Mucosal Hyperplasia Research Articles

Enhancement of erbB2 and erbB3 expression during oral oncogenesis in diabetic rats

The expression of erbB2 and erbB3 receptors was investigated in an experimental model of chemically induced oral carcinogenesis in normal and diabetic (type I) Sprague-Dawley rats. Thirteen diabetic and twelve normal rats developed precancerous and cancerous lesions after 4-nitroquinoline-N-oxide treatment, while six diabetic and six normal animals were used as controls. Sections of biopsies from all animals were classified histologically in the following categories: normal mucosa, hyperplasia, dysplasia, early invasion, well- and moderately-differentiated squamous cell carcinoma. Each section was studied immunohistochemically using monoclonal antibodies against erbB2 and erbB3 proteins and six representative histological regions in each section were analysed. The erbB2 was expressed at very low levels in normal rats, while in diabetic animals its expression was significantly increased during early invasion (P = 0.04). The erbB3 expression was significantly elevated in well-differentiated carcinoma in normal animals (P = 0.01), while in diabetic animals it was significantly increased during oral mucosal hyperplasia and dysplasia (P = 0.03 and 0.0007, respectively). The comparison of erbB2 expression between diabetic and normal rats revealed significant differences in all stages except for the tumor stage of moderately differentiated carcinoma (P = 0.01, 0.00001, 0.00001, 0.003, and 0.00001). In regard to erbB3 expression, significant differences between diabetic and normal rats existed only in normal, non-cancerous and precancerous stages (P = 0.007, 0.0001, 0.0003). It seems that diabetes enhances the expression of both erbB2 and erbB3 in certain stages of oral oncogenesis possibly resulting in promotion of cell proliferation and inhibition of apoptosis.

T-Cell Function Is Critical for Murine Cholesterol Gallstone Formation

The formation of cholesterol gallstones is a complex process involving contributions from genes and environmental factors. Although gallbladder inflammation is believed to be common during cholelithogenesis, the role of immunologic factors is unknown. The role of adaptive immunity in cholesterol cholelithogenesis was analyzed utilizing immunocompetent Helicobacter spp.-infected and -uninfected BALB/c and congenic immunodeficient Rag2(-/-) (Rag) mice. Lymphocyte transfer studies were performed to determine which cellular subset was responsible for cholesterol gallstone formation. Also, gallbladder inflammation was quantified to determine the nature of the inflammatory response associated with cholelilithogenesis. When fed a lithogenic diet for 8 weeks, wild-type mice developed significantly more cholesterol gallstones (27%-80% prevalence) than Rag mice ( approximately 5%, P < .05). Helicobacter spp.-infected BALB/cJ mice displayed statistically significant increases in cholesterol gallstone prevalence compared with uninfected mice (81% vs. 39%; P < .05). Transfer of splenocytes or T lymphocytes to Rag2(-/-) mice increased stone prevalence markedly (26% and 40% respectively; P < .05), whereas transfer of B cells was not appreciably cholelithogenic (13%). The adaptive immune response increased the expression of gallbladder Muc genes and accumulation of mucin gel. In addition, T cells and cholesterol monohydrate crystals induced proinflammatory gene expression in the gallbladder, which likely contributes to gallbladder dysfunction. These studies indicate that T cells are critical in murine cholesterol cholelithogenesis. Furthermore, cholesterol monohydrate crystals induce expression of proinflammatory cytokines in a T-cell-dependent fashion. Acquired immunity and inflammation are likely to be crucial factors in cholesterol gallstone pathogenesis, rather then merely the result of cholelithogenesis.

Gastric Outlet Obstruction due to an Iatrogenic Cause in a Neonatal Period – Report of Two Cases

Gastric mucosa hyperplasia is a rare cause of upper gastrointestinal obstruction in the neonatal period. One of the etiologic factors of this disorder is prolonged prostaglandin E1 (PGE1) therapy of neonates with congenital cyanotic heart diseases. Continuous PGE1 administration ensures patency of the ductus arteriosus, which is essential for stabilizing the general condition until cardiac surgery can be performed. The clinical symptoms of gastric mucosa foveolar hyperplasia due to long-term PGE1 therapy simulate hypertrophic pyloric stenosis. However, the characteristic ultrasound appearance of both pathologies facilitates determination of the final diagnosis and further treatment. We present two cases of neonates with gastric mucosa and submucosa hyperplasia revealed during ultrasound examination. The results of the ultrasound examination combined with clinical anamnesis allowed diagnosis of gastric mucosa foveolar hyperplasia due to prolonged PGE1 therapy.

