Chylous ascites, anti-interferon-gamma autoantibody, and angioimmunoblastic T-cell lymphoma: a rare but intriguing connection over Mycobacterium avium.

We report a case of non-AIDS (acquired immunodeficiency syndrome), non-CAPD (Continuous Ambulatory Peritoneal Dialysis), non-cirrhotic, Mycobacterium avium peritonitis, which is a rare form of mycobacterial infection. A 66-year-old Japanese man who had been treated previously for angioimmunoblastic T-cell lymphoma (AITL), had developed disseminated M. avium infection. Antimycobacterial regimen improved his symptoms; however, following an interruption in treatment, he developed chylous ascites. The patient died of uncontrolled peritonitis despite intensive treatment. Anti-interferon-γ autoantibody was positive, and AITL was presumed to be involved in autoantibody production. A rare coexistence of chylous ascites, autoantibody, and AITL taught us an intriguing lesson on the pathogenesis of M. avium infection. Particularly, we conclude that treatment strategies for M. avium infection should aim to restore immunity.

Plasma presepsin level is an early diagnostic marker of severe febrile neutropenia in hematologic malignancy patients.

BACKGROUND: Febrile neutropenia (FN) is a common infectious complication in chemotherapy. The mortality of FN is higher in hematologic malignancy patients, and early diagnostic marker is needed. Presepsin is a prompt and specific marker for bacterial sepsis, but its efficacy in severe febrile neutropenia (FN) is not well confirmed. We tried to clarify whether it is a useful maker for early diagnosis of FN in patients during massive chemotherapy. METHODS: We measured plasma presepsin levels every 2-3 day in FN cases and evaluated its change during the course of massive chemotherapy. The patients had hematologic malignancy or bone marrow failure, and in all cases, neutropenia was severe during the episode. The baseline levels, onset levels, increase rate at FN onset, and onset / baseline ratio were evaluated for their efficacy of early FN diagnosis. RESULTS: Eleven episodes of bacteremia (six gram negatives and five gram positives) in severe neutropenia were analyzed in detail. While plasma presepsin level was strongly associated to the CRP level (r = 0.61, p < 0.01), it was not associated with the absolute WBC count (r = -0.19, p = 0.19), absolute neutrophil count (r = -0.11, p = 0.41) or absolute monocyte count (r = -0.12, p = 0.40). The average of onset presepsin level was 638 ± 437 pg/mL and the cutoff value (314 pg/mL) has detected FN onset in 9 of 11 cases. The two cases undetected by presepsin were both Bacillus species bacteremia. CONCLUSIONS: Plasma presepsin level is a reliable marker of FN even in massive chemotherapy with very low white blood cell counts. Closer monitoring of this molecule could be a help for early diagnosis in FN. But bacteremia caused by Bacillus species was an exception in our study.

Evidence-based clinical practice guidelines for irritable bowel syndrome.

New strategies for the care of irritable bowel syndrome (IBS) are developing and several novel treatments have been globally produced. New methods of care should be customized geographically because each country has a specific medical system, life style, eating habit, gut microbiota, genes and so on. Several clinical guidelines for IBS have been proposed and the Japanese Society of Gastroenterology (JSGE) subsequently developed evidence-based clinical practice guidelines for IBS. Sixty-two clinical questions (CQs) comprising 1 definition, 6 epidemiology, 6 pathophysiology, 10 diagnosis, 30 treatment, 4 prognosis, and 5 complications were proposed and statements were made to answer to CQs. A diagnosis algorithm and a three-step treatment was provided for patients with chronic abdominal pain or abdominal discomfort and/or abnormal bowel movement. If more than one alarm symptom/sign, risk factor and/or routine examination is positive, colonoscopy is indicated. If all of them, or the subsequent colonoscopy, are/is negative, Rome III or compatible criteria is applied. After IBS diagnosis, step 1 therapy consisting of diet therapy, behavioral modification and gut-targeted pharmacotherapy is indicated for four weeks. Non-responders to step 1 therapy proceed to the second step that includes psychopharmacological agents and simple psychotherapy for four weeks. In the third step, for patients non-responsive to step 2 therapy, a combination of gut-targeted pharmacotherapy, psychopharmacological treatments and/or specific psychotherapy is/are indicated. Clinical guidelines and consensus for IBS treatment in Japan are well suited for Japanese IBS patients; as such, they may provide useful insight for IBS treatment in other countries around the world.

