Guest guest Posted March 14, 2005 Report Share Posted March 14, 2005 awwww darn it Ray, its always something it seems with us heppers.. my mother in law had it, it was cured with radiation, she had it on her face so they didnt want to cut it out.. Keep us posted! hugs jax --- Ray wrote: > Always kinda liked Basil. Toss some in your > spaghetti > sauce, or pizza sauce or lasagne, etc, tastes great! > And Basil Rathbone, one cool Sherlock Holmes. But > basil cell carcinoma... nah, that pretty much sucks! > > But that's what my dermatologist told me today. Not > for sure, have to wait for the biopsy results, but I > figure he knows it when he sees it. AKA basal cell > carcinoma, or skin cancer. And here I was thinking > it > was lichen planus! > > Hard to feel good about that news, but I guess it > isn't that big a deal! It's just the one spot far as > I > can see, and he said the cure rate is 96% or so. > They > either just cut it out, or use radiation. In my case > I'll just go for cutting it out. I already got my Tx > going on, who needs radiation? > > I always seem to relate everything back to music, to > some song or other. Right now I'm thinking of " The > First Cut is the Deepest. " Why? Not talking about > when > they cut that thing out of my forehead. More like > talking about just getting that scary news. I went > through that last year, false reports of cancer and > lymphoma, which really put me through some changes. > So > now I'm not so blown away. Not exactly overjoyed > either though. It sucks! > > But, such is life. It's interesting that this sore > has > been shrinking over the last few weeks. I thought it > was from the protopic I was smearing on it, which is > the ointment they prescribe for lichen planus. Turns > out it's probably due to the interferon. Nice to > know > it " interferes " with something else I need to get > rid > of! > > Ray > Jackie Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 15, 2005 Report Share Posted March 15, 2005 Jackie, nne, Fred: Thanks Jackie! I know a lot of people have had it and were cured ok, I think it's about 97% cure rate, so I'm sure I'll be ok. I was thinking surgery at first, not wanting to deal with radiation while on Tx, but on the other hand it is on my forehead and would leave a scar. I'll decide on that when the time comes, I guess. nne, I know one other person who had it, and was cured and had it come back again but is ok now. Both he and I have spent a lot of time in the sun, at the beach or in his case sailing, so I won't be surprised if I get another one... assuming that is what it is. I'll just have to keep an eye out for it! Fred, Thanks for the info! He did do a biopsy; I'll get the results back tomorrow or the next day. He said it looked like basil cell to him, and it did look the same as this big poster he had on his wall, but I'll see what the biopsy says. Fred, sometimes I think you could be the poster boy for half the diseases known to man! You sure have more than your share of stuff going on! That PCT sounds nasty! There are so many weird things that can happen to you when your liver goes bad. I have a couple of places on my right foot that sound something like what is described below. I'll have the dermatologist take a look at it when I go back in. My wife and I looked over my whole body last night. I do have these funny kinda bright red bumps here and there, very small, not sure what they are. I need to get the derma doc to look me over, just to be sure there is nothing strange going on that I need to worry about. Thanks, Ray --- trimenow1234 wrote: --------------------------------- Sorry to hear that Ray. I have PCT (Porphyria cutanea tarda ). A rare blood disorder. 1 in 25,000 to 50,000. The effects can be related to hepotatic function and can result in scabs on the extremities such as hands face legs. The scabs look like burns at first with blister then at times the scab turns into a scab with distict swirls in them. They took a long time to heal but left a scar. Read the last paragraph. My Demotologist said the only way to diagnose them is with a biopsy of the scab. I too thought I had a form of skin cancer. I have a Phlebotomy (removal of blood) - up to 500 ml blood is removed every one to two weeks until the haemoglobin and iron levels drop to low normal levels. It may take 3 - 6 months to improve. Venesection may need to be repeated after a year or more. I get them now more on my face nowadays. I have some semblance of your feelings. Hope and prayers, Fred Porphyria Cutanea Tarda Last Updated: June 5, 2003 Rate this Article Email to a Colleague Synonyms and related keywords: PCT, hepatic porphyria, chronic porphyria, idiosyncratic porphyria, acquired porphyria, sporadic porphyria, symptomatic porphyria, constitutional porphyria, hereditary porphyria, urocoproporphyria, cutaneous hepatic porphyria, uroporphyrinogen decarboxylase, URO-D, hepatoerythropoietic porphyria, epidemic porphyria AUTHOR INFORMATION Section 1 of 11 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography Author: Maureen B Poh-Fitzpatrick, MD, Professor Emerita and Special Lecturer, Department of Dermatology, Columbia University College of Physicians and Surgeons, Clinical Professor of Medicine, Division of Dermatology, University of Tennessee College of Medicine Maureen B Poh-Fitzpatrick, MD, is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and New York Academy of Medicine Editor(s): Craig A Elmets, MD, Director of Dermatology, Departments of Dermatology, Professor, Pathology, Environmental Health Sciences, The Kirklin Clinic, University of Alabama at Birmingham; Vinson, MD, Chief, Department of Dermatology, Beaumont Medical Center; M Joyce Rico, MD, Consulting Staff, Department of Dermatology, Fujisawa Healthcare, Inc; Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University; and Dirk M Elston, MD, Consulting Staff, Department of Dermatology, Geisinger Medical Center INTRODUCTION Section 2 of 11 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography Background: Porphyria cutanea tarda (PCT) is a term that encompasses a group of related disorders, all of which arise from deficient activity of the heme synthetic enzyme uroporphyrinogen decarboxylase (URO-D) in the liver. PCT has types that are clearly inherited (familial PCT) and acquired types that may occur in the context of genetic predisposition (sporadic PCT). Familial forms most often reflect the presence of one mutation in the gene encoding URO-D in individuals who are affected. A rare familial type due to the presence of 2 such mutations has been termed hepatoerythropoietic porphyria. Clinical expression of both the familial type and the acquired type of PCT often requires exposure to inducing agents or conditions that adversely affect hepatocytes, particularly ethanol, estrogens, hepatitis, and human immunodeficiency viruses, and excess iron in the tissue associated with the presence of hemochromatosis genes or other causes. Excess iron in the tissue is frequently found in patients with PCT and appears to play a major role in its pathophysiology. Environmental exposure to polyhalogenated aromatic hydrocarbon compounds has caused acquired toxic porphyric disorders that have been termed epidemic porphyria when observed among large fractions of exposed populations. Pathophysiology: PCT is a hepatic porphyria; the activity of URO-D within hepatocytes is reduced in all familial and acquired types. Deficient activity of hepatic URO-D results in overproduction of porphyrin by-products of the heme biosynthetic pathway that have 4-8 carboxyl group substituents. These porphyrins are reddish pigments that accumulate in the liver and are disseminated in plasma to other organs. Porphyrins with high carboxyl group numbers are water soluble and excreted primarily by renal mechanisms. The porphyrin with 8 carboxyl groups is termed uroporphyrin; the 4-carboxyl porphyrins include coproporphyrin and isocoproporphyrin, which are chiefly excreted in the feces. These porphyrins are photoactive molecules that absorb light energy strongly in the visible violet spectrum. Photoexcited porphyrins in the skin mediate oxidative damage to biomolecular targets, causing cutaneous photosensitivity reactions. The most common photocutaneous manifestations of PCT are due to increased mechanical fragility of the skin after sunlight exposure; erosions and blistering cause painful indolent sores that eventuate into milia, dyspigmentation, and scarring (see Image 2). Other common features of PCT include hypertrichosis, sclerodermalike plaques that may develop dystrophic calcification, and excretion of discolored urine that resembles port wine or tea because of the presence of porphyrin pigments. Frequency: In the US: No porphyria registry is available in the United States; thus, the incidence of PCT is not accurately known but is estimated at 1 case per 25,000-50,000 people. It is the most common type of porphyria. Internationally: Higher incidences of PCT have been reported in some European populations. A high incidence among South African Bantu people has been linked with a propensity for hepatic siderosis. Mortality/Morbidity: The major morbidity of PCT is due to skin fragility and blistering, which virtually preclude manual