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PubMed2004

[Cloning and expression of the endo-beta-glucanase III cDNA gene from Trichoderma viride AS3.3711].

To study the construction of yeast bioengineering strain which can degrade cellulosic waste, an endo-beta-glucanase III (EG III) cDNA gene of Trichoderma viride AS3.3711 was isolated with RT-PCR protocol. After sequencing it was constructed on S. cerevisiae induceable expression vector pYES2. A L9 (3(4)) orthogonal design was used to optimize yeast sonication assistant transformation. The expression of EG III gene was induced by 2% beta-D-glactose, the transcription and expression of it was detected by Northern blotting and Congo Red method respectively. The endo-beta-glucanase activity was assayed as CMCase activity with CMC-Na as a substrate. The results show that the ORF of EG III was 1254 bp, encoding 418 aa, deducing molecular weight 44.1 x 10(3), group 5 (sonication treat time 60 s, incubate 40 min, SS-DNA 150 microg, heat shock 5 min) was the optimum one of the orthogonal experiment, and EG III transformants can produced clear hydrolysis halos on the Congo-Red-CMC plate. The measure of the enzyme activity show that the expression product can be expressed in active forms and secreted to the medium. The enzyme activity was approached the highest level (0.041 U/mL) when the culture time was 60 h. The optimized enzyme reaction temperature was 50 degrees C and the optimized pH was 5.8.

Cloning, Molecular↗
PubMed1993

Thin, aggregative fimbriae mediate binding of Salmonella enteritidis to fibronectin.

The binding of human fibronectin and Congo red by an autoaggregative Salmonella enteritidis strain was found to be dependent on its ability to produce thin, aggregative fimbriae, named SEF 17 (for Salmonella enteritidis fimbriae with an apparent fimbrin molecular mass of 17 kDa). Two other fimbrial types produced by S. enteritidis, SEF 14 and SEF 21, were not responsible for the aggregative phenotype or for fibronectin binding. SEF 17-negative TnphoA mutants which retained the ability to produce SEF 14 and SEF 21 were unable to bind human fibronectin or Congo red and lost the ability to autoaggregate. Only purified SEF 17 but not purified SEF 14 or SEF 21 bound fibronectin in a solid-phase binding assay. Furthermore, only SEF 17 was able to inhibit fibronectin binding to S. enteritidis whole cells in a direct competition enzyme-linked immunosorbent assay. These results indicate that SEF 17 are the fimbriae responsible for binding fibronectin by this enteropathogen.

Alkaline Phosphatase↗
PubMed1987

Protection of foals against experimental Rhodococcus equi pneumonia by oral immunization.

Two groups of three one to three week old foals were immunized orally on four occasions over five weeks with two strains of Rhodococcus equi, a clinical isolate from a pneumonic foal and a laboratory passaged Congo red negative variant of this strain. Three nonimmunized foals of similar age acted as controls. Three weeks after the last immunization, all foals were challenged on five occasions over seven days by aerosol infection with about 10(10) of the pneumonic foal isolate on each occasion. Control foals became seriously ill and were euthanized. Immunization with either strain protected foals equally against the challenge, and resulted in rapid lung clearance. Oral immunization can thus protect foals against severe challenge with R. equi. The proteins associated with Congo red colony staining appear not to be involved in protective immunity.

Actinomycetales Infections↗
PubMed1990

Monoclonal immunoglobulin deposition disease: light chain and light and heavy chain deposition diseases and their relation to light chain amyloidosis. Clinical features, immunopathology, and molecular analysis.

