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Peliosis hepatis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Farwa Haideri [2]Adenike Eketunde

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Adenike Eketunde

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Overview

Peliosis Hepatis is an uncommon vascular condition characterised by randomly distributed multiple blood-filled cavities throughout liver. Size of the cavities usually ranges between a few millimetres to 3 cm in diameter[1]. In the past it was a mere histological curiosity occasionally found at autopsies but has been increasingly recognised with wide ranging conditions from AIDS to the use of anabolic steroids. It also occasionally affects spleen, lymph nodes, lungs, kidneys, adrenal glands, bone marrow and other parts of gastrointestinal tract.[2].

Peliosis hepatis is often erroneously written “peliosis hepatitis”, despite its not being one of the hepatitides. The correct term arises from the Greek pelios, i.e. discoloured by extravasated blood, livid[3], and the Latinized Genitive case (hepatis[4]) of the Greek hepar, liver[5].

Historical Perspective

There is limited information about the historical perspective of Peliosis hepatis

Classification

There is no established system for the classification of Peliosis hepatis

Pathophysiology

The pathogenesis of peliosis hepatis is unknown. There are several hypotheses, such as, it arise from sinusoidal epithelial damage[6], increased sinusoidal pressure due to obstruction in blood outflow from the liver, or hepatocellular necrosis[1].

Two morphologic patterns of hepatic peliosis were described by Yanoff and Rawson [7]. In the phlebectatic type, the blood-filled spaces are lined with endothelium and are associated with aneurismal dilatation of the central vein; in the parenchymal type, the spaces have no endothelial lining and they usually are associated with haemorrhagic parenchymal necrosis. Some considers both pattern to be one process, initiated by focal necrosis of liver parenchyma observed in parenchymal type progressing into formation of fibrous wall and endothelial lining around haemorrhage of phebectatic type. Fibrosis, cirrhosis, regenerative nodules, and tumours may also be seen.

Causes

Peliosis hepatis may be caused by drugs, toxins, chronic wasting disease, malignancy, and infection. Peliosis Hepatitis may develop in individuals with renal or cardiac transplantation, but in about 20-50% of patients, they are no comorbidities.

common causes include

Differentiating Peliosis hepatis from Other Diseases

Peliosis hepatis must be differentiated from Hepatic Adenoma, Hemangioma, Focal Nodular Hyperplasia, Hepatic Abscess, Hypervascular Metastases, and Hepatocellular Carcinoma.[9] Polycystic liver disease, Congenital hepatic fibrosis, Solitary congenital cysts, Hydatid cyst, Von Meyenburg complexes, Caroli disease (type V choledochal cyst).[10]

Epidemiology and Demographics

The prevalence of Peliosis hepatis is approximately 0.2 percent of patients with pulmonary tuberculosis and about 22 percent in patients following renal transplant. It is most commonly associated with renal transplants. Closing </ref> missing for <ref> tagClosing </ref> missing for <ref> tag

Physical Examination

The condition is typically asymptomatic and is discovered following evaluation of abnormal liver function test. However, when severe it can manifest as jaundice, hepatomegaly, liver failure and haemoperitoneum.

Laboratory Findings

There are no diagnostic laboratory findings associated with Peliosis Hepatis

Imaging Findings

Ultrasound appears non-specific, usually demonstrating an irregular hypoechoic region or mass,[11] and on Computerized Tomography (CT scan) shows multiple hypoattenuating lesions of variable size. Central bleeding may lead to areas of hyperattenuating and even dystrophic calcification.[12] Magnetic resonance imaging (MRI) may typically show hypointense, hyperintense, or enhancement, usually centrifugal (from the center outward). Angiography may show hypervascularity with multiple vascular nodules. [13]

