Re: Re[2]: Re: question for the experts

[Guest guest]

Mold exposure is known to cause substantial amounts of inflammation of

many kinds. The transition from fatty liver to liver necrosis is

influenced substantially by oxidative stress, cytokines, and other

proinflammatory mediators. Also, military reserch frequently cites

liver necrosis as a consequence of numerous mycotoxins.

for example..

" J Surg Res. 2006 Nov;136(1):125-35. Epub 2006 Oct 3.

Molecular pathogenesis of hepatocellular carcinoma.

McKillop IH, Moran DM, Jin X, Koniaris LG.

Department of Biology, University of North Carolina at Charlotte,

Charlotte, North Carolina 28223, USA. imckillo@...

Hepatocellular carcinoma (HCC) is one of the most common

life-threatening malignancies in the world. This cancer generally

arises within the boundaries of well-defined causal factors, of which

viral hepatitis infection, aflatoxin exposure, chronic alcohol abuse,

and nonalcoholic steatohepatitis are the major risk factors. Despite

the identification of these etiological agents, hepatocarcinogenesis

remains poorly understood. The molecular mechanisms leading to the

development of HCC appear extremely complex and only recently have

begun to be elucidated. Currently, surgical resection or liver

transplantation offer the best chance of cure for the patient with

HCC; however, these therapies are hindered by inability of many of

these patients to undergo liver resection, by tumor recurrence and by

donor shortages. A lack of suitable therapeutic strategies has led to

a greater focus on prevention of HCC using antiviral agents and

vaccination. Overall, the current outlook for patients with HCC is

bleak; however, a better understanding of the molecular and genetic

basis of this cancer should lead to the development of more

efficacious therapies.

J Clin Gastroenterol. 2002 Nov-Dec;35(5 Suppl 2):S79-85.

Hepatocellular carcinoma: the high-risk patient.

Nissen NN, P.

Multi-Organ Transplant Program, and the Liver Transplant Program,

Centers for Liver and Kidney Diseases and Transplantation Cedars-Sinai

Medical Center Los Angeles, California 90048, USA. nissenn@...

Hepatocellular carcinoma (HCC) is the most common hepatic

malignancy worldwide. The primary risk factor for the development of

HCC is cirrhosis. Even patients without cirrhosis who develop HCC are

typically found to have some underlying hepatic abnormality, such as

steatohepatitis or chronic viral hepatitis. Although cirrhosis of any

cause increases the risk of developing HCC, cirrhosis associated with

chronic hepatitis B or C virus infection or hemochromatosis carries

the greatest risk. Additional factors such as patient age and sex,

duration and severity of liver disease, concurrent alcohol or

aflatoxin exposure, liver histology, and alpha-fetoprotein levels also

contribute to the relative risk of developing HCC. Vaccination

programs aimed at preventing hepatitis B virus infection have been

very successful in lowering the incidence of HCC in some areas of the

world. Interferon-based therapy, which may control the inflammatory

activity in chronic hepatitis C, also holds promise in preventing HCC.

Other novel chemopreventative agents, such as glycyrrhizin and

polyprenoic acid, may also have a role in preventing HCC, but they

require further study before they can be recommended for widespread

use.

Vet Pathol. 1981 Sep;18(5):652-64.

Related Articles, Links

Mycotoxicosis caused by a single dose of T-2 toxin or

diacetoxyscirpenol in broiler chickens.

Hoerr FJ, Carlton WW, Yagen B.

T-2 toxin (3-hydroxy-4,15-diacetoxy-8-[3-methyl-butyrloxy]-12,13-epoxy-delta

9-trichothecene) and diacetoxyscirpenol, structurally similar

trichothecene mycotoxins, in dimethylsulfoxide:saline (1:9 v/v)

solvent, were given by crop gavage to 7-day-old male broiler chickens.

Selected birds were killed at 1, 6, 12, 18, 24, 72, and 168 hours

post-treatment. The lesions induced by the two toxins were similar,

but were more severe in chicks given T-2 toxin. Necrosis of lymphoid

tissue and bone marrow began one hour after treatment with T-2 toxin,

and was followed by rapid cell depletion. Cell repletion also was

rapid, occurring by hour 24 in mildly injured tissues from birds given

diacetoxyscirpenol and by hours 72 and 168 in more severely injured

tissues from chickens given T-2 toxin. Hepatic lesions were multiple

foci of cell necrosis resolved rapidly and the inflammatory cell

reaction was minimal. Necrosis of gall bladder epithelium and

secondary cholecystitis followed hepatic cell necrosis. In the

alimentary tract, necrosis of the epithelium on the tips of villi in

the duodenum was followed by necrosis of the epithelium of villi and

crypts in the small and large intestine, and of mucosal epithelium of

the proventriculus and ventriculus. Atrophy of intestinal villi and

fewer mitotic figures were seen by 18 hours after treatment. The

alimentary tract epithelium, however, looked normal by hour 72.

Lesions in the integument, including necrosis of feather epidermis and

of the follicular epidermis at the neck of the feather follicle,

occurred at 12 to 24 hours after treatment.

On Sat, Dec 20, 2008 at 11:31 AM, Patilla DaHun <glypella@...> wrote:

> You're right, Carl. I had a liver ultrasound that showed " fatty "

> necrotic lesions. When I asked " Liver Boy " (the liver doctor) if it

> could be mold, that was it! He didn't even want to talk to me.

>

> Barth

>