Monoclonal immunoglobulin deposition occurs in tissues as Congo Red binding fibrils in light chain amyloidosis, as less structured deposits in light chain deposition disease, and as similar but distinct deposits in light and heavy chain deposition disease. The nonamyloid forms were found in 13 patients who had evidence of plasmacytic dyscrasia by the immunohistochemical detection of immunoglobulin light chains of kappa or lambda class (with or without staining for a single heavy chain isotype) and by the absence of amyloid P component in tissue sections that did not show the birefringence characteristic of amyloid after Congo Red staining. All but two of the patients presented with proteinuria with or without azotemia. Clinical syndromes involving other organ systems were less common but occasionally severe. Four patients had overt multiple myeloma. Three others had hypercalcemia and mild bone marrow plasmacytosis but no lytic lesions. Analyses of immunoglobulin synthesis in bone marrow cells from seven patients showed excess light chains in all and incomplete light chains or heavy chain fragments in six, regardless of whether an intact monoclonal protein or related subunit was in the serum or urine. The fibrillar (amyloidotic) and nonfibrillar forms of monoclonal immunoglobulin deposition occur either in overt multiple myeloma or in the course of less neoplastically aggressive plasmacytic dyscrasias. Bone marrow cells from patients with either type produce immunoglobulin fragments that are related to those deposited in the affected tissues.

Adult↗
PubMed1993

Is gastric metaplasia essential for duodenal ulcer?

Multiple biopsies were taken from the duodenum of 100 patients (46 active duodenal ulcer, 14 healed duodenal ulcer, 40 control subjects) to detect duodenitis, gastric metaplasia and Helicobacter pylori (Hp). Histamine-induced congo-red staining of the duodenal bulb was performed in additional 25 cases of active duodenal ulcer to determine the presence of functioning parietal cells in the duodenum. The incidence of duodenitis was 45% in control subjects and 76.7% in patients with duodenal ulcer (active or healed) (p < 0.01). Superficial gastric metaplasia was present in 2.5% of control subjects and 13.3% patients with duodenal ulcer (active or healed) (p > 0.05). Hp in the duodenum was detected in 10% of control subjects and 8.3% of patients with duodenal ulcer. Congo-red test was positive in two of 25 (8%) patients of active duodenal ulcer indicating "functioning" parietal cells in the duodenum. In Indian patients with duodenal ulcer, a low incidence of gastric metaplasia and Hp in the duodenum is observed in contrast to its high incidence in patients from Western countries.

Adult↗
PubMed2006

Alzheimer-like plaque formation by human macrophages is reduced by fibrillation inhibitors and lovastatin.

The cerebral deposition of Abeta-peptide as amyloid fibrils and plaques represents a hallmark characteristic of Alzheimer's disease (AD). AD plaques are defined by their green birefringence after Congo red staining, their spherulite-like superstructure and their association with specific secondary components. Here we show that primary human macrophages promote the formation of amyloid plaques that correspond in all aforementioned characteristics to typical amyloid plaques from diseased tissues: they consist of aggregated Abeta-peptide, they reveal the typical ''Maltese cross" structure and they are associated with the secondary components glycosaminoglycanes, apolipoprotein E (apoE) and the raft lipids cholesterol and sphingomyelin. Plaque formation can be impaired in this cell system by addition of small molecules, such as Congo red, melantonine and lovastatin, suggesting potential applications for the study of cellular amyloid formation and for the identification or validation of drug candidates.

Alzheimer Disease↗
PubMed2000

A beta and perlecan in rat brain: glial activation, gradual clearance and limited neurotoxicity.