[Two cases of successful sorafenib retreatment with the addition of steroid therapy following sorafenib-induced erythema multiforme in two patients with hepatocellular carcinoma].

Erythema multiforme (EM) is a known side effect of sorafenib therapy in cancer patients; at onset, the causative medication should be permanently discontinued. Here we report two cases of hepatocellular carcinoma (HCC) that developed sorafenib-induced EM. In both cases, retreatment with sorafenib combined with steroid therapy achieved effective tumor control without EM recurrence. The first patient was a 72-year-old woman who showed a dramatic response to sorafenib retreatment, with complete remission after 8 months of therapy. There was no rash recurrence after the steroid dose was gradually tapered and stopped. The second patient was a 69-year-old man who responded to sorafenib and exhibited stable disease, with no recurrence of the rash after the steroid dose was tapered. However, mild hand-foot syndrome persisted throughout sorafenib therapy. Although sorafenib should be discontinued if EM occurs, if there is no suitable alternative treatment, retreatment may be considered with steroid cover in patients with unresectable HCC.

Mannan-binding protein, a C-type serum lectin, recognizes primary colorectal carcinomas through tumor-associated Lewis glycans.

Mannan (mannose)-binding protein (MBP) is a C-type serum lectin that plays a key role in innate immunity. MBP forms large multimers (200-600 kDa) and exhibits broad specificity for mannose, N-acetylglucosamine, and fucose. MBP exhibits high affinity for unique oligosaccharides that have been isolated from human colorectal carcinoma (SW1116) cells and characterized as highly fucosylated high m.w. type 1 Lewis glycans. In this study, we first demonstrated that MBP recognizes human primary colorectal carcinoma tissues through tumor-associated MBP ligands. We performed fluorescence-based histochemistry of MBP in human colorectal carcinoma tissues and showed that MBP clearly stained cancer mucosae in a Ca(2+)-dependent manner. Coincubation with plant (Aleuria aurantia) lectin, but not Con A, blocked MBP staining, indicating that fucose, rather than mannose, is involved in this interaction. The expression of MBP ligands was detected in 127 of 330 patients (38.5%), whereas, most significantly, there was no expression in 69 nonmalignant tissues. The MBP-staining pattern in cancer mucosae significantly overlapped with that of Lewis b [Fucα1-2Galß1-3(Fucα1-4)GlcNAc] staining, but the Lewis b staining in normal tissues was not associated with MBP staining. In addition, the MBP staining correlated inversely with the expression of CA19-9 Ag, and MBP stained 11 of 25 (44%) CA19-9 (sialyl Lewis a [NeuAc(α2-3)Galß1-3(Fucα1-4)GlcNAc])(-) colorectal carcinoma tissues. We found a favorable prognosis in patients with MBP ligand(+) tumors. These results suggest that selective recognition of cancer cells by endogenous MBP seems to be associated with an antitumor effect and that tissue staining with MBP in combination with CA19-9 may serve as a novel indicator of colorectal carcinoma tissues.

Cell division cycle-associated protein 1 overexpression is essential for the malignant potential of colorectal cancers.

To identify new cancer biomarkers and therapeutic targets for colorectal cancers (CRCs), we performed immunohistochemical analysis using tissue microarrays covering archival tumor tissue samples from 434 CRC patients and antibodies to cell division cycle-associated protein 1 (CDCA1) that was originally identified as an oncoantigen by our gene expression profile database, and compared its expression with several clinicopathological factors. Strong CDCA1 positivity was associated with poorer prognosis for patients with CRC (P=0.019) and multivariate analysis confirmed its independent prognostic value. In addition, transfection of siRNAs against CDCA1 suppressed its expression and induced apoptosis of CRC cells. These results suggest that CDCA1 could be a prognostic biomarker and a potential therapeutic target for CRCs.

Relationship between serum infliximab trough levels and endoscopic activities in patients with Crohn's disease under scheduled maintenance treatment.