labor and hamper many daily activities. The subsequent erosions represent full-thickness epidermal loss; they are painful and often become thickly crusted and secondarily infected. Healing is slow and leaves pigmentary changes, milia, and scarring. PCT has been associated with the development of hepatocellular carcinoma, chiefly in populations of older men with histories of long-standing active disease, heavy ethanol intake, and associated cirrhosis. Race: PCT occurs in all racial groups. Sex: No sexual predilection exists for PCT. Age: Sporadic PCT typically presents in adulthood. Familial forms of PCT most often present in adults, but they have also been reported in children who are heterozygous for a URO-D gene mutation. In the rare familial cases in which 2 mutations in URO-D genes are present, the onset is typically in childhood. PCT-like disorders resulting from exposure of large numbers of people to hepatotoxic chemicals have afflicted people of all ages. CLINICAL Section 3 of 11 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography History: The most common complaint at initial presentation is of a new onset of cutaneous fragility and blistering of the dorsal aspects of the hands and the arms and sometimes of the face. Dark urine may also have been noted, but this information may need to be elicited. Similarly, changes in hair growth and pigmentation may be recognized by patients only after inquiry. Patients often do not associate sunlight exposure and the subsequent development of lesions. In familial PCT, other individuals who are affected may be known within a patient's kindred, but often, other related carriers of the mutant gene remain silent, such that patients are often unaware of the familial nature of their disease. In both the familial form and the sporadic form of PCT, a history of exposure to environmental factors (eg, ethanol, estrogens, hepatitis) can often be elicited. In symptomatic cases of familial PCT, any of the common inducing agents may be absent. Paradoxically, proven carriers of the same genetic mutation may remain clinically and biochemically silent despite exposure to such agents. Childhood onset of PCT should suggest either heterozygous or homozygous familial forms of the disease, unless observed in the context of environmental exposure to a chemical hepatotoxin. The occurrence of a PCT-like disease in multiple members of populations exposed to polyhalogenated aromatic hydrocarbons should suggest the occurrence of epidemic toxic porphyria. Physical: The most common presenting sign of PCT is fragility of sun-exposed skin after mechanical trauma, leading to erosions and bullae, which are worst on the dorsal aspects of the hands, the forearms, and the face. Healing of crusted erosions and blisters leaves scars, milia, and hyperpigmented and hypopigmented atrophic patches. Hypertrichosis is often observed and is most florid over the temporal and malar facial areas, but it is also sometimes present on the arms and the legs. Pigmentary changes include melasmalike hyperpigmentation of the face, and an erythematous suffusion or plethora of the central part of the face, the neck, the upper part of the chest, and the shoulders may be present. Scarring alopecia and separation of the nail plates from their beds (photo-onycholysis) can be seen in more severely affected cases. Indurated, waxy, yellowish plaques that resemble lesions of scleroderma can develop over the chest and the back but are most often prominent in the preauricular and nuchal areas. These sclerodermoid plaques can develop dystrophic calcification. Rarely, the only physical sign of PCT is a hyperpigmented sclerodermoid appearance. In individuals who are severely affected, particularly in familial hepatoerythropoietic or toxic epidemic cases, digital shortening, atrophy, and contracted hands resembling those of dystrophic epidermolysis bullosa have occurred. A urine sample is often, but not always, grossly discolored with a tea- or wine-colored tint. Causes: The unifying underlying cause of all of the heterogeneous disorders considered to represent various forms of PCT is reduced activity of URO-D in hepatic heme synthesis. Exposure to hepatitis viruses A, B, and C have all been reported in association with PCT. Hepatitis C appears to be the most commonly associated viral infection, with incidences of more than 50% in several populations of patients with PCT studied in European countries and in the United States. It's a pleasure having you join in our conversations. We hope you have found the support you need with us. If you are using email for your posts, for easy access to our group, just click the link-- http://groups.yahoo.com/group/Hepatitis_C_Central/ Happy Posting Quote Link to comment Share on other sites More sharing options...