A beta1-40 and perlecan (A beta + perlecan) were infused into rat hippocampus for 1 week via osmotic pumps. At the end of the infusion a deposit of A beta immunoreactive material was found surrounding the infusion site. No neurons could be identified within this A beta deposit. The neuron-free area resulting from A beta + perlecan was significantly larger than that found after infusions of A beta40-1 and perlecan (reverse A beta + perlecan), perlecan alone or phosphate-buffered saline vehicle. Following infusion of A beta + perlecan, the glial cells segregated in a manner similar to that associated with compacted amyloid plaques in Alzheimer's disease (AD). Activated microglia/macrophages were prevalent within the A beta deposit while the perimeter of the deposit was delimited by reactive astrocytes. Thioflavin S and Congo red staining indicated a beta-pleated sheet conformation of the A beta deposits, implying formation of fibrils. Intact, apparently healthy neurons were found immediately adjacent to the A beta + perlecan deposit. In contrast, reverse A beta peptide did not form congophilic deposits despite the presence of perlecan. Apoptotic profiles visualized with bisbenzamide or TUNEL staining of fragmented DNA were not seen at any of the infusion sites, yet were readily seen in hippocampal sections from animals treated with kainic acid. At 8 weeks, A beta immunoreactivity, Thioflavin S and Congo red staining was reduced, indicating that A beta was being cleared. There also was no evidence of neuron loss by Nissl or TUNEL staining. The zone of apparent necrosis did not expand between 1 and 8 weeks, and in some instances appeared to contract. The consistency of the A beta + perlecan infusion method in producing reliable A beta amyloid deposits permits estimates of the rate at which fibrillar A beta amyloid can be removed from the brain, and may provide a useful model to study this process in vivo. However, the absence of clearly identifiable degenerating/dying neurons at the 1 or 8 week survival times suggests that either fibrillar A beta + perlecan slowly displaced the brain parenchyma during infusion, or neurons were killed very gradually during the process of clearing the A beta.

Amyloid beta-Peptides↗
PubMed2000

Amyloid myopathy masquerading as polymyositis.

OBJECTIVE: It is not well appreciated that the clinical presentation of amyloid myopathy can mimic that of polymyositis. By retrospective clinicopathologic analysis we determined distinctive features of amyloid myopathy that differentiate the 2 diseases. METHODS: Two patients with clinical and histologic evidence of an inflammatory myopathy had fatal outcomes despite appropriate treatment for polymyositis. Their clinical course and original pathologic specimens were reviewed. In addition, original tissue samples were obtained and analyzed using Congo red staining and immunoperoxidase. RESULTS: The initial diagnosis of polymyositis was supported in both cases by muscle biopsies showing inflammatory infiltrates and elevations of creatine phosphokinase and by classic electromyography. Retrospective evaluation of the initial muscle biopsies disclosed subtle but incontrovertible evidence of vascular amyloid. Further analysis of the original specimens confirmed the presence of immunoglobin light chain (AL) amyloid. CONCLUSION: Amyloid myopathy can mimic polymyositis. Both can have similar clinical symptoms, as well as inflammatory infiltrates on muscle biopsy. Failure to recognize amyloid myopathy deprives patients of potentially life prolonging treatment. Congo red staining and immunohistochemical analysis of tissue could prevent misdiagnosis.

Aged↗
PubMed1994

A gene at 59 minutes on the Escherichia coli chromosome encodes a lipoprotein with unusual amino acid repeat sequences.

We report a 1.432-kb DNA sequence at 59 min on the Escherichia coli chromosome that connects the published sequences of the pcm gene for the isoaspartyl protein methyltransferase and that of the katF or rpoS (katF/rpoS) gene for a sigma factor involved in stationary-phase gene expression. Analysis of the DNA sequence reveals an open reading frame potentially encoding a polypeptide of 379 amino acids. The polypeptide sequence includes a consensus bacterial lipidation sequence present at residues 23 to 26 (Leu-Ala-Gly-Cys), four octapeptide proline- and glutamine-rich repeats of consensus sequence QQPQIQPV, and four heptapeptide threonine- and serine-rich repeats of consensus sequence PTA(S,T)TTE. The deduced amino acid sequence, especially in the C-terminal region, is similar to that of the Haemophilus somnus LppB lipoprotein outer membrane antigen (40% overall sequence identity; 77% identity in last 95 residues). The LppB lipoprotein binds Congo red dye and has been proposed to be a virulence determinant in H. somnus. Utilizing a plasmid construct with the E. coli gene under the control of a phage T7 promoter, we demonstrate the lipidation of this gene product by the incorporation of [3H]palmitic acid into a 42-kDa polypeptide. We also show that treatment of E. coli cells with globomycin, an inhibitor of the lipoprotein signal peptidase, results in the accumulation of a 46-kDa precursor. We thus designate the protein NlpD (new lipoprotein D). E. coli cells overexpressing NlpD bind Congo red dye, suggesting a common function with the H. somnus LppB protein. Disruption of the chromosomal E. coli nlpD gene by insertional mutagenesis results in decreased stationary-phase survival after 7 days.

