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Lyme disease with magnesium deficiency
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Magnesium Research. Volume 16, Numéro 4, 287-9, Decembre 2003, ORIGINAL ARTICLE
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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 . |
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
Address for correspondence: Medical Clinic III, 22 Croitorilor
str., 400162 Cluj‐Napoca, ia; Phone: + 40‐64‐532525;
Fax: + 40‐64‐433427; E‐mail: victor_cristeayahoo.com or
vlaicumail.dntcj.ro Address for correspondence: 2 Closca str.,
400039 Cluj‐Napoca, ia; Phone: + 40‐64‐434133;
E‐mail: vlaicumail.dntcj.ro 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) |
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‐‐ Lymphocytoma (lymphadenosis cutis
benigna) |
Early disseminated manifestations |
‐‐ Pseudo‐flu‐like phenomena |
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‐‐ Multiple erythema migrans |
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‐‐ Recurrent arthritis |
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‐‐ Early neuroborreliosis |
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‐‐ Cardiac manifestations |
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‐‐ Ophthalmic manifestations |
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‐‐ Hepatitis, orchitis (less common) |
Chronic Lyme borreliosis |
‐‐ Chronic Lyme arthritis |
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‐‐ Acrodermatitis chronica atrophicans
(Pick‐Herxheimer) |
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‐‐ Neurocognitive disorders |
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Table 2. Main laboratory examinations [1, 2, 5,
11‐14].
Non‐specific |
‐‐ Increased ESR |
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‐‐ Hyperleukocytosis |
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‐‐ Hypertransaminasemia |
Specific |
‐‐ Culture from the biopsy is + in 60% of
acrodermatitis cases |
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‐‐ 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 |
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‐‐ ELISA for IgM and IgG |
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‐‐ Immunoblot (Western blot) |
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‐‐ PCR from skin biopsies, urine, serum, synovial
fluid, cerebrospinal fluid |
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‐‐ 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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