Other Diagnostic Studies

There are no other diagnostic studies associated with Peliosis Hepatis

Treatment

Medical Therapy

  • Bacillary peliosis hepatitis (peliosis hepatis caused by Bartonella spp.)[14]
  • Preferred regimen (1): Clarithromycin 500 mg bid for 4 months
  • Preferred regimen (6): Erythromycin 500 mg PO qid for 4 months
  • Preferred regimen (2): Doxycycline 100 mg PO bid for 4 months
  • Special Consideration
  • Severe disease
  • Preferred regimen: Doxycycline 100 mg PO/IV bid for 4 months AND Rifampin 300 mg PO bid for 4 months

Surgery

Prevention

See Also

References

  1. ↑ 1.0 1.1 Sleisenger, Marvin (2006). Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. Philadelphia: W.B. Saunders Company. ISBN 1416002456. Chapter 80
  2. ↑ Ichijima K, Kobashi Y, Yamabe H, Fujii Y, Inoue Y (1980). “Peliosis hepatis. An unusual case involving multiple organs”. Acta Pathol. Jpn. 30 (1): 109–20. PMID 7361545.
  3. ↑ “Henry George Liddell, Robert Scott, A Greek-English Lexicon”. Retrieved 2007-06-11.
  4. ↑ “Charlton T. Lewis, Charles Short, A Latin Dictionary”. Retrieved 2007-07-02.
  5. ↑ “Henry George Liddell, Robert Scott, A Greek-English Lexicon”. Retrieved 2007-07-02.
  6. ↑ Gushiken FC (2000). “Peliosis hepatis after treatment with 2-chloro-3′-deoxyadenosine”. South. Med. J. 93 (6): 625–6. PMID 10881786.
  7. ↑ YANOFF M, RAWSON AJ (1964). “PELIOSIS HEPATIS. AN ANATOMIC STUDY WITH DEMONSTRATION OF TWO VARIETIES”. Archives of pathology. 77: 159–65. PMID 14088761.
  8. ↑ https://www.ajronline.org/doi/10.2214/AJR.05.0167#:~:text=The%20cause%20of%20peliosis%20hepatis,chronic%20wasting%20diseases%20(e.g.%2C%20tuberculosis
  9. ↑ https://www.ajronline.org/doi/10.2214/AJR.05.0167#:~:text=The%20cause%20of%20peliosis%20hepatis,chronic%20wasting%20diseases%20(e.g.%2C%20tuberculosis
  10. ↑ https://www.ncbi.nlm.nih.gov/books/NBK554470/
  11. ↑ Savastano S, San Bortolo O, Velo E, Rettore C, Altavilla G (2005). “Pseudotumoral appearance of peliosis hepatis”. AJR Am J Roentgenol. 185 (2): 558–9. doi:10.2214/ajr.185.2.01850558. PMID 16037541.
  12. ↑ https://doi.org/10.1148/rg.287085067 /
  13. ↑ https://radiopaedia.org/articles/hepatic-peliosis?lang=us/
  14. ↑ Gilbert, David (2015). The Sanford guide to antimicrobial therapy. Sperryville, Va: Antimicrobial Therapy. ISBN 978-1930808843.

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Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

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Overview

There is limited information about the historical perspective of Peliosis hepatis

Historical Perspective

There is limited information about the historical perspective of Peliosis hepatis

References

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Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Farwa Haideri [2]

Overview

There is no established system for the classification of Peliosis hepatis

Classification

There is no established system for the classification of Peliosis hepatis

References

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Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

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Overview

The pathogenesis of peliosis hepatis is unknown. There are several hypotheses, such as, it arise from sinusoidal epithelial damage[1], increased sinusoidal pressure due to obstruction in blood outflow from the liver, or hepatocellular necrosis[2].

Pathophysiology

The pathogenesis of peliosis hepatis is unknown. There are several hypotheses, such as, it arise from sinusoidal epithelial damage[3], increased sinusoidal pressure due to obstruction in blood outflow from the liver, or hepatocellular necrosis[2].