Amino Acid Sequence↗
PubMed1996

The premortem recognition of systemic senile amyloidosis with cardiac involvement.

PURPOSE: To recognize systemic senile amyloidosis involving the heart and to determine outcome. PATIENTS AND METHODS: All patients with the diagnosis of amyloidosis at the Mayo Clinic from January 1, 1984 through May 1, 1992, were reviewed. Amyloid was confirmed histologically by sulfated alcian blue and alkaline Congo red staining. The labeled streptavidin-biotin immunoperoxidase method was used with antisera against A kappa, A lambda, AA, transthyretin, and beta 2-microglobulin. Anti-P-component and antisera to albumin were used as controls. Chest radiographs, electrocardiograms, transthoracic echocardiograms, and cardiac catheterization data of all patients were reviewed. Serum and urine were examined with immunoelectrophoresis and immunofixation for the presence of a monoclonal protein. Lymphocyte DNA was examined for transthyretin mutations associated with familial amyloidosis. RESULTS: We identified 18 patients with myocardial tissue that stained positive for amyloid with sulfated alcian blue and Congo red and with transthyretin antisera. Congestive heart failure was present at diagnosis in 17 of the 18 patients. Atrial fibrillation was found in 11 patients. No monoclonal protein was found in the serum or urine. The echocardiographic findings were consistent with infiltrative cardiomyopathy due to amyloidosis in 16 patients. Right heart pressures were elevated in all 7 patients who had right-side heart catheterization. No transthyretin mutations were found in the leukocyte DNA from 12 patients. The actuarial median survival was 5 years; in contrast, the median survival was 5.4 months in 147 patients with primary amyloidosis (AL) who presented with congestive heart failure. CONCLUSION: Patients with cardiac amyloid and no monoclonal protein in the serum or urine must have immunohistochemical staining for kappa and lambda light chains and transthyretin to distinguish between systemic senile amyloidosis, familial amyloidosis, and AL. Patients with systemic senile amyloidosis should not be treated with alkylating agents. Their survival is much longer than that of patients with AL (60 versus 5.4 months).

Age Factors↗
PubMed1991

Long-term effect of vagotomy on gastric mucosa and Helicobacter pylori in duodenal ulcer patients.

The purpose of the study was to evaluate the long-term effects of vagotomy on the morphological status and Helicobacter pylori infestation of the gastric mucosa. Endoscopy with biopsies (2 from antrum and 2 from corpus) was performed in 317 patients on whom vagotomy had been performed on an average 8 years earlier. The success of the vagotomy was estimated by the endoscopic Congo Red technique in 270 cases. Non-operated 187 duodenal ulcer patients were examined endoscopically and bioptically in a similar way and used as a reference series. Helicobacter pylori (HP) was determined by Giemsa staining of biopsy specimens in both series. In non-operated dudoenal ulcer patients, gastritis and HP behaved as expected from the data in literature: antral gastritis was present in nearly all cases (96%), while the corpus mucosa was normal or the process was retarded at the stage of superficial gastritis (76%) and atrophic changes were virtually lacking (1%). On the basis of the Congo Red test the vagotomized patients were separated into two groups: successfully operated, i.e., complete vagotomy, and incomplete vagotomy groups. The results of the examinations were independent of the kind of vagotomy performed, but related significantly to its completeness. The incomplete and complete groups differed significantly. The prevalence of atrophic changes (29%) in the corpus was significantly higher and that of superficial gastritis (69%) lower in the complete than in the incomplete vagotomy group, in which the prevalences were 12% and 85%, respectively. Likewise the prevalence and density of HP was lower in the complete vagotomy group but the difference was not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Duodenal Ulcer↗
PubMed2005

Formation of experimental murine AA amyloid fibrils in SAP-deficient mice: high resolution ultrastructural study.

