Nationwide Real-World Data of Microsatellite Instability and/or Mismatch Repair Deficiency in Cancer: Prevalence and Testing Patterns.

Determination of microsatellite instability (MSI)/mismatch repair (MMR) status in cancer has several clinical implications. Our aim was to integrate MSI/MMR status from patients tested in Greece to assess the prevalence of MSI-high (MSI-H)/deficient MMR (dMMR) per tumor type, testing patterns over time and concordance between MSI and MMR status. We retrospectively recorded MSI/MMR testing data of patients with diverse tumor types performed in pathology and molecular diagnostics laboratories across Greece. Overall, 18 of 22 pathology and/or molecular diagnostics laboratories accepted our invitation to participate. In the 18 laboratories located across the country, 7916 tumor samples were evaluated for MSI/MMR status. MSI/MMR testing significantly increased in patients with colorectal cancer (CRC) and other tumor types overtime (p < 0.05). The highest prevalence was reported in endometrial cancer (47 of 225 patients, 20.9%). MSI-H/dMMR was observed in most tumor types, even in low proportions. Among 904 tumors assessed both for MSI and MMR status, 21 had discordant results (overall discordance rate, 2.3%). We reported MSI-H/dMMR prevalence rates in patients with diverse cancers, while demonstrating increasing referral patterns from medical oncologists in the country overtime. The anticipated high rate of concordance between MSI and MMR status in paired analysis was confirmed.

Mucinous adenocarcinoma arising from a tailgut cyst: A case report.

BACKGROUND: Retrorectal hamartomas or tailgut cysts (TCs) are rare. In most cases, they are asymptomatic and benign; however, rarely, they undergo malignant transformation, mainly in the form of adenocarcinoma. CASE SUMMARY: A 55-year-old woman presented to our hospital with lower back pain. On magnetic resonance imaging, a large pelvic mass was found, which was located on the right of the ischiorectal fossa, extending to the minor pelvis. The patient underwent extensive surgical resection of the lesion through the right buttock. Histological examination confirmed the diagnosis of a retrorectal mucinous adenocarcinoma originating from a TC. Surgical resection of the tumour was complete, and the patient recovered without complications. The pilonidal sinus was then excised. One year later, semi-annual positron emission tomography-computed tomography and magnetic resonance imaging scans did not reveal any evidence of local recurrence or metastatic disease. CONCLUSION: Preoperative recognition, histological diagnosis, and treatment of TCs pose significant challenges. In addition, the possibility of developing invasive mucinous adenocarcinoma, although rare, should be considered.

Ampullary Large-Cell Neuroendocrine Carcinoma, a Diagnostic Challenge of a Rare Aggressive Neoplasm: A Case Report and Literature Review.

Ampullary large-cell neuroendocrine carcinomas (LCNECs) are extremely rare, and available data are limited on case reports. They present with jaundice, non-specific abdominal pain, or weight loss, imitating adenocarcinoma. Their incidence increases due to the improved diagnostic techniques. However, preoperative diagnosis remains challenging. We report the case of a 70-year-old man with a history of metabolic syndrome, cholecystectomy, and right hemicolectomy, presenting with jaundice. Laboratory results showed increased liver biochemistry indicators and elevated CA 19-9. Esophagogastroduodenoscopy revealed an ulcerative tumor on the ampulla of Vater, and the biopsy revealed neuroendocrine carcinoma. Although computed tomography (CT) detected enlarged regional lymph nodes, the positron emission tomography (PET) showed a hyperactive lesion only in this area. Pylorus-preserving pancreatoduodenectomy with R0 resection was performed. Pathologic evaluation of the 3.1 × 1.9 cm tumor revealed an LCNEC with immunohistochemical positivity at Synaptophysin, EMA, CD56, and cytokeratin CK8/18. The Ki-67 index was 45%. Two out of the nine dissected lymph nodes were occupied by the neoplasm. The patient was discharged home free of symptoms, and adjuvant chemotherapy with carboplatin + etoposide was initiated. A comprehensive review of the reported cases showed that the preoperative biopsy result was different from the final diagnosis in few cases, regarding the subtypes. Conventional radiology cannot identify small masses, and other methods, such as endoscopy, magnetic resonance cholangiopancreatography (MRCP), and FDG-PET scan, might aid the diagnosis. Diagnosis is based on histology and immunohistochemical markers of the surgical specimens. The treatment of choice is pancreatoduodenectomy, followed by adjuvant chemotherapy. However, recurrence is frequent, and the prognosis remains poor.