Gallbladder disease in Shetland Sheepdogs: 38 cases (1995–2005)

To determine risk, clinical features, and treatment responses for gallbladder disorders in Shetland Sheepdogs. Retrospective case-control study. 38 Shetland Sheepdogs with gallbladder disease. Medical records were reviewed for signalment, history, physical findings, laboratory results, imaging features, coexistent illnesses, histologic findings, treatments, and survival rates. Mature dogs with gastrointestinal signs were predisposed (odds ratio, 7.2) to gallbladder disorders. Gallbladder mucocele was confirmed in 25 dogs. Concurrent problems included pancreatitis, hyperlipidemia, corticosteroid excess, hypothyroidism, protein-losing nephropathy, diabetes mellitus, cholelithiasis, and gallbladder dysmotility. Mortality rate was 68% with and 32% without bile peritonitis. Nonsurvivors had high WBC and neutrophil count and low potassium concentration. Although preprandial hypercholesterolemia, hypertriglyceridemia, and high serum liver enzyme activities were common, gallbladder disease was serendipitously discovered in 11 of 38 dogs. Histologic examination (n=20 dogs) revealed gallbladder cystic mucosal hyperplasia in 20 dogs, cholecystitis in 16, periportal hepatitis in 9, and vacuolar hepatopathy in 7. Surgery included cholecystectomy (n=17) and cholecystoenterostomy (4). In 1 hyperlipidemic dog without clinical signs, gallbladder mucocele resolved 6 months after beginning use of a fat-restricted diet and ursodeoxycholic acid. Shetland Sheepdogs are predisposed to gallbladder disorders, with mucoceles and concurrent dyslipidemia or dysmotility in many affected dogs. Most dogs were without clinical signs during mucocele development. Low survival rate after cholecystectomy in clinically affected dogs suggested that preemptive surgical interventions may be a more appropriate treatment strategy.

Rodent Carcinogenicity Profile of the Antidiabetic Dual PPAR α and γ Agonist Muraglitazar

The carcinogenic potential of muraglitazar, a dual human peroxisome proliferator-activated receptor alpha/gamma agonist, was evaluated in 2-year studies in mice (1, 5, 20, and 40 mg/kg) and rats (1, 5, 30, and 50 mg/kg). Benign gallbladder adenomas occurred at low incidences in male mice at 20 and 40 mg/kg (area under the curve [AUC] exposures > or = 62 times human exposure at 5 mg/day) and were considered drug related due to an increased incidence of gallbladder mucosal hyperplasia at these doses. There was a dose-related increased incidence of transitional cell papilloma and carcinoma of the urinary bladder in male rats at 5, 30, and 50 mg/kg (AUC exposures > or = 8 times human exposure at 5 mg/day). At 30 and 50 mg/kg, the urinary bladder tumors were accompanied by evidence of increased urine solids. Subsequent investigative studies established that the urinary bladder carcinogenic effect was mediated by urolithiasis rather than a direct pharmacologic effect on urothelium. Incidences of subcutaneous liposarcoma in male rats and subcutaneous lipoma in female rats were increased at 50 mg/kg (AUC exposures > or = 48 times human exposure at 5 mg/day) and attributed, in part, to persistent pharmacologic stimulation of preadipocytes. Toxicologically relevant nonneoplastic changes in target tissues included thinning of cortical bone in mice and hyperplastic and metaplastic adipocyte changes in mice and rats. Considering that muraglitazar is nongenotoxic, the observed tumorigenic effects in mice and rats have no established clinical relevance since they occurred at either clinically nonrelevant exposures (gallbladder and adipose tumors) or by a species-specific mechanism (urinary bladder tumors).