BACKGROUND AND AIMS: Few data are available to support the clinical relevance of infliximab (IFX) trough levels for prediction of endoscopic disease activity in Crohn's disease (CD). This study evaluated the endoscopic disease activities in relation to clinical outcome using several laboratory markers including serum IFX trough levels in patients with CD undergoing scheduled IFX maintenance treatment. MATERIALS AND METHODS: A total of 78 sessions of endoscopy were performed on 45 patients with CD. Endoscopic activity was assessed using the modified Rutgeerts scoring system. IFX trough levels and anti-IFX antibodies (ATIs) were determined by immunoassays. RESULTS: Endoscopic activity negatively correlated with serum IFX trough levels (Spearman's rank correlation coefficient (ρ) = -0.54, P < 0.0001) and serum albumin levels (ρ = -0.46, P < 0.0001), and positively correlated with CRP (C-reactive protein) levels (ρ = 0.55, P < 0.0001), ESR (erythrocyte sedimentation rate) (ρ = 0.47, P < 0.0001) and fecal calprotectin levels. IFX trough levels and serum albumin levels were significantly elevated in the mucosal healing (MH) group, but ATIs, CRP, ESR and fecal calprotectin levels were significantly elevated in the nonmucosal healing group. Receiver operation curve revealed that the optimal cutoff value of IFX trough levels for identifying normal laboratory markers was 0.6 µg/ml for CRP, 1.0 µg/ml for serum albumin and 1.1 µg/ml for fecal calprotectin. Identification of mucosal healing needed a higher cutoff value of 4.0 µg/ml. Thiopurine treatment did not affect IFX trough and ATI levels. CONCLUSION: Mucosal healing requires higher IFX trough levels, compared to those to achieve normalization of routine clinical markers.

Clinical utility of newly developed immunoassays for serum concentrations of adalimumab and anti-adalimumab antibodies in patients with Crohn's disease.

BACKGROUND/AIM: The appearance of anti-adalimumab antibodies (AAAs) is associated with low serum adalimumab (ADA) trough levels and a decrease of clinical response. The goal of this study was to assess the accuracy and clinical utility of new immunoassays for serum ADA and AAA levels. PATIENTS AND METHODS: Serum ADA trough levels and AAA levels were measured using new immunoassays in 40 patients with Crohn's disease (CD) receiving ADA maintenance therapy. RESULTS: Serum ADA trough levels were 12.3 ± 9.6 µg/ml (n = 40) in CD patients, and 14 of 40 patients (35 %) were positive for AAAs. A negative correlation was observed between serum AAA levels and ADA trough levels (y = -6.02x + 18.7, r = -0.54, P < 0.001, n = 40). The ROC (receiver-operator curve) analyses indicated that an ADA trough of 5.9 µg/ml was optimal to maintain negative CRP (C-reactive protein) levels (≤0.3 mg/dl). The ADA trough levels were significantly lower in patients positive for AAAs (5.5 ± 5.4 µg/ml, n = 14) than in patients negative for AAAs (16.0 ± 9.5 µg/ml, n = 26). The CRP and ESR levels were significantly higher in AAA-positive patients than in AAA-negative patients. Serum albumin levels were significantly lower in AAA-positive patients. The positive rate for AAAs in patients who lost a response to infliximab (50 %) was significantly higher than that of anti-TNF-α drug naïve patients (12.5 %). CONCLUSIONS: These new assays for serum AAA trough and AAA levels are useful for routine clinical use and may help guide selection of optimal management strategies for IBD patients with a loss of response to ADA.

Predicting Mucosal Healing in Crohn's Disease Using Practical Clinical Indices with Regard to the Location of Active Disease.

BACKGROUND/AIMS: Only a few reports have examined the relationship between balloon-assisted enteroscopy (BAE)-based mucosal lesion severity in Crohn's disease (CD) using clinical variables such as serum levels of disease activity markers and Crohn's Disease Activity Index. We analysed whether clinical variables are useful for predicting mucosal healing (MH) in various CD types. METHODOLOGY: A total of 173 CD patients who underwent BAE were enrolled. Endoscopic findings were assessed using the modified Rutgeerts score (MRS). In this study, all observed samples of intestine, small bowel and large bowel were individually scored. The 'ileum group' included patients with MRS ileum scores greater than or equal to MRS colon scores (n = 139), whereas the 'colon group' included patients who had colon scores greater than or equal to MRS ileum scores (n = 56). RESULTS: Spearman's rank correlation between MRS and practical clinical parameters was stronger in the colon group than in the ileum group. Receiver operating characteristic analysis revealed that the colon group had better correlativity for MH prediction than the ileum group. The MH index using C-reactive protein and serum albumin obtained from logistic regression analysis improved the accuracy of MH prediction by 74.3%. CONCLUSION: A combination of serum albumin and C-reactive protein is useful for MH prediction. However, the reliability of MH prediction can differ depending on the dominant area of the mucosal lesions.

