Part Five, Chapter 1, Section B
DIVERSE APPLICATIONS OF MAGNESIUM THERAPY
by
J. Durlach,
V. Durlach,
SDRM, Hôpital St. Vincent-de-Paul, F-75674 Paris,
France
M. Bara and A. Guiet-Bara
Hôpital Robert Debré, U. 62, F-51092 Reims,
France
Laboratoire de Biologie de la Reproduction,
Université P.M. Curie, F-75252 Paris, France
I. INTRODUCTION
Magnesium has for a long time had only a modest place in
therapeutics, being used only for its cathartic or neutralizing
properties in oral preparations or for its sedative and
antispasmodic properties parenterally.
Today, constantly increasing knowledge of the clinical forms
of magnesium deficit in human beings (Durlach, 1988) has made it
possible to know under which circumstances and in what ways
chronic primary magnesium deficiency can be remedied using
physiological doses of magnesium. That is the main form of
magnesium therapy.
These palliative oral doses of magnesium, meant to balance
chronic magnesium deficiency, are obviously devoid of any
toxicity since their purpose is to ameliorate insufficient
magnesium intakes. Their indications rest on well-founded
epidemiological trials (Durlach et al., 1992a).
Conversely, parenteral or high oral doses of magnesium possess
all the pharmacodynamic properties of magnesium overload and are
capable of inducing toxicity. They must, therefore, always be
administered with caution in more or less specific indications
(Durlach, 1988).
In this review of the diverse applications of magnesium
therapy, we will successively consider:
(i) The uses of physiological oral magnesium - the main form
of magnesium therapy involving, first and foremost, an adequate
knowledge of the sole indication of chronic magnesium deficiency.
The technique of oral physiological magnesium supplementation
will be analyzed.
(ii) The indications for, and techniques of, several
pharmacological applications of magnesium:
- mainly the properties of a magnesium overload induced
through either high doses of oral magnesium, or parenteral
magnesium therapy using soluble magnesium preparations;
- accessorily, laxative and antacid magnesium therapy using
most often non or poorly soluble magnesium salts;
- finally, some types of local magnesium therapy:
mucocutaneous or cytoprotective.
As a conclusion, we will contrast the dangers of using the
pharmacological properties of iatrogenic magnesium overload with
the atoxicity of oral magnesium supplementation at physiological
doses palliative of magnesium deficiencies.
II. PHYSIOLOGICAL ORAL MAGNESIUM THERAPY
Today, the main form of magnesium therapy is oral magnesium
physiological supplementation addressing chronic magnesium
deficiency. It is therefore necessary to be well acquainted with
the clinical pattern of this sole indication.
A. Clinical forms of chronic magnesium
deficiency
Open and controlled trials (Durlach, 1988; 1991; 1992; Durlach
et al., 1992a) have established the clinical and
paraclinical pattern of chronic magnesium deficiency (CMD).
Nervous system consequences irrespective of age can be studied
first: clinical and paraclinical symptoms of latent tetany
(hyperventilation syndrome, chronic fatigue syndrome,
spasmophilia, cryptotetany) with, or more often without,
"idiopathic" mitral valve prolapse (idiopathic Barlow's disease,
Da Costa syndrome, soldier's heart, effort syndrome,
neurocirculatory asthenia) with, or without, pseudo-allergy
(through peripheral hyperreceptivity) more often than allergy
(type I mainly). The non-specific pattern of this symptomatology
brings the patient to consult a wide range of specialists as well
as a general practitioner. It includes non-specific central,
peripheral and autonomic manifestations.
The neurotic, or rather, "central" symptoms consist of
anxiety, hyperemotionality, fatigue, headaches (and sometimes
migraine), insomnia, light-headedness, dizziness, nervous fits,
lipothymiae, sensation of "lump in the throat", of "nuchalgia"
and "blocked breathing". The peripheral signs are
acroparaesthesiae, cramps, muscle fasciculations and myalgiae.