The rare entity of ectopic pancreatic tissue in the gallbladder: A case report.

Introduction: and importance: Ectopic pancreatic tissue (EPT) is a rare clinical entity, which is defined as the presence of pancreatic tissue without any anatomic or vascular connection with the main body of the pancreas. EPT could be found anywhere in the gastrointestinal tract; most commonly in stomach. The aim of this study is to present a rare case report of EPT located in the gallbladder. Case presentation: A 37-year-old woman was scheduled in our surgical department for elective laparoscopic cholecystectomy due to symptomatic chololithiasis. Preoperative ultrasound imaging was indicative only for the presence of multiple stone tin the gallbladder's fundus. The patient had an uneventful recovery and discharged the first postoperative day. Surprisingly, the final pathology report of the specimen referred the existence of EPT in the subserosa territory, as an incidental finding. Clinical discussion: EPT is almost impossible to be diagnosed preoperatively due to its various clinical presentation and the low discriminating power of all the usual imaging tests. However, given the potential malignant transformation of the EPT, physicians should be aware of this clinical entity and consider cholecystectomy immediately when it is highly suspected. Conclusion: EPT in the gallbladder is a very rare finding. There are no established "gold standard" techniques to identify it preoperatively. The patients are either asymptomatic or presenting with non-specific symptoms and almost always the pathology examination, after cholecystectomy, establishes the definite diagnosis.

Prognostic implications of mismatch repair deficiency in patients with nonmetastatic colorectal and endometrial cancer.

BACKGROUND: The clinical relevance of mismatch repair (MMR) status in patients with nonmetastatic cancer across tumour types remains unclear. Our goal was to investigate the prognostic role of MMR deficiency in patients with stage I-III colorectal and endometrial cancer. METHODS: Patients with nonmetastatic colorectal and endometrial cancer with tumour tissue available for analysis were identified through the Hellenic Cooperative Oncology Group (HeCOG)'s tumour repository. Patients had been referred to Departments of Medical Oncology affiliated with HeCOG. MMR protein expression was evaluated by immunohistochemistry. The primary outcome measure was overall survival (OS). RESULTS: From May 1990 to September 2012, 1158 patients with nonmetastatic colorectal (N = 991) and endometrial cancer (N = 167) were identified (median age: 64 years, men: 544). All patients with colorectal and 109 (65%) with endometrial cancer had received adjuvant treatment. MMR deficiency was observed in 114 (11.5%) of colorectal and 80 (47.9%) of endometrial tumours. More commonly deficient proteins were PMS2 (69 patients, 7%) and MLH1 (63 patients, 6.5%) in colorectal cancer and MSH2 (58 patients, 34.7%) in endometrial cancer. Colorectal MMR-deficient (dMMR) tumours were more likely to be right sided (65 % dMMR vs 27 % proficient MMR, pMMR; p < 0.001), high grade (31% vs 15%, χ2, p < 0.001) and with a mucinous component (64% vs 42%, p < 0.001). Endometrial dMMR tumours were more often of endometrioid histology (51.4 % endometrioid vs 20 % serous/clear cell, p = 0.020). Compared with MMR proficiency, MMR deficiency was associated with improved OS in patients with endometrial cancer (HR = 0.38, 95% CI 0.20 to 0.76, p = 0.006), but not in patients with colorectal cancer (HR = 0.73, 95% CI 0.49 to 1.09, p = 0.130). After adjusting for age, stage and grade, MMR deficiency maintained its favourable prognostic significance in patients with endometrial cancer (HR = 0.42, 95% CI 0.20 to 0.88, p = 0.021). CONCLUSIONS: DMMR was associated with improved outcomes in patients with nonmetastatic endometrial cancer, but not in patients with nonmetastatic colorectal cancer who received adjuvant chemotherapy.

