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Texte intégral de l'article
  Version imprimable

Lyme disease with magnesium deficiency

Magnesium Research. Volume 16, Numéro 4, 287-9, Decembre 2003, ORIGINAL ARTICLE

Auteur(s) : Victor Cristea, Monica Crişan, * Professor, Department of Clinical Immunology, University of Medicine and Pharmacy "Iuliu Haţieganu" Cluj‐Napoca. **Department of Immunology, "Ion Chiricuţă" Oncological Institute, Cluj‐Napoca .


Auteur(s) : Victor Cristea*, Monica Crişan **

* Professor, Department of Clinical Immunology, University of Medicine and Pharmacy "Iuliu Haţieganu" Cluj‐Napoca.

**Department of Immunology, "Ion Chiricuţă" Oncological Institute, Cluj‐Napoca

Address for correspondence: Medical Clinic III, 22 Croitorilor str., 400162 Cluj‐Napoca, ia; Phone: + 40‐64‐532525; Fax: + 40‐64‐433427; E‐mail: or Address for correspondence: 2 Closca str., 400039 Cluj‐Napoca, ia; Phone: + 40‐64‐434133; E‐mail: 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.Table I. Main clinical manifestations of the infection with B. burgdorferi [1‐12].
Early localized manifestations  ‐‐ Erythema chronicum migrans (Lipschtz)
 ‐‐ Lymphocytoma (lymphadenosis cutis benigna)
Early disseminated manifestations  ‐‐ Pseudo‐flu‐like phenomena
 ‐‐ Multiple erythema migrans
 ‐‐ Recurrent arthritis
 ‐‐ Early neuroborreliosis
 ‐‐ Cardiac manifestations
 ‐‐ Ophthalmic manifestations
 ‐‐ Hepatitis, orchitis (less common)
Chronic Lyme borreliosis  ‐‐ Chronic Lyme arthritis
 ‐‐ Acrodermatitis chronica atrophicans (Pick‐Herxheimer)
 ‐‐ Neurocognitive disorders

Table 2. Main laboratory examinations [1, 2, 5, 11‐14].
Non‐specific  ‐‐ Increased ESR
 ‐‐ Hyperleukocytosis
 ‐‐ Hypertransaminasemia
Specific  ‐‐ Culture from the biopsy is + in 60% of acrodermatitis cases
 ‐‐ Presence in the urine of antigens by LUAT technique (Lyme Urine Antigen Test) specific for bacterial proteins: 31 kDa, 34 kDa, 39 kDa and 93 kDa in both early and late stages
 ‐‐ ELISA for IgM and IgG
 ‐‐ Immunoblot (Western blot)
 ‐‐ PCR from skin biopsies, urine, serum, synovial fluid, cerebrospinal fluid
 ‐‐ IF techniques (rarely used, as they are not standardized)
. 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) [18]. 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.


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