scholarly journals Apixaban Causing Hepatic Cystic Bleeding: A Rare but a Life-Threatening Complication

2021 ◽  
pp. 904-909
Author(s):  
Elona Shehi ◽  
Ked Fortuzi ◽  
Haider Ghazanfar ◽  
Shehriyar Mehershahi ◽  
Bhavna Balar

Cystic lesions of the liver are a heterogeneous group of disorders with varied etiology, prevalence, and clinical manifestations. Fibropolycystic liver disease encompasses a spectrum of related liver and biliary tract lesions caused by abnormal embryologic development of the ductal plates. These disorders include congenital hepatic fibrosis, biliary hamartomas, polycystic liver disease (PCLD), choledochal cysts, and Carolis disease. PCLD is arbitrarily defined as a liver that contains >20 cysts. Most liver cysts are incidentally found on imaging studies, and the majority of the patients with liver cysts are asymptomatic. Rarely, complications such as compression, infection, and bleeding within the cyst can occur. Under the effect of the increased pressure, the epithelial lining of the cyst undergoes necrosis and sloughing, causing injury of the fragile blood vessels, leading to intracystic bleeding. The bleeding within or from the cyst can be precipitated by anticoagulation. We present a patient with PCLD who developed intracystic bleeding after he was started on apixaban for the prevention of thromboembolism.

2018 ◽  
Vol 2018 ◽  
pp. 1-4 ◽  
Author(s):  
Mohammad Saud Khan ◽  
Zubair Khan ◽  
Toseef Javaid ◽  
Jamal Akhtar ◽  
Abdelmoniem Moustafa ◽  
...  

Isolated polycystic liver disease is a rare disorder. Majority of the patients with isolated polycystic liver disease are asymptomatic with incidental detection of liver cysts on imaging studies done for other purposes. Minority of patients develop symptoms which are mostly secondary to enlarging cysts size and hepatomegaly. Rarely, these patients develop portal hypertension and can present with its clinical manifestations and consequences in the form acute variceal bleeding or recurrent ascites. We present a rare case of 67-year-old female patient with significant history of polycystic liver disease who presented to the hospital with recurrent hematemesis and melena. She underwent esophagogastroduodenoscopy which showed multiple large esophageal varices requiring banding.


2021 ◽  
Vol 49 ◽  
Author(s):  
Isabela Das Neves Piana ◽  
Alexandre Coltro Gazzone ◽  
Luciana Lopes Simplício ◽  
Mariana Isa Poci Palumbo ◽  
Verônica Jorge Babo-Terra

Background: Hepatic cysts are rarely described in association with infections by Platynosomum sp. Infected animals are most often asymptomatic, and the severity of symptoms is associated with the number of biliary tract parasites, which may lead to cholangitis and cholangiohepatitis. Although platinosomiasis is often associated with cholangitis and cholangiohepatitis, it rarely is with polycystic disease. For the parasite’s life cycle to occur, the infected cat must eliminate the eggs in the feces and three intermediate hosts are needed: snails, terrestrial isopods and vertebrates like the frog or the gecko. The eggs are ingested by the snails, then the miracids are released and matured into the mother sporocyst form, which originates child sporocysts containing the cercariae, that leave the mollusks for the soil and are ingested by the terrestrial isopod in which the cercariae matures until metacercariae. Vertebrates ingest terrestrial isopods and are ingested by felines. The present study aimed to report an unusual case of platinosomiasis with the development of multiple hepatic cysts.Case: A mixed breed male kitten was admitted with a history of apathy, hyporexia, increased abdominal volume and jaundice. In the ultrasound examination, we could see hepatomegaly and several hypoecogenic rounded structures, similar to cysts. There was an increase of serum concentration of the hepatic enzymes alanine transaminase and gamma glutamyl transferase enzyme. The parasite’s eggs were investigated in the patient’s feces using the simple sedimentation method, with a negative result. The animal was submitted to celiotomy and it was possible to observe several cystic structures in the liver. The cysts content was sent to cytology and culture. Cytology result was compatible with liver cyst and there was no bacterial growth in the culture. Bile fluid was collected and sent for Platynosomum sp. research using the centrifugal sedimentation test in formalin-ether solution, which allowed the parasite’s eggs to be observed. The cat was treated with praziquantel,silymarin, S-Adenosyl methionine, and ursodeoxycholic acid. The patient gradually improved from jaundice and there was a reduction in abdominal volume. Discussion: This report describes a case of platinossomiasis associated with polycystic liver disease in a domestic cat, which seems to be an uncommon presentation. Most infected cats are asymptomatic, but some animals may exhibit anorexia, apathy, increased abdominal volume due to hepatomegaly and/or ascitis and jaundice. Although infestation in domestic cats is relatively common, its association with liver cysts is rare or poorly reported in the literature, representing a diagnostic challenge, which makes mandatory the inclusion of this differential diagnosis in polycystic liver diseases in cats. The diagnosis of this parasitosis can be made based on the association among clinical signs, laboratory tests and ultrasound examination, but the definitive diagnosis is usually made by visualizing the parasite’s eggs. In the case described, it was not possible to observe parasite’s eggs in the patient’s feces, but in the bile. Platynosomum sp. infection should always be considered as a differential diagnosis in cases of polycystic liver disease in cats, especially in countries with tropical or subtropical climate. Early diagnosis and appropriate treatment were fundamental for the improvement of the patient’s clinical condition.Keywords: feline, liver, platinosomiasis, polycystic disease, jaundice, cystic lesions.


