological examination of the diseased bowel segment revealed an extensive vasculitis with mucosal ulceration attributable to Henoch-Schonlein purpura as well as florid cytomegalovirus infection.

Conservative management of small adenomata in ulcerative colitis.

OBJECTIVE AND METHODS: Patients with chronic ulcerative colitis may develop colitis-related dysplasia and/or sporadic adenomata. Differentiating between these two processes is important because they may dictate different therapeutic approaches. Although distinguishing features of sporadic adenomata versus colitis-related dysplasia have been suggested previously on an a priori basis, they have never been verified by follow-up analysis. We have identified six chronic ulcerative colitis patients whose discrete adenomata were managed conservatively, with subsequent continuation in their surveillance programs. RESULTS: Mean patient age was 69 yr with a mean 21.3 yr of ulcerative colitis. Surveillance endoscopy of 63 patient-yr duration yielded 24 adenomata. A mean follow-up after the initial adenoma diagnosis was 7.2 yr with no carcinoma identified (including the examination of one prophylactic colectomy specimen). One patient, with a 34-yr history of ulcerative colitis and a single sporadic adenoma subsequently developed dysplasia of flat mucosa 14 months later. CONCLUSIONS: Our findings concur with previous reports and indicate that small, discrete adenomata with morphology identical to those seen in the general population occur in patients with ulcerative colitis. Such lesions in patients older than 45 yr, with tubular or tubulovillous architecture and low-grade dysplasia, are effectively treated by polypectomy only and are not necessarily an indication for colectomy. However, sporadic adenomata and colitis-related dysplasia can develop metachronously. It is suggested that subsequent to a diagnosis of sporadic adenoma in a patient with chronic ulcerative colitis, surveillance should increase to colonoscopic examination every 6 to 12 months.

Co-existence of hepatitis A and adult Reye's syndrome.

Reye's syndrome is most frequently seen in children but has also been described in adults. This syndrome is usually associated with ingestion of 5-aminosalicylates (ASA) or infection with influenza A, influenza B, or varicella virus. A case of Reye's syndrome in a 47 year old, previously healthy woman precipitated by ingestion of ASA and acute hepatitis A virus infection is described. Reye's syndrome was diagnosed on the basis of her clinical course, and the presence of hepatic microvesicular steatosis and characteristic electron microscopic changes in the hepatocyte mitochondria. The diagnosis of hepatitis A was based on higher amino-transferase values than would be expected in Reye's syndrome alone, viral serology including the presence of hepatitis A IgM and the demonstration of hepatitis A virus RNA on liver biopsy by in situ hybridisation. Mitochondrial injury has been demonstrated in acute hepatitis A which, in addition to ASA, may have precipitated Reye's syndrome in this patient. The association between hepatitis A and Reye's syndrome has not been reported before. As hepatitis A virus infection is not sought routinely in patients with Reye's syndrome, the frequency of this association is unknown.

Effects of intravenous lipid as a source of energy in parenteral nutrition associated hepatic dysfunction and lidocaine elimination: a study using isolated rat liver perfusion.

The effects on liver function and hepatic lidocaine elimination using 20% Intralipid as a source of non-protein calories (30%) in parenteral nutrition were studied using an isolated rat liver perfusion procedure. Rats were randomly assigned to one of the three treatment groups: PNL group (n = 6), consisting of 16.94% dextrose, 2.46% Intralipid, and 5.2% amino acids; PN group (n = 5), consisting of 24.2% dextrose and 5.2% amino acids; and CF group (n = 6), chow fed (rat chow and water). The rate of lidocaine metabolism was significantly reduced after 7 d in the two PN treated groups when compared to CF. Steatosis was observed in five out of six PNL treated animals and two out of five PN treated animals. Intrinsic clearance was reduced by 80% in the PNL group and by 60% in the PN animals (p < 0.05). Molar metabolite to drug ratios revealed significant reductions in N-dealkylation, m-hydroxylation, and aryl methyl hydroxylation in groups PNL and PN; these values amounted to 67-92% (p < 0.05). These findings suggest that a dextrose-amino acid solution induced steatosis and reduced the rate of lidocaine metabolism. The incorporation of Intralipid caused further deterioration.

Efficacy of lamivudine in chronic hepatitis B patients with active viral replication and decompensated cirrhosis undergoing liver transplantation.