Two morphologic patterns of hepatic peliosis were described by Yanoff and Rawson [4]. In the phlebectatic type, the blood-filled spaces are lined with endothelium and are associated with aneurismal dilatation of the central vein; in the parenchymal type, the spaces have no endothelial lining and they usually are associated with haemorrhagic parenchymal necrosis. Some considers both pattern to be one process, initiated by focal necrosis of liver parenchyma observed in parenchymal type progressing into formation of fibrous wall and endothelial lining around haemorrhage of phebectatic type. Fibrosis, cirrhosis, regenerative nodules, and tumours may also be seen.

References

  1. ↑ Gushiken FC (2000). “Peliosis hepatis after treatment with 2-chloro-3′-deoxyadenosine”. South. Med. J. 93 (6): 625–6. PMID 10881786.
  2. ↑ 2.0 2.1 Invalid <ref> tag; no text was provided for refs named marvin
  3. ↑ Gushiken FC (2000). “Peliosis hepatis after treatment with 2-chloro-3′-deoxyadenosine”. South. Med. J. 93 (6): 625–6. PMID 10881786.
  4. ↑ YANOFF M, RAWSON AJ (1964). “PELIOSIS HEPATIS. AN ANATOMIC STUDY WITH DEMONSTRATION OF TWO VARIETIES”. Archives of pathology. 77: 159–65. PMID 14088761.

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Causes

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

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Overview

Peliosis hepatis may be caused by drugs, toxins, chronic wasting disease, malignancy, and infection. Peliosis Hepatitis may develop in individuals with renal or cardiac transplantation, but in about 20-50% of patients, they are no comorbidities.

Causes

Peliosis hepatis may be caused by drugs, toxins, chronic wasting disease, malignancy, and infection. Peliosis Hepatitis may develop in individuals with renal or cardiac transplantation, but in about 20-50% of patients, they are no comorbidities.

common causes include

References

  1. ↑ https://www.ajronline.org/doi/10.2214/AJR.05.0167#:~:text=The%20cause%20of%20peliosis%20hepatis,chronic%20wasting%20diseases%20(e.g.%2C%20tuberculosis

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Differentiating Peliosis hepatis from Other Diseases

Differentiating Peliosis hepatis from Other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

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Overview

Peliosis hepatis must be differentiated from Hepatic Adenoma, Hemangioma, Focal Nodular Hyperplasia, Hepatic Abscess, Hypervascular Metastases, and Hepatocellular Carcinoma.[1] Polycystic liver disease, Congenital hepatic fibrosis, Solitary congenital cysts, Hydatid cyst, Von Meyenburg complexes, Caroli disease (type V choledochal cyst).[2]

Differential Diagnosis

Peliosis hepatis must be differentiated from Hepatic Adenoma Hemangioma Focal Nodular Hyperplasia Hepatic Abscess Hypervascular Metastases Hepatocellular Carcinoma.[3] Polycystic liver disease, Congenital hepatic fibrosis, Solitary congenital cysts, Hydatid cyst, Von Meyenburg complexes, Caroli disease (type V choledochal cyst).[4] R.|title=Hypervascular Liver Masses on Contrast-Enhanced Ultrasound: The Importance of Washout|journal=American Journal of Roentgenology|volume=194|issue=4|year=2010|pages=977–983|issn=0361-803X|doi=10.2214/AJR.09.3375}}</ref>[5][6][7][8][9][10][11][12][13][14][15][16] [17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33]

Abbreviations: RUQ= Right upper quadrant of the abdomen, LUQ= Left upper quadrant, LLQ= Left lower quadrant, RLQ= Right lower quadrant, LFT= Liver function test, SIRS= Systemic inflammatory response syndrome, ERCP= Endoscopic retrograde cholangiopancreatography, IV= Intravenous, N= Normal, AMA= Anti-mitochondrial antibodies, LDH= Lactate dehydrogenase, GI= Gastrointestinal, CXR= Chest X ray, IgA= Immunoglobulin A, IgG= Immunoglobulin G, IgM= Immunoglobulin M, CT= Computed tomography, PMN= Polymorphonuclear cells, ESR= Erythrocyte sedimentation rate, CRP= C-reactive protein, TS= Transferrin saturation, SF= Serum ferritin, SMA= Superior mesenteric artery, SMV= Superior mesenteric vein, ECG= Electrocardiogram