Jun N-Terminal Protein Kinase Enhances Middle Ear Mucosal Proliferation during Bacterial Otitis Media

Mucosal hyperplasia is a characteristic component of otitis media. The present study investigated the participation of signaling via the Jun N-terminal protein kinase (JNK) mitogen-activated protein kinase in middle ear mucosal hyperplasia in animal models of bacterial otitis media. Otitis media was induced by the inoculation of nontypeable Haemophilus influenzae into the middle ear cavity. Western blotting revealed that phosphorylation of JNK isoforms in the middle ear mucosa preceded but paralleled mucosal hyperplasia in this in vivo rat model. Nuclear JNK phosphorylation was observed in many cells of both the mucosal epithelium and stroma by immunohistochemistry. In an in vitro model of primary rat middle ear mucosal explants, bacterially induced mucosal growth was blocked by the Rac/Cdc42 inhibitor Clostridium difficile toxin B, the mixed-lineage kinase inhibitor CEP11004, and the JNK inhibitor SP600125. Finally, the JNK inhibitor SP600125 significantly inhibited mucosal hyperplasia during in vivo bacterial otitis media in guinea pigs. Inhibition of JNK in vivo resulted in a diminished proliferative response, as shown by a local decrease in proliferating cell nuclear antigen protein expression by immunohistochemistry. We conclude that activation of JNK is a critical pathway for bacterially induced mucosal hyperplasia during otitis media, influencing tissue proliferation.

Alterations in the Brain–Gut Axis Underlying Visceral Chemosensitivity in Nippostrongylus brasiliensis-Infected Mice

Visceral hypersensitivity, a hallmark of irritable bowel syndrome, is generally considered to be mechanosensitive in nature and mediated via spinal afferents. Both stress and inflammation are implicated in visceral hypersensitivity, but the underlying molecular mechanisms of visceral hypersensitivity are unknown. Mice were infected with Nippostrongylus brasiliensis (Nb) larvae, exposed to environmental stress and the following separate studies performed 3-4 weeks later. Mesenteric afferent nerve activity was recorded in response to either ramp balloon distention (60 mm Hg), or to an intraluminal perfusion of hydrochloric acid (50 mmol/L), or to octreotide administration (2 micromol/L). Intraperitoneal injection of cholera toxin B-488 identified neurons projecting to the abdominal viscera. Fluorescent neurons in dorsal root and nodose ganglia were isolated using laser-capture microdissection. RNA was hybridized to Affymetrix Mouse whole genome arrays for analysis to evaluate the effects of stress and infection. In mice previously infected with Nb, there was no change in intestinal afferent mechanosensitivity, but there was an increase in chemosensitive responses to intraluminal hydrochloric acid when compared with control animals. Gene expression profiles in vagal but not spinal visceral sensory neurons were significantly altered in stressed Nb-infected mice. Decreased afferent responses to somatostatin receptor 2 stimulation correlated with lower expression of vagal somatostatin receptor 2 in stressed Nb-infected mice, confirming a link between molecular data and functional sequelae. Alterations in the intestinal brain-gut axis, in chemosensitivity but not mechanosensitivity, and through vagal rather than spinal pathways, are implicated in stress-induced postinflammatory visceral hypersensitivity.

Wideoendoskopowa ocena funkcji gardłowego ujścia trąbki słuchowej u dzieci z chorobami ucha środkowego

Eustachian tube (ET) dysfunction play an important role in the development, persistence and recurrence of otitis media with effusion (OME) and chronic otitis. Evaluation of the type of obstruction in the cartilaginous portion of ET is important for decision concerning methods of treatment and prognosis of surgical outcome. The aim of this study was to identify characteristics of dynamic function of the pharyngeal orifice of ET in children with OME and chronic otitis by video endoscopy. Transnasal endoscopic examination of the nasopharyngeal opening of ET during swallowing was performed on 21 children - 13 with OME, 8 with chronic otitis. Video recording were made for dynamic slow-motion analysis of ET dilation and closing processes. Most cases of ET dysfunction in children were obstrucive (81%), associated with mucosal oedema and hyperplasia. Dynamic type of dysfunction is caused by the reduced movement of the tensor veli palatini. Dynamic video analysis is useful in the identify type of ET dysfunction in children. Obstructive dysfuntion need diagnostic procedures for chronic infection, nasopharyngeal reflux and alergic diseases.

