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T T Wu

Publications and source records attributed to T T Wu.

At least 37 records · Page 2Linked to original sources
PubMed2001

Colchicine toxicity: distinct morphologic findings in gastrointestinal biopsies.

Colchicine is an alkaloid with antimitotic ability used to treat a variety of medical conditions. Colchicine toxicity can result in multiorgan failure and death. The histopathologic features of colchicine toxicity in gastrointestinal biopsies have not been reported. Twenty-one gastrointestinal mucosal biopsies obtained from nine patients receiving oral colchicine therapy were studied. Immunohistochemical staining for Ki67 proliferation antigen was performed, and medical records of each patient were reviewed. All patients had a history of gout. Four patients with chronic renal failure also had clinical evidence of colchicine toxicity, and the other five patients did not. Distinct morphologic changes, seen as metaphase mitoses, epithelial pseudostratification, and loss of polarity, were seen in biopsy material from 4 of 4 (100%) patients with clinical colchicine toxicity. Three of these four cases (75%) also contained abundant crypt apoptotic bodies. These morphologic features were best seen in the biopsies from duodenum and gastric antrum, with relative sparing of the gastric body in the upper gastrointestinal tract. Ki67 staining demonstrated an expansion of the proliferating region in three available cases with clinical colchicine toxicity. These distinctive morphologic features were not seen in the five patients without clinical colchicine toxicity. These results indicate that colchicine toxicity can produce diagnostic morphologic features in gastrointestinal mucosal biopsies. Recognition of these features is important because colchicine toxicity can be fatal if undiagnosed clinically.

Adult↗
PubMed2001

Hyperplastic polyps of the esophagus and esophagogastric junction: histologic and clinicopathologic findings.

Hyperplastic polyps of the esophagus and esophagogastric junction region (EGJ) are uncommon lesions characterized by hyperplastic epithelium (foveolar-type, squamous, or both) with variable amounts of inflamed stroma. They have been reported almost exclusively in the radiologic and clinical literature as occurring predominantly in association with gastroesophageal reflux disease (GERD). Comprehensive histologic and clinicopathologic evaluation of these polyps, their association with background mucosal pathology, and their association with Barrett's esophagus has not been previously performed. We studied 30 hyperplastic polyps from 27 patients and characterized the histologic, endoscopic, and clinical features of both the polyps and the background esophagus. Hyperplastic polyps were most common in the region of the EGJ (67%), followed by the distal esophagus (30%) and mid-esophagus (3%). Most (80%) were composed of predominantly cardiac-type mucosa, predominantly squamous mucosa (17%), or an admixture (3%). Intestinal metaplasia of the polyp was present in only 7% and low-grade dysplasia in only 3%. In the majority of cases (67%) hyperplastic polyps were associated with concurrent or recent ulcers or erosive esophagitis. In most cases (48%) esophageal injury was associated with GERD, but other potential etiologies included medications, infection, anastomotic or polypectomy sites, vomiting, and photodynamic therapy. Four patients (15%) had Barrett's esophagus, three of whom had or developed dysplastic Barrett's mucosa. These results underscore the pathogenesis of esophageal/EGJ region hyperplastic polyps as a mucosal regenerative response to surrounding mucosal injury. Careful clinical history and biopsy of the nonpolypoid mucosa are essential for determining the clinicopathologic context in which the polyps have developed.

Adolescent↗
PubMed2001

Function of Rta is essential for lytic replication of murine gammaherpesvirus 68.

