Undiagnosed Porphria

[andyh]

PORPHYRIN-DEFINITION
Porphyrins are pigments found in both animal and plant life. They are all chelates with metals
(Fe, Mg, Co, Zn, Cu, Ni) and constituents of haemoglobin, chlorophyll, cytochromes.

Increased levels of coproporphyrins can indicate congenital erythropoietic porphyria or sideroblastic
anaemia. Increased protoporphyrins may be seen in infection, thalassaemia, sideroblastic anaemia, iron
deficient anaemia, increased erythropoiesis and lead poisoning. Increased uroporphyrins may indicate
congenital erythropoietic porphyria or erythropoietic protoporphyria.

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It would thus appear that a "porphyrin" is (among other variants) all or part of the molecular structure surrounding iron (in hemoglobin-animals) or magnesium (in chlorphyll-plants). An extraordinary fact is that the structure of chlorophyll and hemoglobin are identical except for the center atom. It is not a stretch to see why "porphyrins" might be both light-sensitive and highly reactive.

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Referenceworks search:
Porphyrin: Beryl., ferr., plb., sulfa., sulfon.,

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Beryl.
Urine, porphyrins increased

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ferr.,
from IFH 1995
excerpt from An Introduction to Evolutionary Metabiochemistry
- In the animal kingdom, Ferrum, the Mars energy, has gained control. Iron has replaced magnesium at the center of the porphyrin ring. The Ferrum atom has taken charge of the porphyrin ring, thereby changing chlorophyll into cytochromes and red-blooded heme groups. In essence, these metamolecules absorb the vital force from other living organisms. Even the most passive animal is still violent in that it must kill plants for food. Thus, death becomes life for all the red-blooded creatures. This animal nature gives us the energy and drive to kill in order to live. The killing
extends to other animals — the loss of one animal life for another.

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plb.,

New toxicology: lead
Peter Fisher, MA, MB, BCHIR, MRCP, MFHOM
The British Homoeopathic Journal, Volume 70, Number 1, January 1988, pp. 1-9.
(excerpt)
A second important biochemical property of lead is its strong affinity for sulphhydryl (-S- H) groups. This is the property which accounts for the so-called "lead line" at the dental margin. Lead precipitates with sulphur-containing compounds produced by bacteria around the teeth. The lead line therefore does not occur if dental hygiene is good, nor in the edentulous. Alkyl lead poisoning does not cause such a line.

thought to account for the remarkable similarity of symptoms and signs in the two conditions.