Changes of energy metabolism, nutritional status and serum cytokine levels in patients with Crohn's disease after anti-tumor necrosis factor-α therapy.

We investigated the effects of treatment with antibodies against tumor necrosis factor (TNF)-α on energy metabolism, nutritional status, serum cytokine levels in patients with Crohn's disease (CD). Twelve patients were enrolled. Resting energy expenditure (REE) levels were measured by indirect calorimetry. Crohn's disease activity index (CDAI) significantly decreased after treatment with anti-TNF-α therapy. Anti-TNF-α therapy did not affect REE, but respiratory quotient (RQ) significantly increased after treatment. Serum interleukin-6 levels were significantly decreased and RQ were significantly increased in high REE (≥25 kcal/kg/day) group as compared to low REE (<25 kcal/kg/day) group. In conclusion, high REE value on admission is a predictive factor for good response to treatment with anti-TNF-α antibodies in active CD patients.

Precursor-derived versus de-novo carcinogenesis depends on lineage-specific mucin phenotypes of intramucosal gland-forming gastric neoplasms.

AIMS: To clarify the lineage-specific carcinogenesis of gland-forming gastric neoplasms, by characterizing mucin phenotypes and proliferation patterns immunohistochemically using monoclonal antibodies against MUC2, MUC5AC, MUC6, CD10 and Ki67. METHODS AND RESULTS: We analysed 49 gland-forming intramucosal neoplasms, including 15 non-invasive low-grade neoplasms (group A), 10 non-invasive high-grade neoplasms (group B) and 24 intramucosal adenocarcinomas (group C). The mode of gland-forming gastric carcinoma development was different between the intestinal and gastric lineages. The pure intestinal-type accounted for 93% of group A, 50% of group B and 4.2% of group C tumours. A zonal pattern of cell proliferation was well retained in group A tumours and was lost size-dependently in group B tumours. These findings suggest that non-invasive low-grade neoplasms of the intestinal lineage progress to non-invasive high-grade neoplasms, but rarely to intramucosal adenocarcinomas. In tumours of the gastric lineage, which exhibited pure gastric or mixed phenotypes, the polarity of cell proliferation and differentiation was well retained in small (≦5 mm) tumours but was lost in larger tumours in groups B and C. CONCLUSIONS: Intramucosal adenocarcinomas of the gastric lineage may often arise de novo, develop in the proper gastric mucosa, and are partially derived from non-invasive high-grade neoplasms.

Genetic lineages of undifferentiated-type gastric carcinomas analysed by unsupervised clustering of genomic DNA microarray data.

BACKGROUND: It is suspected that early gastric carcinoma (GC) is a dormant variant that rarely progresses to advanced GC. We demonstrated that the dormant and aggressive variants of tubular adenocarcinomas (TUBs) of the stomach are characterized by loss of MYC and gain of TP53 and gain of MYC and/or loss of TP53, respectively. The aim of this study is to determine whether this is also the case in undifferentiated-type GCs (UGCs) of different genetic lineages: one with a layered structure (LS+), derived from early signet ring cell carcinomas (SIGs), and the other, mostly poorly differentiated adenocarcinomas, without LS but with a minor tubular component (TC), dedifferentiated from TUBs (LS-/TC+). METHODS: Using 29 surgically resected stomachs with 9 intramucosal and 20 invasive UGCs (11 LS+ and 9 LS-/TC+), 63 genomic DNA samples of mucosal and invasive parts and corresponding reference DNAs were prepared from formalin-fixed, paraffin-embedded tissues with laser microdissection, and were subjected to array-based comparative genomic hybridization (aCGH), using 60K microarrays, and subsequent unsupervised, hierarchical clustering. Of 979 cancer-related genes assessed, we selected genes with mean copy numbers significantly different between the two major clusters. RESULTS: Based on similarity in genomic copy-number profile, the 63 samples were classified into two major clusters. Clusters A and B, which were rich in LS+ UGC and LS-/TC+ UGC, respectively, were discriminated on the basis of 40 genes. The aggressive pattern was more frequently detected in LS-/TC+ UGCs, (20/26; 77%), than in LS+UGCs (17/37; 46%; P = 0.0195), whereas no dormant pattern was detected in any of the UGC samples. CONCLUSIONS: In contrast to TUBs, copy number alterations of MYC and TP53 exhibited an aggressive pattern in LS+ SIG at early and advanced stages, indicating that early LS+ UGCs inevitably progress to an advanced GC. Cluster B (enriched in LS-/TC+) exhibited more frequent gain of driver genes and a more frequent aggressive pattern than cluster A, suggesting potentially worse prognosis in UGCs of cluster B.