Association of Notch and Hedgehog Pathway Activation With Prognosis in Early-stage Colorectal Cancer.

BACKGROUND/AIM: Early-stage colorectal cancer (CRC) carries a wide range of survival probabilities. Novel biomarkers in this setting are eagerly awaited. Cancer stem cells (CSCs) are considered one of the reasons for treatment failure. This study sought to determine whether activation of pathways governing the function of CSC's could correlate with treatment outcomes. MATERIALS AND METHODS: Tumor specimens from 325 patients were analyzed with immunohistochemistry (IHC) for Hedgehog and Notch pathway activation and results were correlated with prognosis. RESULTS: Positive Notch3 protein expression was an unfavorable prognostic factor for disease-free survival (DFS) and overall survival (OS) (HR=2.43, p=0.024 and HR=2.56, p=0.028, respectively). Activation of the Shh pathway showed univariately longer DFS (HR=0.49, p=0.032). Possible crosstalk between the two pathways was indicated. No further associations between pathway activation and outcome were evident. CONCLUSION: Apart from Notch 3, activation of the pathways, as indicated by IHC expression of their components, did not result in differences in terms of DFS or OS.

Mismatch repair deficiency and aberrations in the Notch and Hedgehog pathways are of prognostic value in patients with endometrial cancer.

The aim of this study was to investigate the prognostic value of the Hedgehog (Gli, Patched-1, Shh, Smo) and Notch (Jag1, Notch2, Notch3) pathway members, in comparison to a panel of proteins (ER, PgR, HER2/neu, Ki67, p53, p16, PTEN and MMR) previously suggested to be involved in the pathogenesis of endometrial cancer, in association with clinical outcome and standard clinicopathological characteristics. A total of 204 patients with histological diagnosis of endometrial cancer treated from 2004 to 2013 were included. The evaluation of protein expression was assessed by immunohistochemistry. Univariate analysis showed that higher Ki67 labeling, expression of PTEN, p16, Notch2 and Notch3 proteins, as well as MMR proficiency were associated with increased relapse and mortality rate. Additionally, Patched-1 protein expression was associated with worse DFS, while p53 overexpression was associated with worse OS. In multivariate analyses, patients with MMR proficient tumors had more than double risk for death than patients with MMR deficient (MMRd) tumors (adjusted HR = 2.19, 95% CI 1.05-4.58, p = 0.036). Jag1 positivity conferred reduced mortality risk (HR = 0.48, 95% CI 0.23-0.97, p = 0.042). However, as shown by hierarchical clustering, patients fared better when their tumors expressed high Jag1 protein in the absence of Notch2 and Notch3, while they fared worse when all three proteins were highly expressed. Patched-1 positivity conferred higher risk for relapse (HR = 2.04, 95% CI 1.05-3.96, p = 0.036). Aberrant expression of key components of the Notch and Hedgehog signaling pathways, as well as MMRd may serve as independent prognostic factors for recurrence and survival in patients with endometrial cancer.

Squamous cell carcinoma arising from chronic sacrococcygeal pilonidal disease: a case report.

