When I wrote my book entitled The Top 10 Lyme Disease Treatments, and included a chapter on magnesium deficiency (see the Table of Contents), some people questioned the veracity of my claim that magnesium deficiency is related to Lyme infection. Well, I’ll now share some evidence.
The date is 1997 and the place is Romania, at the Department of Clinical Immunology, University of Medicine and Pharmacy. It was seen that not one, but 3 patients had concurrent magnesium deficiency and Lyme disease, and that furthermore, the patients failed to respond to antibiotics unless magnesium deficiency was addressed first. I’ll let you read the article for yourself:
Excerpted Key Points:
In June 1997 we had under observation a 26‐year‐old man who came to the hospital for articular pain localized in both knees, cephalea, evening subfebrility starting 10 days before. During this time interval, the patient saw his family doctor who prescribed him oral anti‐inflammatory, antipyretic medication, as well as bed rest. As his general status did not improve, he was referred to the hospital with the diagnosis of rheumatoid arthritis. At the objective examination, performed in the ambulatory service, he was pale, subfebrile, sweating, with discrete splenomegaly. History revealed acute endogenous uveitis, treated with retro bulbar injections with cortisone and atropine. Laboratory examinations showed moderate anemia (Hb ∓ 11.4 g\dl; Hct ∓ 34.4%) and leukocytosis of 9.9 K\ìL. A low serum magnesium concentration was also found ‐‐ 1.21 mEq\L (14.7 mg\L). We confirmed the presence of uveitis and arthritis and proposed the continuation of anti‐inflammatory therapy associated with antibiotherapy for 7 days. After another 10 days, the patient came again, complaining of flu‐like phenomena and having an erythematous area of approximately 6 cm on the anterior face of the thigh, with satellite inguinal adenopathy. The clinical and laboratory aspects were suggestive for Lyme disease (table I and II).
Serum and urine samples were tested using the ELISA technique and LUAT test for Borrelia burgdorferi which proved to be positive: IgM and IgG antibodies to the spirochete were shown in the serum, and in the urine 31 kDa, 34 kDa and 93 kDa proteins of the spirochete. Cephalosporin treatment was immediately initiated and anti‐inflammatory therapy was continued. After 5 days the patient was reevaluated and the evolution was slowly favorable, with the disappearance of the inflammatory erythema, but again he had marked hypomagnesaemia (1.20 mEq\L, 14.6 mg\L) and we decided to administer an oral nutritional Mg therapy (5 mg\kg\day). The evolution was rapidly favorable: in the course of 4 days fever, articular pain, asthenia, adynamia gradually disappeared. Leukocytes decreased to 5800\cmm, and Mg was normalized (1.74 mEq\L).
The patient came for follow‐up after 6 months, then after one year. Clinical manifestations did not reappear. During the period April 2001 ‐‐ January 2003, we had under observation other two cases, in which the presence of both IgM and IgG antibodies to Borrelia burgdorferi was serologically confirmed at high titers. In both cases, clinical manifestations were similar: shivering, fever, headache, articular and right hypochondrium pain, and objectively ‐‐ tachycardia and erythema migrans ‐‐ these elements being important for the formulation of Lyme disease suspicion. Borrelia burgdorferi infection can be asymptomatic or have a large spectrum of clinical manifestations, depending on its duration and the organs involved (table I and II) [1‐13]. Humoral tests showed: significantly increased ESR, leukocytosis (> 11 K\ìL) with PMN predominance (> 70%) and with toxic granulations and significant magnesium deficiency (1.20 mEq\L, 1.33 mEq\L, respectively). A specialized laboratory confirmed the presence of both IgM and IgG antibodies to Borrelia burgdorferi at high titers (1\80, 1\160, respectively) and intensely positive PCR (for B. Burgdorferi DNA) The second patient had also slightly increased ASAT, ALAT (45, 62, respectively). A large spectrum of antibiotics with both oral and parenteral administration has been so far used in the treatment of Lyme borreliosis [15‐17]. Among the most frequently used are tetracyclines, betalactamides and cephalosporins.
