Leprosy mailing list – December
3rd, 2005
Ccn: all.
From: G Warren, Sydney,
Australia.
Dear Salvatore,
I would just
like to explain myself a bit more (Silent neuritis, LML Nov. 19th.
2005); and just to thank you again.
I am very
concerned that the highbrow researchers look for all the fancy
things they may be able to do, often they are very expensive and so
the workers cannot afford to supply them; but the clinicians forget
the simple things like low Vit. B1, and mineral deficiencies in
the patients normal diet, or what they can afford.
In many of the
Asian countries rice is the basic diet; but it is only eaten polished
so all the bran is gone and virtually all the B1. In Thailand it
is not uncommon for ordinary, i.e. non-leprosy patients to come
in to outpatients complaining of “air coming out of their ears”; popping I think they say it does.
We have found that one injection of B1 is enough to stop the symptoms
and then daily B complex prevents recurrence.
I have heard it
said that the land has grown rice for so many years it no longer
can produce the B1; but in reality the owners feed the B1 (in the rice
polishings) to the pigs!
In
some of the leprosy programs years ago we always supplied iron and
Multivitamins to the routine patients (as well as treating all
intercurrent diseases); for the chronic LL patients surely this is a
help in the nerve function. I am often distressed by the number of
clinicians who give routine anti-leprosy drugs but do not treat
anaemia, malnutrition, amoeba, typhoid, tapeworms etc! I routinely
give high Multi B, with 10mg of Vit. B1, Calcium, & Magnesium to
all my leprosy patients and all other patients with neuropathy and, in
fact I learnt the value of magnesium from a non leprosy
neuropathy patient who had himself found it reduced the paraesthesia.
Never forget
that emotional problems often precipitate bouts of lepra reaction,
hence we found the use of simple phenobar or, Clhorpromazine
or other tranquilising or mood stabilizing medications
reduced the problem of ENL and, this would help reduce the progress of
the neuritis. Ideally one needs the assistance of Social workers to
help sort out home and family and socio-economic problems, this
often cuts the ENL.
Surely the use
of Clofazimine as it reduces inflammation must reduce the severity of
the silent neuritis that is going on in the LL for so many years
before they have clinical signs of neural deficit. I know
that it is accepted that Clofazimine at 50mgms per day has
adequate bacteriostatic effect for effective treatment. But
one wonders if the higher doses as we give for ENL may in fact
protect the nerves in the early LL leprosy. It would be very hard to
clinically prove it! And in retrospect it would be very
difficult to go back and see the chronic ENL patients that we treated
with Clofazimine in very high doses (we used it for ENL from 1966 on
in Hong Kong.)
I did not use
Thalidomide in the 1960s/1970s; I treated ENL with Clofazimine and
sedatives. And still feel these are better that Thalidomide for
most ENL problems, as long as one treats the other intercurrent
problems. Yes, Clofazimine is no use in the treatment of
acute Type 1 reaction (reversal reaction) but that is a
different problem. The Type I reaction causes a primary anoxia
inside the nerve sheath and that is what causes the acute
neural deficit and it may completely destroy the nerve fibres. The
residue of the nerve will eventually fibrose, and then of course
cannot be reversed. In the tuberculoid end of the spectrum
Clofazimine can certainly help long term in preventing and possibly
reducing the inflammation (oedema) that occurs in Type I reaction but
does not decompress acutely swollen nerves as efficiently as
steroids may do.
Kind regards,
Grace Warren