Citrobacter rodentiuminfection causes iNOS-independent intestinal epithelial dysfunction in mice

Attaching-effacing bacteria are major causes of infectious diarrhea in humans worldwide. Citrobacter rodentium is an attaching-effacing enteric pathogen that causes transmissible murine colonic mucosal hyperplasia. We characterized colonic inflammation and ion transport at 3, 7, 10, 30, and 60 d after infection of C57Bl/6 mice with C. rodentium. Macroscopic damage score was significantly increased 7 and 10 d after infection. Colonic wall thickness was increased at 7, 10, 30, and 60 d. Myeloperoxidase (MPO) activity was significantly increased at 3, 7, and 10 d and returned to control levels by days 30 and 60. The expressions of inducible nitric oxide synthase and cyclooxygenase-2 were increased by C. rodentium infection. Significant reductions in the epithelial secretory response to carbachol, but not to electrical field stimulation or forskolin, were observed at 3 and 10 d of infection. Translocation of enteric bacteria into the mesenteric lymph nodes was observed 10 d following infection. There was no difference in response to infection between animals deficient in inducible nitric oxide synthase and wild-type controls. The COX-2 inhibitor rofecoxib caused decreased wall thickness and MPO activity at day 10. However, COX-2 inhibition did not alter infection-induced changes in ion transport. Citrobacter rodentium infection causes colonic inflammation, mucosal hyperplasia, and nitric-oxide-independent epithelial dysfunction in association with increased permeability to luminal bacteria.

Covered Retrievable Prostatic Urethral Stents: Feasibility Study in a Canine Model

To evaluate the feasibility of use of a covered, retrievable prostatic urethral stent and to determine urethrographic and histologic changes in the prostate induced by the stent in a canine model. Polytetrafluoroethylene-covered retrievable nitinol stents were placed in the normal prostatic urethras of 13 dogs. The stents were removed 8 weeks after placement. The dogs were killed immediately after stent removal (group 1, n = 5) or 8 weeks after stent removal (group 2, n = 8). Retrograde urethrograms were obtained every 2 weeks after stent placement and after stent removal in dogs that had not been killed. The histologic changes in the prostate were compared between the two groups. Stent placement was technically successful in all dogs. In two dogs, a second stent was placed because of migration of the first stent into the urinary bladder. Stent removal was successful in 12 dogs. One stent was removed in its expanded state. On follow-up urethrograms, dilation of the prostatic urethra persisted until animals were killed (P = .14). The mucosal hyperplasia that occurred after stent placement at both ends of the stent gradually decreased after stent removal (P < .001). Histologic examination revealed prostate glandular atrophy and periurethral fibrosis, which did not differ between the two groups (P = .72 and P = .83, respectively). Papillary hyperplasia of the uroepithelium and submucosal inflammatory cell infiltration was decreased significantly in group 2 compared with group 1 (P = .002, P = .011, respectively). Covered retrievable prostatic urethral stents seem to be feasible for use in the canine prostatic urethra. The stent-induced prostatic urethral dilation and prostate glandular atrophy persist until 8 weeks after stent removal.

CONTACT ENDOSCOPY DURING CHOLECYSTECTOMY:A NEW TECHNIQUE FOR STAGING LAPAROSCOPY IN GALLBLADDER CANCERS

Background and study aims: Contact endoscopy is a technique allowing detailed magnified imaging of living epithelium, used extensively to assess tissues of gynecological and laryngeal origan. We used this technique during cholecystectomy to investigate its potential value for staging laparoscopy in gallbladder cancer. Patients and methods: Eight patients with gallbladder cancer, four with mucosal hyperplasia, two with benign polyps and nine with gallstones were evaluated. During surgery, the lens of the contact endoscope (8715AA, 5.5 mm in diameter with a 0° angle) was placed in contact with the serosa of the gallbladder and observations were performed at magnifications of 60 × and 150 ×. Results: Enlarged color images of the subserosal layer of the gallbladder were obtained. In normal mucosa, a fine vascular network with flowing erythrocytes was observed in the subserosal layer. Subserosal fat appeared as tortoiseshell-like markings, shown histologically to be clumps of fat cells surrounded by fine fibrous tissue. A gap between the deep vessels and the superficial vessels in the subserosal fat was also observed. The same findings were detected in gallbladder cancer patients where invasion was limited to the muscular layer. However, in patients with advanced gallbladder cancer, with invasion beyond the muscular layer, both the vessel gap and the fat tissue markings were absent. There was also encasement of the vessels and decreased intravascular flow of erythrocytes. Conclusions: The contact endoscope can be useful in differentiating between early and advanced gallbladder cancer and has some potential for use in staging laparoscopy for gallbladder cancer.

