Guest guest Posted October 19, 2004 Report Share Posted October 19, 2004 Dear Nellie: I've read that high hepatic copper is a problem with PSC, particularly in the later stages, so excluding high copper foods and supplements is a good idea. In primary biliary cirrhosis, D- penicillamine is a medication that has been used to lower hepatic copper and increase urinary excretion of copper. A really good database on the composition of foods [including vitamin and mineral contents] is as follows: http://www.nal.usda.gov/fnic/foodcomp/search/ [You have to search for a specific food item and then select a quantity before it gives you a Table of food composition] ____________________ Gastroenterology. 1985 Aug;89(2):272-8. Abnormalities in tests of copper metabolism in primary sclerosing cholangitis. Gross JB Jr, Ludwig J, Wiesner RH, McCall JT, LaRusso NF. Primary sclerosing cholangitis is a chronic, cholestatic syndrome characterized by fibrosing inflammation of the bile ducts that may lead to cirrhosis and death from liver failure. Previous reports have suggested abnormal hepatic copper metabolism in this disease. Therefore, in 70 patients, we prospectively determined the levels of hepatic copper, serum copper, and serum ceruloplasmin, and the rate of urinary copper excretion to assess the diagnostic and prognostic usefulness of these tests. Virtually all patients had at least one abnormal copper test. Hepatic copper levels were elevated in 87% of patients [292 +/- 38 micrograms/g dry wt (mean +/- SE)] and 24-h urinary copper levels in 64% of patients [135 +/- 15 micrograms/24 h (mean +/- SE)] to values comparable to those seen in 's disease or primary biliary cirrhosis. In advanced histologic stages of primary sclerosing cholangitis, progressively higher mean levels of hepatic and urinary copper were found. In the liver, mean copper content (in micrograms per gram dry weight) in disease stages I and II was 147 +/- 36 (mean +/- SE); in stage III (fibrosis), 302 +/- 68; and in stage IV (cirrhosis), 379 +/- 69. In the urine, mean copper excretion (in micrograms per 24 h) in stages I and II was 72 +/- 14 (mean +/- SE); in stage III, 100 +/- 14; and in stage IV, 207 +/- 30. Higher hepatic and urinary copper levels at initial evaluation were associated with decreased survival during a median follow-up period of 2.6 yr: patients with hepatic copper greater than 250 micrograms/g dry wt and urinary copper excretion greater than 200 micrograms/24 h at initial evaluation had an 18-mo survival of less than 60%. We conclude that abnormal copper metabolism is a universal feature of primary sclerosing cholangitis, that hepatic copper accumulates and urinary copper excretion increases as the disease progresses, and that the hepatic copper concentration and the 24-h urinary copper determination are useful prognostic indicators in this disease. PMID: 4007418 ______________________________ Dig Dis Sci. 1994 Nov;39(11):2416-20. Hepatic copper content is normal in early primary biliary cirrhosis and primary sclerosing cholangitis. Kowdley KV, Knox TA, Kaplan MM. Division of Gastroenterology, New England Medical Center, Boston, Massachusetts. In previous studies, the majority of patients with the cholestatic liver diseases, primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC), had increased hepatic copper (Cu) levels even in early stages of disease. We prospectively measured hepatic copper content by atomic absorption spectrophotometry in 55 patients with PBC, 6 patients with PSC, and 29 patients with other chronic noncholestatic liver diseases. Hepatic Cu content was normal in 22/61 (36%) of patients with PBC or PSC; 18 of the 22 did not have cirrhosis (82%). Hepatic Cu content increased with increasing stage of disease (r = 0.61, P < 0.001) and was positively correlated with serum total bilirubin (r = 0.6, P < 0.0001) and alkaline phosphatase (r = 0.5, P < 0.001). All patients with stage I and II disease had hepatic Cu < 150 micrograms/g dry weight, and all patients with hepatic Cu > 150 micrograms/g dry weight had stage III and IV disease. Hepatic Cu content is normal in early PBC and PSC. Copper accumulation in the liver in these cholestatic liver diseases is secondary to cholestasis rather than a primary phenomenon. PMID: 7956610 ______________________________ Gastroenterology. 