The functional disorders include chest pain, sine materia
dyspnoea, blocked respiration, pre-cordialgia, palpitations,
extrasystolae, dysrhythmias, Raynaud's syndrome, trends to
orthostatic hypotension or conversely to borderline hypertension.
In fact, the dysautonomic disturbances involve both the
sympathetic and the parasympathetic systems.
The evolution may be studied with various acute paroxysmal
manifestations which also can sometimes be seen as initial signs
of the illness. The major crises of acute tetany or of grand mal
- even reduced to a simple loss of consciousness - remain
relatively rare. It is more often a question of nervous crises:
neurotonic, from the ."attack of nerves" to the "hysterical
crises", or autonomic: lipothymia, reactive hypoglycemia,
pseudo-asthmatic crisis, vago-vagal syncope or, on the contrary,
paroxysmal tachycardia. Sometimes, centripetal tingling
sensations and stiffness of the extremities confer on these
nervous crises a tetanoid character. Essentially, they all have
in common the fact that they occur in a context of fits of
anxiety, even sometimes with the impression of imminent death
(panic attack), which causes hyperventilation, gaseous alkalosis,
and self-perpetuation of the crisis. Physical examination must
systematically research the signs of neuromuscular
hyperexcitability as well as the Chvostek's sign as precordial
signs of mitral dyskinesia inducing mitral valve prolapse.
Genuine Chvostek's sign must be systematically sought. With a
small (children's) reflex hammer, the examiner percusses the soft
parts of the cheek at the centre of a line running from ear lobe
to the labial commissure, avoiding the lightning contraction of a
"false Chvostek's sign" by tapping the bone of the zygomatic
apophysis. It is important to consider the quality - and not the
intensity - of this clinical criterion of neuromuscular
hyperexcitability. It is only its presence or its absence which
is significant, respectively quoted 1 or 0.
The examination of the precordial area will be carefully
conducted in order to search either for a non-ejection systolic
click, or for a mid to end systolic or pansystolic murmur, or
both, particularly in orthostatism in complete expiration and in
the left lateral decubitus position.
Two routine tracings should always be made: a
neurophysiological examination (electromyogram (EMG)) and a
cardiological examination (echocardiogram (ECC)).
In EMG testing for latent tetany, a Bronck's needle is
inserted into the first dorsal interosseous muscle of the left
hand. The three classical facilitation tests are used:
tourniquet-induced ischemia lasting 10 min, post-ischemia lasting
10 min after removal of tourniquet and lastly hyperventilation
lasting 5 min. If the EMG shows one (or several) train(s) of
autorhythmic activities, "beating" for more than 2 min of one of
the three tetanic activities (uniplets, multiplets or complex
tonicoclonic tracings) a positive response is defined. As
determined for the clinical criterion of tetanic
hyperexcitability, this neurophysiological criterion is only
considered as a two-class variable. Either its presence or its
absence is significant, respectively quoted 1 or 0.
The "excitability index" (EI) is defined as the sum of the two
criteria of tetany. It allows different classes among tetanies to
be distinguished: one with simultaneous clinical and
neurophysiological criteria (EI=2), the others with only one
criterion of their tetanic state (EI=1) with two sub-groups,
either clinical (through a positive of the Chvostek's sign
alone), or electromyographic (through a positive of EMG
alone).
The ECC is the best tool for detecting mitral valve prolapse
(MVP). With time-motion (TM) mode, three tracings are classical:
a "cuplike" tracing of mesotelesystolic MVP (of more than 2 mm),
a "hammocking" tracing of holosystolic MVP (of more than 3 mm),
an isolated systolic anterior motion (SAM) observed without
obstruction or any septal thickening sign and in the absence of
false systolic anterior motion. Two-dimensional echocardiography
appears to be more accurate than TM echocardiography. It
eliminates a number of artefacts and, particularly, in the
section of parasternal longitudinal cut and the apical cut of the
four heart chamber. The criterion for mitral prolapse is the
billowing of one or both leaflets below the level of the mitral
ring. It is important to assess the leaflet thickness as well as
its whole morphology and to appreciate the ventricular kinetics
by calculating: ΔD = end diastolic diameter - end systolic
diameter / end diastolic diameter. Pulsed Doppler
echocardiography allows the detection of associated mitral
regurgitation.
