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Medical Forum / Diseases and Disorders / Cancer / May 2008Complete Cure Of Aplastic Anemia
"Complete recovery after iron chelation in aplastic anemia" They treated this kid for five years .. aggressively .. and when and ONLY when the kid was failing DUE TO their interventions / iron buildup .. did they finally cure the kid. Removed the iron **totally** .. IE: targeted the iron .. and the kid was cured. --------- Complete hematopoietic recovery after continuous iron chelation therapy in a patient with severe aplastic anemia with secondary hemochromatosis. Park SJ, Han CW J Korean Med Sci 2008 Apr; 23(2):320-3. A 16-yr-old male patient with hemochromatosis due to multiple packed red blood cell transfusions was referred to our emergency center for the treatment of severe aplastic anemia and dyspnea. He was diagnosed with aplastic anemia at 11-yr of age. He had received continuous transfusions because an HLA-matched marrow donor was unavailable. Following a continuous, approximately 5-yr transfusion, he was noted to develop hemochromatosis. He had a dilated cardiomyopathy and required diuretics and digitalis, multiple endocrine and liver dysfunction, generalized bleeding, and skin pigmentation. A total volume of red blood cell transfusion before deferoxamine therapy was about 96,000 mL. He received a regular iron chelation therapy (continuous intravenous infusion of deferoxamine, 50 mg/kg/day for 5 days q 3-4 weeks) for approximately seven years after the onset of multiple organ failures. His cytopenia and organ dysfunctions began to be gradually recovered since about 2002, following a 4-yr deferoxamine treatment. He showed completely normal ranges of peripheral blood cell counts, heart size, and liver function two years ago. He has not received any transfusions for the last four years. This finding suggests that a continuous deferoxamine infusion may play a role in the immune regulation in addition to iron chelation effect. Journal of Korean medical science [J Korean Med Sci] -------------------------------------------------------------------------------- http://en.wikipedia.org/wiki/Aplastic_anemia Treating aplastic anemia involves suppression of the immune system, an effect achieved by daily medicine intake, or, in more severe cases, a bone marrow transplant, a potential cure but a risky procedure.[1] The transplanted bone marrow replaces the failing bone marrow cells with new ones from a matching donor. The pluripotent stem cells in the bone marrow reconstitute all three blood cell lines, giving the patient a new immune system, red blood cells, and platelets. However, besides the risk of graft failure, there is also a risk that the newly created white blood cells may attack the rest of the body ("graft-versus-host disease"). Medical therapy of aplastic anemia often includes a short course of anti-thymocyte globulin (ATG) or anti-lymphocyte globulin (ALG) and several months of treatment with cyclosporin to modulate the immune system. Mild chemotherapy with agents such as cyclophosphamide and vincristine may also be effective. Antibodies therapy, such as ATG, targets T-cells, which are believed to attack the bone marrow. Steroids are generally ineffective. In the past, before the above treatments became available, patients with low leukocyte counts were often confined to a sterile room or bubble (to reduce risk of infections), as in the famed case of Ted DeVita.[2] Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk The Pherrous Phuckwit <halfbaked@my.bbq.com> trolled: > "Complete recovery after iron chelation in aplastic anemia" http://www.youtube.com/watch?v=S524O_XNoLM --Bill Thompson On May 1, 11:55 pm, "wrtho...@ix.netcom.com" <wrthomp...@gmail.com> wrote: http://www.youtube.com/watch?v=S524O_XNoLM << "Complete recovery after iron chelation in aplastic anemia" Now I don't suppose .. complete recovery after iron chelation in aplastic anemia .. actually MEANS anything to .. you .. but it does to some .. sooo .. just in case .. let me cut and paste it .. again .. below .. ok willie .. ? Complete hematopoietic recovery after continuous iron chelation therapy in a patient with severe aplastic anemia with secondary hemochromatosis. Park SJ, Han CW J Korean Med Sci 2008 Apr; 23(2):320-3. A 16-yr-old male patient with hemochromatosis due to multiple packed red blood cell transfusions was referred to our emergency center for the treatment of severe aplastic anemia and dyspnea. He was diagnosed with aplastic anemia at 11-yr of age. He had received continuous transfusions because an HLA-matched marrow donor was unavailable. Following a continuous, approximately 5-yr transfusion, he was noted to develop hemochromatosis. He had a dilated cardiomyopathy and required diuretics and digitalis, multiple endocrine and liver dysfunction, generalized bleeding, and skin pigmentation. A total volume of red blood cell transfusion before deferoxamine therapy was about 96,000 mL. He received a regular iron chelation therapy (continuous intravenous infusion of deferoxamine, 50 mg/kg/day for 5 days q 3-4 weeks) for approximately seven years after the onset of multiple organ failures. His cytopenia and organ dysfunctions began to be gradually recovered since about 2002, following a 4-yr deferoxamine treatment. He showed completely normal ranges of peripheral blood cell counts, heart size, and liver function two years ago. He has not received any transfusions for the last four years. This finding suggests that a continuous deferoxamine infusion may play a role in the immune regulation in addition to iron chelation effect. Journal of Korean medical science [J Korean Med Sci] -------------------------------------------------------------------------------- Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk The Pherrous Phuckwit <nobrains@all> danced to my tune wih: > "wrtho...@ix.netcom.com" <wrthomp...@gmail.com> > brilliantly commented upon Rusty with: > http://www.youtube.com/watch?v=S524O_XNoLM > "Complete recovery after iron chelation in aplastic anemia" > Now I don't suppose .. complete recovery after iron chelation in > aplastic anemia .. actually MEANS anything What's this, Rusty? You posted it and you didn't think it meant anything? Honesty in you is such a surprise! But I knew I could make you dance if I played a little--Heavy Metal! Give us another little dance, Rusty. Do the "TeamTanner Two-Step." Stamp your widdle feet and get red in the face to this song: http://www.youtube.com/watch?v=7E1zE6uH-ng --Bill Thompson On May 2, 10:12 pm, "wrtho...