Targeting mast cells in the treatment of functional gastrointestinal disorders

Enhanced knowledge of the pathophysiological basis of functional gastrointestinal disorders indicates that low-grade mucosal inflammation and mast cell hyperplasia are common findings. Mast cells are multipotent and mucosa-dwelling residents are uniquely located to communicate with host immune and nervous supersystems and with the gut microflora to provide tight microenvironmental conditions. Maintenance of homeostasis within this integrated defense system is crucial for symbiotic health, whereas breakdown of that balance might lead to uncontrolled mucosal and systemic inflammation. Numerous advances have recently emerged in the understanding of regulatory mechanisms of mast cell activation, development and homing to mucosal surfaces, as well as of the role of mast cells in key steps of mucosal inflammation. Such observations have stimulated the development of candidate drugs, such as tryptase or Syk inhibitors, that might be useful for the treatment of gastrointestinal functional disorders.

A repeated 28-day oral dose toxicity study of nonylphenol in rats, based on the ‘Enhanced OECD Test Guideline 407’ for screening of endocrine-disrupting chemicals

A 28-day repeated oral dose toxicity study of nonylphenol (NP) was performed for an international validation of the 'Enhanced OECD Test Guideline 407' paying particular attention to the sensitivity of individual endocrine-related parameters. Sprague-Dawley rats, each group consisting of ten males and ten females, were administered NP once daily by gavage at doses of 0 (control), 10, 50, or 250 mg/kg body weight. At 250 mg/kg, three females died or became moribund during the experiment. At this dose, hepatic and renal toxicity was evident in both sexes with increase of relative liver and kidney weights as well as histopathological changes, such as centrilobular liver cell hypertrophy and a variety of renal tubular lesions, and alteration of serum biochemical parameters, some of them being evident from 50 mg/kg in females (glucose and inorganic phosphates). Hematologically, development of anemia was evident at 250 mg/kg in both sexes. Regarding endocrine-related effects, increase of thyroid weight in males was detected from 50 mg/kg. At 250 mg/kg, males exhibited reduction of relative weights of the ventral prostate and seminal vesicles, and females developed irregular estrous cyclicity and vaginal mucosal hyperplasia. Although changes in serum hormone levels were detected in both sexes, magnitude of the changes was small to be regarded as a low toxicological significance. In summary, repeated oral doses of NP to rats for 28 days resulted in hepato-renal toxicity from 50 mg/kg and anemia at 250 mg/kg. Effects on the endocrine system were observed from 50 mg/kg, and assessment of weights and histopathology of endocrine-related organs and estrous cyclicity may be valid in a battery for detecting endocrine effects of NP. The no-observed-adverse-effect level of NP was estimated to be 10 mg/kg per day.

Strobilocercus fasciolaris infection with hepatic sarcoma and gastroenteropathy in a Wistar colony

Tapeworm cysts were identified in liver of Wistar rats and it induced fibrosarcoma in liver and gastroenteropathy in stomach and intestine. The tapeworm larva was confirmed as Strobilocercus fasciolaris by PCR linked mitochondrial DNA sequencing. Light microscopy, special staining (masson trichrome) and immunoflouresence supported the diagnosis of fibrosarcoma. Infiltration of plasma cells, macrophages and eosinophils were observed in the liver section. Gastric mucosal hyperplasia, dilation of gastric glands with secretion, intestinal mucosal cell hyperplasia, proliferation of duodenal submucosal glands were confirmed by light microscopy and supported by PAS, AB staining. The concomitant development of hepatic sarcoma and gastroenteropathy by larvae of Taenia taeniaeformis ( S. fasciolaris) infection is very rare and is the first reported case in Wistar rats to our knowledge.