Guest guest Posted March 16, 2005 Report Share Posted March 16, 2005 Ray, My mother has basal cell cancers on her body. They usually just take them off, or burn them off. She had one taken off the end of her nose.That one required plastic surgery. But for the most part she has them done right there in the doctor office. She has several taken off her back. I think I have some on my arm and one on my neck. I am going to see the doctor and have them cut off. When you have a parent that has them you tend to know what they look like. When they burn them off it leave very little scarring that is the good thing. Good luck with your doc. Love Janet Ray wrote: Jackie, nne, Fred: Thanks Jackie! I know a lot of people have had it and were cured ok, I think it's about 97% cure rate, so I'm sure I'll be ok. I was thinking surgery at first, not wanting to deal with radiation while on Tx, but on the other hand it is on my forehead and would leave a scar. I'll decide on that when the time comes, I guess. nne, I know one other person who had it, and was cured and had it come back again but is ok now. Both he and I have spent a lot of time in the sun, at the beach or in his case sailing, so I won't be surprised if I get another one... assuming that is what it is. I'll just have to keep an eye out for it! Fred, Thanks for the info! He did do a biopsy; I'll get the results back tomorrow or the next day. He said it looked like basil cell to him, and it did look the same as this big poster he had on his wall, but I'll see what the biopsy says. Fred, sometimes I think you could be the poster boy for half the diseases known to man! You sure have more than your share of stuff going on! That PCT sounds nasty! There are so many weird things that can happen to you when your liver goes bad. I have a couple of places on my right foot that sound something like what is described below. I'll have the dermatologist take a look at it when I go back in. My wife and I looked over my whole body last night. I do have these funny kinda bright red bumps here and there, very small, not sure what they are. I need to get the derma doc to look me over, just to be sure there is nothing strange going on that I need to worry about. Thanks, Ray --- trimenow1234 wrote: --------------------------------- Sorry to hear that Ray. I have PCT (Porphyria cutanea tarda ). A rare blood disorder. 1 in 25,000 to 50,000. The effects can be related to hepotatic function and can result in scabs on the extremities such as hands face legs. The scabs look like burns at first with blister then at times the scab turns into a scab with distict swirls in them. They took a long time to heal but left a scar. Read the last paragraph. My Demotologist said the only way to diagnose them is with a biopsy of the scab. I too thought I had a form of skin cancer. I have a Phlebotomy (removal of blood) - up to 500 ml blood is removed every one to two weeks until the haemoglobin and iron levels drop to low normal levels. It may take 3 - 6 months to improve. Venesection may need to be repeated after a year or more. I get them now more on my face nowadays. I have some semblance of your feelings. Hope and prayers, Fred Porphyria Cutanea Tarda Last Updated: June 5, 2003 Rate this Article Email to a Colleague Synonyms and related keywords: PCT, hepatic porphyria, chronic porphyria, idiosyncratic porphyria, acquired porphyria, sporadic porphyria, symptomatic porphyria, constitutional porphyria, hereditary porphyria, urocoproporphyria, cutaneous hepatic porphyria, uroporphyrinogen decarboxylase, URO-D, hepatoerythropoietic porphyria, epidemic porphyria AUTHOR INFORMATION Section 1 of 11 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography Author: Maureen B Poh-Fitzpatrick, MD, Professor Emerita and Special Lecturer, Department of Dermatology, Columbia University College of Physicians and Surgeons, Clinical Professor of Medicine, Division of Dermatology, University of Tennessee College of Medicine Maureen B Poh-Fitzpatrick, MD, is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and New York Academy of Medicine Editor(s): Craig A Elmets, MD, Director of Dermatology, Departments of Dermatology, Professor, Pathology, Environmental Health Sciences, The Kirklin Clinic, University of Alabama at Birmingham; Vinson, MD, Chief, Department of Dermatology, Beaumont Medical Center; M Joyce Rico, MD, Consulting Staff, Department of Dermatology, Fujisawa