@ix.netcom.com" <wrthomp...@gmail.com> wrote:Stamp your widdle feet and get red in the face to this song: << Let me cut and paste it .. again .. below .. ok willie .. ? Complete hematopoietic recovery after continuous iron chelation therapy in a patient with severe aplastic anemia with secondary hemochromatosis. Park SJ, Han CW J Korean Med Sci 2008 Apr; 23(2):320-3. A 16-yr-old male patient with hemochromatosis due to multiple packed red blood cell transfusions was referred to our emergency center for the treatment of severe aplastic anemia and dyspnea. He was diagnosed with aplastic anemia at 11-yr of age. He had received continuous transfusions because an HLA-matched marrow donor was unavailable. Following a continuous, approximately 5-yr transfusion, he was noted to develop hemochromatosis. He had a dilated cardiomyopathy and required diuretics and digitalis, multiple endocrine and liver dysfunction, generalized bleeding, and skin pigmentation. A total volume of red blood cell transfusion before deferoxamine therapy was about 96,000 mL. He received a regular iron chelation therapy (continuous intravenous infusion of deferoxamine, 50 mg/kg/day for 5 days q 3-4 weeks) for approximately seven years after the onset of multiple organ failures. His cytopenia and organ dysfunctions began to be gradually recovered since about 2002, following a 4-yr deferoxamine treatment. He showed completely normal ranges of peripheral blood cell counts, heart size, and liver function two years ago. He has not received any transfusions for the last four years. This finding suggests that a continuous deferoxamine infusion may play a role in the immune regulation in addition to iron chelation effect. Journal of Korean medical science [J Korean Med Sci] -------------------------------------------------------------------------------- Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk > The Pherrous Phuckwit <nobrains@all> danced to my tune wih: > [quoted text clipped - 16 lines] > > --Bill Thompson Le Phuquewitte de Pherrousse <no.brains@all> danced to my tune with: > "wrtho...@ix.netcom.com" <wrthomp...@gmail.com> wrote: >Stamp your widdle feet and get red in the face to this song: > Let me cut and paste it .. again .. Again, eh? I've noticed somethng about you, Rusty. You claim you're only interested in iron, but somehow you always turn the subject to--blood! And when I post a link to Marlyn Manson, you lose what little self-control you had. It's obvious where you're coming from! Yes, you are--Nosferrousatu! So here's a song going out to you and all the bats in your belfry: http://www.youtube.com/watch?v=ZY-QjUl6Swo --Bill Thompson "Complete recovery after iron chelation in aplastic anemia" Complete hematopoietic recovery after continuous iron chelation therapy in a patient with severe aplastic anemia with secondary hemochromatosis. Park SJ, Han CW J Korean Med Sci 2008 Apr; 23(2):320-3. A 16-yr-old male patient with hemochromatosis due to multiple packed red blood cell transfusions was referred to our emergency center for the treatment of severe aplastic anemia and dyspnea. He was diagnosed with aplastic anemia at 11-yr of age. He had received continuous transfusions because an HLA-matched marrow donor was unavailable. Following a continuous, approximately 5-yr transfusion, he was noted to develop hemochromatosis. He had a dilated cardiomyopathy and required diuretics and digitalis, multiple endocrine and liver dysfunction, generalized bleeding, and skin pigmentation. A total volume of red blood cell transfusion before deferoxamine therapy was about 96,000 mL. He received a regular iron chelation therapy (continuous intravenous infusion of deferoxamine, 50 mg/kg/day for 5 days q 3-4 weeks) for approximately seven years after the onset of multiple organ failures. His cytopenia and organ dysfunctions began to be gradually recovered since about 2002, following a 4-yr deferoxamine treatment. He showed completely normal ranges of peripheral blood cell counts, heart size, and liver function two years ago. He has not received any transfusions for the last four years. This finding suggests that a continuous deferoxamine infusion may play a role in the immune regulation in addition to iron chelation effect. Journal of Korean medical science [J Korean Med Sci] -------------------------------------------------------------------------------- Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk > Le Phuquewitte de Pherrousse <no.brains@all> danced to my tune with: > [quoted text clipped - 12 lines] > > --Bill Thompson On May 4, 7:37 am, ironjustice <teamtan...@hotmail.com> wrote:"Complete recovery after iron chelation in aplastic anemia" << http://tinyurl.com/2nn4q8 Recently, researchers have discovered that most cases of severe aplastic anemia are autoimmune disorders in which the body’s own immune system attacks tissues and organs. ------------------- "The infant died." Aplastic anemia in neonatal lupus erythematosus B. Wolach, L. Choc, A. Pomeranz, Y. Ben Ari, D. Douer and A. Metzker Department of Pediatrics, Meir General Hospital, Sapir Medical Center, Kfar Saba, Israel. OBJECTIVE-- To describe an infant with neonatal lupus erythematosus associated with aplastic anemia. SETTING-- The pediatric department in a tertiary-care hospital. INTERVENTIONS-- Packed red blood cell transfusions and a 3-week course of high-dose steroid therapy. MEASUREMENTS/MAIN RESULTS-- The patient presented with severe anemia and a circumscribed, reticular, macular rash on the face and neck at 5 months of age. Skin lesion biopsy revealed epidermic hyperkeratosis, hydropic degeneration of the basal layer, and deposition of immunoglobulins and granular C1q at the dermoepidermal junction. Ro/SS-A antibodies were present in the infant. BFU-E (erythroid progenitor burst-forming unit) colonies in bone marrow increased by about tenfold when suppressor CD8+ T lymphocytes were removed, indicating immune suppression of hematopoiesis. High-dose steroid therapy failed. The infant subsequently