Lysozyme amyloid related amyloidosis: Difference between revisions
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* Common [[symptoms]] of Lysozyme amyloid related amyloidosis include [[fatigue]], [[weight loss]] and, [[edema]].<ref name="pmid26161016">{{cite journal |vauthors=Lim AY, Lee JH, Jung KS, Gwag HB, Kim DH, Kim SJ, Lee GY, Kim JS, Kim HJ, Lee SY, Lee JE, Jeon ES, Kim K |title=Clinical features and outcomes of systemic amyloidosis with gastrointestinal involvement: a single-center experience |journal=Korean J. Intern. Med. |volume=30 |issue=4 |pages=496–505 |date=July 2015 |pmid=26161016 |pmc=4497337 |doi=10.3904/kjim.2015.30.4.496 |url=}}</ref><ref name="pmid23227278">{{cite journal |vauthors=Baker KR, Rice L |title=The amyloidoses: clinical features, diagnosis and treatment |journal=Methodist Debakey Cardiovasc J |volume=8 |issue=3 |pages=3–7 |date=2012 |pmid=23227278 |pmc=3487569 |doi= |url=}}</ref> | * Common [[symptoms]] of Lysozyme amyloid related amyloidosis include [[fatigue]], [[weight loss]] and, [[edema]].<ref name="pmid26161016">{{cite journal |vauthors=Lim AY, Lee JH, Jung KS, Gwag HB, Kim DH, Kim SJ, Lee GY, Kim JS, Kim HJ, Lee SY, Lee JE, Jeon ES, Kim K |title=Clinical features and outcomes of systemic amyloidosis with gastrointestinal involvement: a single-center experience |journal=Korean J. Intern. Med. |volume=30 |issue=4 |pages=496–505 |date=July 2015 |pmid=26161016 |pmc=4497337 |doi=10.3904/kjim.2015.30.4.496 |url=}}</ref><ref name="pmid23227278">{{cite journal |vauthors=Baker KR, Rice L |title=The amyloidoses: clinical features, diagnosis and treatment |journal=Methodist Debakey Cardiovasc J |volume=8 |issue=3 |pages=3–7 |date=2012 |pmid=23227278 |pmc=3487569 |doi= |url=}}</ref> | ||
*Other [[symptoms]] of Lyzozyme amyloid related amyloidosis include [[Sicca syndrome|sicca]], [[diarrhea]], [[nausea]], [[abdominal discomfort]], [[GI bleeding]], worsening [[kidney function]]. | *Other [[symptoms]] of Lyzozyme amyloid related amyloidosis include [[Sicca syndrome|sicca]], [[diarrhea]], [[nausea]], [[abdominal discomfort]], [[GI bleeding]], worsening [[kidney function]].<ref>{{Cite journal | ||
| author = [[J. G. Lanham]], [[M. L. Meltzer]], [[F. C. De Beer]], [[G. R. Hughes]] & [[M. B. Pepys]] | |||
| title = Familial amyloidosis of Ostertag | |||
| journal = [[The Quarterly journal of medicine]] | |||
| volume = 51 | |||
| issue = 201 | |||
| pages = 25–32 | |||
| year = 1982 | |||
| month = | |||
| pmid = 7111672 | |||
}}</ref><ref name="GillmoreBooth1999">{{cite journal|last1=Gillmore|first1=Julian D.|last2=Booth|first2=David R.|last3=Madhoo|first3=S.|last4=Pepys|first4=Mark B.|last5=Hawkins|first5=Philip N.|title=Hereditary renal amyloidosis associated with variant lysozyme in a large English family|journal=Nephrology Dialysis Transplantation|volume=14|issue=11|year=1999|pages=2639–2644|issn=1460-2385|doi=10.1093/ndt/14.11.2639}}</ref><ref name="PepysHawkins1993">{{cite journal|last1=Pepys|first1=M. B.|last2=Hawkins|first2=P. N.|last3=Booth|first3=D. R.|last4=Vigushin|first4=D. M.|last5=Tennent|first5=G. A.|last6=Soutar|first6=A. K.|last7=Totty|first7=N.|last8=Nguyen|first8=O.|last9=Blake|first9=C. C. F.|last10=Terry|first10=C. J.|last11=Feest|first11=T. G.|last12=Zalin|first12=A. M.|last13=Hsuan|first13=J. J.|title=Human lysozyme gene mutations cause hereditary systemic amyloidosis|journal=Nature|volume=362|issue=6420|year=1993|pages=553–557|issn=0028-0836|doi=10.1038/362553a0}}</ref><ref name="Yood1983">{{cite journal|last1=Yood|first1=Robert A.|title=Bleeding Manifestations in 100 Patients With Amyloidosis|journal=JAMA: The Journal of the American Medical Association|volume=249|issue=10|year=1983|pages=1322|issn=0098-7484|doi=10.1001/jama.1983.03330340064034}}</ref> | |||
