Friday, December 12, 2014

President's Message December 2014

Dear Friends and Colleagues,

I would like to remind you that the HPHS  Companion Society Meeting at Boston is scheduled for March 22, 2015 from 8:30am-12 noon. The title is “Diagnostic Challenges and Update in Hepatopathology”. We have created a program that will not only be very educational to our members but will hopefully be interesting to non-members as well. The topics that will be discussed include new therapeutic interventions for hepatitis and liver cancer and what this means to the pathologist, differential diagnosis of fatty liver diseases, vascular diseases and portal hypertension, the basics of biomedical informatics and its applicability in general practice, diagnosis of mixed hepatocellular-cholangiocarcinoma, and the current methods available to assist in reaching a diagnosis in challenging liver pathology cases. Please see the last page of this Newsletter for the list of speakers and the title of their talks. 

The Business meeting will immediately follow the companion meeting. Members are encouraged to attend, as we will need to vote on some modifications to the bylaws as a result of the tax-exempt status of the HPHS, as well as some changes to the duties and responsibilities of the members of the Executive Committee. Please encourage both your junior and senior colleagues to officially become members of the HPHS. Residents and fellows can become Trainee members without having to pay any dues. They can easily transition to Regular membership once they finish their training. Application to membership is available on the website. Please email completed application to Maha Guindi (Maha.Guindi@cshs.org), chair of the membership committee. 

We have officially created a new Website Committee, and I am grateful that Dr. Arief Suriawinata has graciously agreed to be the Chair of this committee. Please see the website for new updates including the discussion and main learning points for the two interesting cases presented in this Newsletter. I would also like to thank Dr. Bita Naini, past member and the new Chair of the Newsletter Committee as the person behind the scenes in making this Newsletter go out. 

I look forward to seeing you all in Boston.

Sincerely,

Isabel Fiel, M.D.
President, Hans Popper Hepatopathology Society

Interesting Case December 2014 #1

Clinical History:

A 29 year old woman with a 5 year history of insulin dependent diabetes mellitus presented with right flank pain and constipation for the past 2 weeks. During the clinical work up, she was diagnosed with diabetic ketoacidosis and acalculous cholecystitis. Due to elevated liver enzymes and hepatomegaly, liver biopsy was performed during the laparoscopic cholecystectomy.

Labs:

At the time of presentation, the patient’s laboratory values were: blood glucose, 434 mg/dL (normal range [NR] 70-100 mg/dL); alkaline phosphatase, 131 U/L (NR 14-127 U/L); AST, 457 U/L (NR 5-46 U/L); ALT, 230 U/L (NR 4-51 U/L) and total bilirubin, 1.1 mg/dL (NR 0.1-1.5 U/L). 

Microscopic Images:


Figure 1. Low power view showing pale liver parenchyma without steatosis or inflammation.

Figure 2. Swollen and rarified hepatocytes with compressed sinusoids.

Figure 3. Hepatocytes with multiple giant mitochondria and glycogenated nuclei.

Diagnosis

Glycogenic Hepatopathy

Discussion

Glycogenic hepatopathy (GH) is not currently commonly seen in practice due to improved diabetic therapies. The typical clinical presentation is elevated blood glucose, elevated liver enzymes, hepatomegaly and abdominal pain. Other signs and symptoms can include abdominal distension, anorexia, nausea, right upper quadrant pain and shortness of breath. The liver biopsy in GH characteristically shows marked accumulation of glycogen in hepatocytes, but the diagnosis requires close clinicopathological correlation. 

The pathophysiology of GH is incompletely understood, but it is thought to be caused by prolonged periods of hyperglycemia in poorly controlled diabetic patients treated with insulin. The elevated blood glucose passes into hepatocytes independent of insulin. This is then followed by periods of insulin therapy in which the hepatic glucose is converted to glycogen and the glycogen becomes trapped in hepatocytes. It is thought that the excess hepatic glycogen accumulation leads to hepatocyte injury and causes “leakage” of aminotransferases. Significant hepatocellular death is not typical.

GH also been reported in patients with type II diabetes mellitus, urea cycle defects, and medication effects (e.g., short-term high dose steroids). The differential diagnosis includes hereditary glycogen storage diseases, smooth endoplasmic reticulum proliferation due to medication effects, and glycogen pseudoground glass changes associated with the intake of multiple medications (poly- pharmacotherapy). Rarely GH can coexist with NAFLD or steatohepatitis. Minimal fibrosis has rarely been described in GH; significant fibrosis is not characteristic.