Four routine ionic investigations should always be made:
plasma Mg (pMg), erythrocyte Mg (eMg), calcemia and daily
calciuria, which can be completed by the research of daily
magnesuria, proteinuria and urinary infection. These must first
demonstrate normocalcemia and the absence of hypercalciuria
susceptible to induce secondary magnesium deficit. Next, the
evaluation of pMg and eMg with reliable methods such as atomic
absorption spectrophotometry allows the diagnosis of primary
magnesium deficit through hypomagnesemia in one-third of the
cases of latent tetany (LT) due to CMD, with or without MVP.
Normal levels do not rule out the diagnosis of CMD. The
histograms of LT patients (with or without MVP) and of controls
overlap. If the tetanic group reveals gaussian-type magnesemia
curves with significant lower means (p <0.001) both for pMg
and eMg, their constitutive elements can be individually
hypomagnesaemic (one-third of the cases), normomagnesaemic
(almost two-thirds of the cases) and even, occasionally,
hypermagnesaemic. Nevertheless, one must emphasize the remarkable
constancy of magnesemia which lends importance even to small
variations of magnesemia (Whang et al., 1990; Classen
et al., 1991). Lymphocyte Mg/cell appears as the most
interesting static intra-cellular magnesium item (Durlach et
al., 1991a).
In particular clinical forms records should be completed with
corresponding clinical and paraclinical explorations. Rhinoscopy
in rhinitis to discriminate between pseudo-allergic vasomotor and
allergic rhinitis, skin tests not only with allergens but also
with histamine, acetylcholine and plasma IgE in allergic or
pseudo-allergic forms, electroencephalogram and head scan in
convulsive forms, psychometric investigations in psychic forms,
electronystagmogram and optokinetic test in dizziness,
electropolygraphic study of afternoon sleep in dyssomnia, lipid
profile in atheromatous dyslipidemias (Durlach et al.,
1992b; 1992c)
Several risk Populations require special attention: pregnant
women because of the consequences of deficiency on mother,
foetus, neonate and infant (Durlach et al., 1991b) and
infants born of diabetic mothers (Durlach et al.,
1991b). Geriatric (Rayssiguier et al., 1990a; Durlach
et al., 1993) and sporting (Rayssiguier et al.,
1990b) populations where magnesium deficiency is most often
associated with magnesium depletion.
The last two examples illustrate the necessity of
distinguishing between 2 types of
inducing mechanisms of magnesium
deficit (Durlach, 1988; 1992). In the case of
magnesium deficiency, the disorder corresponds to an insufficient
magnesium intake: it merely requires oral physiological magnesium
supplementation. In the case of magnesium
depletion, the disorder which induces magnesium
deficit is related to a dysregulation of the control mechanisms
of magnesium metabolism: either failure of the mechanisms which
insure magnesium homeostatis or intervention of endogenous or
iatrogenic perturbating factors of magnesium status. Magnesium
depletion requires more or less specific correction of its causal
dysregulation. This differential diagnosis between these two
types of magnesium deficit is of major importance in the case of
primary magnesium deficit and it is also interesting in the case
of secondary magnesium deficit. Although both always require
their own specific etiologic treatment initially, these major
therapeutic measures cannot always be performed. It may not be
possible to get an alcoholic to quit drinking or to manage
diabetes mellitus perfectly. In such cases, a careful analysis of
the mechanisms inducing the magnesium deficit can lead to an
effective therapy. In chronic alcoholism, magnesium deficiency
secondary to an insufficient magnesium entry is frequent
(Durlach, 1988), whilst in diabetes mellitus the deficiency
appears as an adjunct to dysregulations inducing magnesium
depletion (Durlach, 1988). In chronic alcoholism, oral magnesium
supplementation frequently constitutes an interesting adjuvant
treatment (Durlach, 1988; Gullestad et al., 1991), while
it is much less efficient in diabetes mellitus. In magnesium
depletion, however, it is always wise to maintain a sufficient
magnesium intake to prevent the dysregulation from having a
substrate. It may thus constitute a necessary adjunct to the
treatment (Durlach, 1988).
