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Recall of brand-name gold sodium thiomalateAre generics reliable.

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5. Cheng HM, Sam C K Bacterial immunity and immunogenesis of
normal salivary IgA and serum IgG, antiphospholipid autoantibody-a link? Immunol Lett 26:7-10, 1990
6. Papadea C, Check IJ: Human IgG and IgG subclasses. Crit Rev
Clin Lab Sci 27:27-58. 1989
To the Editor:
We thank Dr. Cheng for his valuable comments related
to our bone marrow transplantation model of A P S (1). Indeed,
we missed the article by Mizutani et a1 (1). Dr. Cheng is right
indicating that the APS in (B/W)F, mice is a basically genetically determined model, while our model is induced following
active immunization (2). Therefore, a T cell activation must be
involved in this process. Indeed, we (3) and others (4)have
previously shown the transfer of this specific model via T
cell lines (specific for the idiotype), while suppressing its
induction with specific T suppressor cells (5) and anti-CD4
antibodies (6).
We also believe that in humans, some autoimmune
diseases may emerge after infection following endogenous
idiotypic stimulation, with the pathogenic idiotype being harbored on some of the antibacterial antibodies (7-9). In subjects
prone to autoimmunity (due, for example, to genetic background, hormonal suitability, or immunologic deficiencies),
the idiotypic cascade will progress into antibody 3 (anti-antiid), thus simulating antibody 1 in its (auto)antigen binding
characteristics (10,ll).
We also agree that natural antibodies may be pathogenic, as we have shown with both anti-DNA (12) as well as
with anti-cardiolipin antibodies (13). Thus, it is conceivable
that multiple mechanisms may be involved in the pathogenesis
of APS.
Yehuda Shoenfeld, MD
Chaim Sheba Medical Center
Tel-Hashomer, Israel
1. Mizutani H, Engelman RW, Kinjoh K, Kurata Y, Ikehara S, Good
RA: Prevention and induction of occlusive coronary vascular
disease in autoimmune (W/B)F, mice by haploidentical bone
marrow transplantation: possible role for anticardiolipin autoantibodies. Blood 82:3091-3097, 1993
2. Bakimer R, Fishman P, Blank M, Sredni B, Djaldetti M, Shoenfeld
Y: Induction of primary antiphospholipid syndrome in mice by
immunization with a human monoclonal anti-cardiolipin antibody
(H-3). J Clin Invest 89:1558-1663, 1992
3. Blank M, Mendlovic S, Mozes E, Coates ARM, Shoenfeld Y:
Induction of SLE in naive mice with T cell lines specific for human
anti-DNA antibody SA-1 (1616 Idt) and for mouse tuberculous
antibody (TB168) antibody (1616 Id+). Clin Immunol Immunopathol 60:471-483, 1991
4. Fricke H, Mendlovic S, Blank M, Shoenfeld Y, Ben-bassat M,
Mozes E: Idiotype specific T cell lines inducing experimental SLE
in mice. Immunology 73:421-427, 1991
5. Blank M, Ben-Bassat M, Shoenfeld Y: Modulation of SLE induction in naive mice by specific T cells with suppressor activity to
pathogenic anti-DNA antibody idiotype. Cell Immunol 137:474486, 1991
6. Tomer Y, Blank M, Shoenfeld Y: Suppression of experimental
antiphospholipid syndrome and systemic lupus erythematosus in
mice by anti-CD4 monoclonal antibodies. Arthritis Rheum 37:
1236-1244, 1994
Shoenfeld Y: Idiotypic induction of autoimmunity: a new aspect of
the idiotypic network. FASEB J 8:1296-1301, 1994
Shoenfeld Y: Idiotypic induction of autoimmunity: do we need an
autoantigen? Clin Exp Rheumatol 12 (suppl ll):S37-S40, 1994
Shoenfeld Y: Anti-DNA antibodies: is DNA a self antigen or shelf
antigen or are autoimmune rheumatic diseases immunogen
driven? Rheumatol Europe 24 (suppl 2):17-20, 1995
Shoenfeld Y: Idiotypic network, pathogenic autoantibodies and
autoimmunity. Clin Exp Immunol 101 (suppl):26-28, 1995
George J, Shoenfeld Y: Infections, idiotypes and SLE. Lupus
4:333-335, 1995
Mendlovic S, Brocke S, Shoenfeld Y, Ben-Bassat M, Meshorer A,
Bakimer R, Mozes E: Induction of a SLE-like disease in mice by
a common anti-DNA idiotype. Proc Natl Acad Sci U S A
85:2260-2264, 1988
Cohen J, Bakimer R, Blank M, Valesini G, Shoenfeld Y: Pathogenic natural anti-cardiolipin antibodies: the experience from
monoclonal gammopathy. Clin Exp Immunol97:181-186, 1994
Recall of brand-name gold sodium thiomalate: are
generics reliable?
To the Editor:
I recently received a letter from Merck & Co. noting
that they would no longer manufacture gold sodium thiomalate
(Myochrysine). Previously, they had instituted a recall of this
product when it was feared that it might not conform to
“criteria for antimicrobial effectiveness.” Because they would
“be required to assure conformance to the compendia1 specifications,” they stated that they would have to remove the
product from the market for “an extended period” and therefore were instead ceasing production entirely. They noted the
“availability of other therapies” but did not mention that
Myochrysine has been available elsewhere as a generic product. The other injectable gold product, Solganal, remains
available only from Schering.
If I had told my Merck representative a year ago that
I might get a generic form of Myochrysine, he would have told
me of the superiority of branded products and the necessity of
using brands because of the reliability and concern of researchoriented companies like Merck. Physicians who are convinced
of the superiority of branded products (generic gold sodium
thiomalate was not recalled) might consider whether there are
any lessons to be learned from Mercks behavior.
Lonnie B. Hanauer, MD, FACP
Millbum, NJ
To the Editor:
Merck‘s decision to discontinue manufacturing Myochrysine (gold sodium thiomalate) was made reluctantly, and
only after we determined that a variety of effective therapies
remained available to patients with rheumatoid arthritis.
Merck discontinued Myochrysine after determining
that new U S , Pharmacopeia standards related to the preservative content would require extensive, time-consuming, and
costly modifications to our manufacturing process. The development and regulatory approval time needed to make these
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