BACKGROUND: Sacrococcygeal pilonidal disease is a chronic, well-recognized entity, characterized by the recurrent formation of an abscess or draining sinus over the sacrococcygeal area. It is one of the most common surgical problems. Rarely, chronic inflammation and recurrent disease leads to malignant transformation, most commonly to squamous cell carcinoma (SCC). CASE PRESENTATION: We describe an extremely unusual case of SCC developing in a 60-year-old patient with a chronic pilonidal sinus complicated by an anal fistula. After wide surgical excision of the pilonidal sinus and fistulas and because of the poor healing process 6 months later, colonoscopy and a percutaneous fistulography were performed, revealing an anal canal-pilonidal fistula. Patient was treated with a more radical surgical resection with a prophylactic loop colostomy, but healing was not accelerated. Multiple biopsies were then taken from the surgical site at the time, which revealed the development of SCC. CT and MRI imaging techniques revealed SCC partial invasion of the coccyx and sacrum. As a result, aggressive surgical approach was decided. Histological examination revealed moderately to poorly differentiated SCC, and the patient was treated with adjuvant radiation therapy postoperatively. Nine months later, recurrence was found in the sacrum and para-aorta lymph nodes and the patient died shortly after. We discuss the clinical features, pathogenesis, treatment options, and prognosis of this rare malignant transformation. CONCLUSIONS: The development of SCC in chronic pilonidal disease is a rare but serious complication. Symptoms are usually attributed to the sacrococcygeal pilonidal disease (SPD), and diagnosis is often made late by histological examination of biopsies. Malignant transformation should be suspected in chronic SPD with recurrent episodes of inflammation, repeated purulent discharge, poor healing, and chronic complex fistulas.

Immunohistochemical Investigation of HER/AKT/mTOR Pathway and Cellular Adhesion Molecules in Urothelial Carcinomas.

Background. Several investigators have suggested the possibility that the expression of both EGFR and HER2 could be utilized for molecularly targeted therapy in urinary bladder cancer. We tried to evaluate the expression of HER2 and EGFR and activation of the AKT/PTEN/mTOR pathway in urothelial carcinomas and if there is any association between them and cellular adhesion molecules (CAMs). Materials and Methods. Forty-one paraffin-embedded urothelial cancer tissue blocks were collected. Immunostains for HER2, EGFR, MIB1, phospho-AKT, PTEN, phospho-mTOR, e-cadherin, p-cadherin, and b-catenin were performed on tissue microarrays sections. The immunohistochemical results were correlated with clinicopathological parameters. Results. The overexpression of HER2 was found in 19.6% of the cases and it was associated with high grade tumors with a high mitotic index and phosphorylation of AKT and mTOR. Muscle-invasive tumors presented both cytoplasmic and nuclear losses of PTEN expression. There was no association between HER/AKT/mTOR pathway activation and CAM expression. Although cadherins were often coexpressed, only p-cadherin immunoreactivity was associated with tumor grade and high proliferative index. Conclusions. HER2 overexpression is found in a respective proportion of urothelial carcinomas. P-cadherin expression is associated with high grade UCs but it is not affected by HER2 overexpression or by activation of HER/AKT/mTOR pathway.

MYC copy gain, chromosomal instability and PI3K activation as potential markers of unfavourable outcome in trastuzumab-treated patients with metastatic breast cancer.