Disease Clinical Manifestations Diagnosis Comments
Symptoms Signs
Abdominal Pain Fever Rigors and Chills Nausea or Vomiting Jaundice Constipation Diarrhea Weight Loss GI Bleeding Hypotension Guarding Rebound Tenderness Bowel Sounds Lab Findings Imaging
Hepatocellular adenoma RUQ – – – – – – – + + – –
  • Normal
Hepatocellular carcinoma/Metastasis RUQ + − + + + + + + + − +

Other symptoms:

Cholangiocarcinoma RUQ + − + + − − + − − − +
  • Normal
Pancreatic carcinoma MidEpigastric − − + + + − + − − − +
  • Normal

Skin manifestations may include:

Focal nodular hyperplasia Diffuse ± − − ± − − + + − − −
  • Normal
Disease Abdominal Pain Fever Rigors and Chills Nausea or Vomiting Jaundice Constipation Diarrhea Weight Loss GI Bleeding Hypotension Guarding Rebound Tenderness Bowel Sounds Lab Findings Imaging Comments
Gallbladder cancer Midepigastric − − + + − + + − − − −
  • Normal
Liver hemangioma Intermittent RUQ − − + + − − − − − − −
  • Normal
Liver abscess RUQ + − + + − − + − − − −
  • Normal
Cirrhosis RUQ +Bloating + − + + − − + − − − −
  • Normal
Inflammatory lesions RUQ ± − + + − − − − − − −
  • Normal
  • Stigmata of liver disease

