An Unusual Case of Submucosal Invasion of Esophageal Squamous Cell Carcinoma Mistaken as Primary Achalasia

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Abstract

Secondary achalasia due to submucosal invasion of esophageal squamous cell carcinoma (SCC) is a very rare condition. Here, we report a case of secondary achalasia diagnosed after distal esophagectomy, initially mistaken as primary achalasia. A 51-year-old man presented with progressive dysphagia for 2 months and mild weight loss. A barium swallow study, endoscopy, and manometry showed typical findings of primary achalasia. Pneumatic dilatation was performed, but esophageal perforation occurred as a complication. During surgical repair, no abnormalities around distal esophagus were found, and intraoperative esophageal biopsy revealed only inflammatory cells. During the following 8 months, the patient suffered from dysphagia caused by recurrent esophageal obstruction several times although of repeated balloon dilatation and esophageal stent insertion. Finally, he received a distal esophagectomy. The postoperative pathology revealed SCC at the distal esophagus and esophagogastric junction.

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Most cited references 13

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Epidemiology and demographics of achalasia.

Linda J Mayberry (2001)

The incidence and prevalence of achalasia has been reported from a limited number of centers in the US, UK, Israel, Zimbabwe, Singapore, and New Zealand. With two exceptions, the studies have been retrospective. The incidence of the disease is about 0.5/10(5)/year with a prevalence of about 8/10(5) population. However, there appear to be striking international variations and also significant differences within countries. The disease occurs with equal frequency in men and women and is commoner with ageing. The appearance of the disease in the older age groups together with the lack of evidence for an autosomal recessive pattern of inheritance would suggest that environmental factors are important in the cause of the disease.

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Current therapies for achalasia: comparison and efficacy.

M F Vaezi, J Richter (1998)

Achalasia is a primary esophageal motor disorder of unknown etiology producing complaints of dysphagia, regurgitation, and chest pain. The current treatments for achalasia involve the reduction of lower esophageal sphincter (LES) pressure resulting in improved esophageal emptying. Calcium channel blockers and nitrates, once used as initial treatment strategy for early achalasia, are now only used in patients who are not candidates for pneumatic dilation or surgery and those not responding to botulinum toxin injections. By virtue of the more rigid balloons, the current pneumatic dilators are more effective and have better efficacy than the older more compliant balloons. The graded approach to pneumatic dilation using the Rigiflex balloons (3.0, 3.5, and 4.0 cm) are now the most commonly used nonsurgical means of treating patients with achalasia, resulting in symptom improvement in up to 90% of patients. Surgical myotomy, once with high morbidity and long hospital stay, can now be performed laparoscopically with similar efficacy to the open surgical approach (94% vs. 84%, respectively), reduced morbidity, and hospitalization time. Given the advances in both balloon dilation and laparoscopic myotomy, most patients with achalasia can now choose between these two equally efficacious treatment options. Botulinum toxin injection of the LES should be reserved for patients who cannot undergo balloon dilation and are not surgical candidates.

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The pathogenesis of pseudoachalasia: a clinicopathologic study of 13 cases of a rare entity.

J Goldblum, E Achkar, Matthew Rice … (2002)

Pseudoachalasia is an esophageal motor disorder usually associated with malignancy that has clinical, radiographic, and manometric findings that are often indistinguishable from primary achalasia. There are few reports examining the histologic features of the associated neoplasms and their relationship with the esophageal myenteric plexus. We studied the clinical and pathologic features of 13 cases of pseudoachalasia seen at our institution between 1979 and 1999. Detailed clinical and radiographic data were obtained from medical records. In all cases available histologic material was reviewed to confirm the presence and type of associated neoplasm. When possible, the relationship of the neoplasm to the esophageal myenteric plexus was examined. In selected cases immunohistochemical stains were performed to further evaluate this relationship. All patients had clinical, radiographic, and manometric features similar to primary achalasia. The cohort included seven men and six women, age range 24-79 years (median 61 years). Associated neoplasms included esophageal adenocarcinoma arising in Barrett's esophagus (n = 1), adenocarcinoma of the esophagogastric junction (n = 7), metastatic renal cell carcinoma to the esophagogastric junction (n = 1), breast adenocarcinoma (n = 1), pulmonary small cell carcinoma (n = 1), pleural malignant mesothelioma (n = 1), and mediastinal fibrosis (n = 1). The mechanism of pseudoachalasia was consistent with neoplastic infiltration of the esophageal myenteric plexus in 11 cases. Neoplastic cells surrounded myenteric ganglion cells, which appeared normal in number and morphology. In the patient with pulmonary small cell carcinoma, there was no evidence of neoplastic infiltration of the esophagogastric junction, and anti-ANNA-1 antibody was detected, suggesting a paraneoplastic syndrome. Tissue obtained at the time of esophagomyotomy revealed lymphocytic myenteric inflammation and marked depletion of ganglion cells identical to that seen in primary achalasia. The mechanism pseudoachalasia in the patient with breast adenocarcinoma is uncertain, as there was no evidence of direct involvement of the esophagogastric junction. In summary, we describe 13 cases of pseudoachalasia resulting in a clinical syndrome indistinguishable from primary achalasia. The most common mechanism is direct involvement of the esophageal myenteric plexus by neoplastic cells. Rarely, a distant neoplasm may cause this syndrome as a paraneoplastic process.

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Author and article information

Journal

Journal ID (nlm-ta): J Neurogastroenterol Motil

Journal ID (publisher-id): JNM

Title: Journal of Neurogastroenterology and Motility

Publisher: Korean Society of Neurogastroenterology and Motility

ISSN (Print): 2093-0879

ISSN (Electronic): 2093-0887

Publication date (Print): April 2010

Publication date (Electronic): 27 April 2010

Volume: 16

Issue: 2

Pages: 194-198

Affiliations

Department of Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea.

Author notes

Correspondence: Jung Ho Park, MD. Department of Medicine, Sungkyunkwan University School of Medicine, Kangbuk Samsung Hospital, 108 Pyung-dong, Jongno-Gu, Seoul 110-102, Korea. Tel: +82-2-2001-2068, Fax: +82-2-2001-2485, pjho3@ 123456hotmail.com

Article

DOI: 10.5056/jnm.2010.16.2.194

PMC ID: 2879845

PubMed ID: 20535351

SO-VID: 792795cc-4155-42ed-8500-30b2f03630d7

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This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

An Unusual Case of Submucosal Invasion of Esophageal Squamous Cell Carcinoma Mistaken as Primary Achalasia

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Neuronal Signaling

Most cited references 13

Epidemiology and demographics of achalasia.

Current therapies for achalasia: comparison and efficacy.

The pathogenesis of pseudoachalasia: a clinicopathologic study of 13 cases of a rare entity.

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