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I work with patients who cannot tolerate the intense protocols of the alternative lyme docs but who need something more than the standard band-aid approach to what is a chronic illness. 
J Nutr 1998 Jan;128(1):68-72 Related Articles, Links

1,25-Dihydroxycholecalciferol inhibits the progression of arthritis in murine models of human arthritis.

Cantorna MT, Hayes CE, DeLuca HF.

Department of Biochemistry, College of Agricultural and Life Sciences, University of Wisconsin-Madison, Madison, WI 53706, USA.

1,25-Dihydroxycholecalciferol [1,25-(OH)2D3] has been shown to inhibit the progression of experimental autoimmune encephalomyelitis (EAE). Here we tested the possibility that 1, 25-dihydroxycholecalciferol might be therapeutic for another autoimmune disease, arthritis. Two different animal models of arthritis were tested, namely, murine Lyme arthritis and collagen-induced arthritis. Infection of mice with Borrelia burgdorferi (the causative agent of human Lyme arthritis) produced acute arthritic lesions including footpad and ankle swelling. Supplementation with 1,25-dihydroxycholecalciferol of an adequate diet fed to mice infected with B. burgdorferi minimized or prevented these symptoms. Mice immunized with type II collagen also developed arthritis. The symptoms of this disease were also prevented by dietary supplementation with 1,25-dihydroxycholecalciferol. 1, 25-Dihydroxycholecalciferol given to mice with early symptoms of collagen-induced arthritis prevented the progression to severe arthritis compared with untreated controls. These results suggest that 1,25-dihydroxycholecalciferol and/or its analogs may be a valuable treatment approach to this disease.

PMID: 9430604 [PubMed - indexed for MEDLINE]

Int Microbiol 2001 Dec;4(4):209-15 Related Articles, Links



Susceptibility of motile and cystic forms of Borrelia burgdorferi to ranitidine bismuth citrate.

Brorson O, Brorson SH.

Department of Microbiology, Vestfold Sentralsykehus, Tonsberg, Norway.

Gastrointestinal symptoms accompanying Lyme disease have not been considered in the treatment of Lyme patients yet. Here we examine the effect of ranitidine bismuth citrate (RBC) on motile and cystic forms of Borrelia burgdorferi in vitro, to determine whether it could cure this bacterial infection in the gastrointestinal tract. When motile forms of B. burgdorferi were exposed to RBC for 1 week at 37 degrees C, the minimal bactericidal concentration (MBC) was > 64 mg/ml. At 30 degrees C, the MBC was > 256 mg/ml. When the incubation lasted for 2 weeks at 37 degrees C, the MBC dropped to > 2 mg/ml. Bismuth aggregates were present on the surface of B. burgdorferi when RBC > or = MBC, as shown by transmission electron microscopy (TEM). Cystic forms of B. burgdorferi, exposed to RBC for 2 weeks at 37 degrees C, were examined by cultivation in BSK-H medium (Sigma B3528). They were stained with acridine orange (pH 6.4, pH 7.4) and studied by TEM. The MBC for RBC for young cystic forms (1 day old) and old cysts (8 months old) was estimated to be > 0.125 mg/ml and > 2 mg/ml, respectively. Bismuth aggregates were attached to the cysts and, in some, the pin-shaped aggregates penetrated the cyst wall. The bismuth aggregates also bound strongly to blebs and granules of B. burgdorferi when RBC > or = MBC. When B. burgdorferi is responsible for gastrointestinal symptoms, bismuth compounds may be candidates for eradication of the bacterium from the gastrointestinal tract.

PMID: 12051564 [PubMed - indexed for MEDLINE]

N Engl J Med 1997 Jul 31;337(5):289-94 Related Articles, Links



Ceftriaxone compared with doxycycline for the treatment of acute disseminated Lyme disease.

Dattwyler RJ, Luft BJ, Kunkel MJ, Finkel MF, Wormser GP, Rush TJ, Grunwaldt E, Agger WA, Franklin M, Oswald D, Cockey L, Maladorno D.

Department of Medicine, State University of New York, Stony Brook, 11794-8161, USA.