References

  1. ↑ https://www.ajronline.org/doi/10.2214/AJR.05.0167#:~:text=The%20cause%20of%20peliosis%20hepatis,chronic%20wasting%20diseases%20(e.g.%2C%20tuberculosis
  2. ↑ https://www.ncbi.nlm.nih.gov/books/NBK554470/
  3. ↑ https://www.ajronline.org/doi/10.2214/AJR.05.0167#:~:text=The%20cause%20of%20peliosis%20hepatis,chronic%20wasting%20diseases%20(e.g.%2C%20tuberculosis
  4. ↑ https://www.ncbi.nlm.nih.gov/books/NBK554470/
  5. ↑ Tamada T, Ito K, Yamamoto A, Sone T, Kanki A, Tanaka F, Higashi H (2011). “Hepatic hemangiomas: evaluation of enhancement patterns at dynamic MRI with gadoxetate disodium”. AJR Am J Roentgenol. 196 (4): 824–30. doi:10.2214/AJR.10.5113. PMID 21427331.
  6. ↑ Heiken, Jay P. (2007). “Distinguishing benign from malignant liver tumours”. Cancer Imaging. 7 (Special Issue A): S1–S14. doi:10.1102/1470-7330.2007.9084. ISSN 1470-7330.
  7. ↑ Alturkistany, Samira; Jang, Hyun-Jung; Yu, Hojun; Lee, Kyoung Ho; Kim, Tae Kyoung (2011). “Fading hepatic hemangiomas on multiphasic CT”. Abdominal Radiology. 37 (5): 775–780. doi:10.1007/s00261-011-9826-6. ISSN 2366-004X.
  8. ↑ Liu GJ, Lu MD, Xie XY, Xu HX, Xu ZF, Zheng YL, Liang JY, Wang W (2008). “Real-time contrast-enhanced ultrasound imaging of infected focal liver lesions”. J Ultrasound Med. 27 (4): 657–66. PMID 18359914.
  9. ↑ Kim, Kyoung Won; Choi, Byung Ihn; Park, Seong Ho; Kim, Ah Young; Koh, Young Hwan; Lee, Hyun Ju; Han, Joon Koo (2004). “Pyogenic hepatic abscesses: distinctive features from hypovascular hepatic malignancies on contrast-enhanced ultrasound with SH U 508A; early experience”. Ultrasound in Medicine & Biology. 30 (6): 725–733. doi:10.1016/j.ultrasmedbio.2004.03.006. ISSN 0301-5629.
  10. ↑ Invalid <ref> tag; no text was provided for refs named pmid16641791
  11. ↑ Syed MA, Kim TK, Jang HJ (2007). “Portal and hepatic vein thrombosis in liver abscess: CT findings”. Eur J Radiol. 61 (3): 513–9. doi:10.1016/j.ejrad.2006.11.022. PMID 17161932.
  12. ↑ Menias, Christine O.; Surabhi, Venkateswar R.; Prasad, Srinivasa R.; Wang, Hanlin L.; Narra, Vamsi R.; Chintapalli, Kedar N. (2008). “Mimics of Cholangiocarcinoma: Spectrum of Disease”. RadioGraphics. 28 (4): 1115–1129. doi:10.1148/rg.284075148. ISSN 0271-5333.
  13. ↑ Gollapudi P, Chejfec G, Zarling EJ (1992). “Spontaneous regression of hepatic pseudotumor”. Am. J. Gastroenterol. 87 (2): 214–7. PMID 1734701.
  14. ↑ Yoon KH, Ha HK, Lee JS, Suh JH, Kim MH, Kim PN, Lee MG, Yun KJ, Choi SC, Nah YH, Kim CG, Won JJ, Auh YH (1999). “Inflammatory pseudotumor of the liver in patients with recurrent pyogenic cholangitis: CT-histopathologic correlation”. Radiology. 211 (2): 373–9. doi:10.1148/radiology.211.2.r99ma36373. PMID 10228516.
  15. ↑ CHEDID, Marcio F.; KRUEL, Cleber R. P.; PINTO, Marcelo A.; GREZZANA-FILHO, Tomaz J. M.; LEIPNITZ, Ian; KRUEL, Cleber D. P.; SCAFFARO, Leandro A.; CHEDID, Aljamir D. (2017). “HEPATOCELLULAR CARCINOMA: DIAGNOSIS AND OPERATIVE MANAGEMENT”. ABCD. Arquivos Brasileiros de Cirurgia Digestiva (São Paulo). 30 (4): 272–278. doi:10.1590/0102-6720201700040011. ISSN 2317-6326.
  16. ↑ Luigi Grazioli, Lucio Olivetti, Giancarlo Mazza & Maria Pia Bondioni (2013). “MR Imaging of Hepatocellular Adenomas and Differential Diagnosis Dilemma”. International journal of hepatology. 2013: 374170. doi:10.1155/2013/374170. PMID 23606972.
  17. ↑ Lucas Maillette de Buy Wenniger, Valeska Terpstra & Ulrich Beuers (2010). “Focal nodular hyperplasia and hepatic adenoma: epidemiology and pathology”. Digestive surgery. 27 (1): 24–31. doi:10.1159/000268404. PMID 20357448.
  18. ↑ Christian Grieser, Ingo G. Steffen, Daniel Seehofer, Incken-Birthe Kramme, Robert Uktolseya, Christian Scheurig-Muenkler, Bernd Hamm & Timm Denecke (2013). “Histopathologically confirmed focal nodular hyperplasia of the liver: gadoxetic acid-enhanced MRI characteristics”. Magnetic resonance imaging. 31 (5): 755–760. doi:10.1016/j.mri.2012.11.006. PMID 23219272. Unknown parameter |month= ignored (help)
  19. ↑ Shahid M. Hussain, Turkan Terkivatan, Pieter E. Zondervan, Esmee Lanjouw, Sjoerd de Rave, Jan N. M. Ijzermans & Rob A. de Man (2004). “Focal nodular hyperplasia: findings at state-of-the-art MR imaging, US, CT, and pathologic analysis”. Radiographics : a review publication of the Radiological Society of North America, Inc. 24 (1): 3–17. doi:10.1148/rg.241035050. PMID 14730031. Unknown parameter |month= ignored (help)