Rta, encoded primarily by open reading frame 50, is well conserved among gammaherpesviruses. It has been shown that the Rta proteins of Epstein Barr virus (EBV), Kaposi's sarcoma-associated herpesvirus (KSHV, or HHV-8), and murine gammaherpesvirus 68 (MHV-68; also referred to as gamma HV68) play an important role in viral reactivation from latency. However, the role of Rta during productive de novo infection has not been characterized in gammaherpesviruses. Since there are cell lines that can support efficient productive de novo infection by MHV-68 but not EBV or KSHV, we examined whether MHV-68 Rta plays a role in initiating viral lytic replication in productively infected cells. Rta, functioning as a transcriptional activator, can activate the viral promoter of early lytic genes. The amino acid sequence alignments of the Rta homologues suggest that the organizations of their functional domains are similar, with the DNA binding and dimerization domains at the N terminus and the trans-activation domain at the C terminus. We constructed two mutants of MHV-68 Rta, Rd1 and Rd2, with deletions of 112 and 243 amino acids from the C terminus, respectively. Rd1 and Rd2 could no longer trans-activate the promoter of MHV-68 gene 57, consistent with the deletions of their trans-activation domains at the C terminus. Furthermore, Rd1 and Rd2 were able to function as dominant-negative mutants, inhibiting trans-activation of wild-type Rta. To study whether Rd1 and Rd2 blocked viral lytic replication, purified virion DNA was cotransfected with Rd1 or Rd2 into fibroblasts. Expression of viral lytic proteins was greatly suppressed, and the yield of infectious viruses was reduced up to 10(4)-fold. Stable cell lines constitutively expressing Rd2 were established and infected with MHV-68. Transcription of the immediate-early gene, rta, and the early gene, tk, of the virus was reduced in these cell lines. The presence of Rd2 also led to attenuation of viral lytic protein expression and virion production. The ability of Rta dominant-negative mutants to inhibit productive infection suggests that the trans-activation function of Rta is essential for MHV-68 lytic replication. We propose that a single viral protein, Rta, governs the initiation of MHV-68 lytic replication during both reactivation and productive de novo infection.

Animals↗
PubMed2001

Transcription activation of polyadenylated nuclear rna by rta in human herpesvirus 8/Kaposi's sarcoma-associated herpesvirus.

Human herpesvirus 8 (HHV-8) (also known as Kaposi's sarcoma-associated herpesvirus) encodes a novel noncoding polyadenylated nuclear (PAN) RNA (also known as T1.1 or nut-1) during the early phase of lytic replication. PAN RNA is the most abundant transcript of HHV-8, comprising 80% of total poly(A)-selected transcripts in HHV-8-infected cells during lytic replication. We directly measured the abundance of PAN RNA by visualizing 1.1- to 1.2- kb PAN RNA in an ethidium bromide-stained gel from poly(A)-selected RNA. We further pursued the mechanisms by which PAN RNA expression is induced to such high levels. rta, an immediate-early gene of HHV-8, is a transactivator that is sufficient and necessary to activate lytic gene expression in latently infected cells. Ectopic expression of Rta was previously shown to induce PAN RNA expression from the endogenous viral genome and activate the PAN promoter in a reporter system. Here, we have identified the Rta-responsive element (RRE) in the PAN promoter. Deletion analysis revealed that the RRE is present in a region between nucleotides -69 and -38 of the PAN promoter. A promoter construct containing the 69 nucleotides upstream of the transcription start site of the PAN promoter was activated by Rta in the absence or presence of the HHV-8 genome. Rta activated the PAN promoter up to 7,000-fold in 293T cells and 2,000-fold in B cells. Electrophoretic mobility shift assays demonstrated that Rta formed a highly stable complex with the RRE of the PAN promoter. Our study suggests that Rta can induce PAN RNA expression by direct binding of Rta to the RRE of the PAN promoter. This study has highlighted an important mechanism controlling PAN RNA expression and also provides a model system for investigating how Rta transactivates gene expression during lytic replication.

Animals↗
PubMed2001

Should asymptomatic atrophic retinal holes be treated prophylactically in pseudophakic eyes after Nd:YAG laser posterior capsulotomy?

BACKGROUND: Retinal detachment (RD) following cataract extraction is a serious and potentially sight-threatening event that will often necessitate further surgical intervention. Of the several risk factors reported in the literature, Neodymium:YAG laser posterior capsulotomy has been reported to increase the risk of RD following cataract surgery up to 4.9-fold. The purpose of this study is to investigate the difference of characteristics in pseudophakic RD with or without Nd:YAG laser posterior capsulotomy and the possible role of atrophic retinal holes in pseudophakic RD after posterior capsulotomy. METHODS: Retrospective review of 78 cases of pseudophakic RD after uncomplicated extracapsular lens extraction and intraocular lens implantation was done. Twenty-one of them received Nd:YAG laser posterior capsulotomy before RD. We measured the numbers, types, and locations of retinal breaks and several other risk factors associated with RD. Analysis was performed with the system of Statistical Products and Services Solutions (SPSS). RESULTS: The ratio of retinal holes only in retinal breaks that caused retinal detachment was significantly higher in the capsulotomy group than the non-capsulotomy group (12/21 vs 14/57, p = 0.05). Only three patients in the capsulotomy group claimed significant symptoms before the detachment. There was no significant difference in mean number of retinal breaks and break location. Other risk factors predisposing to RD did not differ significantly between the two groups (13/21 vs 23/57, p = 0.12), nor did the interval from cataract surgery to RD (31.20 vs 29.44 months, p = 0.48). CONCLUSIONS: This primitive study suggests that asymptomatic atrophic retinal holes, usually not regarded as an absolute risk factor for RD, might lead to RD preferentially after Nd:YAG laser posterior capsulotomy. Early identification and treatment of such breaks might decrease the incidence of pseudophakic RD. We suggest that it is necessary to perform detailed preoperative and postoperative fundus examination and treat prophylactically any identified breaks, including asymptomatic atrophic retinal holes, in pseudophakic eyes after Nd:YAG laser posterior capsulotomy.

