PART
XX:
THERAPEUTICAL
APPROACH
TO
FLOXED TENDONS
We refer here to the potential
treatments for floxed tendons, ligaments and cartilages. In fact, nobody knows
any therapy with proven eficcacy. So we only make a survey of different
supportive measures that can be of some help in very specific cases only.
While it is true that tendinitis
is among the group of permanent injuries caused by fluoroquinolones, it is also
certain that most people do not take the doses needed to get severely hit and
do recover, as it has been discused before.
We know of people that have been suffering from very
debilitating quinolone-induced elbow epicondylitis for 7 years. It is a tendon
for which quinolones show a predilection. Some doctors are for a surgical
intervention. We believe than in severe cases there are so many tendons so much
affected that surgery had to be performed on several tendons of almost every
joint, rendering the method virtually inviable. The following report, as it
corresponds to a french translation, uses the term "lesion" as a
synonim of injury.
EPICONDYLITIS
AFTER TREATMENT WITH FLUOROQUINOLONE ANTIBIOTICS
JC Le
Huec, T Schaeverbeke, D Chauveaux, J Rivel, J Dehais, and A Le Rebeller
We
report two cases of epicondylitis of the elbow occurring after treatment with
fluoroquinolone antibiotics. Both patients had intense pain which appeared very
shortly after the first dose of the drug and was not relieved by conservative
treatment. Ultrasonography revealed extensive inflammatory lesions with pseudonecrotic areas. MRI confirmed the
lesions and also showed a subclinical abnormality of the adjoining tendons. The
persistent nature of the pain was the indication for surgical release of the
extensor mechanism. After operation pain disappeared completely and the
patients were able to return to their normal activities. Injuries of the tendo
Achillis are a well-known side-effect of treatment with fluoroquinolone. Our
two cases show that such lesions may occur elsewhere. They also indicate the
need for caution when prescribing these antibiotics to patients at risk of
tendon lesions, such as top-level sportsmen or patients on dialysis or steroid
treatment.
There are some authors (Olzi and others), that have compiled proposals to
approach the healing of the connective tissue of normal people through
nutrition (foods and supplements).
For floxed persons things are
different, because the damage is chemical and antinatural, but probably for
mild reactions the following tips could constitute a program that would aid in
healing. For severe floxed persons, none of the following advices has made any
difference, and might even have a negative impact on symptoms.
Many studies demonstrate that
collagen production is sensitive to changes in short and long-term food intake.
Within 24 hours of fasting of some animal models, collagen synthesis in
articular cartilage decreases to 50% of normal. Specific effects of malnutrition
on connective tissue turnover are dependant on many factors such as exercise
activities, injuries, and disease. Replacement of tissue pools of
macronutrients requires weeks to months and certainly affects turnover rates of
tissue components.
Calories provide the body with
cellular energy for normal metabolism, building and repairing tissues and
stimulate hormonal responses. Individuals with injuries or other trauma should
avoid a decrease in calories below maintenance or slightly above, thereby
providing the nutrients and energy needed for healing and repair.
Muscle tissue provides a steady
source amino acids for general body needs. Connective tissue is the second
source, which is reflective of the relative rate of turnover to muscle tissue.
Many studies have demonstrated that a protein deficient diet results in a
reduction of growth and development of the organism as well as delay in wound
healing and repairs.
All of the essential aminoacids
are required for synthesis of proteins and other components and growth factors
in the extracellular matrix. Some studies show that supplementing certain
individual aminoacids (methionine, lysine, arginine, and proline) to a protein
deficient diet may inhibit prolongation of the inflammation phase of connective
tissue healing and aid in fiber cross-linking mechanisms during repair.
Unfortunately, as it is discussed
later, supplementation of floxed persons with arginine or lysine is
controversial with at least as many negative reports as positive ones.
Although countless studies
demonstrate that protein malnutrition is significantly detrimental to normal
turnover and healing of connective tissues, floxed persons do not normally
restrict protein intake, unless they are strictly vegetarian and consume
incorrect proteins like the one derived from soy.