  20. ↑ J. T. Ames, M. P. Federle & K. Chopra (2009). “Distinguishing clinical and imaging features of nodular regenerative hyperplasia and large regenerative nodules of the liver”. Clinical radiology. 64 (12): 1190–1195. doi:10.1016/j.crad.2009.07.015. PMID 19913129. Unknown parameter |month= ignored (help)
  21. ↑ Giovanni Morana, Luigi Grazioli, Miles A. Kirchin, Maria Pia Bondioni, Niccolo Faccioli, Alessandro Guarise & Gunther Schneider (2011). “Solid hypervascular liver lesions: accurate identification of true benign lesions on enhanced dynamic and hepatobiliary phase magnetic resonance imaging after gadobenate dimeglumine administration”. Investigative radiology. 46 (4): 225–239. doi:10.1097/RLI.0b013e3181feee3a. PMID 21102346. Unknown parameter |month= ignored (help)
  22. ↑ I. R. Wanless (1990). “Micronodular transformation (nodular regenerative hyperplasia) of the liver: a report of 64 cases among 2,500 autopsies and a new classification of benign hepatocellular nodules”. Hepatology (Baltimore, Md.). 11 (5): 787–797. PMID 2189821. Unknown parameter |month= ignored (help)
  23. ↑ I. R. Wanless (1996). “Nodular regenerative hyperplasia, dysplasia, and hepatocellular carcinoma”. The American journal of gastroenterology. 91 (5): 836–837. PMID 8633567. Unknown parameter |month= ignored (help)
  24. ↑ T. Ichikawa, M. P. Federle, L. Grazioli, J. Madariaga, M. Nalesnik & W. Marsh (1999). “Fibrolamellar hepatocellular carcinoma: imaging and pathologic findings in 31 recent cases”. Radiology. 213 (2): 352–361. doi:10.1148/radiology.213.2.r99nv31352. PMID 10551212. Unknown parameter |month= ignored (help)
  25. ↑ Jose Traila Campos, Claude B. Sirlin & Jin-Young Choi (2012). “Focal hepatic lesions in Gd-EOB-DTPA enhanced MRI: the atlas”. Insights into imaging. 3 (5): 451–474. doi:10.1007/s13244-012-0179-7. PMID 22700119. Unknown parameter |month= ignored (help)
  26. ↑ Christine Sempoux, Ghalib Jibara, Stephen C. Ward, Cathy Fan, Lihui Qin, Sasan Roayaie, M. Isabel Fiel, Myron Schwartz & Swan N. Thung (2011). “Intrahepatic cholangiocarcinoma: new insights in pathology”. Seminars in liver disease. 31 (1): 49–60. doi:10.1055/s-0031-1272839. PMID 21344350. Unknown parameter |month= ignored (help)
  27. ↑ Nathalie Guedj, Pierre Bedossa & Valerie Paradis (2010). “[Pathology of cholangiocarcinoma]”. Annales de pathologie. 30 (6): 455–463. doi:10.1016/j.annpat.2010.10.004. PMID 21167432. Unknown parameter |month= ignored (help)
  28. ↑ Y. Maetani, K. Itoh, C. Watanabe, T. Shibata, F. Ametani, H. Yamabe & J. Konishi (2001). “MR imaging of intrahepatic cholangiocarcinoma with pathologic correlation”. AJR. American journal of roentgenology. 176 (6): 1499–1507. doi:10.2214/ajr.176.6.1761499. PMID 11373220. Unknown parameter |month= ignored (help)
  29. ↑ Riccardo Manfredi, Brunella Barbaro, Gabriele Masselli, Amorino Vecchioli & Pasquale Marano (2004). “Magnetic resonance imaging of cholangiocarcinoma”. Seminars in liver disease. 24 (2): 155–164. doi:10.1055/s-2004-828892. PMID 15192788. Unknown parameter |month= ignored (help)
  30. ↑ P. Soyer, B. Van Beers, C. Grandin, J. Pringot & M. Levesque (1993). “Primary lymphoma of the liver: MR findings”. European journal of radiology. 16 (3): 209–212. PMID 8508837. Unknown parameter |month= ignored (help)
  31. ↑ E. S. Zafrani & P. Gaulard (1993). “Primary lymphoma of the liver”. Liver. 13 (2): 57–61. PMID 8510487. Unknown parameter |month= ignored (help)
  32. ↑ Saravanan Namasivayam, Diego R. Martin & Sanjay Saini (2007). “Imaging of liver metastases: MRI”. Cancer imaging : the official publication of the International Cancer Imaging Society. 7: 2–9. doi:10.1102/1470-7330.2007.0002. PMID 17293303.
  33. ↑ Daichi Hayashi, Jaroslaw N. Tkacz, Stephen Hammond, Brooke C. Devenney-Cakir, Souhil Zaim, Nadia Bouzegaou, Souhila Ounadjela & Ali Guermazi (2011). “Gastroenteropancreatic neuroendocrine tumors: multimodality imaging features with pathological correlation”. Japanese journal of radiology. 29 (2): 85–91. doi:10.1007/s11604-010-0522-1. PMID 21359932. Unknown parameter |month= ignored (help)