===Physical Examination=== | ===Physical Examination=== | ||
Revision as of 16:17, 20 November 2019
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Homa Najafi, M.D.[2]
Synonyms and keywords:Lysozyme amyloidosis, ALys, Hereditory amyloidosis, autosomal dominant amyloidosis, Hereditary lysozyme amyloidosis, Familial amyloid nephropathy due to lysozyme variant, Familial renal amyloidosis due to lysozyme variant, Hereditary amyloid nephropathy due to lysozyme variant, Hereditary renal amyloidosis due to lysozyme variant
Overview
Four different mutations in lysozyme which are associated with amyloidosis have been defined . Each is associated with adult-onset renal failure due to glomerular deposition of amyloid. The entire 14 500-Dalton lysozyme protein has been found in amyloid deposits and, in some studies, its function as a bacteriolytic enzyme has been preserved after isolation from amyloid-laden tissues.22 Clinical presentation as renal failure may occur in the third or fourth decades, and kidney transplantation has been found to be an effective mode of therapy for a number of patients.
Historical Perspective
- In 1639, Nicolaus Fontanus autopsied a young man who had ascites, jaundice, liver abscess, and splenomegaly and his report has been the first description of amyloidosis.[1]
- In 1854, Rudolph Virchow introduced the term "amyloid" as a macroscopic abnormality in some tissues.[2]
- In 1867, Weber reported the first case of amyloidosis associated with multiple myeloma.[1]
- In 1922, Bennhold introduced Congo Red staining of amyloid that remains the gold standard for diagnosis.[3]
- In 1959, Cohen and Calkins used ultrathin sections of amyloidotic tissues and assessed by electron microscopy, explained the presence of non-branching fibrils with indeterminate length and variable width.[2][1]
- In 1993, Pepys introduced that lysozyme form as an an amyloid fibril protein is a variant of hereditary systemic amyloidosis.[4]
Classification
Apolipoprotein AI amyloidosis is one of the subtypes of familial amyloidosis. Familiar amyloidosis may be classified according to the type of mutant protein into 6 subtypes:[5][6][7]
- Transthyretin (TTR)
- Apolipoprotein AI
- Apolipoprotein AII
- Fibrinogen Aa
- Lysozyme
- Gelsolin
- Cystatin C
| Familial amyloidosis subtypes | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Transthyretin (TTR) | Apolipoprotein AI | Gelsolin | Lysozyme | Cystatin C | Fibrinogen Aa-chain | Apolipoprotein AII | |||||||||||||||||||||||||||||||||||||||||||||||||||
Pathophysiology
- It is understood that amyloidosis is the result of deposition of Amyloid.[8]
- Amyloid is an abnormal insoluble extracellular protein which may cause organic dysfunction and a wide variety of clinical syndromes.
- These abnormal amyloids are derived from misfolding and aggregation of normally soluble proteins.