Aside from protein, carbohydrates
are a major component of an athlete’s diet and supply quick energy for the body
in the form of glucose. Although little information exits on the direct effects
of glucose deficiencies on connective tissues, it is well known that glucose is
an energy source for several components and growth mediators. Tissue cells such
as fibroblasts and chondroblasts require glucose for synthesis of various
macromolecules. Glucose is a building block of glycosaminoglycans and
glycoproteins in the ground substance of the matrix. Arguably, hypoglycemia
(abnormally low level of plasma glucose caused very frequently by quinolones)
impairs normal cell function and delays wound healing. As well, production and
release of several hormones, such as insulin and growth hormone, decline with
low levels of plasma glucose further delaying tissue growth and repair. There
is a suspicion that treating floxed persons with controlled combinations of growth
hormone and anabolic steroids, could contribute to a quick healing process.
Conversely, high levels of plasma
glucose (hyperglycemia, also caused frequenly by quinolones) may also be
detrimental. Decreased insulin function may lead to hyperglycemia which also
impairs wound healing. This is consistent with the high intolerance that many
floxed persons develop to sugar and all kind of sweet foods.
High levels of plasma glucose
reportedly may inhibit the stimulatory action of ascorbic acid on proteoglycan
and collagen production. Furthermore, chronic high plasma and tissue glucose
levels produce advanced glycation products that affect the physical, chemical
and mechanical properties of collagen and elastin protein.
Diets low in carbohydrates
typically cause body water loss. For athletes, the resultant dehydration may
compromise integrity of connective tissues subject to mechanical loading.
Considering that many connective tissues such as in articular joints require a
relatively high water content for optimal functioning under stress, dehydration
may increase incidence of injury or jeopardize healing and repair of injured
tissue. Hence the importance for floxed persons of taking a lot of good quality
water, but avoiding all sort of excesses in order to avoid the negative effects
of too much water intake that for a floxed person can mean an increase in
central nervous system symptoms, among other unwanted effects.
Saturated fats are commonly found
in animal foods and in some vegetable plants and have little direct import in
the physiology of connective tissue. However there are influences of
polyunsaturated fatty acids on injured connective tissue.
The major polyunsaturated fatty
acids are classified as two types: n-3 and n-6 polyunsaturated fatty acids. The
n-6 family is the major polyunsaturated fatty acids in cell membranes and is
derived from vegetable oils. Low levels of n-3 polyunsaturated fatty acids
exist in most individual cell membranes because diets are generally low in fish
oils which are the source of this polyunsaturated fatty acids family.
Polyunsaturated fatty acids are precursors for a family of hormones called
eicosanoids, which are released by macrophages and other cells and mediate many
cellular functions. The major role of eicosanoids is in the inflammatory
response; therefore, dietary polyunsaturated fatty acids may moderate the
length of the inflammatory phase.
A relative excess of n-6
polyunsaturated fatty acids stimulates production of prostaglandin E2 which may
prolong the inflammatory response. Although increasing intake of n-3
polyunsaturated fatty acids may not impact acute inflammation, such nutritional
support quite possibly moderate long-term inflammation related to excessive
prostaglandin E2 production and cytokine release from activated macrophages.
VITAMIN C (ascorbic acid)
Of all the vitamins, ascorbic
acid probably has the most influence on connective tissue metabolism and has
been the most studied.
In connective tissue, ascorbic
acid is involved in several metabolic reactions. Iron is necessary for a
variety of enzymatic reactions, and ascorbic acid protects iron from oxidation.
Vitamin C preserves the enzyme-iron complex that catalyzes the reaction for
intracellular assembly of collagen. Increased intake of dietary Vitamin C may
prevent inhibition induced by high glucose (as seen in quinolone induced
hyperglucemia) on collagen and proteoglycan synthesis.
In addition to collagen, the
influence of Vitamin C extends to proteoglycans. The most commonly known role
of Vitamin C is as an antioxidant. Vitamin C supplementation in surgical and
non-surgical patients resulted in improved wound healing, reduced inflammation
and improved recovery.
Always be aware of the toxic
effects or large quantitites of any vitamin. In particular, Vitamin C excess
can cause, among other disturbances, kidney stones, increased iron absortion
leading to iron overload and liver problems, erosion of dental enamel,
increased oxygen demand and pro-oxidant effects.
VITAMIN B COMPLEX
The B vitamin complex is a large
group of compounds with different structure and biological activity. They are
usually found within the same food sources. The primary role of the B vitamins
is cellular energy metabolism. Any deficit in cellular energy will have adverse
effects on cellular function. Therefore, the B vitamins are essential in
connective tissue metabolism.
