Showing posts with label spleen. Show all posts
Showing posts with label spleen. Show all posts

Wednesday, January 22, 2014

Just For Fun - What Does the Spleen Do?

By Alvin Powell, Harvard Staff Writer

Who knew the spleen was so funny? And popular?
A parody video by a group of Harvard Medical School students went viral in December, garnering a million YouTube hits in just five days and surpassing 1.7 million since.
The video’s creators were astounded at its popularity, according to Ben Rome, a second-year student who filmed and edited the video. Rather than just basking in their 15 minutes of fame, however, the students are trying leverage the video’s popularity for a good cause: science education. They launched the HMS/HSDM Organ Challenge, a contest for primary and secondary school students to create a music video highlighting one of the body’s organs.

Read more here............

Friday, September 7, 2012

Spleen stiffness evaluated portal hypertension, indicated esophageal varices in cirrhosis patients

Spleen stiffness evaluated portal hypertension, indicated esophageal varices in cirrhosis patients

Colecchia A. Gastroenterology. 2012;143:646-654.

September 7, 2012

Results from a recent study suggest that measurement of spleen stiffness can be a noninvasive method of assessing portal hypertension and detecting esophageal varices in patients with HCV-induced cirrhosis.

Researchers evaluated the spleen stiffness (SS) and liver stiffness (LS) in 100 patients with HCV-induced cirrhosis. SS was measured via transient elastography (TE), and the effectiveness of this parameter in diagnosing portal hypertension (PH) and esophageal varices (EV) within the cohort was compared with LS and other noninvasive methods, including the LS-spleen diameter to platelet ratio score (LSPS) and the platelet count to spleen diameter ratio (Plt/Spl).

Esophageal varices were present in 53 participants, including 27 with grade I, 20 with grade II and six with grade III. All patients had hepatic vein pressure gradients (HVPG) of more than 5 mm Hg. Clinically significant portal hypertension was present in 65 patients, with 54 cases considered severe (12 mm Hg or greater).

SS measurements were significantly higher in patients with EV compared with those without (58.6 kPa vs. 39 kPa), and among those with clinically significant PH compared with those with preclinical hypertension (n=35) (56 kPa vs. 37 kPa). Investigators observed correlations between results from different testing methods and HVPG, with the strongest between HVPG and SS (r=0.885) and LS (r=0.836) (P=.0001 for both), and found that the best predictive model for HVPG included both LS and SS (R2=0.85, P<.0001).

AUROC analysis indicated significant differences between SS and other evaluated tests in diagnosing the following:

  • Presence of EV: AUROC=0.941 for SS compared with 0.857 for Plt/Spl (P=.05)
  • HVPG of 10 mm Hg or higher: AUROC=0.966 for SS compared with 0.907 for LSPS (P=.05) and with 0.847 for Plt/Spl (P=.007)
  • HVPG of 12 mm Hg or higher: AUROC=0.959 for SS compared with 0.899 for LSPS (P=.048) and with 0.828 for Plt/Spl (P=.003)
No significant difference was observed between SS and LS in the AUROC for any diagnoses.
“The results of the present study provide advancement and a wide insight into the relevant diagnostic potential of TE in the clinical setting of HCV-induced cirrhosis,” the researchers wrote. “In particular, they suggest for the first time that introduction of SS measurement, possibly associated with LS, may enable clinicians to monitor the evolution of PH from early to late cirrhosis, including the occurrence of EV.”

Monday, December 26, 2011

Hepatitis C News Ticker: Following response-guided therapy guidelines with boceprevir and telaprevir

"Reading the Paper" Lynne Crumpacker

Now Available! CCO Hepatology inPractice™
This special edition includes all the pivotal phase III studies of the HCV protease inhibitors, with a range of commentaries exploring key aspects of the use of these agents, plus Capsule Summaries of each study and downloadable slidesets.

Topics include:
  • Following response-guided therapy guidelines with boceprevir and telaprevir
  • Understanding futility rules and their importance
  • Outcomes and management of anemia
  • Strategies for managing telaprevir rash and anorectal symptoms
  • Using boceprevir and telaprevir in patients with advanced fibrosis or cirrhosis
  • Effect of telaprevir on cyclosporine and tacrolimus pharmacokinetics
  • Antiviral activity with telaprevir in patients with genotype 2 or 3 HCV
  • Evaluation of HBV screening cost effectiveness

*Free Registration Required-Register Here

Sunday, December 11, 2011

Advanced Liver Disease: What Every Hepatitis C Virus Treater Should Know

Advanced Liver Disease Volume 19 Issue 3 August/September 2011

Please click below to listen to podcast and view text.