Adult↗
PubMed2001

p53 mutation and bcl-2 expression in transitional cell carcinoma of the urinary bladder.

BACKGROUND: The purpose of our study was to examine the frequency of p53 mutation and bcl-2 expression in transitional cell carcinoma of the urinary bladder and their clinicopathologic correlates. METHODS: A total of 137 patients who underwent transurethral resection for primary transitional cell bladder carcinomas were enrolled. The paraffin-embedded tissue blocks were recut and stained by monoclonal anti-p53 (DO7) and anti-bcl-2 (124) antibodies. The bcl-2 and p53 immunoreactivity was correlated to tumor grade and pathological stage. RESULTS: p53 mutation was identified in 102 patients (78.5%). The mutation was most common in grade 3 tumors (95%) as compared to grade 2 (74%) and grade 1 (80%) tumors, but the difference was not statistically significant (p = 0.289). Stage pT2 tumors had higher incidence of p53 mutation (97%) as compared to pTa-1 tumors (71%, p = 0.0003). Only 17 tumors (13%) expressed bcl-2; the grade 3 tumors had significantly higher incidence of bcl-2 expression (p = 0.04). The bcl-2 expression was not related to pathological stage (p = 0.083). There was no interrelation between p53 mutation and bcl-2 expression (p = 0.97). Grade 3 tumors correlated well with invasive disease (p < 0.00001). When grade 2 tumors were evaluated separately, p53 mutation was positively correlated with disease invasion (p = 0.001). CONCLUSIONS: Grade 3 tumor was the most important variable associated with tumor invasion in transitional cell carcinoma of the urinary bladder. p53 mutation was positively correlated with invasive disease. Grade 2 tumors with p53 mutation had greater probability of disease invasion. Expression of bcl-2 positively correlated with tumor grade but not pathological stage.

Adult↗
PubMed2001

Frequency doubling technology perimetry in retinal diseases--preliminary report.

The role of frequency doubling technology perimetry (FDT) in glaucoma has been promising in speed and simplicity as well as in its high sensitivity and specificity compared to conventional automatic perimetry. In this study, we evaluate the role of frequency doubling technology perimetry (FDT) in a variety of retinal diseases. FDT using full-threshold C-20 mode was performed in thirty-three patients with a variety of retinal diseases [16 cases of rhegmatogenous retinal detachment (RRD), nine cases of age-related maculopathy (AMD) and eight cases of central serous chorioretinopathy (CSCR)]. The fundus was scored by the extent of disease on each quadrant and macular area (central five degree visual angle). Then the retinal scores were compared with the points depressed to 2% on total deviation plots in FDT C-20 full-threshold mode using Spearman's rank correlation method. The correlation was statistically significant in the group of RRD (R = 0.57, P = 0.01), whereas the correlation was not significant in the group of macular diseases (AMD & CSCR, R = 0.47 & 0.32, P = 0.12 & 0.20). In conclusion, our results suggest that FDT might be a useful and simple technique for functional evaluation in RRD, but not in the macular disease group under this scoring system.

Adult↗
PubMed2001

Frequent hypermethylation of the 5' CpG island of E-cadherin in esophageal adenocarcinoma.