1977 Jun;72(6):1208-12. Effect of D-penicillamine on copper retention in patients with primary billiary cirrhosis. Deering TB, Dickson ER, Fleming CR, Geall MG, McCall JT, Baggenstoss AH. As part of a double blind, randomized trial evaluating D- penicillamine in primary biliary cirrhosis, we monitored urinary copper excretion and hepatic copper concentration during the 1st year of therapy in 46 patients with this disease. The retention of copper in primary biliary cirrhosis was confirmed by finding abnormally high levels of standard copper measurements in almost all patients before treatment. The hepatic copper was elevated in 43 of 45 patients, the urinary copper in 42 of 46, and the ceruloplasmin in 46 of 46. Urinary copper excretion correlated with the hepatic copper concentration (r = 0.68, P less than or equal to 0.001). No significant correlation occurred between hepatic copper and ceruloplasmin. Hepatic copper concentrations greater than 400 microng per g of dry weight were found almost exclusively in patients with advanced histological disease (P less than or equal to 0.01). Therapy with D-penicillamine and a low copper diet sustained increased urinary copper excretion for 1 year in almost all patients (P less than or equal to 0.001). Among patients taking placebo, the median hepatic copper concentration increased 13 microng per g of dry weight after 1 year. In contrast, among the patients taking D-penicillamine, the median hepatic copper concentration decreased 99 microng per g of dry weight (P less than or equal to 0.02). Continued observation of this therapeutic trial may help to clarify the relationship of copper retention and liver injury in primary biliary cirrhosis. Publication Types: Clinical Trial Randomized Controlled Trial PMID: 870369 ________________________ Best regards, Dave (father of (19); PSC 07/03; UC 08/03) Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 19, 2004 Report Share Posted October 19, 2004 Thanks so much, . I had read the first abstract you included and found it a bit scary. The food table link is very helpful. I'm also going to visit some of the 's disease sites, as I know they have some good lists of high-copper foods. I'm starting to wonder why the GI would put Larry on a supplement that contains copper, though. I'll be asking about that tomorrow for sure. Thanks again, Nellie > > Dear Nellie: > > I've read that high hepatic copper is a problem with PSC, > particularly in the later stages, so excluding high copper foods and > supplements is a good idea. In primary biliary cirrhosis, D- > penicillamine is a medication that has been used to lower hepatic > copper and increase urinary excretion of copper. > > A really good database on the composition of foods [including vitamin > and mineral contents] is as follows: > > http://www.nal.usda.gov/fnic/foodcomp/search/ > > [You have to search for a specific food item and then select a > quantity before it gives you a Table of food composition] > > ____________________ > > Gastroenterology. 1985 Aug;89(2):272-8. > > Abnormalities in tests of copper metabolism in primary sclerosing > cholangitis. > > Gross JB Jr, Ludwig J, Wiesner RH, McCall JT, LaRusso NF. > > Primary sclerosing cholangitis is a chronic, cholestatic syndrome > characterized by fibrosing inflammation of the bile ducts that may > lead to cirrhosis and death from liver failure. Previous reports have > suggested abnormal hepatic copper metabolism in this disease. > Therefore, in 70 patients, we prospectively determined the levels of > hepatic copper, serum copper, and serum ceruloplasmin, and the rate > of urinary copper excretion to assess the diagnostic and prognostic > usefulness of these tests. Virtually all patients had at least one > abnormal copper test. Hepatic copper levels were elevated in 87% of > patients [292 +/- 38 micrograms/g dry wt (mean +/- SE)] and 24-h > urinary copper levels in 64% of patients [135 +/- 15 micrograms/24 h > (mean +/- SE)] to values comparable to those seen in 's disease > or primary biliary cirrhosis. In advanced histologic stages of > primary sclerosing cholangitis, progressively higher mean levels of > hepatic and urinary copper were found. In the liver, mean copper > content (in micrograms per gram dry weight) in disease stages I and > II was 147 +/- 36 (mean +/- SE); in stage III (fibrosis), 302 +/- 68; > and in stage IV (cirrhosis), 379 +/- 69. In the urine, mean copper > excretion (in micrograms