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Epidemiology and Demographics

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

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Overview

Epidemiology and Demographics

The epidemiology of Peliosis hepatis is not completely understood, Peliosis Hepatis is usually asymptomatic, thus most cases go undiagnonised. [1]

Multiple studies associate Peliosis Hepatis with pulmonary tuberculosis, carcinomatosis, HIV infection, aplastic anemia treated with anabolic steroids, systemic lupus erythematosus treated with high-dose glucocorticoids, and patients who underwent renal transplantation. [2].

  • The prevalence was 0.2 percent in patients with pulmonary tuberculosis
  • Five cases of PH were observed in a study of 17,000 patients with HIV infection
  • The prevalence ranged from 0 to 22 percent in patients who underwent renal transplantation. [3]

References

  1. ↑ https://somepomed.org/articulos/contents/mobipreview.htm?26/61/27615/abstract/2
  2. ↑ https://somepomed.org/articulos/contents/mobipreview.htm?26/61/27615/abstract/2
  3. ↑ https://somepomed.org/articulos/contents/mobipreview.htm?26/61/27615/abstract/2

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Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

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Overview

Common risk factors in the development of Peliosis Hepatis include certain drugs, malignancy, infections, and chronic conditions.

Risk Factors

Common risk factors in the development of Peliosis Hepatis include certain drugs [1], malignancy, infections, and chronic conditions.

A study of Molecular Epidemiology of Bartonella Infections in Patients with Bacillary Angiomatosis–Peliosis show that peliosis hepatis was associated exclusively with B. henselae. Some chronic conditions like Kidney transplant.[2] Some chronic conditions like Kidney transplant. [3]

  • Infections: HIV, Bacillary peliosis (caused by genus Bartonella, bacteria responsible for cat-scratch disease which are identified histologically adjacent to the peliotic lesions.[2]

Prognosis

Depending on if the right diagnosis was made, the prognosis may vary. Peliosis hepatis should not be drained. If mistaken for hepatic abscess and drained, it can lead to life-threatening hemorrhage. However, the prognosis is generally regarded as excellent.[8]