- Amyloid depositions also have glycosaminoglycans and serum amyloid P component (SAP) which alter the propensity for amyloid formation.[9][10][11]
- Amyloid deposition can disrupt tissue structure of involved organ and consequently leads to organ failure.[12]
Genetics
There are four genetic mutations which are associated with lysozyme amyloid related amyloidosis. include:[4]
- Ile56Thr
- Asp67His
- Trp64Arg
- Phe57Ile
Causes
Common cause of lysozyme amyloid related amyloidosis is genetic mutations.[13][5][6][14]
Differentiating ((Page name)) from Other Diseases
[Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as [differential dx1], [differential dx2], and [differential dx3].
OR
[Disease name] must be differentiated from [[differential dx1], [differential dx2], and [differential dx3].
Epidemiology and Demographics
- The incidence of amyloidosis is approximately 1.2 per 100,000 individuals per year worldwide.[15]
- The mortality rate of systemic amyloidosis is approximately 100 per 100,000 deaths in developed countries.[16]
- Lysozyme amyloid related amyloidosis commonly affects individuals in their third to fourth decades of life.[5]
- Hereditary amyloidosis subtypes include a substitution of an amino acid that is detected in approximately 4% of the african american population.[3]
- Men are more commonly affected by amyloidosis than women.[17]
Risk Factors
The most potent risk factor in the development of lysozyme amyloid related amyloidosis is positive familial history. Other risk factors include older age, male gender, and African-American race.[17][3][18]
Screening
There is insufficient evidence to recommend routine screening for lysozyme amyloid related amyloidosis.
Natural History, Complications, and Prognosis
- Important complication of lysozyme amyloid related amyloidosis is heavy bleeding caused by hepatic rupture and/or hemorrhagic lymph node rupture.[19]
Note: Because the risk of bleeding in this patients, liver biopsy should not be performed in suspected ones.[20]
Diagnosis
Diagnostic Study of Choice
The diagnosis of lysozyme amyloid related amyloidosis is based on the familial history, histologic analysis of affected organs and immunohitochemistry.
OR
The diagnosis of [disease name] is based on the [criteria name] criteria, which include [criterion 1], [criterion 2], and [criterion 3].
OR
The diagnosis of [disease name] is based on the [definition name] definition, which includes [criterion 1], [criterion 2], and [criterion 3].
OR
There are no established criteria for the diagnosis of [disease name].
First, a careful family history is needed to search for a hereditary form of amyloidosis. After questioning, many relatives may have similar syndromes, without a precise diagnosis, but in fact related to lysozyme amyloidosis. Diagnosis of amyloidosis depends on evaluation of tissue biopsy specimens with Congo red staining by demonstration of the pathognomonic red-green birefringence when viewed under cross-polarized light. Most of the time, histologic analysis is performed on affected organs such as kidneys and digestive tract. Due to the high risk of bleeding complications observed in the family described by Harrison et al16, liver biopsy should not be performed in suspected cases of lysozyme amyloidosis. Amyloid deposits can frequently be observed in labial salivary glands. To our knowledge there are no data in the literature concerning abdominal fat pad aspirate. The definitive technique for typing amyloid fibril proteins is direct amino-acid sequencing in vitro, but the isolation of fibrils requires substantial amounts of tissue available only after surgical resection or at autopsy. Thus, immunohistochemistry using a polyclonal antibody against lysozyme is the usual method to identify the nature of the protein. The third step is DNA testing to screen for genetic mutations associated with lysozyme amyloidosis; unfortunately, DNA sequencing for lysozyme amyloidosis is available only in research laboratories. As classically reported for other forms of systemic amyloidoses, the presence of the amyloid P component in deposits is the basis for the use of the radioisotope-labeled SAP tracer in diagnosis and evaluation. SAP scintigraphy has a high sensitivity for the detection of amyloid deposits in the liver, spleen, kidney, adrenal glands, and bone marrow and can be used to evaluate the extent of lysozyme amyloid deposits. Organs may be positive by SAP scintigraphy, without evidence of clinical disease.
History and Symptoms
- Common symptoms of Lysozyme amyloid related amyloidosis include fatigue, weight loss and, edema.[21][22]
- Other symptoms of Lyzozyme amyloid related amyloidosis include sicca, diarrhea, nausea, abdominal discomfort, GI bleeding, worsening kidney function.[23][24][4][25]
Physical Examination
Physical examination of patients with Lyzozyme amyloid related amyloidosis is usually remarkable for renal impairment, petechiae, purpura, lymphadenopathy, and splenomegaly.