Advanced Liver Disease: What Every Hepatitis C Virus Treater Should Know

Audio Will Include Moments Of Hesitation/Silence During Podcast.....

Patients with advanced fibrosis need to be regularly monitored for evidence of decompensated disease, and complications need to be aggressively managed.....

This article summarizes a presentation by Kenneth E. Sherman, MD, at the IAS–USA live continuing medical education course, Management of Hepatitis C Virus in the New Era, held in New York City in April 2011.

Friday, March 11, 2011

Esophageal varices' presence can be better predicted if both spleen and liver stiffness measurements are used

New Chronic Hepatitis Study Findings Reported from H. Stefanescu and Co-Authors


According to recent research from Romania, "Splenomegaly in a common finding in liver cirrhosis that should determine changes in the spleen's density because of portal and splenic congestion and/or because of tissue hyperplasia and fibrosis. These changes might be quantified by elastography, so the aim of the study was to investigate whether spleen stiffness measured by transient elastography varies as liver disease progresses and whether this would be a suitable method for the noninvasive evaluation of the presence of esophageal varices."

"One hundred and ninety-one patients (135 liver cirrhosis, 39 chronic hepatitis and 17 healthy controls) were evaluated by transient elastography for measurements of spleen and liver stiffness. Cirrhotic patients also underwent upper endoscopy for the diagnosis of esophageal varices. Spleen stiffness showed higher values in liver cirrhosis patients as compared with chronic hepatitis and with controls: 60.96 vs 34.49 vs 22.01 KPa (P Chronic Hepatitis).

The researchers concluded: "Esophageal varices' presence can be better predicted if both spleen and liver stiffness measurements are used."

Stefanescu and colleagues published their study in the Journal of Gastroenterology and Hepatology (Spleen stiffness measurement using fibroscan for the noninvasive assessment of esophageal varices in liver cirrhosis patients. Journal of Gastroenterology and Hepatology, 2011;26(1):164-170).

For additional information, contact H. Stefanescu, Iuliu Hatieganu University of Medicine & Pharmacy, Medical Clinic 3, 19-21 Croitorilor St., Cluj Napoca 400162, Romania.

Publisher contact information for the Journal of Gastroenterology and Hepatology is: Wiley-Blackwell Publishing, Inc., Commerce Place, 350 Main St., Malden 02148, MA, USA.

Keywords: Country:Romania, Chronic Hepatitis, Digestive System Diseases, Fibrosis, Gastroenterology, Hemic and Immune Systems, Hepatology, Human, Immunology, Infectious Disease, Liver Cirrhosis, Liver Diseases, Spleen, Varicose Vein

This article was prepared by Gastroenterology Week editors from staff and other reports. Copyright 2011, Gastroenterology Week via

To see more of the, or to subscribe, go to .

Thursday, November 25, 2010

Facts About Decompensated Liver Disease

Facts About Decompensated Liver Disease
In order to understand what happens in decompensated liver disease, you need to understand some of the many functions of the liver and what happens in liver disease. Decompensated when used in this way, really means unstable. Someone can have liver disease for many years, and while they may not be in great health, they are not in immediate risk of liver failure.

This liver is the only organ that has the ability to regenerate itself after it is injured in some way. When the liver is injured repeatedly, but still regenerates, it becomes fibrous in texture. When enough damage has occurred and the liver can no longer repair itself, that is called cirrhosis. At that point, the liver damage is permanent.

The liver makes bile. Bile is necessary to break down fats and therefore a healthy liver is needed for the body to be able to use fat soluble vitamins. The fat soluble vitamins that doctors worry about are A, D, E, and K. Most people with compensated, or stable, liver disease will take supplements of those vitamins in order to avoid deficiencies.
Another major function of the liver is to clean the blood. Blood flows from the spleen through the portal vein to the liver. It then profuses through the liver like water goes through a sponge.

If the liver is cirrhotic, it will be too hard and the blood can’t go through it as fast as the body needs. The main chemical that builds up in the blood that causes problems for people is ammonia.