Previously, the role of the serum amyloid P component (SAP) in the deposition of murine AA amyloid has been examined in SAP-deficient mice in which the deposition was significantly retarded. In this study, AA amyloid fibrillogenesis in SAP-deficient mice was examined ultrastructurally. The fibrils of wild type mice were made up of a microfibril-like main body composed of SAP, chondroitin sulfate proteoglycan (CSPG), and outermost heparan sulfate proteoglycan (HSPG), and associated on its surface were 3 nm wide AA protein 'helical rods', a possible suitable form for Congo red staining. In SAP-deficient mice, fibrils of a similar appearance were also noted among an overwhelming amount of amorphous material, but the AP-containing main body of the fibril was replaced by elongated irregular aggregates of CSPG. The mechanism of retardation of AA amyloid induction in SAP-deficient mice has not yet been clear. It may be caused by possible slower formation of a 'substitute' core. Also, slower formation of AA helical rods may be possible due to the difference in the core material to which AA protein is attached. If it is so, it may limit the extent of Congo red staining, resulting in underestimation of the actual amount of AA protein.

Amyloid↗
PubMed1999

[Pseudotumoral adenopathies, an unusual means of detecting systemic amyloidosis].

INTRODUCTION: It is uncommon that lymph node enlargement is diagnostic of systemic amyloidosis as found in the case reported in this study. EXEGESIS: This study examined the case of a 49-year old male with chronic bronchitis in whom in 1990 the presence had been detected of an isolated cervical lymphadenopathy, 2 cm in diameter, and which had previously remained unnoticed. In 1993, a significant number of other peripheral adenopathies also appeared in various locations, i.e., cervical, axillary, inguinal. Chest and abdominal CT-scans revealed several mediastinal and abdominal lymphadenopathies. The histological study with Congo red stain of a cervical lymph node biopsy determined the diagnosis of amyloidosis. The patient was at that time asymptomatic. In September 1997, upon physical examination the following were found: lower limb edema, superior vena cava syndrome, and several cervical lymphadenopathies. Abdominal ultrasonography showed enlarged kidneys, and homogeneous splenomegaly. Biological examination determined the existence of a nephrotic syndrome with renal failure and creatinemia of 350 mumol/L. Due to superior vena cava syndrome worsening, cervical lymph node removal was performed. However, the patient died after rapid renal failure. CONCLUSION: Although it is a rare occurrence, amyloidosis should be taken into consideration in the differential diagnosis of isolated lymphadenopathy. Congo red stain amongst others, and an immunohistochemical study should be performed in cases of uncertain diagnosis.

Amyloidosis↗
PubMed2006

Screening of different adjuvants for wastewater/wastewater sludge-based Bacillus thuringiensis formulations.