Pharmacokinetic interaction between sorafenib and prednisolone in a patient with hepatocellular carcinoma.

PURPOSE: Sorafenib is primarily metabolized in the liver, by CYP3A4-mediated oxidation and UGT1A9-mediated glucuronidation. However, there is little information about the pharmacokinetic interaction of sorafenib. Here, we report a pharmacokinetic interaction between sorafenib and the CYP3A4 inducer prednisolone in a patient with hepatocellular carcinoma (HCC). PATIENTS AND METHODS: The patient was a 72-year-old woman diagnosed with HCC. She was treated with sorafenib at 400 mg daily. On day 9, sorafenib was discontinued due to drug eruption. Nine months later, she was rechallenged with sorafenib at 400 mg daily concurrently with oral prednisolone. Prednisolone was started at 20 mg daily and was tapered by 5 mg every 14 days. We assessed the pharmacokinetics of sorafenib and its major metabolite M-2. RESULTS: The concentration of sorafenib was gradually increased following tapering of prednisolone. On day 56 after rechallenge, she developed G3 oral mucositis. At this time, serum trough concentrations of sorafenib and M-2 were at 5.9 and 1.1 µg/ml, respectively. Consequently, sorafenib dosage was reduced to 200 mg daily, and the oral mucositis was attenuated. The subsequent concentrations of sorafenib and M-2 obtained with a dose of 200 mg daily ranged from 1 to 3 µg/ml and from 0.1 to 0.4 µg/ml, respectively. Computed tomography scan showed a complete response of the liver tumor with no further recurrence of the rash. CONCLUSIONS: We have demonstrated for the first time that prednisolone stimulates the sorafenib metabolism and that therapeutic drug monitoring could be useful during sorafenib therapy.

Threaded biliary inside stents are a safe and effective therapeutic option in cases of malignant hilar obstruction.

BACKGROUND: Although endoscopic biliary stents have been accepted as part of palliative therapy for cases of malignant hilar obstruction, the optimal endoscopic management regime remains controversial. In this study, we evaluated the safety and efficacy of placing a threaded stent above the sphincter of Oddi (threaded inside plastic stents, threaded PS) and compared the results with those of other stent types. METHODS: Patients with malignant hilar obstruction, including those requiring biliary drainage for stent occlusion, were selected. Patients received either one of the following endoscopic indwelling stents: threaded PS, conventional plastic stents (conventional PS), or metallic stents (MS). Duration of stent patency and the incident of complication were compared in these patients. RESULTS: Forty-two patients underwent placement of endoscopic indwelling stents (threaded PS = 12, conventional PS = 17, MS = 13). The median duration of threaded PS patency was significantly longer than that of conventional PS patency (142 vs. 32 days; P = 0.04, logrank test). The median duration of threaded PS and MS patency was not significantly different (142 vs. 150 days, P = 0.83). Stent migration did not occur in any group. Among patients who underwent threaded PS placement as a salvage therapy after MS obstruction due to tumor ingrowth, the median duration of MS patency was significantly shorter than that of threaded PS patency (123 vs. 240 days). CONCLUSIONS: Threaded PS are safe and effective in cases of malignant hilar obstruction; moreover, it is a suitable therapeutic option not only for initial drainage but also for salvage therapy.

[A case report: feasible treatment of adalimumab for Crohn disease during pregnancy].

A 33-year-old woman with Crohn disease complained of diarrhea and hematochezia from the fifth week of her third pregnancy and was hospitalized. Because her CDAI indicated 307.1 points and colonoscopy showed multiple longitudinal ulcers in the distal colon, adalimumab therapy was initiated. The CDAI had decreased to 160.0 points and the colonic ulcers improved by 22 days after beginning the administration of adalimumab. Although adalimumab therapy was continued every 2 weeks during the third trimester, fetus growth was not affected and the woman delivered a healthy child. Adalimumab should be considered as one treatment for Crohn disease during pregnancy.