The Value of Myenteric Plexitis to Predict Early Postoperative Crohn’s Disease Recurrence

Early ileocolonoscopy allows detection of recurrence after surgically induced remission of Crohn's disease (CD). Unequivocal histologic markers predicting recurrence have not been identified. We assessed the predictive value of neural lesions for early endoscopic CD recurrence and long-term reintervention risk. Ileocolonic resection specimens from 59 patients with CD and 21 control patients were histologically scored for typical inflammatory bowel disease lesions, neural hypertrophy, and presence and severity of inflamed ganglia and nerve bundles. Endoscopic recurrence was determined at 3 months in all patients and at 1 year in 32 patients as part of 2 prospective clinical trials. Myenteric plexitis of the proximal resection margin was present in 32 patients with CD (54%) in absence of surrounding inflammation. Patients with this feature had a higher endoscopic recurrence (Rutgeerts score >/=2) at 3 months (75% vs 41%; odds ratio, 4.36; 95% confidence interval, 1.44-13.23; P = .008) and at 1 year (93% vs 59%; odds ratio, 9.80; 95% confidence interval, 1.04-92.70; P = .041) and had a trend toward an earlier reintervention (mean, 7.00 vs 5.30 years; P = .174). The severity of myenteric plexitis in the proximal resection margin correlated with the severity of endoscopic recurrence at 3 months (r = 0.334, P = .010) and 1 year (r = 0.560, P = .001). Myenteric plexitis was the only consistent predictor of endoscopic recurrence. The presence of myenteric plexitis in proximal margins of ileocolonic resection specimens is predictive of early endoscopic CD recurrence.

Short bowel syndrome and intestinal transplantation in children

This review summarizes recent knowledge and clinical practice for pediatric patients suffering extensive intestinal resection causing short bowel syndrome. This condition requires the use of parenteral nutrition, as long as intestinal failure persists, and may be, in some selected cases, an indication for intestinal transplantation. Biological evaluation of intestinal failure is becoming possible with the use of plasma citrulline as a marker of intestinal mass. Few epidemiological data are available; some indicate an increased incidence of short bowel syndrome-related gastroschisis and persistent high incidence of necrotizing enterocolitis. Morbidity and mortality data in pediatric patients with short bowel syndrome are limited, while long-term outcome is better documented from recently reported cohorts. Non-transplant surgery is one of the best options for patients with unadapted short bowel syndrome. Isolated liver transplantation may be avoided. The use of trophic factors for enhancing mucosal hyperplasia still remains disappointing. The management should include therapies adapted to each stage of intestinal failure, based on a multidisciplinary approach in centers involving pediatric surgery, pediatric gastroenterology, parenteral nutrition expertise, home-parenteral nutrition program, and liver-intestinal transplantation experience. If managed appropriately, the prognosis of short bowel syndrome is excellent, with limited indications for intestinal and/or liver transplantation. Timing for patient referral in specialized centers remains an issue.

Cytokeratin‐20 and seminal vesicle secretory protein VI as possible marker proteins in urinary bladder preneoplastic lesions induced by N‐butyl‐N‐(4‐hydroxybutyl) nitrosamine

A simple and non-invasive methods for the diagnosis of transitional cell carcinoma of the bladder are needed for the prevention of invasive tumor. A proteomic technology has recently been developed to facilitate protein profiling of biological mixtures. We tried to detect the marker proteins by proteomic approach during the initiation stages on N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN)-induced bladder carcinogenesis in rats. Ten rats in group A were given 0.05% BBN in drinking water for 12 weeks. Other 10 rats in group B with 10 rats were designated as a control group and were not given BBN. Whole urinary bladders of all rats were excised at 12 weeks from the beginning of the experiment. Conventional proteomics was performed with high resolution 2-dimension gel electrophoresis followed by computational image analysis and protein identification using mass spectrometry. A comparison of urinary bladder hyperplasia tissue with control tissue showed that five proteins; actin gamma2 propeptide, cytokeratin-20 (CK-20), proapolipoprotein, alpha2 actin (alpha-cardiac actin) and heat shock 27 kDa protein-1 were over-expressed in hyperplastic tissues. Three proteins; transcription factor myocardin, seminal vesicle secretory protein VI (SVS-VI) precursor and hypothetical protein RMT-7 were under-expressed in hyperplastic tissues. In our animal mode, BBN-induced urinary bladder mucosal hyperplasia resulted in an increase in the expression of five proteins and a decrease in the expression of three proteins. Of these, CK-20 and SVS-VI seem to be of particular interest. However other method such as Western blotting seems to be needed for confirmation of these proteins and more information on human bladder tissue is needed for clinical application.