BACKGROUND: There is an unmet need for more efficient patient stratification for receiving trastuzumab in the metastatic breast cancer (mBC) setting, since only part of such patients benefit from the addition of this agent to chemotherapy. The aim of this study was to investigate the prognostic value of biomarkers including MYC and MET in mBC patients treated with trastuzumab-based regimens. METHODS: mBC patients, locally tested as HER2-positive, treated with trastuzumab and chemotherapy between 1998 and 2010 were evaluated. Paraffin tumors (n = 229) were retrospectively centrally assessed by immunohistochemistry (IHC) for HER2, ER, PgR and Ki67; fluorescence in situ hybridization (FISH) for HER2, TOP2A and centromere (CEN) 17, MYC and CEN8, MET and CEN7; qPCR for MYC, MET copy number (CN); and, for PI3K activation (PIK3CA mutations; PTEN and phospho-mTOR protein expression). Increased CEN CN was assessed based on normal cut-offs. Time to progression (TTP) and survival were evaluated from the initiation of trastuzumab as first line treatment. RESULTS: Among all tumors, 90 were HER2-negative upon central testing (ambiguous HER2) and the rest were true HER2-positive. Further, 156 patients presented with mBC upon relapse of pre-treated disease (R-mBC) and 65 were diagnosed at stage IV (de novo mBC). Concordance between FISH and qPCR on gene CN status was fair for MYC (Kappa = 0.458) and absent for MET. The presence of MYC CN gain with qPCR and the absence of PI3K activation were infrequent events (7 and 8 % of evaluable tumors, respectively), while 41 % of tumors had increased CEN CN in one or more chromosomes, indicative of chromosomal instability. The most consistent finding in the entire cohort and in the above patient subgroups with respect to outcome was the unfavourable effect of MYC CN gain, which was retained upon multivariable analysis (e.g., survival in the entire cohort, HR 6.02; 95 % CI 2.67-13.6; p < 0.001). Further unfavourable prognosticators were increased CEN CN in one chromosome in R-mBC but not in de novo mBC (multivariable interaction p = 0.048), PI3K activation in R-mBC (multivariable p = 0.004) and increased Ki67 for patient TTP. CONCLUSIONS: MYC gene copies, centromere status and PI3K activation may adversely impact trastuzumab treated mBC patient outcome and seem worthy validating in larger series.

Evaluation of CpG Island Methylator Phenotype as a Biomarker in Colorectal Cancer Treated With Adjuvant Oxaliplatin.

BACKGROUND: The CpG island methylator phenotype (CIMP) is a promising biomarker for irinotecan/5-fluorouracil/leucovorin chemotherapy for stage III colon cancer. In the present study, we evaluated whether CIMP is a prognostic biomarker for standard-of-care oxaliplatin-based adjuvant therapy. MATERIALS AND METHODS: The HE6C/05 trial randomized 441 patients with stage II-III colorectal adenocarcinoma to adjuvant XELOX (capecitabine, oxaliplatin) or modified FOLFOX6 (5-fluorouracil, leucovorin, oxaliplatin). The primary and secondary objectives were disease-free and overall survival, respectively. CIMP status was determined using the DNA methylation status of CACNA1G, IGF2, NEUROG1, RUNX3, and SOCS1. Cox models were used to assess the association of CIMP with survival. RESULTS: Of the 293 available tumors, 28 (9.6%) were CIMP(+). On univariate Cox regression analysis, no significant differences in survival were observed between individuals with CIMP(+) versus CIMP(-) tumors. CIMP(+) tumors were more likely to be right-sided and BRAF mutant (χ(2), P < .001). In the multivariate model, TNM stage II (vs. stage III) was associated with a reduced risk of relapse (hazard ratio [HR], 0.25; 95% confidence interval [CI], 0.11-0.55; Wald's P < .001), and a colon primary located on the left side and earlier TNM stage were associated with a reduced risk of death (HR, 0.48; 95% CI, 0.28-0.81; P = .006; and HR, 0.22; 95% CI, 0.10-0.49; P < .001, respectively). CONCLUSION: In the present exploratory analysis, CIMP did not appear to be a prognostic biomarker in oxaliplatin-treated patients with resected colorectal cancer.

Immune response gene expression in colorectal cancer carries distinct prognostic implications according to tissue, stage and site: a prospective retrospective translational study in the context of a hellenic cooperative oncology group randomised trial.

