Platelet E-News – September 16, 2004

This e-newsletter is a monthly publication of The Platelet Disorder Support Association. The information in this newsletter is for educational purposes only. For advice on your unique medical condition, please consult a health care professional.


  • Clinical Trial Registration: Medical Journal Editors Speak
  • H pylori Eradication Therapy for ITP: Thoughts on the Different Results
  • NIH Expands Health Information Web Site
  • Blood Cells Excitable Just Like Nerve Cells
  • Platelets Feel Your Pain
  • Infliximab Associated with Risk of Thrombocytopenia
  • New Immunosuppressive Drug May Help Patients with Autoimmune Disease



The International Committee of Medical Journal Editors (ICMJE) has proposed comprehensive clinical trial registration as a solution to the problem of the selective announcing of the initiation, progress, and results of clinical trials. The proposal was made in an editorial published simultaneously in all member journals. It was signed by 12 editors of medical journals and the editor of Medline, a service of the National Library of Medicine. The editorial calls for a registry that is accessible to the public at no charge, open to all prospective registrants, and managed by a not-for-profit organization. It must have a mechanism to insure the validity of registration data and be electronically searchable. The editorial also specifies the minimum data elements that must be included and makes registration of a clinical trial at or before patient registration a necessary condition for publication in the journals that make up the ICMJE.

New England Journal of Medicine, September 9, 2004, pp1250-1251


Some years ago, Italian researchers reported the recovery from ITP in a large percentage of patients treated to eradicate H pylori infection. Other researchers, in the United States and elsewhere, have had difficulty duplicating these results. A recent communication reported in “Blood” (The journal of the American Society of Hematology) suggests that this discrepancy in the clinical response to eradication therapy might be due to differences in the bacterial strains. In the patients who responded to the eradication therapy, the level of an antibody associated with H pylori declined. The level of H pylori antibody did not decline in the patients who did not respond. The H pylori antibody is specific to different strains of H pylori. The authors of the “Blood” correspondence suggest “that molecular mimicry between the H pylori antibody and a platelet antigen might mediate the autoimmunity in some chronic ITP patients (the ones who respond to the eradication therapy).”

Blood, July 15, 2004, p 594


The National Institutes of Health (NIH) has launched an expanded health information Web site It includes three new sections. The Healthy Lifestyles section addresses nutrition and weight loss; the Research in Action section provides information on stem cells and genetics; and the Now Online section deals with current topics of interest. The new site provides links to popular health databases and information for people of all ages, including children and teens.

Orphan Disease Update, Summer 2004, p 16.


In 1978 it was shown that a Guinea pig megakaryocyte (cell in the bone marrow that gives rise to platelets) when stimulated with an electric current fired exactly as a neuron (brain cell) would under the same conditions. We now recognize that blood cells, like neurons, generate and store electric potential energy. It is also accepted in the scientific community that when a blood cell like a platelet performs any of its functions, electric energy is spent through many of the same chemical steps or pathways that exist in brain and muscle cells. Current research published in the journal “Blood” reports that human stem cells (primary human CD34+ hematopoietic stem and progenitor cells) “express not only genes encoding many of the ion channels (chemical pathways) found in the brain, but also a variety of other proteins whose roles have been primarily defined in the nervous system.” Sullivan goes on to say that “in their paper, Steidl et al go to great lengths to show that many neurobiologic genes are not only expressed at both the mRNA (messenger RNA) and protein level in CD34+ cells, some of them exhibit their predicted functions in these cells. …The blood-brain barrier is weakening”

Richard Sullivan, “Blood Cells: Excitable at Last”, Blood, July 2004, vol 104, n 1, p 5.


Recent research shows that the brain and body both respond to the same family of stimulating peptides. Tachykinins, stimulating peptides, are widely expressed in central and peripheral nervous systems and participate in neurotransmission. Recent research has addressed the possibility that platelets respond to tachykinins. This possibility was raised because a high concentration of a tachykinin, neurokinin B, by the placenta has been linked to pre-eclampsia, a hypertensive (high blood pressure) disorder occurring during pregnancy. Since platelet dysfunction is associated with pre-eclampsia, Graham and colleagues addressed the possibility that platelets respond to tachykinins. Their work forms strong evidence that tachykinins influence platelet function. Robert Flaumenhaft of the Harvard Medical School in commenting on the work of Graham and colleagues says, “It is conceivable that under certain physiologic conditions tachykinins mediate cross talk between these 2 cell types (platelets and neurons).

Robert Flaumenhaft, “Platelets Feel Your Pain”, Blood, August 2004, vol 104, n 4, p 913.


Additional warnings have been added to the labeling of infliximab (Remicade). According to the notification letter, postmarketing cases of lekopenia, neutropenia, thrombocytopenia, and pancytopenia, some with fatal outcome, have been reported in patients treated with infliximab for rheumatoid arthritis and Crohn’s disease. Infliximab was approved in the US on August 24, 1998 and since that time 508 cases of hematologic and neurologic problems have been reported by the approximately 509,000 patients who have used the drug. Infliximab is an anti-TNF drug that works by blocking the tumor necrosis factor (TNF), a protein involved in causing inflammation. Other ant-TNF drugs on the market, Enbrel and Humira, carry similar label warnings regarding blood disorders.


A drug that presently carries the name CP-690,550, shows promise as a therapy for quieting the overactive immune system in patients with autoimmune disease. Dr. Borie, who is studying the drug, said it holds promise of suppressing the immune system without major side effects. This drug inhibits the enzyme Jak3 that is found only in immune cells. Studies show that inhibiting this enzyme suppresses the immune system while not affecting other systems of the body. Much work remains.

NIH News, October 30, 2003
“Preventing Transplant Rejection ---Research Summary” July 9, 2004

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