PURPOSE: E-cadherin, a M(r) 120,000 transmembrane glycoprotein, mediates calcium-dependent intercellular adhesion that is essential for normal tissue homeostasis. Loss of E-cadherin occurs in a variety of epithelial tumors and is correlated with invasion and metastasis. In esophageal adenocarcinoma, reduction of E-cadherin expression has been demonstrated previously, but mutations of the gene (CDH1) are rare. EXPERIMENTAL DESIGN: In this study, we used a nested PCR approach to examine the methylation status of the 5' CpG island of E-cadherin in esophageal specimens obtained from individuals with and without a history of esophageal cancer. RESULTS: In four individuals without esophageal cancer, E-cadherin was completely unmethylated in normal squamous cell-lined esophageal mucosa. In contrast, in patients with esophageal adenocarcinoma, E-cadherin was methylated in 26 of 31 (84%) tumor specimens. In the majority of cases, matched normal tissue (esophagus or stomach) from each patient was completely unmethylated. By immunostaining, methylated tumor samples demonstrated heterogeneously decreased membranous E-cadherin staining. CONCLUSIONS: These data suggest that epigenetic silencing via aberrant methylation of the E-cadherin promoter is a common cause of inactivation of this gene in esophageal adenocarcinoma.

Adenocarcinoma↗
PubMed2001

Correlation of acoustic velocity of synovial fluid with markers of inflammation in arthritic patients.

Analysis of synovial fluid is important in the evaluation and treatment of arthritic conditions. This study measured the acoustic velocity of synovial fluids in patients with degenerative joint diseases, crystal arthropathy, and other inflammatory arthropathies using the ultrasonic pulse-echo method. The measured acoustic velocities of these bio-fluids were then correlated with clinical parameters including the synovial white blood cell count (WBC), clarity, viscosity, string test, erythrocyte sedimentation rate (ESR), and serum C-reactive protein (CRP). Results showed that the acoustic velocities were correlated with ESR (p = 0.0016) and CRP (p = 0.0001). The mean acoustic velocity of inflammatory synovial fluids, defined as synovial fluids with WBCs of more than 2000/mm3, was greater than that of synovial fluids with WBCs of less than 2000/mm3 (1550 +/- 4.5 m/s vs 1544 +/- 1.5 m/s, p = 0.007). This study demonstrated that the acoustic velocity of synovial fluid correlates well with severity of inflammation. These findings suggest that measurement of acoustic velocity may be useful in the clinical evaluation and management of arthritic conditions.

Arthritis↗
PubMed2000

LNCaP progression model of human prostate cancer: androgen-independence and osseous metastasis.

BACKGROUND: Clinically, the lethal phenotypes of human prostate cancer are characterized by their progression to androgen-independence and their propensity to form osseous metastases. We reported previously on the establishment of androgen-independent (AI) human prostate cancer cell lines derived from androgen-dependent (AD) LNCaP cells, with androgen independence defined as the capability of prostate cancer cells to grow in castrated hosts. One of the sublines, C4-2, was found to be AI, highly tumorigenic, and metastatic, having a proclivity for metastasis to the bone. METHODS: We established the AI and bone metastatic cell sublines B2, B3, B4, and B5 from the parental C4-2 subline, using a previously established coinoculating procedure. We determined the biologic behavior of the parental and derivative LNCaP sublines in vivo and in vitro, as well as their molecular and cytogenetic characteristics. RESULTS: Unlike other human prostate cancer models, the LNCaP progression model shares remarkable similarities with human prostate cancer. We observed a comparable pattern of metastasis from the primary to the lymph node and to the axial skeleton, with a predominant phenotype of osteoblastic reaction; 25-37.5% of the animals developed paraplegia. Cytogenetic and biochemical characterizations of LNCaP sublines also indicate close similarities between human prostate cancer and the LNCaP progression model. Additional chromosomal changes were detected in B2-B5 sublines derived from C4-2 bone metastases. These LNCaP sublines were found to grow faster under anchorage-dependent but not -independent conditions. The in vitro invasion and in vivo metastatic potential of these LNCaP sublines surprisingly correlated with anchorage-dependent and not -independent growth. The derivative LNCaP sublines when cultured in vitro produced a substantially higher (20-30-fold) amount of basal steady-state concentrations of PSA than that of the parental LNCaP cells. PSA production was high initially, but was markedly reduced when the derivative cell lines were inoculated and allowed to grow long-term in vivo for the establishment of tumors and metastasis, suggesting that unknown host factors derived either from the prostate or the bone can effectively downregulate PSA expression by prostate tumor epithelium. CONCLUSIONS: The LNCaP model of human prostate cancer progression will help improve our understanding of the mechanisms of androgen-independence and osseous metastasis, and tumor-host determinants of PSA expression.