developed gram-negative sepsis, severe metabolic acidosis, and consumptive coagulopathy and died. CONCLUSIONS-- Neonatal lupus erythematosus may present as part of a spectrum. The disease may range from mild and transient to a severe, life- threatening condition requiring immediate intervention, as in the case reported here. This is the first report of neonatal lupus associated with aplastic anemia due to immune-mediated suppression of hematopoiesis. Infants Born to Mothers With Anti-SSA/Ro Autoantibodies: Neonatal Outcome and Follow-up Zuppa et al. CLIN PEDIATR 2008;47:231-236. http://www.aamds.org/aplastic/ MedlinePlus Aplastic anemia is a life-threatening condition. http// www.nlm.nih.gov/medlineplus/ency/article/000554.htm http://www.nhlbi.nih.gov/health/dci/Diseases/aplastic/aplastic_whatis.html Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk > "Complete recovery after iron chelation in aplastic anemia" > [quoted text clipped - 59 lines] > > - Show quoted text - Rusty the Nosferroustu <no.brains@all> danced this little dance for me: > Complete recovery after iron chelation in aplastic anemia" > Recently, researchers have discovered that most cases of severe > aplastic anemia are autoimmune disorders in which the body’s own > immune system attacks tissues and organs. In other words, iron has nothing to do with the problem. It's a good thing you read my posts, Rusty. My common sense is beginning to rub off on you. > Jesus Was A Vegetarian! Not at all! Don't you remember how he went to Hell after he died? He went there because his uncle, Satan, loves to throw a good barbeque! And after the day he'd had, Jesus really needed to unwind. Thus vented the Lord, "Uncle S., why did I let my old man talk me into going into the family business? Here it is a Friday and I had to work late, when even those Roman soldiers got to sit around and shoot craps like they were at Vegas. And you should hear my mom kvetch! 'My son, he could have been a rabbi! Instead he went and became a Christian!' And what about my mates? Twelve blokes and only Judas hung around!" At this point Satan passed Jesus a plate of spare ribs, and yea verily did the Lord eat heartily of them, annointing them with A-1 Steak Sauce. Thus did he fortify himself against the sad knowledge that he had to get up at dawn on Easter Sunday. http://www.youtube.com/watch?v=8iJDtAqHO-s --Bill Thompson On May 4, 8:38 pm, "wrtho...@ix.netcom.com" <wrthomp...@gmail.com> wrote: snip << :"Complete recovery after iron chelation in aplastic anemia" << http://tinyurl.com/2nn4q8 Recently, researchers have discovered that most cases of severe aplastic anemia are autoimmune disorders in which the body’s own immune system attacks tissues and organs. ------------------- "The infant died." Aplastic anemia in neonatal lupus erythematosus B. Wolach, L. Choc, A. Pomeranz, Y. Ben Ari, D. Douer and A. Metzker Department of Pediatrics, Meir General Hospital, Sapir Medical Center, Kfar Saba, Israel. OBJECTIVE-- To describe an infant with neonatal lupus erythematosus associated with aplastic anemia. SETTING-- The pediatric department in a tertiary-care hospital. INTERVENTIONS-- Packed red blood cell transfusions and a 3-week course of high-dose steroid therapy. MEASUREMENTS/MAIN RESULTS-- The patient presented with severe anemia and a circumscribed, reticular, macular rash on the face and neck at 5 months of age. Skin lesion biopsy revealed epidermic hyperkeratosis, hydropic degeneration of the basal layer, and deposition of immunoglobulins and granular C1q at the dermoepidermal junction. Ro/SS-A antibodies were present in the infant. BFU-E (erythroid progenitor burst-forming unit) colonies in bone marrow increased by about tenfold when suppressor CD8+ T lymphocytes were removed, indicating immune suppression of hematopoiesis. High-dose steroid therapy failed. The infant subsequently developed gram-negative sepsis, severe metabolic acidosis, and consumptive coagulopathy and died. CONCLUSIONS-- Neonatal lupus erythematosus may present as part of a spectrum. The disease may range from mild and transient to a severe, life- threatening condition requiring immediate intervention, as in the case reported here. This is the first report of neonatal lupus associated with aplastic anemia due to immune-mediated suppression of hematopoiesis. Infants Born to Mothers With Anti-SSA/Ro Autoantibodies: Neonatal Outcome and Follow-up Zuppa et al. CLIN PEDIATR 2008;47:231-236. http://www.aamds.org/aplastic/ MedlinePlus Aplastic anemia is a life-threatening condition. http// www.nlm.nih.gov/medlineplus/ency/article/000554.htm http://www.nhlbi.nih.gov/health/dci/Diseases/aplastic/aplastic_whatis... Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk "Complete recovery after iron chelation in aplastic anemia" << Well it seems in dogs .. females are "overrepresented" and in dogs they 'coincidentally' have a high **iron** .. load. Might explain why iron chelation works .. "Hyperferremia and high percentage saturation of transferrin" -------------------------------------------------- Pure erythrocyte aplasia is a recognised feature of systemic lupus erythematosus (SLE) http://lup.sagepub.com/cgi/content/refs/4/5/407 -------------------------------------------------- Abstract Journal of the American Veterinary Medical Association May 1, 2000, Vol. 216, No. 9, Pages 1429-1436 Idiopathic pure red cell aplasia and nonregenerative immune-mediated anemia in dogs: 43 cases (1988–1999) Tracy Stokol , BVSc, PhD, DACVP Julia T. Blue , DVM, PhD, DACVP Tracy W. French , DVM, DACVP Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853-6401. (Stokol, Blue, French) Objective—To examine clinical features, laboratory test results, treatment, and outcome of dogs with pure red cell aplasia (PRCA) and idiopathic nonregenerative immune-mediated anemia (NRIMA). Design—Retrospective study. Animals—43 dogs with severe nonregenerative anemia. Procedure—Medical records of dogs determined to have PRCA, NRIMA, or ineffective erythropoiesis on the basis of bone marrow analysis between 1988 and 1999 were reviewed. Criteria for inclusion were ≥ 5- day history of severe nonregenerative anemia (Hct < 20%; < 60.0 X 103 reticulocytes/µl) with no underlying diseases. Information was retrieved on signalment, clinical signs, laboratory