References

  1. ↑ Schmoldt A, Benthe HF, Haberland G (1975). “Digitoxin metabolism by rat liver microsomes”. Biochem Pharmacol. 24 (17): 1639–41. PMID https://doi.org/10.1016/B978-0-12-387817-5.00033-9 Check |pmid= value (help).
  2. ↑ 2.0 2.1 Koehler JE, Sanchez MA, Garrido CS, Whitfeld MJ, Chen FM, Berger TG; et al. (1997). “Molecular epidemiology of bartonella infections in patients with bacillary angiomatosis-peliosis”. N Engl J Med. 337 (26): 1876–83. doi:10.1056/NEJM199712253372603. PMID 9407154.
  3. ↑ Schmoldt A, Benthe HF, Haberland G (1975). “Digitoxin metabolism by rat liver microsomes”. Biochem Pharmacol. 24 (17): 1639–41. PMID https://doi.org/10.1016/S0168-8278(05)80479-9 Check |pmid= value (help).
  4. ↑ Haboubi NY, Ali HH, Whitwell HL, Ackrill P (1988). “Role of endothelial cell injury in the spectrum of azathioprine-induced liver disease after renal transplant: light microscopy and ultrastructural observations”. Am. J. Gastroenterol. 83 (3): 256–61. PMID 3278593.
  5. ↑ Izumi S, Nishiuchi M, Kameda Y, Nagano S, Fukunishi T, Kohro T, Shinji Y (1994). “Laparoscopic study of peliosis hepatis and nodular transformation of the liver before and after renal transplantation: natural history and aetiology in follow-up cases”. J. Hepatol. 20 (1): 129–37. PMID 8201214.
  6. ↑ Cavalcanti R, Pol S, Carnot F, Campos H, Degott C, Driss F, Legendre C, Kreis H (1994). “Impact and evolution of peliosis hepatis in renal transplant recipients”. Transplantation. 58 (3): 315–6. PMID 8053054.
  7. ↑ Goldman, Lee (2003). Cecil Textbook of Medicine — 2-Volume Set, Text with Continually Updated Online Reference. Philadelphia: W.B. Saunders Company. ISBN 0721645631.
  8. ↑ Cohen GS, Ball DS, Boyd-Kranis R, Gembala RB, Wurzel J (1994). “Peliosis hepatis mimicking hepatic abscess: fatal outcome following percutaneous drainage”. J Vasc Interv Radiol. 5 (4): 643–5. doi:10.1016/s1051-0443(94)71572-4. PMID 7949724.

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Screening

Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

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Overview

There is insufficient evidence to recommend routine screening for Peliosis Hepatis.

Screening

There is insufficient evidence to recommend routine screening for Peliosis Hepatis.

References

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Natural History, Complications, and Prognosis

Natural History, Complications, and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

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Overview

If left untreated, some patients with Peliosis Hepatis may progress to develop hemoperitoneum.

Natural History

Complications

If left untreated, some patients with Peliosis Hepatis may progress to develop hemoperitoneum. [1]

Prognosis

Prognosis is uncertain, and most patients will remain asymptomatic. In some individuals, it can lead to a life-threatening complication with a high rate of mortality. [2]

References

  1. ↑ “Correction to Lancet Infectious Diseases 2020; published online April 29. https://doi.org/10.1016/ S1473-3099(20)30064-5”. Lancet Infect Dis. 20 (7): e148. 2020. doi:10.1016/S1473-3099(20)30370-4. PMID 32595044 Check |pmid= value (help). External link in |title= (help)
  2. ↑ Choi SK, Jin JS, Cho SG, Choi SJ, Kim CS, Choe YM; et al. (2009). “Spontaneous liver rupture in a patient with peliosis hepatis: a case report”. World J Gastroenterol. 15 (43): 5493–7. doi:10.3748/wjg.15.5493. PMC 2778108. PMID 19916182.

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Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | Chest X Ray | CT | MRI | Echocardiography or Ultrasound | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1

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