Animals↗
PubMed2000

Kabat database and its applications: 30 years after the first variability plot.

The Kabat Database was initially started in 1970 to determine the combining site of antibodies based on the available amino acid sequences at that time. Bence Jones proteins, mostly from human, were aligned, using the now-known Kabat numbering system, and a quantitative measure, variability, was calculated for every position. Three peaks, at positions 24-34, 50-56 and 89-97, were identified and proposed to form the complementarity determining regions (CDR) of light chains. Subsequently, antibody heavy chain amino acid sequences were also aligned using a different numbering system, since the locations of their CDRs (31-35B, 50-65 and 95-102) are different from those of the light chains. CDRL1 starts right after the first invariant Cys 23 of light chains, while CDRH1 is eight amino acid residues away from the first invariant Cys 22 of heavy chains. During the past 30 years, the Kabat database has grown to include nucleotide sequences, sequences of T cell receptors for antigens (TCR), major histocompatibility complex (MHC) class I and II molecules and other proteins of immunological interest. It has been used extensively by immunologists to derive useful structural and functional information from the primary sequences of these proteins. An overall view of the Kabat Database and its various applications are summarized here. The Kabat Database is freely available at http://immuno.bme.nwu.edu

Animals↗
PubMed2000

The role of laparoscopy in preoperative staging of esophageal cancer.

BACKGROUND: Diagnostic laparoscopy has been used to determine resectability and to prevent unnecessary laparotomy in patients with advanced esophageal cancer. The objective of this prospective study was to evaluate the role of laparoscopy in conjunction with computed tomography (CT) scan in staging patients with esophageal cancer. METHODS: From March 1995 to October 1998, 59 patients with biopsy-proven esophageal cancer underwent diagnostic laparoscopy with concurrent vascular access device and feeding jejunostomy tube placement. RESULTS: Laparoscopy changed the treatment plan in 10 of 59 patients (17%). Of the patients with normal-appearing regional or celiac nodes, 78% were confirmed by biopsy to be tumor free, whereas 76% of patients with abnormal-appearing nodes were confirmed by biopsy to have node-positive disease. CONCLUSIONS: Diagnostic laparoscopy is useful for detecting and confirming nodal involvement and distant metastatic disease that potentially would alter treatment and prognosis in patients with esophageal cancer.

Adult↗
PubMed2000

Fundic gland polyps in familial adenomatous polyposis: neoplasms with frequent somatic adenomatous polyposis coli gene alterations.

Fundic gland polyps (FGPs) are the most common gastric polyps in patients with familial adenomatous polyposis (FAP). FGPs have traditionally been regarded as nonneoplastic, possibly hamartomatous lesions, but the pathogenesis of FGPs in both FAP and sporadic patients remains unclear. FGPs in FAP can show foveolar dysplasia, and rarely invasive gastric adenocarcinoma has been reported in patients with FAP and fundic gland polyposis. Using direct gene sequencing and allelic loss assays at 5q, we analyzed somatic adenomatous polyposis coli (APC) gene alterations in 41 FAP-associated FGPs (20 with foveolar dysplasia, six indefinite for dysplasia, and 15 nondysplastic) and 13 sporadic FGPs. The foveolar epithelium and dilated fundic glands of the polyps were separately microdissected and analyzed in 25 of 41 FAP-associated FGPs and 13 of 13 sporadic FGPs. Somatic APC gene alterations were identified frequently (21 of 41 cases, 51%) in FAP-associated FGPs. Both the foveolar epithelium and the dilated fundic gland epithelium comprising the FGPs were shown to carry the same somatic APC gene alteration in 24 (96%) of 25 cases. Furthermore, there was no difference in the frequency of somatic APC gene alterations between FGPs with foveolar dysplasia (10 of 20, 50%), indefinite for dysplasia (four of six, 67%), and nondysplastic (seven of 15, 47%) in FAP patients (P: = 0.697). In contrast, FGPs from non-FAP patients showed infrequent (one of 13, 8%) APC gene alterations (P: = 0.008). These results show that FGPs in FAP patients are pathogenetically distinct from sporadic FGPs. Somatic, second-hit APC gene alterations, which precede morphological dysplasia in many FAP-associated FGPs, indicate that FGPs arising in the setting of FAP are neoplastic lesions.