per 24 h) in stages I and II was 72 +/- 14 > (mean +/- SE); in stage III, 100 +/- 14; and in stage IV, 207 +/- 30. > Higher hepatic and urinary copper levels at initial evaluation were > associated with decreased survival during a median follow-up period > of 2.6 yr: patients with hepatic copper greater than 250 micrograms/g > dry wt and urinary copper excretion greater than 200 micrograms/24 h > at initial evaluation had an 18-mo survival of less than 60%. We > conclude that abnormal copper metabolism is a universal feature of > primary sclerosing cholangitis, that hepatic copper accumulates and > urinary copper excretion increases as the disease progresses, and > that the hepatic copper concentration and the 24-h urinary copper > determination are useful prognostic indicators in this disease. > > PMID: 4007418 > ______________________________ > > Dig Dis Sci. 1994 Nov;39(11):2416-20. > > Hepatic copper content is normal in early primary biliary cirrhosis > and primary sclerosing cholangitis. > > Kowdley KV, Knox TA, Kaplan MM. > > Division of Gastroenterology, New England Medical Center, Boston, > Massachusetts. > > In previous studies, the majority of patients with the cholestatic > liver diseases, primary biliary cirrhosis (PBC) and primary > sclerosing cholangitis (PSC), had increased hepatic copper (Cu) > levels even in early stages of disease. We prospectively measured > hepatic copper content by atomic absorption spectrophotometry in 55 > patients with PBC, 6 patients with PSC, and 29 patients with other > chronic noncholestatic liver diseases. Hepatic Cu content was normal > in 22/61 (36%) of patients with PBC or PSC; 18 of the 22 did not have > cirrhosis (82%). Hepatic Cu content increased with increasing stage > of disease (r = 0.61, P < 0.001) and was positively correlated with > serum total bilirubin (r = 0.6, P < 0.0001) and alkaline phosphatase > (r = 0.5, P < 0.001). All patients with stage I and II disease had > hepatic Cu < 150 micrograms/g dry weight, and all patients with > hepatic Cu > 150 micrograms/g dry weight had stage III and IV > disease. Hepatic Cu content is normal in early PBC and PSC. Copper > accumulation in the liver in these cholestatic liver diseases is > secondary to cholestasis rather than a primary phenomenon. > > PMID: 7956610 > ______________________________ > > Gastroenterology. 1977 Jun;72(6):1208-12. > > Effect of D-penicillamine on copper retention in patients with > primary billiary cirrhosis. > > Deering TB, Dickson ER, Fleming CR, Geall MG, McCall JT, Baggenstoss > AH. > > As part of a double blind, randomized trial evaluating D- > penicillamine in primary biliary cirrhosis, we monitored urinary > copper excretion and hepatic copper concentration during the 1st year > of therapy in 46 patients with this disease. The retention of copper > in primary biliary cirrhosis was confirmed by finding abnormally high > levels of standard copper measurements in almost all patients before > treatment. The hepatic copper was elevated in 43 of 45 patients, the > urinary copper in 42 of 46, and the ceruloplasmin in 46 of 46. > Urinary copper excretion correlated with the hepatic copper > concentration (r = 0.68, P less than or equal to 0.001). No > significant correlation occurred between hepatic copper and > ceruloplasmin. Hepatic copper concentrations greater than 400 microng > per g of dry weight were found almost exclusively in patients with > advanced histological disease (P less than or equal to 0.01). Therapy > with D-penicillamine and a low copper diet sustained increased > urinary copper excretion for 1 year in almost all patients (P less > than or equal to 0.001). Among patients taking placebo, the median > hepatic copper concentration increased 13 microng per g of dry weight > after 1 year. In contrast, among the patients taking D-penicillamine, > the median hepatic copper concentration decreased 99 microng per g of > dry weight (P less than or equal to 0.02). Continued observation of > this therapeutic trial may help to clarify the relationship of copper > retention and liver injury in primary biliary cirrhosis. > > Publication Types: > Clinical Trial > Randomized Controlled Trial > > PMID: 870369 > > ________________________ > > Best regards, > > Dave > (father of (19); PSC 07/03; UC 08/03) Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 19, 2004 Report Share Posted October 19, 