Case contributed by

Jie Ouyang, M.D. 
Florida Hospital Center for Diagnostic Pathology 
Orlando, Florida 

References



Interesting Case December 2014 #2

Clinical history

This biopsy is from a 62 year old male who underwent liver transplantation 6 months prior for decompensated hepatitis C cirrhosis and multifocal hepatocellular carcinoma. Two months prior to this biopsy (4 months post-transplant) the patient’s laboratory studies were abnormal with ALT 57, AST 69, ALP 149, total bilirubin 17.3 mg/dL (296 umol/L) and the liver biopsy at that time showed features consistent with fibrosing cholestatic recurrent hepatitis C. The patient was urgently treated with Simeprevir and Sofosbuvir, in addition to his other medications which included prednisone and Tacrolimus. At the time of this biopsy, two months after commencing HCV treatment, his viral RNA was down to 1 log but his liver enzymes began to rise with mainly a cholestatic pattern with ALT 13 U/L, AST 26 U/L, ALP 1032 U/L, total bilirubin 2.7 mg/dL (46 umol/L). Imaging showed no evidence of bile duct dilatation, however, he was deemed too ill for MRCP or ERCP. A liver biopsy was obtained; representative pictures are shown below.

Microscopic images

Figure 1

Figure 2

Figure 3A
Figure 3B

Figure 4
The liver shows mild portal and scanty lobular inflammation (Figure 1-3). The portal tracts, however, are expanded by mild edema, a mild ductular reaction, and the inflammation includes neutrophils. Overall these findings simulate those of biliary obstruction. Fibrosis is mild in the subsinusoidal and periportal areas, but not progressed significantly compared to the biopsy obtained two months earlier. Additionally there is less severe hepatocellular injury compared to the prior biopsy. No viral inclusions are apparent, but occasional foci of neutrophilic microabscesses are identified. The patient was known to have been CMV mismatched with his donor (recipient negative anti-CMV Ab; donor positive). CMV immunohistochemistry was obtained and many cells were positive, most of which were neither “megalic” nor apparent on routine stains, even in hindsight (Figure 4).

Diagnosis

Post-transplant CMV syndrome presenting biochemically and histopathologically as biliary obstruction.

Main Learning Points:


  • A combination of immunosuppression, a “sick” patient and unfavorable serology (e.g., CMV recipient-donor mismatch) should always prompt a search for CMV.
  • Histopathologically, “classical” CMV inclusions have low sensitivity and are typically rare even in the most severe cases. 
  • Diagnosis of CMV infection post-transplant therefore depends more on clinical suspicion rather than initial identification of possible viral inclusions.
  • In the liver, biliary epithelia are known targets of CMV either directly or indirectly via injury to peribiliary plexus endothelial cells.
  • Biliary strictures from mechanical causes are more common than CMV-induced biliary injury, but one should consider CMV infection in the differential diagnosis especially in a suggestive clinical context as described above.

Discussion

With the use of prophylactic and pre-emptive antiviral therapy, cytomegalovirus symptomatic infection now occurs in only about 2-10% of transplanted patients. It usually occurs in the first few months after transplantation and the most important risk factor for the development of the disease is the combination of a seropositive donor with a seronegative recipient. In solid organs transplantation, the graft is particularly prone to infection.

The characteristic and most common histological finding in CMV hepatitis, in our experience, is the presence of neutrophilic aggregates/microabscesses or satellitosis within the parenchyma. Viral inclusions can be seen in hepatocytes, endothelial cells and biliary epithelial cells, but they are often sparse. When suspected, the use of deeper levels and immunohistochemistry should be performed.  

CMV infection has been associated with an increased risk for other allograft complications such as chronic rejection and biliary compromise. Biliary complications due to CMV have been reported to occur at a mean post-transplant period of 8.4 months (Liver Transplantation. 2013;19(10):1142-1150), and in this series CMV was detected in the tissues of some patients with undetectable virus in the peripheral blood by PCR. Biliary strictures could also result in part from damage to endothelium of small size hepatic arteries and/or peribiliary plexus. 