Adenomatous Polyposis Coli↗
PubMed2000

The role of bcl-2, p53, and ki-67 index in predicting tumor recurrence for low grade superficial transitional cell bladder carcinoma.

PURPOSE: We assess the prognostic significance of bcl-2 expression, p53 mutation and ki-67 index for low grade, superficial transitional cell bladder carcinoma. MATERIALS AND METHODS: The medical records of 93 cases of primary, low grade (24 G1, 69 G2), superficial (70 pTa, 23 pT1) transitional cell carcinoma of the bladder were reviewed. Association of bcl-2, p53 and ki-67 index immunoreactivity with tumor grade and stage was examined. Prognostic significance of tumor grade, pathological stage, bcl-2 expression, p53 mutation and ki-67 index in predicting tumor recurrence was assessed. RESULTS: Of the tumors 60 (70%) had p53 mutation and 9 (10.5%) expressed bcl-2. These 2 markers did not relate to tumor grade or pathological stage. Median ki-67 index was 10.9% and positively correlated with tumor grade. Recurrence was noted in 34.9% of patients with a median followup of 26 months (range 1 to 84). The ki-67 index was the only significant prognostic indicator in univariate and multivariate analyses. This marker can further distinguish grade 2 tumors with a favorable prognosis from those with an unfavorable outcome. CONCLUSIONS: The ki-67 labeling index is an independent predictor of tumor recurrence for patients with primary superficial, low grade bladder cancers.

Carcinoma, Transitional Cell↗
PubMed2000

Mutations in beta-catenin and APC genes are uncommon in esophageal and esophagogastric junction adenocarcinomas.

Beta-catenin plays important roles in both intercellular adhesion and signal transduction. Mutations in the beta-catenin or adenomatous polyposis coli (APC) gene can alter the degradation of beta-catenin and cause aberrant accumulation of beta-catenin result in increased transcription of target genes. The dysregulated APC/beta-catenin pathway has been recently discovered as an important mechanism of tumorigenesis in various cancers, but its role in esophageal adenocarcinomas is not clear. Therefore, we studied the beta-catenin gene mutation, allelic loss of chromosome 5q, and APC gene mutation in esophageal and esophagogastric junction adenocarcinomas. Two (2%) somatic mutations in exon 3 of the beta-catenin gene, encompassing the region for glycogen synthase kinase-3beta phosphorylation, were detected from 109 adenocarcinomas. Chromosomal allelic loss on 5q was frequent in 45.3% (44/97) of tumors. Only one missense mutation in the mutation cluster region of the APC gene was detected from 38 esophageal and esophagogastric junction adenocarcinomas with the 5q allelic loss. Our results based on partial screening mutational analyses indicate that mutations of APC/beta-catenin pathway, unlike in colorectal carcinoma, involve only a small subset of esophageal and esophagogastric junction adenocarcinoma.

Adenocarcinoma↗
PubMed2000

Investigation of the association of esophageal carcinoma with human papillomaviruses.

The role of human papillomavirus (HPV) in esophageal cancers was evaluated in patients seen at Johns Hopkins University Hospital. Frozen esophageal tumor tissues from 22 cases with squamous cell carcinoma (SCC) and 24 cases with adenocarcinoma (AC), diagnosed between 1988 and 1998, were assayed for HPV sequences by reverse line blot polymerase chain reaction. HPV sequences (HPV-54) were detected in a single specimen; the other 45 specimens were negative. The HPV sequences in the positive specimen may represent infection of the epithelium. Our results suggest that genital HPVs may sometimes infect the esophagus, but there is no evidence to indicate that these infections contribute substantially to the development of esophageal cancer in North America.

Adenocarcinoma↗
PubMed2000

Esophageal lichen planus: case report and review of the literature.

Involvement of the esophagus by lichen planus is a rarely reported condition. The histologic features of esophageal lichen planus, which may differ from those of cutaneous disease, have only rarely been illustrated. We describe a 58-year-old woman with skin and oral lichen planus who presented with dysphagia and an esophageal stricture that were ultimately diagnosed as esophageal lichen planus. Multiple esophageal biopsies demonstrated a lichenoid, T cell-rich lymphocytic infiltrate, along with degeneration of the basal epithelium and Civatte bodies. Correct diagnosis of esophageal lichen planus is critical because of its prognostic and therapeutic distinction from other more common causes of esophagitis and stricture formation.

Deglutition Disorders↗