Laboratory Findings
An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name].
OR
Laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].
OR
[Test] is usually normal among patients with [disease name].
OR
Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].
OR
There are no diagnostic laboratory findings associated with [disease name].
Electrocardiogram
There are no ECG findings associated with [disease name].
OR
An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
X-ray
There are no x-ray findings associated with [disease name].
OR
An x-ray may be helpful in the diagnosis of [disease name]. Findings on an x-ray suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
OR
There are no x-ray findings associated with [disease name]. However, an x-ray may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
Echocardiography or Ultrasound
There are no echocardiography/ultrasound findings associated with [disease name].
OR
Echocardiography/ultrasound may be helpful in the diagnosis of [disease name]. Findings on an echocardiography/ultrasound suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
OR
There are no echocardiography/ultrasound findings associated with [disease name]. However, an echocardiography/ultrasound may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
CT scan
There are no CT scan findings associated with [disease name].
OR
[Location] CT scan may be helpful in the diagnosis of [disease name]. Findings on CT scan suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
OR
There are no CT scan findings associated with [disease name]. However, a CT scan may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
MRI
There are no MRI findings associated with [disease name].
OR
[Location] MRI may be helpful in the diagnosis of [disease name]. Findings on MRI suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
OR
There are no MRI findings associated with [disease name]. However, a MRI may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].
Other Imaging Findings
There are no other imaging findings associated with [disease name].
OR
[Imaging modality] may be helpful in the diagnosis of [disease name]. Findings on an [imaging modality] suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
Other Diagnostic Studies
There are no other diagnostic studies associated with [disease name].
OR
[Diagnostic study] may be helpful in the diagnosis of [disease name]. Findings suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].
OR
Other diagnostic studies for [disease name] include [diagnostic study 1], which demonstrates [finding 1], [finding 2], and [finding 3], and [diagnostic study 2], which demonstrates [finding 1], [finding 2], and [finding 3].
Treatment
Medical Therapy
There is no treatment for lysozyme amyloid related amyloidosis; the mainstay of therapy is supportive care.[26]
Surgery
- Kidney transplant may be effective in patients with minor or absent extrarenal visceral involvement.[27][28]
- Liver transplant may be used as a palliative treatment.[29][30]
Primary Prevention
There are no established measures for the primary prevention of lysozyme amyloid related amyloidosis.
Secondary Prevention
Effective measures for the secondary prevention of lysozyme amyloid related amyloidosis include:[19]
References
- ↑ 1.0 1.1 1.2 Kyle RA (June 2011). "Amyloidosis: a brief history". Amyloid. 18 Suppl 1: 6–7. doi:10.3109/13506129.2011.574354001. PMID 21838413.
- ↑ 2.0 2.1 Sipe JD, Cohen AS (June 2000). "Review: history of the amyloid fibril". J. Struct. Biol. 130 (2–3): 88–98. doi:10.1006/jsbi.2000.4221. PMID 10940217.
- ↑ 3.0 3.1 3.2 Khan MF, Falk RH (November 2001). "Amyloidosis". Postgrad Med J. 77 (913): 686–93. PMC 1742163. PMID 11677276.
- ↑ 4.0 4.1 4.2 Pepys, M. B.; Hawkins, P. N.; Booth, D. R.; Vigushin, D. M.; Tennent, G. A.; Soutar, A. K.; Totty, N.; Nguyen, O.; Blake, C. C. F.; Terry, C. J.; Feest, T. G.; Zalin, A. M.; Hsuan, J. J. (1993). "Human lysozyme gene mutations cause hereditary systemic amyloidosis". Nature. 362 (6420): 553–557. doi:10.1038/362553a0. ISSN 0028-0836.
