An unusual association of diffuse adenomyomatosis with dysplastic adenoma in chronic calculous cholecystitis: case presentation

<p>Abstract</p> <p>Background</p> <p>Gallbladder adenomyomatosis is an epithelial proliferation and hypertrophy of the muscularis mucosae of the gallbladder. Rokitansky-Aschoff sinuses are a characteristic of this condition. The segmental adenomyomatosis has a higher risk of developing into gallbladder carcinoma, especially in the fundal region of elderly patients.</p> <p>We report the case of a patient affected by chronic calculous cholecystitis with diffuse adenomyomatosis associated with dysplastic adenoma.</p> <p>Case presentation</p> <p>An 81-year-old woman presented at our hospital with a 1-year history of intermittent pain localized at the right upper abdominal quadrant, without diffusion to any other body part. On physical examination the abdomen was soft, not distended, and tender to palpation in the right upper quadrant. Murphy sign was negative. Laboratory tests were normal. The patient was scheduled for a laparoscopic cholecystectomy, and neither endoscopic ultrasonographic scan nor magnetic resonance imaging was performed. The operation, performed after obtaining informed consent, was uncomplicated and the intra-operative pathological examination showed no malignancy. The definitive pathological examination of the gallbladder showed: multiple stones of cholesterol origin; diffuse mucosal adenomyomatosis; and a 1.1 cm pedunculated mass localized at the fundus, whose surface was lumpy. This mass was diagnosed as an adenoma with multiple areas of severe dysplasia.</p> <p>Conclusions</p> <p>The adenoma of the gallbladder, together with the dysplasia, represents a biological carcinogenetic model. Carcinoma has rarely been reported in adenomyomatosis. Degenerative risk suggests surgery should be mandatory when there is a concomitant presence of large adenoma and adenomyomatosis.</p

Crisi parziali complesse in un paziente affetto da insulinoma: l’importanza di una diagnosi precoce

L’insulinoma, solitamente benigno (90%), è clinicamente caratterizzato da sintomi quali tremori, tachicardia, debolezza, sudorazione, fatica, fame, emicrania, vertigini e perdita della coscienza. Il tumore raramente può presentare una sintomatologia atipica. Presentiamo un caso di insulinoma in cui era stata posta diagnosi errata di patologia neurologica primitiva. Un uomo di 48 anni giunge al Pronto Soccorso in seguito a un incidente stradale causato da un’ improvvisa perdita di coscienza. Un anno prima era stata posta diagnosi di crisi parziali complesse. Il paziente appare pallido, tachicardico con pressione arteriosa 130/85 mmHg. Le analisi dimostrano una severa ipoglicemia (30 mg/dl): viene somministrata una glucosata con successiva risoluzione della sintomatologia. I dosaggi dell’insulina e del peptide-C, la TC e la RMN confermano la diagnosi di insulinoma. Le crisi neurologiche scompaiono dopo l’intervento chirurgico. Nei casi atipici la diagnosi di insulinoma può essere ritardata fino a più di 20 anni. Sintomi neurologici o psichiatrici, quali disorientamento, alterazione della personalità, amnesia, irritabilità, crisi convulsive, comportamenti bizzarri, difficoltà visive, neuropatia possono essere causa di un’errata diagnosi. La diagnosi di insulinoma deve essere considerata anche in questi casi, soprattutto se non responsivi a terapia specifica. L’insulinoma è curabile nella gran parte dei casi e una precoce diagnosi può evitare gravi conseguenze incluso il danno neurologico

Systemic allergic reactions induced by labile plant‐food allergens: Seeking potential cofactors. A multicenter study

Background: Heat-and-pepsin-sensitive plant food allergens (PR-10 and profilin) sometimes cause systemic reaction.Objective: To detect the risk factors for systemic reactions induced by labile food allergens.Methods: A retrospective multicenter study was performed on patients with a documented history of systemic allergic reaction to labile plant food allergens and on age-matched controls with a history of oral allergy syndrome (OAS) induced by the same foods. Offending foods, their amount, and state (solid or liquid), and potential cofactors (nonsteroidal anti-inflammatory drugs, protonic pump inhibitors, exercise, alcohol, and fasting) were considered.Results: We studied 89 patients and 81 controls. Sensitization to PR-10 or profilin, IgE to Bet v 1 and/or Bet v 2, and foods causing OAS were similar in the two groups. Twenty patients experienced &gt;1 systemic allergic reaction. Tree nuts, Rosaceae, Apiaceae, and soymilk were the main offending foods. Seventeen (19%) patients were taking a PPI when the systemic reaction occurred (vs 5% in controls; P &lt; .025). The ingestion of the offending food in liquid form (soymilk) was frequent among patients (15%) but unusual among controls (2%; P &lt; .025). Soy milk-induced systemic reactions were independent of PPI treatment. Fasting and excess of allergen, but not NSAID and exercise, were other relevant cofactors for systemic reactions. Systemic reactions occurred without any identifiable cofactor in 39 (44%) cases.Conclusion: PR-10- and profilin-induced systemic reactions are facilitated by PPI, ingestion of large amounts of unprocessed foods, and fasting. Soybean beverages represent a risk for PR-10 hypersensitive patients and should be avoided