The histological alterations associated with hepatic CMV infection may cause differential diagnostic problems as inclusions are rarely found. Other infections (bacterial, fungal and viral) or non-infectious conditions (graft ischemia and biliary obstruction) can be associated with neutrophilic microabscesses.  Nevertheless a high index of clinical suspicion and occasional neutrophilic microabscesses (arrows in figure 3) in the appropriate clinical setting should prompt immunohistochemistry for the virus. In our practice we tend to order CMV immunohistochemistry on most liver biopsies performed for cause in the first 6 months post-transplant (including liver, bone marrow or other solid organ transplant) irrespective of the clinical presentation. It is also worth noting that inflammation is typically sparse in CMV “hepatitis”. Indeed, abundant inflammation may be indicative of CMV occurring together with some other condition.

In this patient, response to HCV treatment was characterized by improved bilirubin, drop in viral RNA load, and less prominent hepatocellular swelling/disarray. However, CMV PCR in the peripheral blood soon after the second biopsy showed a titer of 4 logs and the CMV titer had been undetectable prior to HCV treatment 2 months earlier. The preceding biopsy had been negative when stained for CMV. The question therefore is: do these new antiviral agents come with increased risk for CMV infection specifically and/or for opportunistic infections in general? The answer is not known but as we gain increasing experience with these drugs, new issues will certainly emerge for the pathologist to consider, and CMV reactivation may be one to keep an eye on. Also the question of a biliary stricture not related to CMV (e.g., anastomotic) cannot be ruled out on the basis of histopathology alone, even with a positive CMV, and the possibility further exploring other causes biliary stricture should be raised.

Case contributed by

Aude Roussel-Jobin, M.D. Fellow, Liver Pathology University of Toronto

References:

Hübscher SG, and Clouston AD, Transplantation pathology. In: Burt A, Portmann L, and Ferrell L, MacSween’s Pathology of the Liver. 6th edition. Churchill Livingstone Elsevier, 2012: 877-878.

Adeyi O, Fischer S and Guindi M. Liver allograft pathology: approach to interpretation of needle biopsies with clinicopathological correlation. J Clin Pathol 2010; 63:47-74.

Gotthardt DN1, Senft J, Sauer P, Weiss KH, et al. Occult cytomegalovirus cholangitis as a potential cause of cholestatic complications after orthotopic liver transplantation? A study of cytomegalovirus DNA in bile. Liver Transpl. 2013;19(10):1142-1150.

Adeyi O. Liver Transplant Pathology. In: Ferrell LD, Kakar S, editors. Consultant Pathology: Liver Pathology. 1st ed. New York City: Demos Medical, 2011:307-342.

Wednesday, September 3, 2014

Annual Membership Dues via PayPal is now LIVE!

Dear Hans Popper Hepatopathology Society Members,

We are happy to inform everyone that you may now contribute your annual membership dues via PayPal within the HPHS website.

As you know, we will continue to have dedicated speakers each year, which, of course, requires ongoing funding. We appreciate your attention to our dues notice.

Once again, thank you for your exceptional support of the HPHS.

Grace E. Kim, MD
Secretary –Treasurer,
Hans Popper Hepatopathology Society

Tuesday, August 26, 2014

President's Message August 2014

Dear Friends and Colleagues,

I am delighted to inform you that, thanks to Grace Kim’s hard work and dedication, the Hans Popper Hepatopathology Society is now officially a Non-Profit Organization and has garnered 501(3)(c) tax-exempt status officially recognized by the IRS. Additionally, the HPHS bank account has been set up locally in California. Further details from Grace are found in this newsletter.

The HPHS Companion Society Meeting is scheduled for March 22, 2015 from 8:30am-12noon. The title is “Diagnostic Challenges and Update in Hepatopathology”. We have created a program that will not only be very educational to our members but will hopefully be interesting to non-members as well.

The Business meeting will immediately follow the companion meeting. Members are encouraged to attend as we will need to vote on some modifications to the bylaws as a result of the tax-exempt status of the HPHS, as well as some changes to the duties and responsibilities of the members of the Executive Committee, and finally to officially create a Website Committee. In the meantime, I would like members to volunteer to serve on this committee. Please email me directly (mariaisabel.fiel@mountsinai.org) if you are interested.  In the near future, we will have the ability to check off on-line our interest in committee membership when we pay our yearly dues. Currently, Arief Suriawinata is overseeing the website with the help of Vince Hoang, Grace Kim’s Administrative Assistant. Vince has replaced Julie Gutierrez, who was an invaluable help to Beth Brunt with the membership dues, correspondence, and all other HPHS matters for many years. We thank Julie for all of her efforts throughout the years!