Neutralization of complement component C5 ameliorates the development of dextran sulfate sodium (DSS)-colitis in mice.

The complement system is a potent effector of innate immunity. To elucidate the pathophysiological role of the complement system in inflammatory bowel disease, we evaluated the effects of anti-C5 antibodies on the development of dextran sulfate sodium-induced colitis in mice. Dextran sulfate sodium-colitis was induced in BALB/c mice with intraperitoneal administrations of anti-C5 antibodies (1 mg/body [DOSAGE ERROR CORRECTED]) every 48 h. Tissue samples were evaluated by standard histological procedures. The mucosal mRNA expression of the inflammatory cytokines was analyzed by real-time PCR. Body weight loss in the mice was completely blocked by the administration of anti-C5 antibody. The disease activity index was significantly lower in the anti-C5 antibody-treated mice than the dextran sulfate sodium mice. The colonic weight/length ratio, histological colitis score and mucosal myeloperoxidase activity were significantly lower in the anti-C5 antibody-treated mice than the dextran sodium sulfate mice. The administration of the anti-C5 antibody significantly reduced the mucosal expression of mRNAs for tumor necrosis factor-α, interleukin-1ß and interleukin-6. In conclusion, the complement system plays a role in the development of dextran sodium sulfate-induced experimental colitis.

Decreased abundance of Faecalibacterium prausnitzii in the gut microbiota of Crohn's disease.

BACKGROUND AND AIMS: Dysbiosis is thought to be relevant to the etiology and pathogenesis of Crohn's disease (CD). In this study, we investigated the abundance of Faecalibacterium prausnitzii, as well as Bilophila wadsworthia, in the gut microbiota of Japanese CD patients. METHODS: Forty-seven CD patients and 20 healthy controls were enrolled. Abundance of F. prausnitzii in fecal samples was quantified by real-time polymerase chain reaction. The gut microbiota profile was evaluated by terminal restriction fragment length polymorphisms. RESULTS: The abundance of F. prausnitzii significantly decreased in CD patients compared with healthy subjects. B. wadsworthia was scarcely detected in the same samples. Among CD patients, the Crohn's Disease Activity Index, C-reactive protein levels, and erythrocyte sedimentation rate were significantly lower, and serum albumin levels were significantly higher in the high F. prausnitzii group compared with the low group. Terminal restriction fragment length polymorphisms analysis showed that fecal bacterial communities of CD patients differed from those of healthy individuals. The changes in simulated bacterial composition indicated that class Clostridia, including genus Faecalibacterium, was significantly less abundant in CD patients as compared with healthy individuals. The bacterial diversity measured by the Shannon Diversity Index was significantly reduced in CD patients compared with healthy individuals. CONCLUSION: The decreased abundance of class Clostridia, including F. prausnitzii, may translate into a reduction of commensal bacteria-mediated, anti-inflammatory activities in the mucosa, which are relevant to the pathophysiology of CD. In contrast, the role of B. wadsworthia was suspected to be minimal.

CD8(+) mycosis fungoides with esophageal involvement: A case report.

Mycosis fungoides (MF) is the most common type of cutaneous T-cell lymphoma and is characterized clinically by an indolent course with slow progression. MF is limited to the skin with widespread distribution, however, extracutaneous involvement of MF occurs during the advanced stages of the disease. Esophageal involvement of MF is a rare event. In the present study, we describe the first documented case of CD8(+) MF with esophageal involvement that was endoscopically diagnosed antemortem. A 70-year-old male with a 15-year history of MF presented with difficulty in swallowing. Endoscopic examination revealed a tumorous lesion with ulceration in all regions of the esophagus. Esophagus biopsy demonstrated atypical lymphocytic infiltrates with ulceration. Immunohistochemically, these atypical lymphocytes were positive for CD3, CD8 and cytotoxic granules. Therefore, a diagnosis of CD8(+) MF involving the esophagus was made. Extracutaneous involvement of the esophagus in MF is extremely rare and the majority of previously reported cases have been diagnosed postmortem. Only two cases of MF with esophageal involvement endoscopically diagnosed antemortem have been previously reported and this is the first documented case of CD8(+) MF with esophageal involvement diagnosed by this method. Early detection of extracutaneous involvement of MF is important for accurate treatment and endoscopic examination is a useful tool for detection of this pathology.