test results, treatment, and outcome. Results—Median age of the dogs was 6.5 years. Spayed females and Labrador Retrievers were significantly overrepresented. Median Hct was 11% with no evidence of regeneration (median, 1.5 X 103 reticulocytes/ µl). Direct Coombs' test results were positive in 57% of dogs. Biochemical abnormalities included hyperferremia and high percentage saturation of transferrin. Bone marrow findings ranged from PRCA (5%) to erythroid hyperplasia (55%). Myelofibrosis was common. Dogs were treated with immunosuppressive drugs and the response was complete, partial, and poor in 55, 18, and 27% of the dogs, respectively. Mortality rate was 28%. Conclusion and Clinical Relevance—An immunemediated pathogenesis should be considered in dogs with severe, nonregenerative anemia, normal WBC and platelet counts, hyperferremia, mild clinical signs, and no evidence of underlying disease. Bone marrow findings range from the rare PRCA to erythroid hyperplasia. Myelofibrosis is often detected in affected dogs and may prevent bone marrow aspiration. (J Am Vet Med Assoc 2000;216:1429–1436) doi: 10.2460/javma.2000.216.1429 ----------------------------------- In Europe, the focus is on stem cell transplant http://www.hopkins-arthritis.org/arthritis-info/lupus/ Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk > On May 4, 8:38 pm, "wrtho...@ix.netcom.com" <wrthomp...@gmail.com> > wrote: snip << [quoted text clipped - 66 lines] > > DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk The Ferrous Fuckwit <ironjust...@bullshitte.com> netkooked: > Well it seems in dogs .. females are "overrepresented" and in dogs > they 'coincidentally' have a high **iron** .. load. Do you have any idea what you're saying, or are you in fact a bit of software that strings together words at random? > Might explain why iron chelation works .. You're stll talking off-topic nonsense, Rusty. Try to explain why anyone with lupus, fibro, cancer or chronic pain would want to undergo a treatment for an utterly irrelevant condition. But you can't do that, so you'll just repost the exact same twaddle, which is fine. Your bizarre spews do nothing but show newbies that you're nuts. Meanwhile, the voices in your head are getting bored with your inane drivel, so they phoned in this request: http://www.youtube.com/watch?v=i4qrBtavjEQ --Bill Thompson On May 7, 8:49 pm, "wrtho...@ix.netcom.com" <wrthomp...@gmail.com> wrote: utterly irrelevant condition<< Try to read to comprehend. Pure erythrocyte aplasia is a recognised feature of systemic lupus erythematosus (SLE) http://lup.sagepub.com/cgi/content/refs/4/5/407 Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk > The Ferrous Fuckwit <ironjust...@bullshitte.com> netkooked: > [quoted text clipped - 19 lines] > > --Bill Thompson The Ferrous Fuckwit <injust...@horseshitte.com> put this twist on reality: > Try to read to comprehend. Yes, Rusty, why don't you try that? You might enjoy the change of pace. > Pure erythrocyte aplasia is a recognised feature of systemic lupus > erythematosus (SLE)http://lup.sagepub.com/cgi/content/refs/4/5/407 No, I'm not going to waste my time reading something that amounts to "We don't really understand this problem, but if we've guessed right, iron might be involved somewhere in the process and maybe you could, uh, chelate it or something and that might not kill the patient, but don't blame us if we're mistaken." Stick it back up your a.s, if your head doesn't block the entry. You keep offering medical advice. I say you are not qualified to do that. Everyone agrees with me on that. Let's see you post your qualifications to give medical advice, Fuckwit. > Who loves ya. > Tom the Telly Savalas Worshipper > Jesus Was A Vegetarian! No, he wasn't. > Man Is A Herbivore! No, he isn't. Neither is Woman. You are a herbivore, Fuckwit, but that's because you're not a man. You're a mouse. Hey, Rusty, Joni Mitchell is playing your song! Dance Fuckwit dance! http://www.youtube.com/watch?v=IKIQSo7JbKQ --Bill Thompson On May 8, 8:45 pm, "wrtho...@ix.netcom.com" <wrthomp...@gmail.com> wrote: Fuckwit Stick it back up your a.s, Fuckwit. Fuckwit, Fuckwit No, I'm not going to waste my time reading something << "Erythrocyte aplasia is a feature of lupus" Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk On May 9, 7:29 am, ironjustice <ironjust...@cashette.com> wrote:"Erythrocyte aplasia is a feature of lupus" << PEDIATRICS Vol. 22 No. 5 November 1958, pp. 910-922 This Article STUDIES OF CONGENITAL HEMOLYTIC SYNDROMES I. Rates of Destruction and Production of Erythrocytes in Thalassemia Marion E. Erlandson M.D.1, Irving Schulman M.D.1, Gertrude Stern M.D. 1, and Carl H. Smith M.D.1 1 Department of Pediatrics, the New York Hospital-Cornell Medical Center Rates of destruction of erythrocytes and of effective production of erythrocytes and hemoglobin have been determined in 10 patients with homozygous Cooley's anemia. The method employed was based upon survival of Cr51-labeled cells in patients in whom a state of equilibrium of erythrocytes was present. While a marked hemohytic defect is present, this defect does not, by itself, determine the degree of anemia present. Rates of effective production of erythrocytes are increased above normal but are not increased to the same degree found in patients with other hemolytic diseases. Rates of effective synthesis of hemoglobin were found to be less than those obtained for production of erythrocytes. The rates of production of fetal hemoglobin in these patients are remarkably elevated but cannot be directly correlated with the rate of destruction of erythrocytes, rate of production of erythrocytes, or the degree of anemia present. The hemolytic defect in patients with intermediate Cooley's anemia was comparable to that in the majority of the patients with the severe form of disease. However, the most marked hemolytic defects were among patients with the severe and not with the intermediate form of disease. Production of erythrocytes and hemoglobin did not differ significantly in the two forms of this disease. Results in two splenectomized patients did not differ significantly from results in the non-splenectomized group of patients. However, since pre-splenectomy data were not available, no statement may be made as to possible