Mucinous cystadenoma of the appendix associated with adenocarcinoma of the sigmoid colon and hepatocellular carcinoma of the liver: Report of a case

Mucinous cystadenoma of the appendix is a rare condition and represents one of the three entities with the common name mucocele of the appendix. It is characterized by a cystic dilatation of the lumen with stasis of mucus inside it. Histopathologically mucocele is divided into three groups: focal or diffuse mucosal hyperplasia, mucinous cystadenoma and mucinous cystadenocarcinoma. This condition is often associated with other neoplasia, especially adenocarcinoma of the colon and ovaries. We here describe a 57 year old male patient who presented with abdominal discomfort, constipation, fresh blood in stool and frequent urination. He had a big cystadenoma of the appendix associated with adenocarcinoma of the colon and hepatocellular carcinoma of the liver. The patient underwent right haemicolectomy, sigmoid colon resection and segmental resection of the liver. Now 3 years later he has no evidence of disease relapse. According to this, we stress the need of accurate preoperative diagnosis and intraoperative exploration of the whole abdomen in these patients.

Estrogen receptor expression in anomalous arrangement of the pancreaticobiliary duct

Background/Purpose Anomalous arrangement of the pancreaticobiliary duct (AAPBD) is a malformation of the bile and pancreatic ducts which is commonly associated with congenital biliary dilatation and predominantly occurs in girls. Estrogen receptor (ER) is reported to modulate cholangiocyte proliferation and play a role in tumorigenesis of estrogen-dependent malignancies. The present study investigated the presence of ER in the gallbladder of patients with AAPBD to elucidate whether ER expression is correlated with sexual specificity and biliary histology. Methods Specimens comprised samples of 29 gallbladders from patients with AAPBD (21 girls and 8 boys; mean age at surgery, 5.3 years). Medical records were retrospectively reviewed, and sex, age, radiographic parameters, and laboratory data were collected for this study. Immunohistochemistry was performed using anti-ER and anti–MIB-1 antibodies, and MIB-1 score was calculated for evaluation of cell proliferation. Results ER expression was observed in both the nuclei and cytoplasm of gallbladder epithelium in 12 of 29 specimens. No difference in background characteristics were noted between ER-positive and ER-negative groups. Mucosal hyperplasia was found in 17 specimens. ER-positive cases were significantly more common in AAPBD with mucosal hyperplasia than without ( P <0.03). MIB-1 score did not differ significantly between ER-positive and ER-negative groups. Conclusions ER expression seems to be related to hyperplastic mucosa of the gallbladder in AAPBD. ER might play a role in the proliferation of gallbladder epithelium.

ACUTE GASTRIC OUTLET OBSTRUCTION DUE TO AN IATROGENIC CAUSE

Methods and Materials: Mucosa hyperplasia is an uncommon cause of gastric outlet obstruction in neonatal period. The main etiologic factor of this disorder is long-term prostaglandin E1 (PGE1) infusion. PGE1 administration is used to maintain the patency of the ductus arteriosus in neonates with ductal-dependent cyanotic congenital heart diseases. The treatment although life saving is limited with possible side effects. The pathophysiology of prostaglandin induced gastric mucosa hyperplasia is based on delayed senescence and exfoliation of foveolar cells. Supposition of this disorder is possible on the basis of some clinical features, results of chest radiographs, contrast gastrointestinal imaging or ultrasound examination. We present two cases of neonates with tetralogy of Fallot, pulmonary trunk hypoplasia and PDA hospitalised in Pediatric Cardiology Departament of Medical University in Gdansk, for who prostaglandin E1 therapy was started on the second day of life. After around 3–3,5 weeks of these treatment clinical features of acute gastric outlet obstruction were noticed. Therefore ultrasound examination was carried out using Unit GE Logiq 500, with microconvex transducer 3–7MHz and linear transducer 8,2–11,0MHz.