The Call for Abstracts for the “Pathologist-in-Training Award” is now official. Deadline for submission to Dele Odeyi (oyedele.adeyi@uhn.ca), Chair of the Education Committee, is March 6, 2015. Please encourage your residents and fellows to submit their work to the HPHS.

Finally, please encourage both your junior and senior colleagues to officially become members of the HPHS. Residents and fellows can become Trainee members without having to pay any dues. They can easily transition to Regular membership once they finish their training. Application to membership is available on the website. Please email completed application to Maha Guindi (Maha.Guindi@cshs.org), chair of the membership committee.

I hope everyone is having a great summer. I look forward to seeing you in Boston.

M. Isabel Fiel
President,
Hans Popper Hepatopathology Society

Time to support the Hans Popper Hepatopathology Society - Membership dues for 2014-2015 or Donations

The Hans Popper Hepatopathology Society has an EIN (Federal Tax Identification Number for use to identify a business entity) and has become incorporated as:  Hans Popper Hepatopathology Society, Inc.  We are also tax-exempt (501(c)(3)); therefore your membership dues and donations are now tax-deductible. 

Membership categories:

Regular Member:  Any individual who has completed a postdoctoral program in Pathology or another specialty of Medicine, and has earned certification as a specialist in Pathology or another specialty of Medicine, with demonstrated interest and involvement in hepatobiliary pathology.  Dues: $50/year

Associate Member:   Any person holding a doctorate, or doctorate equivalent, degree, who is enrolled in a post-doctoral educational program in Pathology (PhD, post-doctoral fellowship, residency or fellowship) or another specialty of Medicine, and who has demonstrated interest in hepatobiliary pathology.  Dues:  None; limited to five years only.

Corresponding Member:  Any individual who satisfies the requirements for Regular Membership or Associate Membership, but does not reside in the United States or Canada.  No dues.  Corresponding members can apply for regular membership.

Ways you can contribute (membership dues or donations).

1.      Bank Transfer: If you have a Wells Fargo account, you can transfer funds using the following bank information:
a.    Routing #: 121042882
b.    Account #: 8558608389

2.      PayPal: You may now contribute via PalPay using your personal credit card.

Membership Dues - 2014


Donations:

3.     Bank Checks: You can send a check via U.S. mail:  Make checks payable to: Hans Popper Hepatopathology Society, Inc. Include “membership dues” or “general donation” in the memo line of your check. Send checks to:

Grace E. Kim, Secretary-Treasurer
Hans Popper Hepatopathology Society, Inc.
505   Parnassus Avenue M561 Box 0102
San Francisco, CA 94143-0102

When using option 1 and 3, you will receive an electronic receipt from the Hans Popper Hepatopathology Society, Inc. to file your tax deductions.


Monday, August 11, 2014

Interesting Case August 2014


Clinical history

The patient is an 81 year old male with no significant past medical history who presented with abdominal pain, nausea and weight loss of several months duration.

Labs

ALT 15 U/L, AST 55 U/L, ALK PHOS 81 U/L, total bilirubin 0.3 mg/dl. Tumor makers: AFP 1 IU/ml, CEA 2.4 ng/ml CA19-9 55 U/ml, PSA 11.35 ng/ml.

Radiology

CT scan showed four liver masses which measured up to 3.6 cm, a 6.9 cm left kidney mass and an 8.9 cm mesenteric mass. A CT-guided biopsy of the liver mass was performed.

Microscopic images


Figure 1
Figure 2
Figure 3
Figure 4
Figure 5, HMB-45
Figure 6, Melan A
Figure 7, CD10
Figure 8, AE1/AE3
Figure 9, S-100

Diagnosis

Metastatic malignant epithelioid angiomyolipoma.

Discussion

This tumor demonstrates a proliferation of predominantly large epithelioid cells with abundant eosinophilic cytoplasm, vesicular nuclei, and prominent nucleoli (Figure 1). Focal tumor cell spindling is seen (Figure 2). Scattered ganglion-like cells and multinucleated giant cells are present (Figure 3). Mitoses, including atypical mitotic figures, are present (Figure 3 and Figure 4). No necrosis is identified. The tumor cells are positive by immunohistochemistry (IHC) for HMB45 (Figure 5), Melan A (Figure 6), CD10 (Figure 7), MiTF, and CD68; they are negative for cytokeratin AE1/AE3 (Figure 8), S100 (Figure 9), CAM 5.2, CD117, CD34, SMA, desmin, calponin, myogenin, and inhibin.