individual benefit derived from the operation. The final status of each patient is determined by the particular balance obtained between rates of destruction and production. Neither production nor destruction alone determines the degree of anemia. The compensation index, as a measure of final status in each patient, was lowest in the severe form of Cooley's anemia. It is presumed to be lower still in many patients who could not be studied because transfusion therapy was in progress. The compensation index is somewhat higher in patients with intermediate Cooley's anemia and in two splenectomized individuals not requiring frequent transfusions. Values in these patients approach the higher levels found in patients with sickle cell anemia and congenital spherocytosis. Submitted on April 7, 1958 Accepted on May 15, 1958 -------------------- Association of systemic lupus erythematosus and hemolytic uremic syndrome in a child Journal Pediatric Nephrology SpringerLink Date Monday, January 03, 2000 Brief Report Association of systemic lupus erythematosus and hemolytic uremic syndrome in a child T. Ogawa1, H. Arai1, K. Maruyama1, T. Watanabe1, Y. Kobayashi1, O. Kikuchi1 and A. Morikawa1 (1) Department of Pediatrics, Gunma University School of Medicine, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan Tel.: +81-27-220-8205, Fax: +81-27-220-8215, JP Abstract We describe a 10-year-old girl with systemic lupus erythematosus (SLE) who first presented with hemolytic uremic syndrome (HUS). Diagnoses were based on the classic HUS triad, including the observation of fragmented red blood cells, and on the American College of Rheumatology criteria for SLE. Plasma exchange may have been effective against both HUS and SLE in this patient, as it was associated with improvement of platelet counts, renal function, and serological findings. Key words Systemic lupus erythematosus - Hemolytic uremic syndrome - Plasma exchange Received: 24 September 1998 / Revised: 4 January 1999 / Accepted: 4 January 1999 --------------- Blood, 1952, Vol. 7, No. 3, pp. 350-357. © 1952 American Society of Hematology, Inc. Publisher Springer Berlin / Heidelberg ISSN 0931-041X (Print) 1432-198X (Online) Issue Volume 14, Number 1 / January, 2000 Category Brief Report DOI 10.1007/s004670050016 Pages 62-64 -------------------------------------------------------------------------------- Chronic Hemolytic Anemia Associated with Thalassemia and Sickling Traits PHILLIP STURGEON M.D.1, HARVEY A. ITANO M.D., PH.D.1, and WILLIAM N. VALENTINE M.D.1 1 Department of Research, Los Angeles Childrens’s Hospital, and the Department of Pediatrics, University of Southern California School of Medicine, Los Angeles; the Gates and Crellin Laboratories of Chemistry (Contribution No. 1602), California Institute of Technology, Pasadena; and the Department of Medicine, School of Medicine, University of California Medical Center, Los Angeles. The family history, case history and genealogy of a 6 year old girl suffering from a chronic hemolytic anemia is presented. The disease, resulting from her inheritance of both the gene for sickle trait and that for thalassemia trait, is compared to a similar case in a 38 year old male reported by Powell, et al. To date the child has had no clinical evidence of an hemolytic anemia, except for an enlarged spleen. Hematologically, however, all findings indicate the presence of a brisk hemolytic process. Electrophoretic analysis of the patient’s hemoglobin reveals a unique pattern intermediate between the usual sickle cell trait and sickle anemia patterns. Submitted on August 20, 1951 Accepted on November 7, 1951 ------------------------ Hematology 2005 © 2005 The American Society of Hematology Cardiopulmonary Complications of Sickle Cell Disease: Role of Nitric Oxide and Hemolytic Anemia Mark T. Gladwin and Gregory J. Kato Correspondence: Dr. Mark T. Gladwin, Head, Vascular Therapeutics Section, Cardiovascular Branch, NHLBI, Critical Care Medicine Department, Clinical Center, National Institutes of Health, Building 10-CRC, Room 5-5140, 10 Center Drive, MSC 1476, Bethesda MD 20892-1476; Phone (301) 435-2310; Fax (301) 451-7091; mgladwin@nih.gov Abstract Medical advances in the management of patients with sickle cell disease, thalassemia, and other hemolytic anemias have led to significant increases in life expectancy. Improved public health, neonatal screening, parental and patient education, advances in red cell transfusion medicine, iron chelation therapy, penicillin prophylaxis for children, pneumococcal immunization, and hydroxyurea therapy have all likely contributed to this effect on longevity.1,2 Importantly, as a generation of patients with sickle cell disease and thalassemia ages, new chronic complications of these hemoglobinopathies develop. In this context, pulmonary hypertension is emerging as one of the leading causes of morbidity and mortality in adult sickle cell and thalassemia patients, and likely in patients with other hemolytic anemias. A common feature of both sickle cell disease and thalassemia is intravascular hemolysis and chronic anemia. Recent data suggest that chronic intravascular hemolysis is associated with a state of endothelial dysfunction characterized by reduced nitric oxide (NO) bioavailability, pro-oxidant and pro-inflammatory stress and coagulopathy, leading to vasomotor instability and ultimately producing a proliferative vasculopathy, a hallmark of which is the development of pulmonary hypertension in adulthood.3–5 In conclusion, pulmonary hypertension is common in patients with hereditary hemolytic anemias and is associated with a high risk of death in patients with sickle cell disease. New therapies targeting this vasculopathy and aimed at normalizing the vasodilator:vasoconstrictor balance are discussed. Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk > On May 8, 8:45 pm, "wrtho...@ix.netcom.com" <wrthomp...