- ↑ 5.0 5.1 5.2 Benson, Merrill D (2003). "The hereditary amyloidoses". Best Practice & Research Clinical Rheumatology. 17 (6): 909–927. doi:10.1016/j.berh.2003.09.001. ISSN 1521-6942.
- ↑ 6.0 6.1 Benson, Merrill D (2003). "The hereditary amyloidoses". Best Practice & Research Clinical Rheumatology. 17 (6): 909–927. doi:10.1016/j.berh.2003.09.001. ISSN 1521-6942.
- ↑ Scriver, Charles (2001). The metabolic & molecular bases of inherited disease. New York: McGraw-Hill. ISBN 978-0079130358.
- ↑ Wechalekar AD, Gillmore JD, Hawkins PN (June 2016). "Systemic amyloidosis". Lancet. 387 (10038): 2641–2654. doi:10.1016/S0140-6736(15)01274-X. PMID 26719234.
- ↑ Pepys MB, Rademacher TW, Amatayakul-Chantler S, Williams P, Noble GE, Hutchinson WL, Hawkins PN, Nelson SR, Gallimore JR, Herbert J (June 1994). "Human serum amyloid P component is an invariant constituent of amyloid deposits and has a uniquely homogeneous glycostructure". Proc. Natl. Acad. Sci. U.S.A. 91 (12): 5602–6. doi:10.1073/pnas.91.12.5602. PMC 44044. PMID 8202534.
- ↑ Tan SY, Pepys MB (November 1994). "Amyloidosis". Histopathology. 25 (5): 403–14. doi:10.1111/j.1365-2559.1994.tb00001.x. PMID 7868080.
- ↑ Botto M, Hawkins PN, Bickerstaff MC, Herbert J, Bygrave AE, McBride A, Hutchinson WL, Tennent GA, Walport MJ, Pepys MB (August 1997). "Amyloid deposition is delayed in mice with targeted deletion of the serum amyloid P component gene". Nat. Med. 3 (8): 855–9. doi:10.1038/nm0897-855. PMID 9256275.
- ↑ Wechalekar AD, Gillmore JD, Hawkins PN (June 2016). "Systemic amyloidosis". Lancet. 387 (10038): 2641–2654. doi:10.1016/S0140-6736(15)01274-X. PMID 26719234.
- ↑ Pepys MB, Hawkins PN, Booth DR, Vigushin DM, Tennent GA, Soutar AK, Totty N, Nguyen O, Blake CC, Terry CJ (April 1993). "Human lysozyme gene mutations cause hereditary systemic amyloidosis". Nature. 362 (6420): 553–7. doi:10.1038/362553a0. PMID 8464497.
- ↑ Scriver, Charles (2001). The metabolic & molecular bases of inherited disease. New York: McGraw-Hill. ISBN 978-0079130358.
- ↑ Khan MF, Falk RH (November 2001). "Amyloidosis". Postgrad Med J. 77 (913): 686–93. PMC 1742163. PMID 11677276.
- ↑ Pepys MB (2006). "Amyloidosis". Annu. Rev. Med. 57: 223–41. doi:10.1146/annurev.med.57.121304.131243. PMID 16409147.
- ↑ 17.0 17.1 Shin YM (March 2011). "Hepatic amyloidosis". Korean J Hepatol. 17 (1): 80–3. doi:10.3350/kjhep.2011.17.1.80. PMC 3304630. PMID 21494083.
- ↑ Shin YM (March 2011). "Hepatic amyloidosis". Korean J Hepatol. 17 (1): 80–3. doi:10.3350/kjhep.2011.17.1.80. PMC 3304630. PMID 21494083.
- ↑ 19.0 19.1 Granel, Brigitte; Valleix, Sophie; Serratrice, Jacques; Chérin, Patrick; Texeira, Antonio; Disdier, Patrick; Weiller, Pierre-Jean; Grateau, Gilles (2006). "Lysozyme Amyloidosis". Medicine. 85 (1): 66–73. doi:10.1097/01.md.0000200467.51816.6d. ISSN 0025-7974.