The differential diagnosis includes, but is not limited to, renal cell carcinoma with sarcomatoid differentiation, adrenal cortical carcinoma, melanoma, malignant GIST, undifferentiated/sarcomatoid carcinoma and malignant epithelioid angiomyolipoma. Combined epithelioid and spindle cell morphology, large ganglion-like cells and multinucleated giant cells are characteristic of epithelioid angiomyolipoma (E-AML). Positive IHC for HMB45, Melan A, MiTF and CD68, together with negative IHC for epithelial markers and S100 help confirm the diagnosis.  However, as we are always taught, “melanoma is the great mimicker” and rarely melanoma can be S-100 negative.

The usual renal angiomyolipoma (AML) is considered a benign mesenchymal tumor composed of a variable portion of fat, smooth muscle cells, and abnormal thick-walled vessels. E-AML is a rare variant and potentially malignant neoplasm composed partially or entirely of epithelioid cells. Up to one-third of E-AML patients experience local recurrences and/or distant metastases. Features that favor malignant E-AML include nuclear atypical in ≥70% of the epithelioid cells, ≥2 mitotic figures per 10 high power fields, atypical mitotic figures, and necrosis; the presence of 3 or all of these features is predictive of aggressive behavior (Brimo F, Robinson B, Guo C et al. Am J Surg Pathol 2010;34:715-722). E-AMLs are immunoreactive for one or more melanocytic markers (e.g., HMB45, Melan A, and MiTF). They often express smooth muscle markers such as SMA and desmin. The absence of S100 staining can help distinguish E-AML from melanoma. The absence of staining for epithelial markers can help distinguish E-AML from carcinoma.

Patient follow up:
Shortly after the diagnosis of malignant E-AML was made in August of 2013, the patient was started on Afinitor 10 mg daily (also called everolimus, an established medication for AML). He had an excellent initial response (CT scan in early 2014 showed significantly reduced size of the mesenteric mass with stable liver and kidney masses). However, the treatment was held several times due to severe side effects including hyponatremia, diarrhea and fevers. Afinitor was re-started in July of 2014 at a very low dose. Currently, one year since diagnosis, the patient is doing reasonable well with no new masses.

Contributed by
Wendy Cao, MD

Wednesday, June 4, 2014

President's Message May 2014

Dear Friends and Colleagues,

It is with great pleasure and honor that I assumed the position of President of the Hans Popper Hepatopathology Society (HPHS) during the United States and Canadian Academy of Pathology (USCAP) Annual Meeting this past March. I took over this position from Matthew Yeh who remains a member of HPHS Executive Committee. We thank Matthew for having ably led the HPHS for the last two years and particularly for having organized two excellent companion meetings at the USCAP. The attendance during these sessions was among the highest in the society’s history. Recruitment of new members also increased during Matthew’s stint as president.

Beth Brunt has stepped down from her position of Secretary-Treasurer, a position she has adeptly held for many years. Beth was instrumental in increasing the society membership and was key in keeping our society in an extremely sound financial state. I would like to express my sincere thanks not only for her past accomplishments and dedication but also for her continued support of the society. Grace Kim has now stepped into Beth’s shoes as our Secretary-Treasurer. She has enthusiastically taken on this challenging task from the get go. Lastly, Michael Torbenson has been elected as Vice President during the USCAP meeting. He will assume the position of HPHS president in 2016.

I expect that 2014 will be a busy one for our society. The HPHS will be participating in the International Academy of Pathology 2014 Congress to be held in Bangkok on October 5-10, 2014. The society was invited through the USCAP’s Bruce Smoller with the help of Beth Brunt and Matthew Yeh. The Scientific Committee of the IAP has requested the HPHS to conduct a two and a half hour seminar on liver pathology on Thursday, October 9.  

The Executive Committee is in the process of applying for a Non-Profit Organization status for the HPHS. Subsequent to this, we will be able to apply for a 5013C tax-exempt status with the IRS. This will enable the members to claim the annual HPHS dues as a tax deduction.

The website is up and running, courtesy of the Newsletter Committee. Details as to how to access the website are found in this newsletter. Cases that are interesting, challenging and have educational value will be regularly posted. The Education Committee, chaired by Oyedele Adeyi, is actively recruiting and encouraging submission of such cases. In addition, applications for membership will be made available in the website. We are working on having the ability to pay member dues via PayPal as well, and for payment to go directly into a secure web server that can be accessed from the website.