@gmail.com> > wrote: [quoted text clipped - 11 lines] > > DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk proliferative vasculopathy is associated with a high risk of death << http://rheumatology.oxfordjournals.org/cgi/content/full/39/1/108 Letters to the Editor Antiphospholipid syndrome with proliferative vasculopathy and bowel infarction Y. I. Patel, A. St John1 and N. J. McHugh2 Department of Medicine, Groote Schuur Hospital, J47 Old Main Building, Cape Town, South Africa, 1 Directorate of Pathology, Royal United Hospital, Bath BA1 3NG and 2 Royal National Hospital for Rheumatic Diseases, Bath BA1 1RL, UK Correspondence to: Y. I. Patel. Sir, Since antiphospholipid syndrome (APS) was first described in 1983 [1], many complications have been reported which result from vascular occlusion as a result of thrombosis [2]. More recently, a few cases have been described where a proliferative vasculopathy appears to have been the major mechanism of vascular occlusion rather than thrombosis or vasculitis [3–5]. The patient developed pulmonary complications and died 6 weeks later. --------------------------------- Widespread vasculopathy with hemolytic uremic syndrome, perimyocarditis and cystic pancreatitis in a young woman with mixed connective tissue disease Journal Rheumatology International Publisher Springer Berlin / Heidelberg ISSN 0172-8172 (Print) 1437-160X (Online) Issue Volume 13, Number 1 / April, 1993 Category Case Report DOI 10.1007/BF00290331 Pages 31-36 SpringerLink Date Tuesday, November 30, 2004 Case Report Widespread vasculopathy with hemolytic uremic syndrome, perimyocarditis and cystic pancreatitis in a young woman with mixed connective tissue disease Case report and review of the literature J. Braun1 , J. Sieper1, A. Schwarz1, F. Hiepe3, T. Lenz1, F. Keller1, H. Herbst2 and A. Distler1 (1) Abteilung für Allgemeine Innere Medizin und Nephrologie, Klinikum Steglitz FU Berlin, Germany (2) Abteilung für Pathologie, Klinikum Steglitz FU Berlin, Germany (3) Arbeitsbereich Rheumatologie, Universitätsklinik für Innere Medizin, Charité HU Berlin, Germany (4) Med. Klinik und Poliklinik, Abteilung für Allgemeine Innere Medizin und Nephrologie, Univ-Klinikum Steglitz, Hindenburgdamm 30, 1000 Berlin 45 Received: 5 October 1992 Accepted: 14 January 1993 Summary A 15-year-old girl had severe Raynaud's phenomenon and arthralgias. A high ANA-IF titer was found and undifferentiated connective tissue disease was diagnosed. After 7 years of moderately flaring disease the patient deteriorated and presented with congestive heart failure, pleuropericardial effusion, hemolytic uremic syndrome, proteinuria and moderate hypertension. Autoantibodies against DNA, Sm- protein, and very high titers against U1RNP were detected. Therapy with high steroid doses, a cyclophosphamide pulse and 4 weeks of plasmapheresis with plasma exchange improved the heart, but not the renal condition. Symptomatic pancreatitis became the dominant problem of a progressively consuming process that resulted in the death of the patient. Postmortem examination revealed widespread vasculopathy with intima proliferation and only minimal fibrosis involving the kidneys, heart and other main organs, including the pancreas. Taken together, the clinical picture was of an overlap between scleroderma and systemic lupus crythemathosus; the serologic and histopathologic findings suggest a diagnosis of a severe form of mixed conective tissue disease (MCTD). Key words Vasculopathy - Hemolytic uremic syndrome - Mixed connective tissue disease -------------------------------------------------------------------------------- Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk > On May 9, 7:29 am, ironjustice <ironjust...@cashette.com> > wrote:"Erythrocyte aplasia is a feature of lupus" << [quoted text clipped - 195 lines] > > - Show quoted text - http://www.nature.com/bmt/journal/v27/n7/full/1702992a.html Case Report Recovery of erythropoiesis following allogeneic bone marrow transplantation for chronic lymphocytic leukaemia-associated pure red cell aplasia M P de Vetten, M van Gelder and G E de Greef Department of Hematology, University Hospital Rotterdam/Daniel den Hoed Cancer Center, Rotterdam, Netherlands Correspondence to: Dr G E de Greef, Department of Hematology, University Hospital Rotterdam/Daniel den Hoed Cancer Center, PO Box 5201, 3008 AE Rotterdam, Netherlands Abstract Pure red cell aplasia is a rare condition, that can be either idiopathic or associated with a lymphoproliferative disorder. The latter is considered to result from T cell-mediated suppression of haematopoiesis, and usually responds well to treatment with immunosuppressive medication. We describe a patient with B-CLL- associated pure red cell aplasia who did not respond to several courses of immunosuppressive treatment. Erythropoiesis was finally restored after allogeneic bone marrow transplantation. Bone Marrow Transplantation (2001) 27, 771-773. Keywords pure red cell aplasia; allo-BMT; CLL -------------------------------- Rheumatology 2000; 39: 1155-1157 © 2000 British Society for Rheumatology -------------------------------------------------------------------------------- Letters to the Editor Successful treatment of pure red cell aplasia associated with systemic lupus erythematosus with cyclosporin A C. Duarte-Salazar, J. Cazarín-Barrientos, M. V. Goycochea-Robles, J. Collazo-Jaloma and R. Burgos-Vargas Rheumatology Service, Haematology Laboratory and Research Division, Hospital General de México and Faculty of Medicine Universidad Nacional Autónoma de México SIR, We report the first case of a patient with pure red cell aplasia (PRCA) and systemic lupus erythematosus (SLE) failing to respond to corticosteroids and then being successfully treated with cyclosporin A (CyA), with no recurrence of the disease in the last 4 yr. A 21-yr-old female was admitted to our ward with anaemia. Previously, she had had polyarthritis of the small joints of the hands, knees and ankles, photosensitivity, and a malar rash that responded well to non- steroidal anti-inflammatory drugs, which were used from October 1994 to April 1995. She was later seen in the emergency department and diagnosed with severe anaemia (haemoglobin 3.8 g/dl, haematocrit 11.1%, fatigue, tiredness, cephalalgia and low blood pressure), and she received two units of red blood cells. After initial improvement, her clinical condition worsened in the following 2 weeks. Her haemoglobin level and haematocrit fell to 2.8 g/dl and 8.8%, respectively. She was transfused again with two units of red blood cells and transferred to our service. She was dyspnoeic and semiconscious, with paleness and swelling of the