A person with too much ammonia in their blood will become, lethargic and confused and this can even lead to coma. This is called hepatic encephalitis (Encephalopathy)
Dr. Johnson provides commentary on minimal hepatic encephalopathy
Do patients with minimal hepatic encephalopathy have insight into their impaired
driving skills?
Portal Hypertension

Another complication of the blood not being able to adequately flow through the portal vein and through the liver (called portal hypertension) is an enlarged spleen. In itself, an enlarged spleen is not a large concern, but as the spleen enlarges it tends to attract platelets and white blood cells. This, and the vitamin K deficiency, will cause the blood to not be adequately able to clot. It also causes the immune system to be compromised.
. .
The human body is an amazing thing and will always try to find a way to make things work. When a person with liver disease has portal hypertension the blood backs up into the spleen. The spleen can only handle so much, but the pressure is still in the portal vein.
That’s when the body creates new veins to carry the blood. .
These are called varices. .

These veins can be seen on the stomach of someone with severe portal hypertension. They seem to radiate from the belly button and are called caput medusai, because they look the Medusa’s hair. Varices become a concern because they tend to rupture and bleed. The varices that are most likely to bleed are the ones surrounding the esophagus. A bleed of this sort can be massive and life threatening.

Decompensated liver disease is when any of these complications become a problem, or when the complications begin to deteriorate at a fast rate. Many people live with cirrhosis and portal hypertension for years at a time. When a person has decompensated liver disease, the only available medical intervention is a liver transplant. In most cases this will be a cure and many of the complications will disappear. Unfortunately not everyone that is listed for a liver transplant receives an organ in time.

Also See:

Wednesday, November 10, 2010

Cirrhosis: What Happens When The Spleen Is Enlarged ?

Q- What happens when the spleen is enlarged ?
Spleen is an important organ of the lymphatic system. It is found on the left upper side of the abdomen, between the 9th and 12th rib. The primary function of the spleen is to produce lymphocytes and plasma cells, which are used in humoral and cellular immune defense. Approximately half of the body’s monocytes are stored in this organ. These cells can easily transform into macrophages and dendritic cells, and assist in wound repair. Additionally, the spleen filters the blood and removes all the unwanted materials like cell debris and microorganisms as bacteria, viruses and fungi.

Furthermore, it monitors the red blood cells, eliminating those that are abnormal, damaged or too old to function properly. It also serves as a storehouse for various elements of the blood like platelets and white blood cells. In the absence of the spleen, the body becomes susceptible to diseases caused by bacteria and protozoa, and responsiveness to certain vaccines also decreases.Whenever the normal functioning of the body is hampered by disorders like cancer, anemia, malaria, tuberculosis, amyloidosis, cirrhosis, hepatitis and the like, the spleen becomes hyperactive, and starts entrapping and storing a large number of blood cells and platelets.

As the result, the platelet and blood cell count in the bloodstream begins to fall dramatically. Due to entrapment, the spleen grows in size, and as it grows, it traps in more and more blood cells and platelets. Eventually the overgrown spleen starts capturing and destroying the normal blood cells together with the abnormal ones. These blood cells and platelets clog the spleen and interfere with its normal function.

The characteristic symptom of spleen enlargement is severe pain in the abdomen and back. At times, the pain shoots up to the left shoulder. This happens when certain parts of the spleen begin to bleed and die due to inadequate supply of blood. The enlarged spleen also starts pressing the stomach, which leads to the feeling of fullness after eating a small amount of food or even without eating anything. Furthermore, as too many blood cells and platelets have been removed from the bloodstream, the body’s immune response begins to dwindle, symptoms of anemia emerge, and normal blood clotting process is also slows down.

Recommended Reading
May 2017
The spleen in liver cirrhosis: revisiting an old enemy with novel targets
The spleen is a secondary lymphoid organ which can influence the progression of multiple diseases, notably liver cirrhosis. In chronic liver diseases, splenomegaly and hypersplenism can manifest following the development of portal hypertension. These splenic abnormalities correlate with and have been postulated to facilitate the progression of liver fibrosis to cirrhosis, although precise mechanisms remain poorly understood. In this review, we summarize the literature to highlight the mechanistic contributions of splenomegaly and hypersplenism to the development of liver cirrhosis, focusing on three key aspects: hepatic fibrogenesis, hepatic immune microenvironment dysregulation and liver regeneration. We conclude with a discussion of the possible therapeutic strategies for modulating splenic abnormalities, including the novel potential usage of nanomedicine in non-surgically targeting splenic disorders for the treatment of liver cirrhosis.

SVR leads to decreased spleen size in patients with HCV, cirrhosis
Researchers observed a decrease in spleen size over time after patients with hepatitis C virus infection and cirrhosis achieved successful sustained virologic response, according to findings presented at the Society of Hospital Medicine Annual Meeting.

Current categorized article directory;
Staging Cirrhosis

Page edited May 2017 to included article published in Journal of Translational Medicine