Healthcare, Inc; Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University; and Dirk M Elston, MD, Consulting Staff, Department of Dermatology, Geisinger Medical Center INTRODUCTION Section 2 of 11 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography Background: Porphyria cutanea tarda (PCT) is a term that encompasses a group of related disorders, all of which arise from deficient activity of the heme synthetic enzyme uroporphyrinogen decarboxylase (URO-D) in the liver. PCT has types that are clearly inherited (familial PCT) and acquired types that may occur in the context of genetic predisposition (sporadic PCT). Familial forms most often reflect the presence of one mutation in the gene encoding URO-D in individuals who are affected. A rare familial type due to the presence of 2 such mutations has been termed hepatoerythropoietic porphyria. Clinical expression of both the familial type and the acquired type of PCT often requires exposure to inducing agents or conditions that adversely affect hepatocytes, particularly ethanol, estrogens, hepatitis, and human immunodeficiency viruses, and excess iron in the tissue associated with the presence of hemochromatosis genes or other causes. Excess iron in the tissue is frequently found in patients with PCT and appears to play a major role in its pathophysiology. Environmental exposure to polyhalogenated aromatic hydrocarbon compounds has caused acquired toxic porphyric disorders that have been termed epidemic porphyria when observed among large fractions of exposed populations. Pathophysiology: PCT is a hepatic porphyria; the activity of URO-D within hepatocytes is reduced in all familial and acquired types. Deficient activity of hepatic URO-D results in overproduction of porphyrin by-products of the heme biosynthetic pathway that have 4-8 carboxyl group substituents. These porphyrins are reddish pigments that accumulate in the liver and are disseminated in plasma to other organs. Porphyrins with high carboxyl group numbers are water soluble and excreted primarily by renal mechanisms. The porphyrin with 8 carboxyl groups is termed uroporphyrin; the 4-carboxyl porphyrins include coproporphyrin and isocoproporphyrin, which are chiefly excreted in the feces. These porphyrins are photoactive molecules that absorb light energy strongly in the visible violet spectrum. Photoexcited porphyrins in the skin mediate oxidative damage to biomolecular targets, causing cutaneous photosensitivity reactions. The most common photocutaneous manifestations of PCT are due to increased mechanical fragility of the skin after sunlight exposure; erosions and blistering cause painful indolent sores that eventuate into milia, dyspigmentation, and scarring (see Image 2). Other common features of PCT include hypertrichosis, sclerodermalike plaques that may develop dystrophic calcification, and excretion of discolored urine that resembles port wine or tea because of the presence of porphyrin pigments. Frequency: In the US: No porphyria registry is available in the United States; thus, the incidence of PCT is not accurately known but is estimated at 1 case per 25,000-50,000 people. It is the most common type of porphyria. Internationally: Higher incidences of PCT have been reported in some European populations. A high incidence among South African Bantu people has been linked with a propensity for hepatic siderosis. Mortality/Morbidity: The major morbidity of PCT is due to skin fragility and blistering, which virtually preclude manual labor and hamper many daily activities. The subsequent erosions represent full-thickness epidermal loss; they are painful and often become thickly crusted and secondarily infected. Healing is slow and leaves pigmentary changes, milia, and scarring. PCT has been associated with the development of hepatocellular carcinoma, chiefly in populations of older men with histories of long-standing active disease, heavy ethanol intake, and associated cirrhosis. Race: PCT occurs in all racial groups. Sex: No sexual predilection exists for PCT. Age: Sporadic PCT typically presents in adulthood. Familial forms of PCT most often present in adults, but they have also been reported in children who are heterozygous for a URO-D gene mutation. In the rare familial cases in which 2 mutations in URO-D genes are present, the onset is typically in childhood. PCT-like disorders resulting from exposure of large numbers of people to hepatotoxic chemicals have afflicted people of all ages. CLINICAL Section 3 of 11 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography History: The most common complaint at initial presentation is of a new onset of cutaneous fragility