B. Technique of physiological oral magnesium
therapy
The effect of oral physiological magnesium supplementation is the
best tool for establishing the diagnosis of magnesium deficiency.
Physiological oral doses of magnesium are totally devoid of the
pharmacodynamic effects of parenteral magnesium which are
observed irrespective of magnesium status: they are without
clinical effects when magnesium status is normal. But correction
of symptoms by this oral magnesium load will not only be studied
on extra - and intra - cellular magnesium parameters, but also on
all the well known - but non specific -
clinical and paraclinical items. For example, the stigma of
neuromuscular hyperexcitability should be integrated in the
protocol of physiological oral magnesium supplementation
concerning allergic, vascular, aging of sport patients (Durlach,
1988; Durlach et al., 1992a; 1993; Rayssiguier et
al., 1990a; 1990b).
Chronic primary magnesium deficit affects a large proportion
of the population (15 to 20 %). This prevalence seems consistent
with the estimation of nutrient deficiency using probability
analysis in populations where the mean magnesium daily intake is
slightly above 4 mg/kg/day vs recommended dietary amounts of
magnesium set at 6 mg/kg/day (Durlach, 1988; 1989; Durlach and
Mareschi, 1991). The first step of physiological oral
supplementation should be achieved through dietetic means. But
usually magnesium and energy contents of food correlate (Durlach,
1988; Durlach et al., 1992a; Classen et al.,
1991): magnesium-rich products are also rich in energy. Except
for some vegetarian diets (Durlach, 1988; Durlach et
al., 1993), supplementation should be achieved using a
high-magnesium density nutrient with the best possible
availability (Durlach, 1988; 1989; Durlach and Mareschi, 1991;
Fine et al., 1991). This requirement is met by magnesium
in water, which is probably in relation to the importance of its
hydrated form in biological systems (Durlach, 1988; 1989; Durlach
and Mareschi, 1991; Bara et al., 1989; Theophanides
et al., 1990; Meyer and Classen,1991). In practice, this
is rarely the case in tap water,sometimes in bottled mineral
water.
Most often, the treatment is medicinal using the addition of
soluble magnesium salts to ordinary water (Durlach, 1988; 1989;
Durlach and Mareschi, 1991; Classen, 1990; Fehlinger, 1990;
1991). If it is only a question of correcting an experimental
magnesium deficiency in vivo, all highly soluble
magnesium salts have a comparable bioavailability, either mineral
salts, (i.e. chloride) or organic salts, (i.e.
acetate, citrate, methionate, aspartate, lactate, glutamate,
pyrrolidone-carboxylate). Evidently, the specific properties of
their anions may have their own importance: for example a supply
of chloride is interesting in the case of concomitant
hypochloremic alkalosis (Durlach, 1988; Classen, 1990) or the
anions may act differently at the membrane level (Durlach et al.,
1992d).
Tolerance of these physiological doses is excellent.
Acceleration of intestinal transport is observed only in
susceptible subjects: for example patients with colitis (Durlach,
1988).
The contraindications are obvious (Durlach, 1988). Two are
exceptional: myasthenia and hypermagnesemic periodic paralysis.