Many of the B complex serve as
cofactors in process of collagen and elastin cross-linking. Deficiencies in
several of the B vitamins influence expression of collagen genes and induce
decreased mechanical strength of repaired and remodeled tissue.
Since most all B vitamins are
found together in similar food groups, deficiencies of one singular vitamin is
uncommon. However, deficiencies may exist if overall dietary intake is reduced.
A mixture of all B vitamins should adequately provide for daily needs.
Always be aware of the toxic
effects or large quantitites of any vitamin. In particular, Vitamin B1 excess
can cause, among other disturbances. Niacin excess can be hepatotoxic (liver
toxicity). Vitamin B6 excess causes NEUROPATHY. Vitamin B12 excess may cause
insomnia, leukemia, kidney damage and also hypertiroidysm.
VITAMIN A
Retinoids are a group of
compounds of which some have vitamin A activity and others do not. Vitamin A is
often referred to as retinol in much of the literature and will be used
interchangeably here. Although carotenoids are commonly mistaken for vitamin A,
only a fraction of them have any vitamin A activity. b -Carotene is the most
significant because in the body it can be broken down into two retinol
molecules and therefore supply vitamin A when needed. Retinol is stored in the
liver and distributed to peripheral tissues by strict regulatory mechanisms and
metabolized in several pathways.
Retinol is converted to retinoic
acid inside cells and both are potent regulators of specific genes, including
expression of fibronectin and type I procollagen. Other metabolites of retinol
regulate cell differentiation and are associated with glycosaminoglycan,
glycoprotein and proteoglycan synthesis. Although still unclear, the role of
vitamin A in proteoglycan synthesis may be involved in sulfation of
glycosaminoglycan s. Tissue from animals deficient in vitamin A typically
displays decreased synthesis of highly sulfated glycosaminoglycan.
Few in vivo studies exist
documenting specific roles of retinoids in connective tissue, except for those
studying wound healing in animal models. That rapidly growing tissues are
sensitive to vitamin A deficiency is well known. Deficiency of other nutrients,
such as zinc and protein, that assist in transport and metabolism of retinol
may induce deficiency symptoms. Therefore, since retinol distribution from the
liver is tightly regulated, functional deficiencies may result with normal
vitamin A intake and stores. Additionally, extra-physiological doses of vitamin
A may counteract the inhibitory effects of systemic corticosteroids on plasma
retinol transport.
Because vitamin A is fat-soluble,
toxicity is also a concern in connective tissue metabolism. High levels may
inhibit collagen synthesis, as seen in the skin, and increase catabolism of
cartilage. This may be concentration dependent since excessively high levels
affect ascorbate induced lipid peroxidation, which in turn inhibits vitamin
C-induced collagen synthesis.
Always be aware of the toxic
effects or large quantitites of any vitamin. In particular, Vitamin A excess
causes liver abnormalities and is teratogenic for the foetus. It also causes
blurred vision, muscular incoordination, nervous system changes anb bone and
skin abnormalities. In fact we recommend you to avoid any kind of
supplementation with vitamin A above the daily recomendation of just one
milligram (1 mg).
VITAMIN E
Vitamin E is a group of compounds
comprising of two major classes: tocopherols and tocotrienols. The basic
chemical structure in each class is similar with variations of substituents and
confirmation resulting in different relative activity. We use the term vitamin
E as a reference primarily to the tocopherols, as they have the greatest
activity in the body.
Literature information on the
role of vitamin E in connective tissue metabolism is controversial. The major
function of vitamin E is as an antioxidant and in the maintenance of cell
membrane integrity. Its role as an antioxidant is thought to require vitamin C
and selenium. Although no specific disease of connective tissue can be
attributed to vitamin E deficiency, it is no doubt needed for life and cell
processes.
Animal model studies have shown that severe deficiency in vitamin E influence collagen cross-linking and an increase in susceptibility of insoluble collagen to degradation by proteinases. Conversely, excessive doses of vitamin E elicit effects similar to those of corticosteroids: inhibition of collagen synthesis and wound repair. Rats given supra-physiological doses of vitamin E exhibited less tensile strength in skin of healed wounds. Indeed, vitamin E may potentiate adverse effects of corticosteroids. We do not recommend to take supplemented vitamin E to treat a floxing because some floxed persons have reported increased hemorrhages probably due to