metacarpophalangeal and hand proximal interphalangeal joints, knees and ankles. Her laboratory test results were as follows: haemoglobin 6.9 g/dl; haematocrit 20%; reticulocytes 0.2%; erythrocyte sedimentation rate 75 mm/h. Immunological studies showed a direct Coombs test result of 1:4, a speckled pattern of antinuclear antibodies at a titre of 1:320, DNA binding (radioimmunoassay) of 84.3% (normal value <52%), and IgG and IgM anti-cardiolipin antibodies 2.5 U (normal value <2.0 U) and 5.0 U (normal value <2.2 U), respectively. The following tests were normal: bilirubin, total proteins and albumin, prothrombin and partial thromboplastin; VDRL was negative. An additional search for serum IgG and IgM anti-B12 parvovirus antibodies was negative. Chest X-rays and computed tomography were normal. A bone marrow sample revealed the absence of erythroid precursors cells, without significant abnormalities of the megakaryocytic, granulocytic or lymphocytic cell lines. A diagnosis of PRCA associated with SLE was established, and treatment with 60 mg prednisone (l mg/ kg) daily was started. Ten days later, her haemoglobin level was 5.9 g/ dl, haematocrit 17.6% and reticulocyte count 0.4%; her clinical symptoms were unchanged. She was transfused for a third time with two units of red blood cells and treated with 1 g methylprednisolone intravenously for 3 consecutive days (Fig. 1). Haemoglobin rose to 9.2 g/dl and haematocrit to 27.1%; reticulocyte count remains without change. She continued with 60 mg of prednisone per day, but 4 weeks later (5 weeks after starting corticosteroids) symptoms reappeared and laboratory values dropped again (haemoglobin 6.2 g/dl, haematocrit 17.0%, reticulocyte count 0.4%). She was again transfused and started on CyA at a dose of 200 mg/day (3.5 mg/kg). Twenty-one days later, her clinical condition had improved significantly, as had her laboratory test values, with an increased reticulocyte count (haemoglobin 9.8 g/ dl, haematocrit 31.6%, reticulocyte count 11%). Investigations during the following 6 months showed continuous improvement in her clinical condition and laboratory values. CyA was then stopped and azathioprine was introduced at a dose of 150 mg/day. Since then, the patient was followed for a mean of 4 yr; there was a favourable clinical outcome with remission of PRCA but with mild intermittent episodes of arthralgia and arthritis, which were treated with chloroquine. At the start of CyA, the patient's serum creatinine value was 0.7 mg/dl and glomerular filtration rate 101.5 ml/min. Currently, her creatinine level is 1.0 mg/dl and glomerular filtration rate 112.0 ml/min. During follow-up, these parameters were monitored closely and remained within normal limits. Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk > proliferative vasculopathy is associated with a high risk of death << > [quoted text clipped - 231 lines] > > - Show quoted text - On May 9, 9:09 am, ironjustice <ironjust...@cashette.com> wrote:bone marrow transplantation << "Early institution of iron reduction in ex-thalassaemia is safe." March 2000, Volume 25, Number 6, Pages 653-656 Iron Overload Early iron reduction programme for thalassaemia patients after bone marrow transplantation C K Li, D H Lai, M M K Shing, K W Chik, V Lee and P M P Yuen Department of Paediatrics, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong Correspondence to: Dr C K Li, Department of Paediatrics, Prince of Wales Hospital, Shatin, NT, Hong Kong Abstract Thirty thalassaemia patients received iron reduction starting at around 3 months post transplant. Sixteen received desferrioxamine and nine had phlebotomy, five patients had desferrioxamine followed by phlebotomy. The desferrioxamine group had higher serum ferritin levels at the start of iron reduction as compared to the phlebotomy group (5292 vs 2453 g/l, P EQ 0.001). After 444 and 407 days of iron reduction, serum ferritins at cessation of iron reduction in both groups was similar (665 vs 588 g/l). The rate of decline of serum ferritin in both groups was similar. There was no graft rejection during the programme. Early institution of iron reduction in ex- thalassaemia is safe. Bone Marrow Transplantation (2000) 25, 653-656. Keywords desferrioxamine; phlebotomy; ferritin http://www.nature.com/bmt/journal/v25/n6/full/1702212a.html Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk > http://www.nature.com/bmt/journal/v27/n7/full/1702992a.html > [quoted text clipped - 214 lines] > > - Show quoted text - "Complete recovery after iron chelation in aplastic anemia" << "Where clinical trials are not feasible, data from observational studies may be the best available evidence to guide practice." Sooo .. the observation is .. iron chelation cured the kid therefore the treatment works. Pretty simple to .. observe .. Anyone disagree with the .. observation .. ? These guys aren't really .. surrrre .. how to treat this problem .. Originally published as JCO Early Release 10.1200/JCO.2007.15.0169 on March 31 2008 Journal of Clinical Oncology, Vol 26, No 13 (May 1), 2008: pp. 2162-2170 © 2008 American Society of Clinical Oncology. Individual Physician Practice Variation in Hematopoietic Cell Transplantation Stephanie J. Lee, Steven Joffe, Andrew S. Artz, Richard E. Champlin, Stella M. Davies, Madan Jagasia, Nancy A. Kernan, Fausto R. Loberiza, Jr, Robert J. Soiffer, Mary Eapen From the Division of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, WA; Departments of Pediatrics, Medicine, and Medical Oncology, Dana-Farber Cancer Institute, Children's Hospital, Boston, MA; Department of Medicine, University of Chicago, Chicago, IL; Department of Stem Cell Transplantation and Cellular Therapy, M.D. Anderson Cancer Center, Houston, TX; Division of Hematology/Oncology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH; Division of Hematology-Oncology, Vanderbilt University Medical Center, Nashville, TN; Pediatric Bone Marrow Transplantation Service, Memorial Sloan-Kettering Cancer Center, New York, NY; Department of Medicine, University of Nebraska, Omaha, NE; and the Center for International Blood and Marrow Transplant Research, Medical College of Wisconsin, Milwaukee, WI Corresponding author: Stephanie Lee, MD, MPH, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave N, D5-290, Seattle, WA 98109; e- mail: sjlee@fhcrc.org Purpose: Previous studies have evaluated practice variation in hematopoietic cell transplantation (HCT) among transplant centers and countries. There are no studies investigating individual physician practice variation in HCT. Methods: An international Internet-based survey of transplant physicians collected data on medical decisions made by adult and pediatric HCT physicians. Multivariable analyses identified practitioner and transplant center characteristics predictive of medical decision making. Results: Analysis of 526 assessable respondents showed a wide variation in management approaches to specific clinical scenarios. Pediatric and adult transplant physicians differed significantly in their management strategies for chronic myeloid leukemia, acute and chronic graft-versus-host disease, and choice of graft source for patients with aplastic anemia. Among adult transplant physicians, there was little agreement on the patient factors favoring reduced intensity conditioning or myeloablative conditioning. Conclusion: These results emphasize the heterogeneity of worldwide transplant practices. Local preferences or biases likely result in similar patients being offered different transplant and treatment procedures. The degree of practice variation also highlights the need for clinical trials to clarify areas of controversy. Where clinical trials are not feasible, data from observational studies may be the best available evidence to guide practice. published online ahead of print at www.jco.org on March 31, 2008. Presented in part at the 48th Annual Meeting of the American Society of Hematology, December 9-12, 2006, Orlando, FL. Authors' disclosures of potential conflicts of interest and author contributions are found at the end of this article. Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk > On May 9, 9:09 am, ironjustice <ironjust...@cashette.com> wrote:bone > marrow transplantation << [quoted text clipped - 220 lines] > > - Show quoted text - "Complete recovery after iron chelation in aplastic anemia" << "Iron restriction healed a leg ulcer." Am J Hematol. 1994 Oct;47(2):74-81. Links Comment in: Am J Hematol. 1995 Sep;50(1):68-9. Improvement of sickle cell anemia by iron-limited erythropoiesis. Castro O, Poillon WN, Finke H, Massac E. Center for Sickle Cell Disease, Howard University College of Medicine, Washington, D.C. 20059. We report the hematologic and clinical features of four adult patients (Pts.) with sickle cell anemia and iron-limited erythropoiesis. Two of the Pts. had spontaneous iron deficiency (chronic GI bleeding, low-grade hemoglobinuria). In the other two Pts. iron restriction was induced by periodic RBC aphereses as part of a pilot protocol designed to decrease intracellular HbS polymerization by MCHC reduction. Iron-limited erythropoiesis was defined by reduction in red cell indices (MCV range 60.4-67 fl) in the presence of low serum ferritin (range < 10-20 ng/ml). In these Pts. iron restriction did not cause clinically significant worsening of the anemia (Hb 7.8-9.0 g/dl). In two Pts. the anemia actually improved. Other hematologic effects of iron restriction were: decreased MCHC, reticulocyte count, RDW, and dense cells. A reduced hemolytic rate was suggested by a lowering of serum bilirubin and LDH. In one of the Pts. the 51Cr RBC T1/2 survival increased from 12 to 16 days. The intracellular HbS polymer fractions (fp) were determined at 25% O2 by Csat and with the use of the conservation of mass equation. The baseline fp values ranged from 0.48-0.53. After iron restriction they ranged from 0.33-0.48. The fp decreased even though iron-limited erythropoiesis also lowered the Hb F concentration in three of our Pts. In one of the two Pts. with induced iron depletion, hospitalization days for pain crises decreased from an average of 4.5 days/month (2 year baseline period) to an average of 0.5 days/month in the 3 year follow-up after iron depletion. The second patient with induced iron restriction experienced the rapid healing of a leg ulcer. Controlled iron restriction should be explored as a therapeutic strategy in selected SS patients. PMID: 7522396 [PubMed - indexed for MEDLINE] Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/a3cc3 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk > "Complete recovery after iron chelation inaplasticanemia" << > [quoted text clipped - 225 lines] > > - Show quoted text - The Ferrous Fuckwit <trembling@the.truth> netkooked: <snip of the Artless Dodger's clumsy avoidance of a question> Answer this question, Fuckwit: What are your qualifications to give medical advice? --Bill Thompson The Pherrous Phuckwit <nobrains@all> danced to my tune wih: > "wrtho...@ix.netcom.com" <wrthomp...@gmail.com> > brilliantly commented upon Rusty with: > http://www.youtube.com/watch?v=S524O_XNoLM > "Complete recovery after iron chelation in aplastic anemia" > Now I don't suppose .. complete recovery after iron chelation in > aplastic anemia .. actually MEANS anything What's this, Rusty? You posted it and you didn't think it meant anything? Honesty in you is such a surprise! But I knew I could make you dance if I played a little--Heavy Metal! Give us another little dance, Rusty. Do the "TeamTanner Two-Step." Stamp your widdle feet and get red in the face to this song: http://www.youtube.com/watch?v=7E1zE6uH-ng Marilyn Manson--very entertaining! I've not seen/heard him before, so I guess I should crawl out from under my rock more often...hopefully at the same time when this character is out from under his. Mair > wrthomps06@gmail.com wrote >> Give us another little dance, Rusty. Do the "TeamTanner >> Two-Step." Stamp your widdle feet and get red in the face to >> this song: >> http://www.youtube.com/watch?v=7E1zE6uH-ng > Marilyn Manson--very entertaining! I've not seen/heard him before, so I > guess I should crawl out from under my rock more often...hopefully at the > same time when this character is out from under his. Funny, I found Marilyn Manson by crawling under rocks. These days you have to go out of your way to find good music, and he fills the void left by Alice Cooper. What impresses me is the way Rusty enjoys him. Who'd have thought? --Bill Thompson |
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