There is only one frequent contraindication: overt renal
insufficiency (creatinine clearance < 15 ml/mn). Urinary
infection with elevated urinary phosphates is a transient
contraindication, with the risk of the precipitation of
ammonium-magnesium phosphates. Urinary residues must be cleared
prior to any magnesium therapy (Durlach, 1988). Magnesium may
impair the properties of several drugs: for example 4-quinolones,
tetracyclines, several aminoglycosides and vancomycine. The use
of these antibiotics constitutes another transient
contraindication (Durlach, 1988; Günther, 1991). Finally,
within the limits of our present knowledge, solid tumors in a
state of development may also be considered as a contraindication
of magnesium therapy since magnesium may stimulate their growth
(Durlach, 1988; Durlach et al., 1990). However,
palliative control of poorly tolerated magnesium deficiency is
permissible if it coincides with an effective cytostatic
treatment - such as Cisplatin - which prevents the risk of
inducing magnesium excess in the sites where magnesium excess is
noxious (Durlach, 1988; Durlach et al., 1990).
If one finds at the first monthly monitoring of a treatment of
chronic magnesium deficit that a simple increase in oral
magnesium intake is ineffective or insufficient, it is necessary
to proceed to the treatment of this magnesium depletion (Durlach,
1988): in the case of renal loss of magnesium, using agents that
reduce urinary magnesium, either magnesium-sparing diuretics,
i.e. amiloride (5 to 10 mg/day), spironolactone (100 to
200 mg/day), or anti-stress hygienic or medicinal prescriptions;
if these fail (or immediately in the case of no urinary magnesium
leakage) magnesium-fixing agents are indicated, i.e.
pharmacological doses of vitamin B6 and physiological doses of
vitamin D, progesterone in particular cases of luteal
insufficiency or high risk pregnancies (Durlach, 1988). After
failure of these 2 initial stages of therapy for magnesium
depletion, we use either partial magnesium "analogues",
i.e. propranolol, verapamil, several anticonvulsants as
phenytoin, baclofen..., anti-oxidants, i.e. sulfur
compounds, vitamin C and E (Durlach, 1988; Durlach et al., 1992b;
1992c; 1993; Günther, 1991; Freedman et al., 1991;
Rayssiguier et al., 1992) or parenteral magnesium
therapy.
III. PHARMACOLOGICAL MAGNESIUM THERAPY
A. Induced
magnesium overload
In order to induce a therapeutic magnesium overload and to use
the pharmacological properties of the ion, it is necessary to go
beyond the mechanisms of magnesium homeostasis. Large doses of
magnesium given orally are advisable for chronic indications, and
the parenteral route is suitable for acute applications. The
pharmacodynamic properties of magnesium are curariform and
ganglioplegic, bradycardic, antiarrhythmic and hypotensive,
antithrombotic, antianoxic, stabilizing, antitoxic vs several
pollutants (Durlach, 1988; Classen, 1990; Durlach et
al., 1990; Guiet-Bara et al., 1991; Zdanowicz and
Barletta, 1991; Cordova et al., 1992).
1. Indications
There are three types of indications: specific,
pharmacological or mixed.
a. Specific indications
Parenteral magnesium treatment is specifically used for the
treatment of magnesium deficit in its acute form, often with
magnesium-dependent hypocalcemia and/or hypokalemia, when the
oral route is prohibited (parenteral nutrition, anesthesias,
coma) or after the failure of oral magnesium therapy.
b. Pharmacological indications
The pharmacological properties of magnesium apply in many
illnesses where no magnesium deficit has been described:
intoxication with anticholinesterases (especially TEPP or DFP),
aconitine or strychnine; treatment for convulsions in hyperoxia,
decompression disorders (caisson disease), or gas embolism and
treatment in porphyria that does not increase ALA synthetase
activity; treatment for certain forms of migraine and hiccups; as
a relaxant that facilitates certain kinds of psychological or
neurologic examination, in anesthesiology or during
kinesitherapy; anti-hypoxic treatment, especially with high
altitude sickness or for carbon monoxide poisoning; treatment in
any kind of tachyarrhythmia, for example, in lithium poisoning
and particularly in ventricular dysrhythmia such as in "torsade
de pointes"; and treatment of cases of tissue calcinosis such as
ossifying myositis (neurotic, traumatic or progressive) or
para-articulatory ossification after the implantation of
articular endoprostheses (Durlach, 1988; Durlach and Durlach,
1992; Durlach et al., 1992b; 1992c; Classen, 1990;
Günther, 1991).
