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Background: Littoral cell angioma (LCA) is a rare vascular primary tumor of the spleen with no more than 440 cases described so far. Although often seen as benign, it is described to have malignant potential and to be associated with other immunologic disorders or malignancies., Case Presentation: We present the case of LCA in a 75-year old man with a concomitant non-Hodgkin lymphoma and medical history of malign melanoma. The tumor was discovered incidentally after splenectomy for splenomegaly and refractory thrombocytopenia. The post-operative period was uneventful., Conclusion: Our case is the first to report an association of LCA with both lymphoma and melanoma thus far. It emphasizes the need for a thorough total body examination for synchronous diseases and close follow-up to reveal associated malignancies or immunologic disorders. Further research is required to identify etiologic and pathogenetic mechanisms behind this tumor and a common basis between the three diseases., Key Words: Littoral Cell Angioma, Neoplasm, Splenectomy, Solid Spleen Tumor.

Aim: Laparoscopic Nissen fundoplication represents the gold standard in GERD therapy, although, a frequent failure of this primary repair is represented by the breakdown of the hiatoplasty. Aim of our work is to evaluate if ultrastructural alterations of the diaphragmatic pillars in patients with hiatal hernia, can explain the physiopathology of hernia recurrence., Material of Study: The patients were divided into two groups: group A comprised 51 patients affected by hiatal hernia and group B (control) included 30 patients not affected by hiatal hernia.. Each patient underwent four biopsies, two from the phrenoesophageal membrane and two from the diaphragmatic pillars during laparoscopic procedures. Three hundred and twenty-four specimens, 204 from the group A and 120 from the group B, were processed and analyzed by transmission electron microscopy., Results: No alterations were found in the phrenoesophageal membrane in both groups; samples from the diaphragmatic pillars showed no alteration in the group without hiatal hernia (group B). Instead, 90,2% of the muscular samples from the crura of group A patients presented ultrastructural alterations: in almost 75% of the cases the lesions were considered severe with extended disruption-degeneration of the muscle architecture., Discussion: Patients with hiatal hernia have ultrastructural abnormalities of the muscular tissue of the diaphragmatic pillars that are absent in patients with normal gastroesophageal junction., Conclusions: The outcome of GERD surgery could depend not only on a correct technique but also on the underlying status of the diaphragmatic crura.

Actually, achalasia can be defined as a primary esophageal motor disorder characterized by esophageal aperistalsis and abnormal post-deglutitive lower esophageal sphincter (LES) relaxation. Its incidence varies from 0.03 to 1.63 cases per 100,000 people per year and increases with age, while the prevalence is almost 10/100,000 with no difference between the sexes. Regarding etiology, the most frequent histologic alteration is represented by the loss of the myenteric nerve fibers regulating inhibitory nitrergic neurotransmission in the LES, with the presence of a lymphocytic infiltrate and collagen deposition. The cause of this loss remains unclear. Among the theories proposed, the infectious, hereditary and autoimmune etiologies have been widely investigated. The only infectious agent identified as a cause of achalasia is Trypanosoma Cruzi, responsible of Chagas' disease. Regarding hereditary component, in rare cases achalasia presents as part of a genetic syndrome such as Down syndrome, Allgrove syndrome and familial visceral neuropathy. Although, no disease-specific gene has been identified. The autoimmune hypothesis has focused on the association of specific HLA classes with achalasia. However, no consistent association has been observed across studies. Despite increasing understanding of the physiopathology of achalasia, its etiology remains largely unknown. The onset of the disease is characterized by chronic inflammation of the myenteric plexus of the esophagus secondary to an environmental insult. Probably, genetic factors are involved in the development of achalasia, although the precise molecular basis of the disease has not been identified.