ALA is known to interfere with synaptic transmission mediated by gamma amino butryic acid (GABA) and also interfere with GABA synthesis. The so-called GABA-ergic neuronal pathways mediate inhibitory functions in the central nervous system, increasing liability to seizures of lead poisoned rats. It is tempting to ascribe the hyperactivity observed in chronically lead poisoned children to the same cause. Lead has many other effects on nerve conduction and synaptic transmission. Blocking effects have been observed at both cholinergic and adrenergic synapses. In the case of
cholinergic transmission part of the effect, at least, is due to inhibition by lead of the enzyme cholinesterase which normally inactivates acetylcholine. This block can be reversed like that of the nerve gases, by pralidoxime. In the adrenergic pathway, lead blocks the receptors, particularly B preceptors, and this can result in hypertension. An aspect of lead toxicity which is of great clinical significance is the reduction of conductive velocity which it produces in motor nerves, particularly the radial nerve, resulting in wrist drop (acute intermittent porphyria can also
cause wrist drop). This effect is probably due to a combination of depressed cholinergic transmission and a lead-induced defect in myelin synthesis (which has been demonstrated experimentally in rats).
Lead colic (also known as painter's colic and saturnine colic) is, in common with the abdominal pain of acute intermittent porphyria, a notorious imitator of acute abdomen, although in both conditions the abdominal pain is accompanied by tenderness and guarding only in the minority of cases.
Lead, Motor Neurone Disease and Mental Retardation
Despite some conflict between the results of different studies of children exposed to lead from different sources - waterborne, paint, lead smelters, etc. - there is no doubt that lead can cause a variety of behaviour problems ("non-adaptive" and "hyperkinetic" behaviour patterns in children, as well as reduced IQ and poorer performance than non-lead exposed contemporaries in a variety of tests of coordination, visual and motor functions. These effects are particularly pronounced if lead exposure is in the perinatal period. Similar findings have been reported from adult lead
workers, despite the fact that their blood lead levels were regularly checked and never reached levels considered dangerous. Pica has sometimes been described as a feature of childhood lead intoxication (the word refers to the magpie's Pica pica pica Linn., a bird proverbial for its capricious appetite!). However, recent work by Needleman makes this seem unlikely. Statistical analysis of his results shows that pica is no more associated with lead intoxication than with mental retardation in general. It has also been argued that pica is a symptom of some deficiency, and lead pica
has been induced in rats by calcium deprivation. A diet high in calcium reduces lead absorption, probably because the two elements compete for the same binding protein in the small intestine. Lead also has an important interaction with alcohol; the effects of lead and of alcohol on the central nervous system and porphyrin metabolism are synergistic (alcohol can precipitate acute intermittent porphyria). The constellation of low calcium intake, lead and alcohol may be of particular significance in areas such as Glasgow, where the water is soft, there is much old lead plumbing and
high alcohol intake is not unknown!
However perhaps the most important recent advance in this field is the recognition that lead can cause a syndrome clinically indistinguishable from motor neuron disease, particularly one of its subtypes, amyotrophic lateral sclerosis (ALS). Indeed, it appears that a proportion of the cases formerly diagnosed as classical idiopathic motor neuron disease were in fact due to occult lead poisoning. Campbell and his collaborators have demonstrated a statistically significant correlation between bone fractures and wasting bone disease and the onset of motor neuron disease. They
propose that this is due to the release of lead from bone, as over 90% of total body lead is stored in bone.
From the homoeopathic point of view this is a most exciting discovery for, if the similia doctrine is true, it raises the possibility of treatment for what is surely one of the cruellest, most relentless and distressing diseases encountered in medical practice.
Although lead can cause a demyelinating encephalopathy in subhuman primates, it is not involved in the pathogenesis of multiple sclerosis. The clinical picture seems to resemble more closely that of subacute sclerosing panencephalitis (SSPE) a disease due to measles virus which affects children in the tropics. The possible role of lead in the various "senile", "pre - senile" and arteriosclerotic" dementias which are now so common has not been investigated. It is currently fashionable to attribute pre-senile dementias to "slow" viruses (on very slender evidence) but some
degree of osteoporosis is virtually universal with ageing, and this must presumably by accompanied by release of lead from bone, and lead certainly has effects on cerebral capillaries.
Other effects of lead
Lead has a large number of other pathological effects. It can cause hypertension (particularly in men) and gout, and has been found experimentally to cause changes resembling congestive cardiomyopathy in rat hearts. It also causes acute and chronic kidney disease. In the acute form, the lesion is in the proximal convoluted tubule, causing aminoaciduria. The chronic form of lead nephropathy is seen particularly among fair-skinned people living in the tropical regions (e.g. Queensland, Australia). It is thought that the effects of lead on the kidney are aggravated by the high
Vitamin D levels of such individuals. Chronic lead nephropathy presents with hypertension, nephritis, proteinuria and hyperuricaemia disproportionate to the degree of renal damage. Histologically, many nephrons are totally destroyed, leaving interstitial scarring. The surviving nephrons are hypertrophied.
Conclusion
We have seen that lead is an ancient, widespread, cumulative and pernicious toxin. It can cause or mimic a wide range of diseases. Recent work on the effects of porphyrias and lead on porphyrin metabolism has shown in detail that the effects of the two conditions are not identical but are certainly very similar. This should stimulate us to consider the meaning of the term "similar"; a term more bandied about than thought about in homoeopathic circles. Lead poisoning has taken on a new guise in recent years with the large scale use of volatile lead containing "anti-knock"
fuel additives, which have toxic properties distinct from those of inorganic lead. There have been great advances in the understanding of lead toxicity of which the most important have been the recognition that lead can cause or stimulate a variety of central nervous system dysfunctions and diseases, particularly mental retardation in children and motor neuron disease in adults. Lead can cause a variety of other complaints ranging from colic to hypertension, gout and renal disease. The use of lead in homoeopathy should be extended on the basis of these findings, and the alkyl
lead compounds introduced as remedies.

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sulfa.,
Presence of porphyrin in the urine.

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sulfon.,
murphy
COMMENTS - Prominent symptoms of Sulfon. were: Stupor. Headache with noises in ears. Vomiting and diarrhea. Urine retained or secretion arrested, claret-colored, containing albumen, porphyrin. Ataxic gait and diminished or abolished reflexes point to locomotor ataxia. Ascending paralysis has been observed. The heart is weak, fainting occurs and death takes place by heart failure.
Rashes have been noticed on the skin, purpura, erythematous, etc. One man observed uniform skin effects every time he took Sulfon., more intense the larger the dose. This occurred from 5 grains: Patches of erythema appeared (1) first on inner side of first phalanx of right little finger, (2) next over proximal ends of metacarpal bones of left thumb and index, (3) on posterior surface of left forearm a little below elbow, (4) fourth on prepuce. The symptoms were better by cold douches.