Pylephlebitis is an uncommon entity characterized by septic thrombophlebitis of the portal vein and its tributaries, with more frequent involvement of the right portal vein branch. In 1846, Waller first described it as a possible origin of liver abscesses.1,2 The literature on pylephlebitis is restricted to case reports. The estimated incidence is 2.7 cases per 100,000 people per year. It is closely associated with intra-abdominal inflammatory and infectious processes, especially pancreatitis, diverticulitis, and peritonitis. Cholecystitis, as observed in our case, was identified in approximately 7% of pylephlebitis cases. The main risk factors associated with its development are smoking, previous abdominal surgeries, and the use of antiplatelet agents.2 Although the pathogenesis of pylephlebitis is not yet well-established, it has been associated with a hypercoagulability state and bacterial translocation, specially by gram-negative bacteria such as Bacteroides fragilis, Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis and Enterobacter spp.3 The clinical picture of pylephlebitis is nonspecific, with fatigue, abdominal pain, fever, nausea, and vomiting, which contributes to a delay in diagnosis and the initiation of therapy, leading to high rates of morbidity and mortality. The typical pathological findings of pylephlebitis are polymorphonuclear inflammatory infiltrate causing venulitis in the portal veins, with endothelial tumefaction, desquamation, and fibrinoid necrosis. The suppurative inflammatory reaction frequently invades the adjacent parenchyma.4 Figure 1 refers to the autopsy finding of a 56-year-old man, diagnosed with hypertension, diabetes, and dyslipidemia, who presented with nonspecific abdominal pain, evolving 2 weeks later with fever and loss of appetite. He was admitted to the emergency department with jaundice, septic shock, and encephalopathy, dying one day after admission despite the intensive care treatment. The autopsy revealed an enlarged, congested, and friable liver that weighed 2789 g (reference range: 1500-1800); the gallbladder had a thick wall filled with multiple blackened calculi, compatible with calculous cholecystitis. The histologic exam showed portal venulitis, with fibrino- leukocytic exudate sparing the biliary tract and the hepatic artery associated with numerous hepatic abscesses (Figure 1). Figure 1 A - Gross examination of the congested and friable liver (weight: 2789,0 g); B - Gallbladder with chronic inflammation due to calculi; C - Photomicrograph of the liver shows portal venulitis, with a suppurative inflammatory reaction and fibrin (black arrow), sparing the biliary tract (blue arrow) and the hepatic artery (red arrow) (H&E, 400X).:
Melanoma arising in the hard palate is an exceedingly rare entity, comprising a minute fraction of all melanoma cases. The absence of specific clinical signs often leads to delayed diagnosis and subsequent challenges in treatment planning. We discussed the existing literature to elucidate the epidemiology, risk factors, and molecular pathways associated with melanoma of the hard palate. Additionally, we discuss the importance of a multidisciplinary approach involving dermatologists, otolaryngologists, oncologists, and pathologists in diagnosing and managing this condition. A 62-year-old male patient presented with a pigmented lesion on the hard palate mucosa, which was initially asymptomatic but gradually increased in size. Biopsy revealed melanoma, confirmed through immunohistochemical staining. Staging investigations indicated a metastatic disease. Surgery followed by adjuvant therapy was planned; however, he was lost for the follow-up. Melanoma originating from the hard palate mucosa is exceedingly rare, posing diagnostic and therapeutic challenges. Early detection, accurate diagnosis, and prompt multidisciplinary management are crucial for optimal outcomes. This case underscores the importance of comprehensive evaluation and tailored treatment strategies in patients with uncommon mucosal melanomas.
Biliary atresia (BA) is a progressive inflammatory cholangiopathy of infancy that results in fibrous obliteration of the extrahepatic and intrahepatic bile ducts. In untreated patients, this leads to biliary-type cirrhosis within the first two years of life. Timely diagnosis of BA with a lack of significant hepatic fibrosis is critical and surgical drainage (Kasai procedure) within the first two months of life is the initial treatment modality with the highest success rate. Ultimately, liver transplantation is required due to surgical drainage complications, such as recurrent cholangitis, failure to thrive, and portal hypertension (PHTN). Histopathological findings of hepatectomy specimens after failed and successful Kasai procedures are vastly different depending on the subsequent course of liver disease. Bile flow is inadequate following a failed Kasai procedure with rapid development of biliary cirrhosis. Explants from patients with successful Kasai procedure may show cholestatic (recurrent cholangitis), vascular (obliterative venopathy, regenerative hyperplasia, and PHTN), or an interplay of both cholestatic and vascular abnormalities. Pathologists need to be aware of explant histopathology (post-successful Kasai procedures) with a clinical course dominated by PHTN for precise documentation of vascular abnormalities.
Schistosomiasis is an infectious disease caused by parasitic flatworms of the genus Schistosoma. The species Schistosoma mansoni is associated with hepatosplenic disease. Schistosomiasis involving the gallbladder alone is highly unusual, with a few cases reported. Herein, we present the case of a woman from a region with endemic schistosomiasis who presented with a painless solid lesion and wall thickening of the gallbladder. She underwent an uneventful laparoscopic cholecystectomy. Microscopic examination of the surgical specimen revealed Schistosoma mansoni eggs associated with granulomatous reaction, leading to the diagnosis of schistosomiasis of the gallbladder, prompting subsequent treatment with praziquantel and follow-up. This case illustrates the importance of suspicion for this diagnosis in endemic areas, as it can be misdiagnosed with malignancy if not examined microscopically. Complications and treatment strategies are poorly characterized for the few cases of schistosomiasis; reporting this case can serve as a helpful reminder of a rare presentation of this disease.
Castleman disease (CD) is a rare, benign lymphoproliferative disorder, mostly involving the mediastinal lymph nodes, but can occur wherever lymphoid tissue is found. With only a few published case reports, there needs to be more literature on its cytological findings. We report the case of a 63-year-old female presenting with left upper cervical swelling. Fine needle aspiration cytology smears showed variably sized lymphoid follicles with diminished germinal centers, prominence of follicular dendritic cells, and capillaries traversing some of the follicles. The possibility of a hyaline-vascular type of Castleman disease was suggested. Histopathology confirmed the cytological diagnosis. The index case is being presented to discuss the cytological features of the CD along with its histological and immunohistochemical correlation.