Screening of different adjuvants, namely, suspending agents, phagostimulants, stickers, antimicrobial agents, and UV screens to develop aqueous biopesticidal suspensions of Bacillus thuringiensis (Bt) variety kurstaki HD-1 fermented broths, specifically, nonhydrolyzed sludge, hydrolyzed sludge, starch industry wastewater, and soya (commercial medium), were investigated. The selected suspending agents [20% (wt:vol)] included sorbitol, sodium monophosphate, and sodium metabisulfite with corresponding suspendibility of 74-92, 69-85, and 71-82%, respectively. Molasses [0.2% (wt:vol)] increased adherence by 84-90% for all fermented broths. The optimal phagostimulants [0.5% (wt:vol)], namely, soya and molasses, caused entomotoxicity increase of 3-13 and 7-13%, respectively. Sorbic and propionic acids showed high antimicrobial action [0.5% (wt:vol)], irrespective of fermentation medium. Sodium lignosulfonate, molasses, and Congo red, when used as UV screens [0.2% (wt:vol)], showed percent corresponding entomotoxicity losses of 3-5, 0.5-5 and 2-16, respectively. The Bt formulations, when exposed to UV radiation, showed higher half-lives (with and without UV screens) than the fermented broths or semisynthetic soya medium and commercial Bt formulation. UV screen-amended nonhydrolyzed, hydrolyzed, and starch industry wastewater formulations showed 1.3-1.5-fold higher half-lives than commercial Bt formulation. Thus, the recommended formulation comprises sorbitol, sodium monophosphate, sodium metabisulfite (suspending agents); molasses, soya flour (phagostimulants); molasses and skimmed milk powder (rainfasteners); sorbic and propionic acids (antimicrobial agents) and sodium lignosulfate; and molasses and Congo red (UV screens). These waste-based Bt formulations offer better UV resistance in comparison with commercial formulation.

Adhesives↗
PubMed2000

Immunohistology of kerato-epithelin in corneal stromal dystrophies associated with R124 mutations of the BIGH3 gene.

PURPOSE: To investigate corneal deposits associated with kerato-epithelin (KE) in three corneal dystrophies harboring mutations at Arg-124 in the BIGH3 gene. METHODS: Six patients with Avellino corneal dystrophy (ACD) associated with R124H, one patient with superficial granular corneal dystrophy (SGCD) associated with R124L, and seven patients with lattice corneal dystrophy type 1 (CDL1) associated with R124C were examined. Corneal buttons obtained during keratoplasties were stained with Masson's trichrome and with Congo red, and immunostained with antibodies specific for N-terminal and C-terminal portions of KE (KE-15 and KE-2, respectively). RESULTS: In all corneas with ACD, subepithelial to midstromal deposits of granular material stained with KE-2 and KE-15. However, deep stromal deposits containing amyloid reacted with KE-2, but not KE-15. Granular deposits in the subepithelial layer observed in SGCD stained intensely with KE-2 and KE-15. In all corneas with CDL1, subepithelial and midstromal amyloid deposits stained with KE-2; these deposits did not stain with KE-15. Deposits between the epithelial layer and Bowman's layer stained with Masson's trichrome but not with Congo red in five of the seven corneas; these deposits were stained with both KE-2 and KE-15. CONCLUSIONS: Deposits in corneal buttons involved by ACD, SGCD, and CDL1 included forms of the BIGH3 gene product, KE. An N-terminal sequence of KE may be related to formation of amyloid associated with R124 mutations.

Amyloid↗
PubMed2003

Amyloid in surgical pathology.

Amyloid is defined as a proteinaceous tissue deposit that shows a typical green birefringence in polarized light after staining with Congo red, the presence of non-branching linear fibrils of indefinite length with a mean diameter of 10 nm, and a distinct X-ray diffraction pattern consistent with Pauling's model of a cross beta-fibril. Amyloid may deposit locally or may present as a systemic disease. The origin of amyloid is diverse: 25 different fibril proteins have been described so far. The precursor proteins differ from each other in their primary structures and functions. The only common denominator is the propensity to form anti-parallel cross beta-fibrils under certain circumstances. Early diagnosis of amyloid is still a major challenge in surgical pathology. Histological proof can be obtained using Congo-red staining and polarization microscopy. However, small deposits may be difficult to discern, and sensitivity can be improved using fluorescence microscopy. Classification of amyloid is mandatory, since amyloid is treatable and different treatment regimens are applied to different amyloid diseases. This review focuses on the epidemiology, clinical features, pathology and diagnosis of amyloid in surgical pathology.

Amyloid↗
PubMed2002

[Differential diagnosis of amyloidosis].