and blistering of the dorsal aspects of the hands and the arms and sometimes of the face. Dark urine may also have been noted, but this information may need to be elicited. Similarly, changes in hair growth and pigmentation may be recognized by patients only after inquiry. Patients often do not associate sunlight exposure and the subsequent development of lesions. In familial PCT, other individuals who are affected may be known within a patient's kindred, but often, other related carriers of the mutant gene remain silent, such that patients are often unaware of the familial nature of their disease. In both the familial form and the sporadic form of PCT, a history of exposure to environmental factors (eg, ethanol, estrogens, hepatitis) can often be elicited. In symptomatic cases of familial PCT, any of the common inducing agents may be absent. Paradoxically, proven carriers of the same genetic mutation may remain clinically and biochemically silent despite exposure to such agents. Childhood onset of PCT should suggest either heterozygous or homozygous familial forms of the disease, unless observed in the context of environmental exposure to a chemical hepatotoxin. The occurrence of a PCT-like disease in multiple members of populations exposed to polyhalogenated aromatic hydrocarbons should suggest the occurrence of epidemic toxic porphyria. Physical: The most common presenting sign of PCT is fragility of sun-exposed skin after mechanical trauma, leading to erosions and bullae, which are worst on the dorsal aspects of the hands, the forearms, and the face. Healing of crusted erosions and blisters leaves scars, milia, and hyperpigmented and hypopigmented atrophic patches. Hypertrichosis is often observed and is most florid over the temporal and malar facial areas, but it is also sometimes present on the arms and the legs. Pigmentary changes include melasmalike hyperpigmentation of the face, and an erythematous suffusion or plethora of the central part of the face, the neck, the upper part of the chest, and the shoulders may be present. Scarring alopecia and separation of the nail plates from their beds (photo-onycholysis) can be seen in more severely affected cases. Indurated, waxy, yellowish plaques that resemble lesions of scleroderma can develop over the chest and the back but are most often prominent in the preauricular and nuchal areas. These sclerodermoid plaques can develop dystrophic calcification. Rarely, the only physical sign of PCT is a hyperpigmented sclerodermoid appearance. In individuals who are severely affected, particularly in familial hepatoerythropoietic or toxic epidemic cases, digital shortening, atrophy, and contracted hands resembling those of dystrophic epidermolysis bullosa have occurred. A urine sample is often, but not always, grossly discolored with a tea- or wine-colored tint. Causes: The unifying underlying cause of all of the heterogeneous disorders considered to represent various forms of PCT is reduced activity of URO-D in hepatic heme synthesis. Exposure to hepatitis viruses A, B, and C have all been reported in association with PCT. Hepatitis C appears to be the most commonly associated viral infection, with incidences of more than 50% in several populations of patients with PCT studied in European countries and in the United States. It's a pleasure having you join in our conversations. We hope you have found the support you need with us. If you are using email for your posts, for easy access to our group, just click the link-- http://groups.yahoo.com/group/Hepatitis_C_Central/ Happy Posting Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 7, 2011 Report Share Posted August 7, 2011 .......perhaps a little like blueberry yogurt?.......... Re: OT: Aerogarden sale HI. I have a water question. When I give my sprouts a DRINK two times a day, can I use the liquid whey that I have leftover from when I make greek yogurt? I am now putting this liquid in my basil plants. But I was wondering if it would have any beneficial properties to either the soak water, or when I rinse and drain my sprouts.???? Thanks much to anyone who knows. Melody > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 7, 2011 Report Share Posted August 7, 2011 My basil is WONDERFUL. Still growing and I eat it every day in my sprout salad. Now can I use the leftover whey to rinse my sprouts with, OR NOT?? Because the next time I make home-made greek yogurt and I have leftover whey, I wonder if it would benefit my sprouts? Melody > > > > > > > Quote Link to comment Share on other sites More sharing options...
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