c. Mixed indications: pharmacological and etiopathoenic
These types constitute very interesting indications for
magnesium therapy. The list of possible types of treatment is
quite long: treatment for delirium tremens and the different
acute complications of alcoholism, most often in hypertonic form
and associated with vitamins B1 and B6; treatment of the various
withdrawal syndromes; treatment for many nervous crises, not only
the tetanic forms but also "grand mal", loss of consciousness,
hypoglycemic episodes, vago-vagal syncope, swooning, "panic
attacks"; treatment for hypertensive diabetic and atherosclerotic
vasculopathy or for various types of central and peripheral
arteriopathies (cerebral, ocular, of the lower limbs, coronary
and especially for myocardial infarction); treatment for acute
intoxication by citrates, by aluminum phosphide, by ricin and
fluoride compounds as well as for intoxication by the major
pollutants, Pb and Cd, and perhaps Hg, ultimately alternating
with chelation treatment; treatment for dilutional hyponatremia
and ketosis. The rarity of gynecologic indications, which, in
practice, are limited to a few cases of severe dysmenorrhea,
contrasts with the importance of obstetrical indications:
treatment for pre-eclampsia and eclampsia, tocolysis in premature
labor, tetanization of the uterus, fetal distress syndrome and
meconial contamination, and even, by virtue of magnesium's role
in the synthesis of surfactant, prevention of hyaline membrane
disease. Finally, parenteral magnesium is interesting in the
treatments of anaphylactic shock and of asthmatic crisis, whereas
the effects of magnesium aerosols are dubious for the latter
indication (Durlach, 1988; Durlach and Durlach, 1992; Durlach
et al., 1992b; 1992c; Classen, 1990; Günther, 1991;
Rasmussen, 1988; Kaplan et al., 1990; Tetikkurt et
al., 1992).
2. Technique
Curiously the most widely used preparations involve magnesium
sulfate. Among the soluble salts of magnesium, sulfate has the
least advantageous pharmacological properties (Durlach, 1988;
Classen, 1990; Durlach et al., 1992d). It is better to
use isotonic preparations of other soluble salts of magnesium,
for example chloride (MgCl2.6H2O), acetate
(Mg[C2H3O2]2.
4H2O), pyrrolidone carboxylate, aspartate, etc. The
intravenous route is customary because of the painful character
of the intramuscular route. A bolus, inducing a sensation of
increased warmth, should never exceed 100 mg (0.1 mmol/kg/day);
one or two boluses per day are possible. For venous perfusions we
use as a normal well tolerated dose 100 mg per hour for
perfusions of 4 to 6 hours: 400 to 600 mg (17 to 25 mmol) for
each perfusion. Massive doses reach 4 perfusions per day: 2400 mg
(or 100 mmol).
It is obvious that such forms of therapy are possible only in
intensive care units, with careful monitoring of pulse, arterial
pressure, deep tendon reflexes, hourly diuresis and
electrocardiogram and respiratory rhythm recordings (Durlach,
1988). Contraindications for this form of pharmacological therapy
are the same as for oral magnesium therapy but one must be even
more cautious because of the toxicity (approaching lethality) of
iatrogenic magnesium overload.