Author(s):  
René M. M. van Aerts ◽  
Tom J. G. Gevers ◽  
Joost P. H. Drenth

In a subset of autosomal dominant polycystic kidney disease patients, hepatic cysts dominate the clinical picture. These patients may develop polycystic liver disease, and enlargement of the liver leads to compression of adjacent abdominal and thoracic organs. The main risk factors for growth of liver cysts are female sex, exogenous oestrogen use, multiple pregnancies, and severity of renal disease. Treatment is only indicated in those with symptoms, and choice of treatment depends on total liver volume, size, and location of the liver cysts. Current radiological and surgical therapies include aspiration-sclerotherapy, fenestration, segmental hepatic resection, and liver transplantation. They all are palliative in nature and are partially effective and have non-negligible morbidity and mortality. Somatostatin analogues are still in development for polycystic liver disease.


Kidney360 ◽  
2020 ◽  
Vol 1 (10) ◽  
pp. 1066-1074
Author(s):  
Whitney Besse ◽  
Charlotte Roosendaal ◽  
Luigi Tuccillo ◽  
Sounak Ghosh Roy ◽  
Anna-Rachel Gallagher ◽  
...  

BackgroundA major difference between autosomal recessive polycystic kidney disease (ARPKD) and autosomal dominant polycystic kidney disease (ADPKD) lies in the pattern of inheritance, and the resultant timing and focality of cyst formation. In both diseases, cysts form in the kidney and liver as a consequence of the cellular recessive genotype of the respective disease gene, but this occurs by germline inheritance in ARPKD and somatic second hit mutations to the one normal allele in ADPKD. The fibrocystic liver phenotype in ARPKD is attributed to abnormal ductal plate formation because of the absence of PKHD1 expression during embryogenesis and organ development. The finding of polycystic liver disease in a subset of adult PKHD1 heterozygous carriers raises the question of whether somatic second hit mutations in PKHD1 in adults may also result in bile duct-derived cyst formation.MethodsWe used an adult-inducible Pkhd1 mouse model to examine whether Pkhd1 has a functional role in maintaining bile duct homeostasis after normal liver development.ResultsInactivation of Pkhd1 beginning at 4 weeks of age resulted in a polycystic liver phenotype with minimal fibrosis at 17 weeks. Increased biliary epithelium, which lines these liver cysts, was most pronounced in female mice. We assessed genetic interaction of this phenotype with either reduced or increased copies of Pkd1, and found no significant effects on the Pkhd1 phenotype in the liver or kidney from altered Pkd1 expression.ConclusionsSomatic adult inactivation of Pkhd1 results in a polycystic liver phenotype. Pkhd1 is a required gene in adulthood for biliary structural homeostasis independent of Pkd1. This suggests that PKHD1 heterozygous carrier patients can develop liver cysts after somatic mutations in their normal copy of PKHD1.


2016 ◽  
Vol 34 (6) ◽  
pp. 654-658 ◽  
Author(s):  
Masahiro Takita ◽  
Mina Iwanishi ◽  
Tomohiro Minami ◽  
Masashi Kono ◽  
Hirokazo Chishina ◽  
...  

Objective: The objective of treatment for polycystic liver disease is to reduce the liver volume and reduce or resolve compression symptoms such as abdominal fullness and abdominal pain due to hepatomegaly. Liver cysts are treated internally by puncture and aspiration of the cyst contents or hepatic artery embolization and surgically by cyst fenestration or hepatectomy, but no clear consensus has been reached concerning their selection. We introduced monoethanolamine oleate (EO) sclerotherapy therapy for liver cysts in 1999 and reported its effectiveness. In this study, cases were added, and the results including those of long-term follow-up were evaluated. Subjects: Twenty-two patients (5 males and 17 females, mean age 65.2) who underwent EO infusion therapy for liver cysts between January 1999 and June 2011 were evaluated. Methods: Liver cysts were punctured under ultrasound guidance, and a 7Fr pigtail catheter was inserted. After aspirating the cyst contents, EO was infused, and a clamp was applied for 24 h. Then, the catheter was declamped, cyst contents were aspirated again, and the catheter was removed. After the treatment, the cyst size was measured, and the patients were followed up. Results: Eight simple cysts in 8 patients (simple cyst group) and 21 cysts in 14 patients with multiple cysts (polycystic liver disease group) were treated and followed up over a median of 78 months (0-203 months). The mean volume reduction rate was 99% in the simple cyst group and 91% in the polycystic liver disease group (p = 0.04). One procedural accident resulting in liver abscess formation was observed in 1 patient 1 week after discharge, and it required drain placement and antibiotic administration. While mild abdominal pain was observed in a few patients, it was resolved spontaneously under observation. Conclusion: EO infusion therapy achieves fairly high treatment response in the volume reduction (99%) and sustained shrinkage over long-term follow-up. Therefore, this is a breakthrough technique in the treatment of polycystic liver disease as well as simple cyst and should be a standard of care in the treatment of this disease.


2014 ◽  
Vol 39 (1) ◽  
pp. 59-61 ◽  
Author(s):  
Jeffrey Alan Belair ◽  
Judith Marie Joyce ◽  
Eun Jeong Kwak

2007 ◽  
Vol 12 (3) ◽  
pp. 477-482 ◽  
Author(s):  
Loes van Keimpema ◽  
Jelle P. Ruurda ◽  
Miranda F. Ernst ◽  
Hendrikus J. A. A. van Geffen ◽  
Joost P. H. Drenth

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