2004 I have heard hepatologists suggesting a low copper diet for pscer's in general when discussing nutrition that is why iam surprised how his doctor did not restrict his diet to try to decrease the insults on his comromised liver specially that he has accumulated a good amount of copper. But personally i still think that us pscer's need to somehow watch for copper, specially in the latest stages of the disease. The Mayo Clinic has a very good detailed copper food list [mayoclinic.com]. I know that also provided a link for that I don't blame you for being concerned about the vitamin supplement that contains copper. I beleive that it should be avoided and in case of Larry, definitely but iam glad that you will be consulting a hepatologist tomorrow. It is great that some of his symptoms are improving. Good luck with his Tx evaluation. PSC/UC --- lilnellawafer wrote: > > Hello, all, > > Larry and I are heading for Birmingham tomorrow to > begin the tx > evaluation. Larry got all of his lab and pathology > reports yesterday > and one thing struck me -- his liver bx report > showed that way too > much copper had accumulated in his liver > (originally, the GI suspected > he might have 's disease) and yet the dr. > didn't say anything > about restricting copper in Larry's diet. > > Have any of you been told to cut out copper-rich > foods? I know that > the copper accumulation leads to cirrhosis and I'm > concerned that not > addressing this problem could further his cirrhosis. > In any case, I > removed all the nuts and chocolate (which Larry > loves) from the house > just in case. I plan to ask the hepatologist > tomorrow about this, but > wondered if anyone in the group had any info on > this. > > By the way, since Larry started all his meds, he > seems to be improving > some -- certainly his moods and fatigue -- I wonder > if it's because > some of the copper is making its way out of his > system. But I'm > concerned that one of the vitamin supplements the GI > put him on also > has copper. > > As always, any insight is appreciated. > Nellie > Wife of Larry (31) PSC 9/04, UC 10/04 > > > > __________________________________________________ Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 20, 2004 Report Share Posted October 20, 2004 Hey Nellie, I have been on a copper restricted diet and water filtered to remove all heavy metals for 24 years. Most copper people take in comes not from food, but from drinking water. It's interesting; when I was very ill in about 1980, there was a research project at Mayo that my liver specialist asked that I participate in. It was conducted by Dr. LaRusso ( I think was the spelling) and studied copper and other heavy metal accumulations and use of pellicilimine to remove them. My copper content was not appreciably high in my liver, but was in my blood. Just so happens that my dad is a chemist, specifically, a water and food chemist. He immediately went crazy testing the well water and plumbing at our farm where we lived. The plumbing was old copper plumbing and the well water was acidic, beautiful delightful water, but leaching the copper out of the pipes. From then until now, I have resin water filters on all my water that you may drink from at home. They are Continential Water supplied commercial filters and take just about everything out, especially all metals and have an alarm light to tell when they stop working and need to be replaced. I have done very well over the years, and that is one thing I think has been a factor. I was evaluated for the study and contributed my records and interviews, but my liver doctor did not want me to have the periodic liver biopsies they required. Tee ( T. McCoy, CEBS-- psc 35 + years) > > Hello, all, > > Larry and I are heading for Birmingham tomorrow to begin the tx > evaluation. Larry got all of his lab and pathology reports yesterday > and one thing struck me -- his liver bx report showed that way too > much copper had accumulated in his liver (originally, the GI suspected > he might have 's disease) and yet the dr. didn't say anything > about restricting copper in Larry's diet. > > Have any of you been told to cut out copper-rich foods? I know that >> As always, any insight is appreciated. > Nellie > Wife of Larry (31) PSC 9/04, UC 10/04 Quote Link to comment Share on other sites More sharing options...
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