The use of high oral doses of magnesium for inducing chronic
magnesium overload for example to treat extrasystoles or vascular
hypertension (Durlach and Durlach, 1992) appears very
questionable because of its potential toxicity (Durlach and
Durlach, 1992; Ganguli et al., 1990). Conversely, the
use of induced acute magnesium overload appears well-founded
after control with double-blind studies: for example in acute
myocardial infarction, ventricular tachycardias, tocolysis and in
asthma crises (Durlach, 1988; Durlach and Durlach, 1992; Durlach
et al., 1992b; 1992c; Classen, 1990; Rasmussen, 1988;
Kaplan et al., 1990; Tetikkurt et al.,
1992).
B. Laxative and antacid magnesium
therapy
Laxative magnesium therapy traditionally uses the irritative
osmotic strength of large doses of magnesium salts, for example
hydrated MgSO4 or magnesium hydroxide. Any renal or
digestive tract lesion formally rules out its use because of the
risk of a fatal magnesium overload. When cautiously used,
however, laxative magnesium may also constitute an efficient
therapy for magnesium-dependent disturbances of lipid,
carbohydrates and electrolyte metabolism, in geriatric patients
particularly (Durlach et al., 1993; Kinnunen et
al., 1989; Kinnunen and Salokannel, 1989).
Antacid therapy uses the neutralizing capacity of
Mgo or Mg carbonate. The more widespread use of
magnesium-containing phosphate binders creates the risk of
hypermagnesemia. Its interest in hemodialysis patients is
controversial. Theoretically, its use, coupled with a
low-magnesium dialysate, may reduce phosphorus absorption. It
appears better than aluminum salts with their risk of aluminum
encephalopathy (Durlach, 1988), but it is difficult to determine
the use of magnesium-containing antacids with an optimal
magnesium dialysate to efficiently avoid hyper- as well as
hypomagnesemia (Gonelia and Calabrese, 1989).
C. Local magnesium therapy
1. Topical applications of magnesium
During the first world war, P. Delbet stressed the interest of
irrigating wounds with a "cytophylactic" solution of 1.2%
MgCl2 (Durlach, 1988). Today, the topical use of
magnesium is proposed as the best possible antagonist for
hydrofluoric acid burns: bathing with a saturated ice cold
solution of magnesium sulfate associated with local injections of
a 10% solution of magnesium acetate (Harris and Rumack, 1981). An
ointment containing 25% MgSO4 has local decongestive
osmotic effects which make it useful as a non specific
anti-inflammatory agent (Durlach, 1988).
Such an ointment could be used associated with local treatment
of soft tissue calcifications (Steidl and Ditmar, 1990). Finally,
in ophtalmology an eye wash with 10% MgSO4 appears to
have a significant effect on herpetic superficial dentritic
keratitis (Durlach, 1988).
2. Magnesium and cytoprotection
The cytoprotective properties of magnesium make it a
theoretically important element in solutions for the irrigation
and perfusion of organs destined for transplant: cornea, lungs,
liver, pancreas, kidney and especially the heart. The role of
magnesium in cardioplegy is still subject to discussion (Durlach,
1988; Classen, 1990). The protective role of magnesium in insulin
secretion (Ziegler et al., 1983) makes it logical to
consider its use in cultures of the islets of Langerhans to make
this promising treatment for insulin-dependent diabetes more
effective (Durlach, 1988).
IV. CONCLUSION
The applications of magnesium therapy are constantly
progressing. The range of the indications for pharmacological
magnesium therapy is widening: for example in intensive care as
well as in cardiologic emergencies such as myocardial infarctions
and torsades de pointe, and in toxicological emergencies such as
acute intoxication by aluminum phosphide.
Its main indication still concerns the control of chronic
primary magnesium deficiency through physiological oral magnesium
therapy. The pattern of this therapy has now been clearly
delineated, but epidemiological intervention trials are still
needed to better assess its importance. There should be a
follow-up of the effects of the physiological oral magnesium
supplementation not only on magnesium items but also on
all the well-known--but
nonspecific--clinical and paraclinical signs. Its specific
efficiency should contribute to the importance of the clinical
forms of chronic marginal magnesium deficiency, which constitutes
the sole indication for oral physiological magnesium
application.
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