Liver transplantation for endstage hepatitis B virus (HBV) infection has been associated with survival inferior to that of liver transplantation in other chronic liver diseases due to HBV reinfection of the graft. Lamivudine is a new nucleoside analog with potent antiviral effects against hepatitis B. Our aim was to test its efficacy when used pre- and posttransplantation in HBV-DNA positive patients with endstage liver disease. Patients received oral lamivudine 100 mg daily both pretransplant and posttransplant. Viral serology, serum and tissue HBV-DNA and liver histology were assessed sequentially. Five consecutive patients with endstage hepatitis B were entered into the trial. Serum HBV-DNA was cleared pretransplant in all patients. Three of four transplanted patients cleared HBeAg and HBsAg postoperatively, whereas all four became negative for serum HBV-DNA (dot-blot and PCR). Liver biopsies were negative for HBV-DNA by PCR in 3 of 4 cases. Lymphocytes were negative for HBV-DNA by PCR in all cases. With follow-up of 3, 14, 16, and 26 months, two patients have normal liver enzymes and normal liver histology and two have developed recurrent hepatitis B. No significant side effects were seen. This pilot study shows that lamivudine can effectively inhibit hepatitis B virus in cirrhotic patients pretransplant and posttransplant. A lamivudine resistant mutant developed in two patients. Transplant recipients with actively replicating HBV related cirrhosis may achieve a good outcome after liver transplantation using lamivudine, but viral resistance is likely to be a significant problem.

Immunocytochemical and morphometric studies of gastrin-, somatostatin- and serotonin-producing cells in the stomach and duodenum of patients with acid peptic disorders.

Gastric and duodenal biopsies from 90 patients with various acid peptic disorders-reflux esophagitis (n = 24), gastric ulcer (n = 13), duodenal ulcer (n = 47) and nonulcer dyspepsia (n = 6)-were examined. Seven patients with minimal dyspeptic symptoms and an endoscopically and histologically normal stomach and duodenum served as controls. Immunoperoxidase staining for gastrin-producing G cells, somatostatin-producing D cells and serotonin-producing EC cells was carried out on fundic, antral and duodenal biopsies, and was quantified using a Zeiss MOP Videoplan using the peroxidase-antiperoxidase technique of Sternberger. In the gastric antrum, a G:D:EC cell ratio of approximately 1.6:1:1-was observed. In the duodenum the corresponding ratio was 1:1:2.4. No significant differences were observed within any of the major diagnostic categories. Patient age, sex, duration of symptoms, smoking habits, alcohol consumption and nonsteroidal anti-inflammatory drug use had no effect on endocrine cell densities. Reduced G cell density in the descending duodenum was observed in the presence of mild duodenitis in four patients. In four patients with evidence of antral intestinal metaplastic changes, a significant increase in duodenal G cell densities was found. These results suggest that a change in the number of G, D or EC cells does not play a primary role in the pathophysiology of acid peptic disorders in the majority of patients.

Effects of light-exposed parenteral nutrition on hepatic function and lidocaine metabolism: a study using isolated rat liver perfusion.

Effects of light-exposed parenteral solutions on hepatic function and lidocaine metabolism were studied. Male rats (190-220 g) were randomly assigned to one of the three isocaloric treatment groups: parenteral nutrition (PN) (+L) group (n = 6), animals received a solution of 24.2% dextrose and 5.2% amino acids with light exposure; PN(-L) group (n = 5), animals received the same solution without light exposure; and CF group, chow-fed animals (n = 6) that received rat chow and water. Average energy intake in these animals was approximately 33 kcal/100 g/d. Lidocaine metabolism was studied in livers isolated from animals 7 d after treatment. Liver morphology indicated that five livers from PN(+L) animals developed steatosis. The lidocaine metabolism rate was the slowest in PN(+L) animals; this is marked by changes in the steady state levels (% dose) of lidocaine [PN(+L), 47.9 +/- 17.6; PN(-L), 25.9 +/- 2.1; versus CF, 11.3 +/- 5.3; p < 0.05]. The extraction ratio and intrinsic clearance values were reduced by 41 and 86% in PN(+L) group and 16 and 70% in PN(-L) group, respectively, when compared with CF (p < 0.05). Metabolite to drug ratios indicated that N-dealkylation, ring-hydroxylation, and aryl methyl hydroxylation of lidocaine were severely impaired, particularly in the PN(+L) animals. The extents of reduction in metabolic pathways were in the ranges 79-95% in the PN(+L) group and 44-90% in the PN(-L) (p < 0.05). These findings suggest that parenteral nutrition infusion induces steatosis and reduces the rate of lidocaine metabolism and exposure of parenteral nutrition solutions to light exacerbates this change.

Effects of taurine supplementation in parenteral nutrition-associated hepatosteatosis and lidocaine metabolism. A study using isolated rat liver perfusion.