BACKGROUND: Although host immune response is an emerging prognostic factor for colorectal cancer, there is no consensus on the optimal methodology, surrogate markers or tissue for study. PATIENTS AND METHODS: Tumour blocks were prospectively collected from 344 patients with stage II/III colorectal cancer (CRC) treated with adjuvant chemotherapy. Whole section lymphocytic infiltration was studied along with mRNA expression of CD3Z, CD8, CD4, CXCL9, CXCL13, IGHM, FOXP3, SNAI2 and ESR1 by qRT-qPCR in tissue microarray (TMA) cores from the centre of tumour, invasive margin and adjacent normal mucosa. RESULTS: Lymphocytic infiltration, deficient MMR (10.9%), KRAS (40.7%) and BRAF (4.9%) mutations or single mRNA gene expression were not prognostic. Tumour ESR1 gene expression (Hazard Ratio [HR] for relapse 2.33, 95% CI 1.35-4.02; HR for death 1.74, 95% CI 1.02-2.97) and absence of necrosis (HR for relapse 1.71, 95% CI 1.05-2.71; HR for death 1.98, 95% CI 1.14-3.43) were adverse prognostic features. We used CD3Z and CD8 expression in order to devise the mRNA-based Immune Score (mIS) and proceeded to partitioning analysis in 267 patients, with age, stage, tumour site (Right vs Left CRC), KRAS mutation and tumour mIS as input factors. Only in patients with stage III right-sided colon cancer, a low immune response was associated with inferior disease-free survival (mIS-low, HR for relapse 2.28, 95% CI 1.05-8.02). No prognostic significance was seen for tumour mIS in any other stage or site of CRC, or for a similar mIS score derived from adjacent normal mucosa. Independent adverse prognostic significance was retained in multivariable analysis for absence of necrosis, tumour ESR1 expression in all patients and low tumour mIS in stage III right-sided CRC. CONCLUSIONS: In localised CRC, mRNA-based CD3Z/CD8 profiling of tumour immune response may have stage, site and tissue-specific prognostic significance, along with ESR1 expression. TRIAL REGISTRATION: ANZCTR.org.au ACTRN12610000509066.

Randomized phase III clinical trial comparing the combination of capecitabine and oxaliplatin (CAPOX) with the combination of 5-fluorouracil, leucovorin and oxaliplatin (modified FOLFOX6) as adjuvant therapy in patients with operated high-risk stage II or stage III colorectal cancer.

BACKGROUND: The aim of the trial was to compare two active adjuvant chemotherapy regimens in patients with early stage colorectal cancer (CRC). METHODS: Patients were assigned to oxaliplatin, leucovorin and 5-FU for 12 cycles (group A, FOLFOX6) or oxaliplatin and capecitabine for eight cycles (group B, CAPOX). Primary endpoint was disease-free survival (DFS). Tumors were classified as mismatch repair proficient (pMMR) or deficient (dMMR) according to MLH1, PMS2, MSH2 and MSH6 protein expression. KRAS exon two and BRAF V600E mutational status were also assessed. RESULTS: Between 2005 and 2008, 441 patients were enrolled, with 408 patients being eligible. After a median follow-up of 74.7 months, 3-year DFS was 79.8 % (95 % CI 76.5-83.4) in the FOLFOX group and 79.5 % (95 % CI 75.9-83.1) in the CAPOX group (p = 0.78). Three-year OS was 87.2 % (95 % CI 84.1-91.1) in the FOLFOX and 86.9 % (95 % CI 83.4-89.9) in the CAPOX group (p = 0.84). Among 306 available tumors, 11.0 % were dMMR, 34.0 % KRAS mutant and 4.9 % BRAF mutant. Multivariate analysis showed that primary site in the left colon, earlier TNM stage and the presence of anemia at diagnosis were associated with better DFS and overall survival (OS), while grade one-two tumors were associated with better OS. Finally, a statistically significant interaction was detected between the primary site and MMR status (p = 0.010), while KRAS mutated tumors were associated with shorter DFS. However, the sample was too small for safe conclusions. CONCLUSIONS: No significant differences were observed in the efficacy of FOLFOX versus CAPOX as adjuvant treatment in high-risk stage II or stage III CRC patients, but definitive conclusions cannot be drawn because of the small sample size. TRIAL REGISTRATION: ANZCTR 12610000509066 . Date of Registration: June 21, 2010.

Ixabepilone administered weekly or every three weeks in HER2-negative metastatic breast cancer patients; a randomized non-comparative phase II trial.