BACKGROUND: Localized Lyme disease, manifested by erythema migrans, is usually treated with oral doxycycline or amoxicillin. Whether acute disseminated Borrelia burgdorferi infection should be treated differently from localized infection is unknown. METHODS: We conducted a prospective, open-label, randomized, multicenter study comparing parenteral ceftriaxone (2 g once daily for 14 days) with oral doxycycline (100 mg twice daily for 21 days) in patients with acute disseminated B. burgdorferi infection but without meningitis. The erythema migrans skin lesion was required for study entry, and disseminated disease had to be indicated by either multiple erythema migrans lesions or objective evidence of organ involvement. RESULTS: Of 140 patients enrolled, 133 had multiple erythema migrans lesions. Both treatments were highly effective. Rates of clinical cure at the last evaluation were similar among the patients treated with ceftriaxone (85 percent) and those treated with doxycycline (88 percent); treatment was considered to have failed in only one patient in each group. Among patients whose infections were cured, 18 of 67 patients in the ceftriaxone group (27 percent) reported one or more residual symptoms at the last follow-up visit, as did 10 of 71 patients in the doxycycline group (14 percent, P > or = 0.05). Mild arthralgia was the most common persistent symptom. Both regimens were well tolerated; only four patients (6 percent) in each group withdrew because of adverse events. CONCLUSIONS: In patients with acute disseminated Lyme disease but without meningitis, oral doxycycline and parenterally administered ceftriaxone were equally effective in preventing the late manifestations of disease.

PMID: 9233865 [PubMed - indexed for MEDLINE]

Curr Opin Rheumatol 2002 Jul;14(4):388-93 Related Articles, Links

Development of autoimmunity in Lyme arthritis.

Guerau-de-Arellano M, Huber BT.

Tufts University School of Medicine, Boston, Massachusetts 02111, USA.

Treatment-resistant Lyme arthritis (TRLA) develops in 10% of Lyme arthritis patients and is characterized by continuous joint inflammation that does not resolve with antibiotic therapy. TRLA is associated with HLA-DRB1*0401 and related alleles, as well as with an immune response to the Borrelia burgdorferi (Bb) outer surface protein A (OspA). The immunodominant epitope of OspA in the context of HLA-DRB1*0401 corresponds to amino acids 165-173 (OspA165-173). The human Lymphocyte Function Antigen-1 (hLFA1alpha) contains a peptide with homology to OspA165-173. Treatment-resistant Lyme arthritis patients' T cells, cloned based on their ability to bind OspA165-173-loaded HLA-DRB1*0401 tetramers, respond to OspA and hLFA1alpha with a different cytokine profile, suggesting that hLFA1alpha acts as a partial agonist with a potential role in the perpetuation of joint inflammation.

PMID: 12118172 [PubMed - indexed for MEDLINE]

Epidemiol Mikrobiol Imunol 2002 Apr;51(2):60-5 Related Articles, Links



[Lyme borreliosis--incidence of serum anti-myelin antibodies]

[Article in Czech]

Ryskova O, Vyslouzil L, Honegr K, Lesna J, Horacek J, Skrabkova Z.

Ustav klinicke mikrobiologie, UK Praha, LF Hradec Kralove. ryskovao@lfhk.cuni.cz

The method of enzyme immunoassay (ELISA) was used for detection of antibodies against the basic protein myelin (antimyelin antibodies) for a group of serum samples (n 36) with positive anti-borrelia immunoglobulins IgG and IgM (ELISA-Borrelia afzelii) and their immune complexes (ELISA-PEG). Antimyelin antibodies (ELISA-Doxa Kit-Myelin Basic Protein Antibodies) were assessed in 31% (n 11) of examined serum samples of patients with the working diagnosis of Lyme borreliosis. Statistical analysis (p 0.07) confirmed a more frequent incidence of antimyelin antibodies in younger female subjects (age 31 years) as compared with a group of sera (n 25) where the authors did not record the formation of immunoglobulins against the basic myelin protein (age 51 years). Neither the value of titres nor the frequency of detected anti-borrelia IgG and IgM and immune complexes did not differ significantly in the two groups. From the assembled results ensues that in the course of Lyme borreliosis, in chronic affection of organs an autoimmune reaction may develop where the basic myelin protein is damaged (demyelinizatio) and subsequently antimyelin antibodies are formed.

PMID: 11987581 [PubMed - indexed for MEDLINE]

 (207) 623-1681 Maloney Medical, 4 Drew St., Augusta ME 04330 docleroymaloney@hotmail.com 
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