Amyloid is defined as a proteinaceous tissue deposit that shows a typical green birefringence in polarized light after staining with Congo red, the presence of non-branching linear fibrils of indefinite length with an approximate diameter of 10-12 nm, and a distinct X-ray diffraction pattern consistent with Pauling's model of a cross-beta fibril. Amyloid may deposit locally, organ-limited, tumor-like, or may present as a generalized disease. The origin of amyloid is diverse: twenty different fibril proteins have been described so far. The precursor proteins differ from each other in their primary structures and functions. The only common denominator is the propensity to form anti-parallel cross beta-fibrils under certain circumstances. Early diagnosis of amyloid is still a major challenge in surgical pathology. Histological proof can be obtained using Congo red staining and polarisation microscopy. However, small deposits may be difficult to discern and sensitivity can be improved by using fluorescence microscopy. Classification of amyloid is mandatory, since amyloid is treatable and different treatment regimens are applied to different amyloid diseases. AA amyloidosis requires intensified treatment of the underlying disease. Patients with generalized AL amyloidosis receive high dose chemotherapy and stem cell transplantation. Familial amyloidoses (AApoAI, AFib, ATTR) may undergo liver transplantation.

Amyloidosis↗
PubMed1998

Postoperative function following laparoscopic collis gastroplasty for shortened esophagus.

BACKGROUND: Collis gastroplasty is indicated when tension-free fundoplication is not possible. Few studies have described the physiological results of this procedure, and no studies have evaluated outcomes of the endoscopic approach. OBJECTIVE: To assess the long-term outcomes of patients treated with laparoscopic Collis gastroplasty and fundoplication. DESIGN: Case series. SETTING: Tertiary care teaching hospital and esophageal physiology laboratory. PATIENTS: Fifteen consecutive patients with refractory esophageal shortening diagnosed at operation. Complicated gastroesophageal reflux disease or type III paraesophageal hernia (or both) was preoperatively diagnosed with esophagogastroduodenoscopy, 24-hour pH monitoring, esophageal motility, and barium esophagram. Fourteen (93%) of the 15 patients were available for long-term objective follow-up. INTERVENTIONS: Laparoscopic Collis gastroplasty with fundoplication and esophageal physiological testing. OUTCOME MEASURES: Preoperative and postoperative symptoms, operative times, and complications were prospectively recorded on standardized data forms. Late follow-up at 14 months included manometry, 24-hour pH monitoring, and esophagogastroduodenoscopy with endoscopic Congo red testing and biopsy. RESULTS: Presenting symptoms included heartburn (13 patients [87%]), dysphagia (11 patients [73%]), regurgitation (7 patients [47%]), and chest pain (7 patients). An endoscopic Collis gastroplasty was performed, followed by fundoplication (12 Nissen and 3 Toupet). There were no conversions to celiotomy and no deaths. Long-term follow-up occurred at 14 months. Esophagogastroduodenoscopy revealed that all wraps were intact with no mediastinal herniations. Manometry demonstrated an intact distal high-pressure zone with a 93% increase in resting pressure over the preoperative values. Two (14%) of these patients reported heartburn, and 7 (50%) patients had abnormal results on postoperative 24-hour pH studies (mean DeMeester score, 100). Biopsy of the neoesophagus revealed gastric oxyntic mucosa in all patients. Endoscopic Congo red testing showed acid secretion in only those patients with abnormal DeMeester scores. Of these 7 patients, 5 (36%) had persistent esophagitis and 6 (43%) had manometric evidence of distal esophageal body aperistalsis that was not present preoperatively. CONCLUSIONS: Collis gastroplasty allows a tension-free fundoplication to be performed to correct a shortened esophagus. It results in an effective antireflux mechanism but can be complicated by the presence of acid-secreting gastric mucosa proximal to the intact fundoplication and a loss of distal esophageal motility. These patients require close objective follow-up and maintenance acid-suppression therapy.

Adult↗