The decision to initiate antibiotic therapy can be difficult because in the majority of the cases acute infection is self‐limited. Since in the first case antibiotic therapy alone did not lead to the expected results, magnesium derivatives were also associated. In both cases, following combined therapy, symptomatology significantly improved at 14 days, and laboratory examinations were restored to normal values after 6‐8 weeks‐‐ disappearance of IgM to B. Burgdorferi and significantly increased magnesemia (1.74 mEq\L, 1.72 mEq\L, respectively). Three more cases have been described in the literature since 1997, in which Lyme disease was associated with magnesium deficiency, according to the data presented by EUCALB (European Union Concerted Action on Lyme Borreliosis) . We believe that in certain diseases, Mg deficiency can cause a decrease in immune response.
The appearance of recurrences, which are frequently reported in the literature, in spite of adequate antibiotic therapy, could represent an argument for this. This is why the use of Mg derivatives in therapy can represent an immunostimulating factor. The peculiarities of the cases are the following: a) patients had in addition to fever, articular pain and erythema migrans, Mg deficiency; b) the supplementation of therapy with Mg derivatives had an immediate beneficial effect that was maintained in time. In conclusion, Borrelia burgdorferi infection can have non‐specific symptoms, but the presence of acrodermatitis chronica atrophicans and multiple migratory erythema facilitates clinical diagnosis.
A certainty diagnosis can only be performed by the detection of Borrelia burgdorferi anti‐antigen Ig and\or evidencing of spirochete DNA. The presence of Mg deficiency causes the appearance of a secondary immunodeficiency syndrome which requires the treatment of the patient not only with large spectrum antibiotics but also with magnesium in order to obtain efficient results in the long term.
1 .Cutler SJ. Lyme borreliosis: an update. Br J Hosp Med 1996; 56: 581‐4.
2 .Evans J. Lyme disease. Curr Opin Rheumathol 1997; 9: 328‐36.
3 .Hoxeng K. Lyme disease mimics many other diseases. J Emerg Nurs 1997; 23: 516.
4 .Merkle T, Landthaler M, Neubert U. Pigmentierte urtikarielle Erytheme mit schlaffer Atrophie als Ausdruck einer ungewöhnlichen Manifestation de Lyme‐Borreliose. Der Hautartz 1992; 43: 89‐91.
5 .Sigal LH. Pitfalls in the diagnosis and management of Lyme disease. Arthritis Rheum 1998; 41: 195‐204.
6 .Bujak DI, Weinstein A, Dornbush RL. Clinical and neurocognitive features of the post Lyme syndrome. J Rheumathol 1996; 23: 1392‐7.
7 .Balcer LJ, Winterkorn JM, Galetta SL. Neuro‐ophtalmic manifestations of Lyme disease. J Neuroophtalmol 1997; 17: 108‐21.
8 .Scott IU, Silva‐Lepe A, Siatkowski RM. Chiasmal optic neuritis in Lyme disease. Am J Ophtalmol 1997; 123: 136‐8.
9 .Briant C, Kutcher AH, Roye KJ. Pericarditis as a manifestation of Lyme disease. Emerg Nurs 1997; 23: 525‐9.
10 .Nagi KS, Joshi R, Thakur RK. Cardiac manifestations of Lyme disease: a eview. Can J Cardiol 1996; 12: 503‐6.
11 .Horowitz HW, Wormser GP, Calmann M, et al. Liver function in early Lyme disease. Hepatology 1996; 23: 1412‐7.
12 .Halperin JJ. Neuroborreliosis: Central nervous system involvement. Semin Neurol 1997; 17: 19‐24.
13 .Mouritsen CL, Wittwer CT, Litwin CM, et al. Polymerase chain reaction detection of Lyme disease: correlation with clinical manifestations and serologic responses. Am J Clin Pathol 1996; 105: 647‐54.
14 .Wormser GP, Pavia C, Cooper D, et al. Improving the yield of blood cultures for patients with early Lyme disease. J Clin Micobiol 1997; 36: 296‐8.
15 .Wormser GP. Controversies in the use of antimicrobials for the prevention and treatment of Lyme disease. Infection 1996; 24: 178‐81.
16 .Dattwyler RJ, Luft BJ, Kunkel MJ, et al. Ceftriaxone compared with doxycycline for the treatment of acute disseminated Lyme disease. N Engl J Med 1997; 337: 289‐94.
17 .Donta ST. Tetracycline therapy for chronic Lyme disease. Clin Infect Dis 1997; 25 (Suppl 1): 52‐6.
18 .European Union Concerted Action on Lyme Borreliosis (EUCALB) WWW document. URL http:\\www.dis.strath.ac.uk\lymeeu\index.htm