The number of liver specimens we all see has steadily declined because fewer biopsies are being performed by clinicians for hepatitis C staging. This is primarily due to the newly approved medications for hepatitis C wherein treatment can be initiated regardless of the stage of fibrosis. However, the role of liver pathology has shifted to evaluating biopsies from patients with metabolic liver diseases and drug-induced liver injury, and other more challenging cases. Additionally, molecular diagnostic modalities are being incorporated into the work up of liver tumors. We will try to continue to disseminate advances in the diagnosis of such entities via the website, newsletter and future companion meetings. The Executive Committee is also planning to propose an increased involvement and greater visibility of liver pathology in the American Association for the Study of Liver Diseases (AASLD). In the next few months, we will reach out to the AASLD Governing Board and the Education Committee to add a new liver pathology session during its Annual Meeting. When these meetings  were held in previous years they were well-attended not just by pathologists but also by clinicians. Having a liver pathology session at national meetings such as the AASLD will increase awareness and further promote liver pathology.

Lastly, I encourage you to advocate for greater membership and foster education and interest amongst your junior hepatopathology colleagues.

Thank you for your continued support of the HPHS. I look forward to seeing you at the Companion Meeting during the USCAP Annual Meeting in Boston on March 22, 2015.

Sincerely,

M. Isabel Fiel, M.D.
President,
Hans Popper Hepatopathology Society

Tuesday, June 3, 2014

Interesting Case May 2014

Clinical History 
This 23 year old woman is status post allogeneic BMT for Fanconi anemia 15 years prior. She was generally doing well, but was lost to follow up at our institution since 5 years ago. She presented to an outside pediatrician with complaint of fatigue, malaise, abdominal pain and pruritus for the past couple of months.

Labs
At the time of presentation her alkaline phosphatase >700 U/L, AST 100-200 U/L, ALT 200-300 U/L and total bilirubin 18-20 mg/dL.

Microscopic Images
Figure 1

Figure 2 

Figure 3

Figure 4

Figure 5

Figure 6
Diagnosis
Chronic graft versus host disease

Discussion
Figure 1 shows a large portal area with several vascular profiles and lack of interlobular bile duct. Figure 2 shows the only bile duct identified on multiple levels. This duct shows features of injury including loss of nuclear polarity and nuclear hyperchromasia.
Figure 3 shows marked canalicular cholestasis.
Figure 4 is the keratin 19 stain confirming a lack of interlobular bile duct and essentially no ductular reaction.
Figures 5 and 6 show portal-portal bridging fibrosis at least.

The paucity of interlobular bile ducts and lack of ductular reaction raises several possibilities. The top of the list in this setting would be chronic graft versus host disease (GVHD). However, advanced fibrosis with chronic GVHD is rarely described. From the available clinical records, this patient has a history of chronic skin and liver GVHD that has responded well to immunosuppression in the past. Furthermore, the patient intermittently electively takes herself off immunosuppressive therapy with resultant flares, as happened in this case.

The differential diagnosis would also include drug/medication induced “vanishing bile duct syndrome”. The lack of a history of drug induced cholestatic hepatitis, the presence of what appears to be well documented chronic cutaneous GVHD, along with prompt symptomatic and laboratory improvement with reestablishment of immunosuppression support chronic liver GVHD. In this age group, the differential diagnosis would also include primary sclerosing cholangitis. Although no cholangiogram was performed, the patient underwent abdominal MRI with and without contrast which showed no evidence of intra- or extrahepatic biliary ductal dilation and she has no history of inflammatory bowel disease.

As the outcomes for BMT patients continue to improve and the duration of patient survival is extended, perhaps we will see more cases of chronic GVHD with advanced fibrosis.

Contributed by
Cynthia D. Guy, MD

Sunday, March 2, 2014

Hans Popper Hepatopathology Society Best Trainee Abstract Award, 2014 USCAP Annual Meeting, San Diego, CA

Hans Popper Hepatopathology Society Best Trainee Abstract Award was presented to Juan Putra, M.D. (PGY-2, Dartmouth-Hitchcock Medical Center, Lebanon, NH).

Abstract title:
Altered Expression of MiR-21, MiR-27b, MiR-10b and MiR-146a in Different Stages of Nonalcoholic Fatty Liver Disease
Putra J, Abreu FB, Burchard P, Toor A, Tsongalis GJ, Suriawinata AA

Juan Putra and the MiR abstract
Award presentation by Dr. Matthew Yeh