The effects of taurine in parenteral nutrition (PN)-related hepatic dysfunction are controversial. The aims of the present study were to evaluate the effects of taurine on hepatic function and on lidocaine metabolism, using two strengths of taurine (15 and 50 mg/dl) that are present in commercially available preparations. Animals (N > or = 4) were randomly assigned to one of the four 7-day treatment groups: chow-fed (CF); dextrose/amino acids (PN); dextrose/amino acids and taurine, 15 mg/dl (T15); dextrose/amino acids and taurine, 50 mg/dl (T50). Between 40-75% of the animals treated with PN developed steatosis. The origin of steatosis was zonal specific and dependent on taurine treatment. All livers in the CF group had a normal cellular architecture. Lidocaine metabolism was found to be impaired in groups PN, T15, and T50. This was indicated by a significant reduction in the intrinsic clearance values: 70%, 76%, and 85% in groups PN, T15, and T50, respectively (p < 0.05). Metabolites-to-drug ratios indicated that N-dealkylation, m-hydroxylation, and aryl methyl hydroxylation were significantly reduced in all treatment groups; the most pronounced effect was observed in the T50 group. These findings suggest that PN infusion results in impaired liver function, and the reduction of drug elimination rate is exacerbated by the addition of taurine.

Long-term results of total abdominal colectomy for chronic idiopathic constipation. Value of preoperative assessment.

PURPOSE: A small proportion of patients with chronic idiopathic constipation are incapacitated by the problem. We have assessed 1) the efficacy of total abdominal colectomy, and 2) the predictive value of preoperative testing. METHODS: Preoperative testing included complete history and physical examination, appropriate biochemical and hematologic assessment, psychiatric interview, colon transit studies using ingested radiopaque pellets, anorectal manometry, colonic intraluminal manometry, and measurement of colon diameters and length on barium enema examination. All patients were followed for 65 +/- 40 months. RESULTS: Seventy-one percent had excellent or very good results. Twenty-one percent were satisfied, had improved the quality of their life, and felt the operation was worthwhile despite frequent residual or new symptoms. Two (8 percent) patients did not improve. Patients with a psychiatric history or physiologic evidence of an afferent nerve defect had poorer results (P < 0.05). CONCLUSIONS: Total abdominal colectomy with ileorectal anastomosis is highly effective in alleviating symptoms in patients with chronic idiopathic constipation.

Colonic delivery of dexamethasone from a prodrug accelerates healing of colitis in rats without adrenal suppression.

BACKGROUND/AIMS: Dexamethasone-beta-D-glucuronide, a colon-specific prodrug of dexamethasone, may be useful in the treatment of ulcerative colitis and Crohn's colitis. The aim of this study was to evaluate colonic delivery and efficacy of this prodrug in the rat. METHODS: Distribution of dexamethasone in luminal contents and tissues of the gastrointestinal tract and in plasma was measured after oral administration of dexamethasone-beta-D-glucuronide or free dexamethasone. Efficacy of the prodrug and free drug was tested in an acetic acid-induced rat colitis model. Healing of induced colitis was assessed by measuring net intestinal fluid absorption, colonic surface area of ulceration, histology, and myeloperoxidase activity. Glucocorticosteroid toxicity was evaluated with serum corticosterone and plasma adrenocorticotropic hormone levels. RESULTS: The drug delivery index (a measure of relative targeting efficiency) was 6.7 and 8.6 in the cecal and colonic mucosa, respectively. The prodrug was significantly more potent than free drug in improving net colonic fluid absorption while significantly reducing surface area of ulceration and histological grade in colitic rats. Treatment with free dexamethasone significantly reduced serum corticosterone levels to subnormal levels, and treatment with the prodrug maintained serum corticosterone and plasma adrenocorticotropic hormone levels near control levels. CONCLUSIONS: The prodrug dexamethasone-beta-D-glucuronide delivers efficacious amounts of dexamethasone to the large intestine from lower doses than free dexamethasone.

Case report: mesenteric mixed haemangioma and lymphangioma; report of a case with 10 year follow-up after radiation treatment.

A patient with massive mixed haemangioma and lymphangioma of the mesentery first presented in childhood with ascites which subsided spontaneously and, subsequently, at 21 years of age, presented with gastrointestinal bleeding. At laparotomy, the lesion was found to involve 90% of the mesentery and was unresectable due to its bulk. Hence he was treated by radiotherapy (15 Gy/15 fractions/3 weeks followed by a boost of 5 Gy/4 fractions/4 days). He responded to the treatment. 10 years later he again experienced mild gastrointestinal bleeding which subsided spontaneously. This case illustrates the efficacy of radiotherapy in massive mesenteric haemolymphangiomas. Review of the literature revealed that surgical excision, embolization, and radiotherapy have been used in the treatment of haemangiomas and lymphangiomas. In unresectable cases, radiotherapy has a definite role in the management. A variety of doses has been employed in the literature. No definite dose-response relationship was identified.