- ↑ Harrison, R F; Hawkins, P N; Roche, W R; MacMahon, R F; Hubscher, S G; Buckels, J A (1996). "'Fragile' liver and massive hepatic haemorrhage due to hereditary amyloidosis". Gut. 38 (1): 151–152. doi:10.1136/gut.38.1.151. ISSN 0017-5749.
- ↑ Lim AY, Lee JH, Jung KS, Gwag HB, Kim DH, Kim SJ, Lee GY, Kim JS, Kim HJ, Lee SY, Lee JE, Jeon ES, Kim K (July 2015). "Clinical features and outcomes of systemic amyloidosis with gastrointestinal involvement: a single-center experience". Korean J. Intern. Med. 30 (4): 496–505. doi:10.3904/kjim.2015.30.4.496. PMC 4497337. PMID 26161016.
- ↑ Baker KR, Rice L (2012). "The amyloidoses: clinical features, diagnosis and treatment". Methodist Debakey Cardiovasc J. 8 (3): 3–7. PMC 3487569. PMID 23227278.
- ↑ J. G. Lanham, M. L. Meltzer, F. C. De Beer, G. R. Hughes & M. B. Pepys (1982). "Familial amyloidosis of Ostertag". The Quarterly journal of medicine. 51 (201): 25–32. PMID 7111672.
- ↑ Gillmore, Julian D.; Booth, David R.; Madhoo, S.; Pepys, Mark B.; Hawkins, Philip N. (1999). "Hereditary renal amyloidosis associated with variant lysozyme in a large English family". Nephrology Dialysis Transplantation. 14 (11): 2639–2644. doi:10.1093/ndt/14.11.2639. ISSN 1460-2385.
- ↑ Yood, Robert A. (1983). "Bleeding Manifestations in 100 Patients With Amyloidosis". JAMA: The Journal of the American Medical Association. 249 (10): 1322. doi:10.1001/jama.1983.03330340064034. ISSN 0098-7484.
- ↑ Pleyer, Christopher; Flesche, Jan; Saeed, Fahad (2015). "Lysozyme amyloidosis – a case report and review of the literature". Clinical Nephrology Case Studies. doi:10.5414/CNCS108538. ISSN 2196-5293.
- ↑ Yazaki, Masahide; Farrell, Sandra A.; Benson, Merrill D. (2003). "A novel lysozyme mutation Phe57Ile associated with hereditary renal amyloidosis". Kidney International. 63 (5): 1652–1657. doi:10.1046/j.1523-1755.2003.00904.x. ISSN 0085-2538.
- ↑ Valleix, Sophie; Drunat, Séverine; Philit, Jean-Baptiste; Adoue, Daniel; Piette, Jean-Charles; Droz, Dominique; MacGregor, Brigitte; Canet, Denis; Delpech, Marc; Grateau, Gilles (2002). "Hereditary renal amyloidosis caused by a new variant lysozyme W64R in a French family". Kidney International. 61 (3): 907–912. doi:10.1046/j.1523-1755.2002.00205.x. ISSN 0085-2538.
- ↑ Sattianayagam, P. T.; Gibbs, S. D. J.; Rowczenio, D.; Pinney, J. H.; Wechalekar, A. D.; Gilbertson, J. A.; Hawkins, P. N.; Lachmann, H. J.; Gillmore, J. D. (2012). "Hereditary lysozyme amyloidosis - phenotypic heterogeneity and the role of solid organ transplantation". Journal of Internal Medicine. 272 (1): 36–44. doi:10.1111/j.1365-2796.2011.02470.x. ISSN 0954-6820.
- ↑ Loss, Martin; Ng, Wa S.; Karim, Rooshdiya Z.; Strasser, Simone I.; Koorey, David J.; Gallagher, Peter J.; Verran, Deborah J.; McCaughan, Geoffrey W. (2006). "Hereditary lysozyme amyloidosis: Spontaneous hepatic rupture (15 years apart) in mother and daughter. role of emergency liver transplantation". Liver Transplantation. 12 (7): 1152–1155. doi:10.1002/lt.20803. ISSN 1527-6465.