Re: Alcohol Issue

[Guest guest]

Hi ;

This study from Indiana University suggests there is a risk

associated with alcohol consumption and cholangiocarcinoma in PSC

patients:

__________________

Hepatology. 2000 Jan;31(1):7-11.

Cholangiocarcinoma in patients with primary sclerosing cholangitis:

a multicenter case-control study.

Chalasani N, Baluyut A, Ismail A, Zaman A, Sood G, Ghalib R,

McCashland TM, Reddy KR, Zervos X, Anbari MA, Hoen H.

Indiana University School of Medicine, Indianapolis, IN 46202, USA.

nchalasa@...

Patients with primary sclerosing cholangitis (PSC) have a

significantly increased risk of developing cholangiocarcinoma (CCA).

Risk factors for developing such a complication are not well

defined. We conducted a multicenter, case-control study to determine

the risk factors and possible predictors for CCA in patients with

PSC. The demographic, clinical, and laboratory features of 26 PSC

patients with CCA diagnosed over a 7-year period at eight academic

centers were compared with 87 patients with PSC but no CCA

(controls). There was no statistically significant difference in

demographics, smoking, signs or symptoms or complications of PSC,

indices of disease severity (Mayo Risk score or Child-Pugh score),

frequency or duration or complications of inflammatory bowel disease

(IBD), frequency of biliary surgery, or therapeutic endoscopy

between the two groups. Alcohol consumption was significantly

associated with CCA in patients with PSC (odds ratio: 2.95; 95% CI:

1.04-8.3). Serum carbohydrate antigen 19-9 (CA 19-9) was

significantly higher in patients with CCA than those without (177 +/-

89 and 61 +/- 58 U/mL, respectively; P =.002). A serum CA 19-9

level > 100 U/mL had 75% sensitivity and 80% specificity in

identifying PSC patients with CCA. In conclusion, alcohol

consumption was a risk factor for having CCA in PSC patients. The

indices of severity of liver disease were not associated with CCA in

patients with PSC. Serum CA 19-9 appeared to have good ability to

discriminate PSC patients with and without CCA.

Publication Types:

Multicenter Study

PMID: 10613720

____________________

If you are interested, I could look up the full paper and try to

find out how much alcohol consumption they are talking about?

Best regards,

Dave

(father of (20); PSC 07/03; UC 08/03)

> Anyone out there know if they have scientifically made any

> significant connections to alcohol consumption and significantly

> increased incidents of cholangecarcinoma (I know the spelling is

> probably way off!) ?

>

[Guest guest]

Hi Joan;

Looking at the full paper of Chalasani et al (2000), this is how they

defined alcohol consumption:

" Alcohol Consumption. Alcohol consumption was separated into three

categories: never, those who never had regular alcohol intake; past,

those who have been abstinent for longer than 6 months; and current,

those who are currently consuming regular amounts of alcohol. The

precise definition of 'regular alcohol consumption' was dependent on

the individual health care provider's practice. The data on alcohol

consumption were extracted from the primary physician's initial

assessment, and in the majority of the subjects (~85%), this was

confirmed by the transplantation psychologist or psychiatrist. "

In the discussion, they say:

" In this study, alcohol consumption was a risk factor for

having CCA. Patients with PSC who consumed alcohol were almost three

times as likely to have CCA than those without alcohol consumption.

We lacked sufficient data to evaluate the influence of the quantity

of alcohol consumed on the risk of CCA. "

So basically, the data does allow distinguishing between the types of

alcohol consumption that you describe.

The article was accompanied by an editorial, which has this to say

about the topic:

de Groen PC 2000 Cholangiocarcinoma in primary sclerosing

cholangitis: who is at risk and how do we screen? Hepatology 31: 247-

248.

" In this issue of HEPATOLOGY, Chalasani et al. report the

results of a multicenter, case control study aimed at identifying

risk factors and indicators of cholangiocarcinoma in patients with

PSC. Unlike other studies, they do not find a correlation with a

history of smoking8 or evidence of a 'rapid clinical and biochemical

deterioration,'7 but instead report a significant correlation between

the development of cholangiocarcinoma and the presence of alcohol

consumption. How should we interpret this finding? On the one hand,

the findings make sense. Alcohol has been found to be a risk

factor for numerous cancers, including cancers of the larynx,

esophagus, lung, and breast.9 Alcohol abuse results in cirrhosis and

hepatocellular cancer, and alcohol consumption also is known to

accelerate the development of cirrhosis and probably hepatocellular

cancer in other liver diseases, most notably hepatitis C. Finally,

prolonged high alcohol consumption was present in nearly half of 112

patients with cholangiocarcinoma reported by Altaee et al.10

However, one needs to be careful not to over-interpret the findings.

First, this is a retrospective study with all its associated flaws,

as acknowledged by the authors. It is uncommon to find a group of

mostly men of whom 78% never used alcohol. In addition, patients tend

to give lower estimates of the amount of alcohol they consume than

their family members. In fact, in a prospective study of patients

with pancreatic and distal biliary tree cancers, patient and family

members disagreed most on the history regarding the consumption of

alcoholic drinks.11 Second, the actual numbers in this study were

small: 11 of 26 patients with cholangiocarcinoma were using alcohol,

where as 17 of 78 used alcohol in the noncancer group.

Misclassification of 1 or 2 patients in either group could have made

the observed difference nonsignificant. Third, analysis of a dose-

response relationship was not possible because of insufficient data.

In general, a cause-effect relationship is strengthened by a dose-

effect relationship, as has been described for alcohol in other

cancers, such as breast cancer.12,13 Furthermore, recent extensive

alcohol consumption—that is, within the years immediately leading up

to the diagnosis of cancer—may be more important than having ever

used alcohol.13,14 Fourth, other investigators have been unable to

find a correlation between alcohol consumption and the development of

cholangiocarcinoma in patients with PSC.8 Alcohol use is not

universally associated with an increased risk for cancer. On the

contrary, Moerman et al.14 concluded that long-term moderate alcohol

use might be protective against cancer of the biliary tract. The type

of alcohol consumed also may be important with wine reported to have

the most beneficial effects.15 Fifth, Chalasani et al. may have

studied a selected group of PSC patients with cholangiocarcioma,

because all patients with cholangiocarcinoma without previously

documented PSC were excluded from the study. In addition, the

duration of disease was significantly shorter in the

cholangiocarcinoma group, suggesting that possibly 2 groups of PSC

patients exist: those who have a rather rapid course toward

cholangiocarcinoma, and those who slowly progress toward

end-stage liver disease. Finally, it is of interest that cases had a

longer history of inflammatory bowel disease, although this

difference was not statistically significant. "

Dave R.

(father of (20); PSC 07/03; UC 08/03)

>

> Dave,

> This article refers very generally to alcohol consumption

increasing the odds of getting cca. Is there any info on very

occasional, or once weekly glass of wine type of drinking. This

could totally negate the relationship that is presented.

> Joan

[Guest guest]

Thanks, Dave. The devil is always in the details, and the details for

this study clearly don't draw a rock-solid conclusion. You need to

see the data details and validate the conclusions.

Arne

54, UC 1977 - PSC 2000

Hi Joan;

Looking at the full paper of Chalasani et al (2000)...