UNLABELLED: To explore the activity and safety of two schedules of ixabepilone, as first line chemotherapy, in patients with metastatic breast cancer previously treated with adjuvant chemotherapy, a randomized non-comparative phase II study was conducted. From November 2008 until December 2010, 64 patients were treated with either ixabepilone 40 mg/m(2) every 3 weeks (Group A, 32 patients) or ixabepilone 20 mg/m(2) on days 1, 8 and 15 every 4 weeks (Group B, 32 patients). Overall response rate (the primary end point) was 47% in Group A and 50% in Group B. The most frequent severe adverse events were neutropenia (32% vs. 23%), metabolic disturbances (29% vs. 27%) and sensory neuropathy (12% vs. 27%). Two patients in Group A and 3 in Group B developed febrile neutropenia. After a median follow-up of 22.7 months, median progression-free survival (PFS) was 9 months in Group A and 12 months in Group B. Median survival was 26 months in Group A, whereas it was not reached in Group B. Multiple genetic and molecular markers were examined in tumor and peripheral blood DNA, but none of them was associated with ORR or drug toxicity. Favorable prognostic markers included: the T-variants of ABCB1 SNPs c.2677G/A/T, c.1236C/T and c.3435C/T, as well as high MAPT mRNA and Tau protein expression, which were all associated with the ER/PgR-positive phenotype; absence of TopoIIa; and, an interaction between low TUBB3 mRNA expression and Group B. Upon multivariate analysis, tumor ER-positivity was a favorable (p = 0.0092) and TopoIIa an unfavorable (p = 0.002) prognostic factor for PFS; PgR-positivity was favorable (p = 0.028) for survival. In conclusion, ixabepilone had a manageable safety profile in both the 3-weekly and weekly schedules. A number of markers identified in the present trial appear to deserve further evaluation for their prognostic and/or predictive value in larger multi-arm studies. TRIAL REGISTRATION: ClinicalTrials.gov NCT 00790894.

Severe eosinophilic cholangitis with parenchymal destruction of the left hepatic lobe due to hydatid disease.

Hydatid cysts of the liver are known to occasionally rupture into the bile ducts and cause cholangitis. The histological features of this complication have not been adequately described in the literature. Herein is reported a case of severe eosinophilic cholangitis of the left hepatic lobe, occurring in a 24-year-old man with a large (16 cm) hydatid cyst, which obstructed and eroded the left hepatic duct. The patient presented with upper abdominal discomfort and low-grade fever of 3 weeks' duration. Sections of the left lobectomy specimen showed marked inflammatory infiltrates in the portal tracts, predominantly composed of eosinophils, extensively involving bile ducts of all sizes. Occasional small bile ducts were replaced by epithelioid cell granulomas surrounding eosinophilic microabscesses. The inflammatory infiltrates extended into the lobules, resulting in marked hepatocyte loss. This case demonstrates that echinococcosis may cause severe eosinophilic cholangitis with extensive parenchymal destruction, apparently resulting from a hypersensitivity reaction to parasitic antigens.

Anterior chest wall tuberculous abscess: a case report.

The granulomatous inflammation of tuberculosis usually involves the lungs and the hilar lymph nodes. Musculoskeletal tuberculosis (TB) occurs in 1-3% of patients with TB, while TB of the chest wall constitutes 1% to 5% of all cases of musculoskeletal TB. Furthermore, nowadays it is rarer to find extrapulmonary TB in immunocompetent rather that non-immunocompetent patients. The present case reports a fifty-six-year-old immunocompetent man with an anterior chest wall tuberculous abscess. The rarity of the present case relates both to the localization of the tuberculous abscess, and to the fact that the patient was immunocompetent. The diagnosis of musculoskeletal tuberculous infection remains a challenge for clinicians and requires a high index of suspicion. The combination of indolent onset of symptoms, positive tuberculin skin test, and compatible radiographic findings, strongly suggests the diagnosis. TB, however, must be confirmed by positive culture or histologic proof. Prompt diagnosis and treatment are important to prevent serious bone and joint destruction.