Glyoxal compositum

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Urenus

in

INJECTION SOLUTION
Composition: 2.2 ml containing: Methylglyoxalum D10, Glyoxalum D10 22 mg each.

Indications:
Stimulation of the defensive mechanisms against toxins in blocked and defective enzymatic systems, disturbed glandular functions, degenerative diseases (cellular phases).

Dosage:
Standard dosage: Adults (and children 12 yrs. and older): 1 ampoule 1 to 3x weekly.
Glyoxal compositum injection solution may be administered by the s.c., i.d., i.m. or i.v. route.

Note:
If the patient briefly experiences temperature rise or local pain after administration, this should be interpreted as a positive response to therapy. These reactions should, however, be allowed to subside before repeated injection.

Package sizes:
Packs containing 10 and 100 ampoules of 2.2 ml each. (8521)

Pharmacoclinical notes

Methylglyoxalum D10 (a glyoxyl with the addition of a methyl group):
A key reactive intermediate that is an α-oxoaldehyde (also termed an α-dicarbonyl) formed as an early glycation end product partly from the nonenzymatic reaction between reducing sugars and amine residues on proteins, lipids, and nucleic acids; can be formed from the spontaneous degradation of glucose during short periods of hyperglycemia, as can occur in impaired glucose tolerance; also can be formed from catabolism of ketone bodies and threonine, as well as from breakdown of triosephosphates; finally, can be formed from tobacco smoke and diet, especially with prolonged heating of food products. It is metabolized to D-lactate in a process that requires glutathione; unlike glyoxal, it also can be formed in an enzymatic process, such as from aldose reductase and glyoxalase reactions, and has 4 different pathways that can be involved in its detoxification.

It has well-established roles in the development of complications of diabetes; the development of advanced glycation end products (AGEs) is accelerated by hyperglycemia; these products accumulate in the sites, such as the retina, kidney, and atherosclerotic plaques, that are the most common sites for damage from diabetic complications.

Involved in the development of diabetic peripheral neuropathy, nephropathy, ocular disease, atherosclerotic disease, cardiomyopathy, and peripheral arterial disease; possibly provides the link between hyperglycemia and immune suppression; in particular, it is a potent suppressor of myeloid and T-cell immune function, such as the loss of interferon-a and interleukin 10.

AGEs also might activate monocytes to increase the expression of adhesion molecules and promote the production of cytokines and the proliferation of T cells. AGEs have been linked to the development of chronic diseases, such as the retinopathy, neuropathy, and nephropathy associated with long-term diabetes mellitus, macrovascular disease, Alzheimer disease, cataracts, and premature aging.

AGEs act through their receptor, which is termed receptor for AGEs (which is an immunoglobulin superfamily receptor) or via cross-links of the extracellular matrix to promote the oxidative stress and proinflammatory signaling components contributing to the neuronal and vascular complications of long-term diabetes. AGEs also directly cross-link type I collagen and elastin proteins of the vascular walls to increase vascular stiffness and resistance to proteolytic degradation and promote cardiovascular complications, as well as cross-link with myelin, tubulin, plasminogen activator, and fibrinogen to promote further intracellular and extracellular damage.

The composition of the extracellular matrix is modified by AGEs, with an increased expression of certain proteins, such as fibronectin, types III, IV, and VI collagen, and laminin, as well as through the upregulation of transforming growth factor-β and connective tissue growth factor; is cytotoxic to neuroglial cells.

Glyoxalum D10:
An α-oxoaldehyde formed as an early glycation end product from the product of the nonenzymatic glycosylation of proteins; can be formed from the spontaneous degradation of glucose during short periods of hyperglycemia, as can occur in impaired glucose tolerance; also can be formed in lipid peroxidation; is part of the AGE-receptor for AGE process previously described for methylglyoxalum.

Glyoxal and methylglyoxal are members of the carbonyl group series. According to Prof. W. F. Koch, they have the ability to depolymerize toxic material by acting as a hydrogen receptor. The same action is seen with the quinones. Glyoxal is one of the dangerous by-products of abnormal glucose metabolism in diabetics and is implicated in the formation of the so-called AGEs. These are immunogenic and stimulate an inflammatory response, which leads to tissue destruction. Glyoxal in a D10 may facilitate the excretion of this glyoxal and protect the tissues. Furthermore, through the carbonyl group, it acts as a hydrogen receptor, resulting in the formation of free radicals. Intracellular free radicals are especially dangerous to cancer cells, because they have poor antioxidant protection. Glyoxal was classically used infrequently, and only repeated when its action had worked. However, in modern homotoxicology, it is often used in a much more frequent manner because of the increase in intoxication and the dysregulation of modern patients.

References

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