Shame: the elephant in the room

The entire Endocrinological world should hang their heads in total
shame at the way they treat Thyroid patients and ignore with contempt
their ongoing suffering

The obstinate insistance that Thyroxine / Synthyroid and Thyroid
Blood tests especially TSH are PERFECT and must be defended at all costs
is doing a huge diservice to countless millions of suffering patients

Those very few enlightened Doctors who have dared to speak out on the
subject and use lateral thinking or unconventional treatments/ medications
on their patients and have suceeded in restoring to health those patients
whom the Establishment Endocrinologists have thrown on the scrapheap have
been witchunted into oblivion by sheer jealousy of success and an arrogant
refusal by the Establishment to admit that they are WRONG

Far far too many thyroid patients are "Sick and tired of feeling Sick
and Tired " on useless Thyroxine

Start giving them T3 or Armour Thyroid and just see those patients
regaine their lives
Then reinstate pioneering doctors who showed the way back into a
profession they loved and a disease they actually understood

Mitch Abrahams - 25 March 2002 - writes about his middle-ground
position where HIV is neither 'sole-cause' nor 'non-existent' in relation
to AIDS, he however makes an awkward comment in relation to AIDS in
Africa.

He seems to promote the idea that some action should be taken against
this 'unknown' disease in Africa, though it is uncertain exactly what
action he would suggest should be done. It appears as though he's
advocating that this action should take place in precedence over
determining the actual cause of the death and sickness. This I find
totally irresponsible. He only needs to put himself in the following
position to see how he would feel...

"You go to see your doctor, but unfortunately there is no-one you can
speak to. Fortunately though, you're in luck, because there's a very
qualified team of doctors and statisticians from the first world who are
sitting at a desk with a fancy computer behind a large glass window. All
you need to do - along with everyong else from your village - is stand in
line and walk past the window. Then, come back tomorrow once they've
analysed the results of the (visual) test and developed the latest and
greatest cure for your illness - One pill to cure all ills! Don't worry if
it doesn't work, or makes you feel even more sick, they'll come up with a
new 'better' pill soon enough."

Africa's problems are great:

* They've got bigger things to deal with than AIDS - how about
poverty first? Then development that creates jobs, health and education?
Of course, in the meantime you still need to make sure they have the
medication for REAL, TREATABLE, IDENTIFIABLE diseases like TB, maleria,
syphalis, etc.

The only pill that will cure Africa is the triple-cocktail-therapy
of:

* CANCEL THIRD-WORLD DEBT,

* PROVIDE RELEVANT INVESTMENT FOR DEVELOPMENT,

* ENSURE CONTINUED EQUAL FAIR TRADE.

After all, it's the pill that first-world countries offer to their
citizens and neighbours all the time.

ALSO;

Munir E. Nassar M.D. - 26 March 2002 - writes that "blame" is a
better word than "shame" if applied to who he sees as the problem -
researchers and pharmaceutical big-business (not physicians).

I can't see how physicians get to avoid blame. A lawyer who advises
a client on old or not-quite-up-to-date law cannot claim ignorance when
the client blames him for shoddy work. Similarly, it is physicians'
responsibility to keep informed of ALL areas of research pertaining to
their skills as well as the GOOD AND BAD of drugs available (not only
those that big-business markets). It is surely the physicians'
responsibility to know what others are saying about the efficacy of drugs
- not only what the pharmaceutical firm tells them.

Further, I don't think that society (NOTE - and therefore also the
individuals in society) should take blame in those places where society
has set up organisations to provide assistance to physicians in keeping up
to date with medical developments (in both formal research and practical
consensus remedies). Provided that there are also organisations that
provide assistance to patients in recognising where and when they might be
getting bad advice from physicians, drug companies and the general media.

Phew... what a lot to say!!

Professor Davidoff is quite right to point out that great harm is
often done by inappropriate treatments whose safety and efficacy were
established as often by anecdotal evidence than by rigorous review. We are
now learning, for instance, that the coxibs that selectively inhibit
inducible prostaglandins also inhibit a physiologically important pathway.
Parts of the COX-2 pathway are physiologic - especially for kidney and
heart function - and therefore not only pathologic. This has led to
ongoing changes in the guidelines for selective COX inhibitors.

With respect to harm, some of the earlier hypoglycemic drugs may be
similar to the triple-drug anti-HIV therapies now used in the developed
world to treat AIDS. In fact, the harm from HIV treatment may turn out to
be a much bigger tragedy than that from older hypoglycemic drugs,
selective COX inhibitors, or for that matter, treatments like out-patient
anti-arrhythmics and all the teratogens. AIDS physicians spend far too
much of their time managing the often horrific side effects of the current
anti-retroviral regimens, such as dislipidaemia, hypertension,
lipodistrophy, heart attack, stroke, kidney failure, cytochrome P-450
interference/liver failure, fatigue, anaemia, depression, etc.

In addition, these regimens, while seemingly reducing the number of
deaths in the short-term, have resulted in unusual and unexpected changes
in AIDS-defining events. (1, 2) This has cast confusion as to when - or
even if - to initiate these triple-drug treatments. (3) We may be
witnessing a repeat of the situation with zidovudine ten years ago when,
despite early hopes, the largest and longest study in asymptomatic
individuals with HIV demonstrated little - if any - survival benefit, (4)
with the earlier higher dosages causing substantial morbidity.

The lack of progress in achieving sustainable benefits with the HIV-
based lifelong regimens, and in developing an efficacious HIV vaccine, has
led AIDS "dissidents" such as David Rasnick and Peter Duesberg to posit
that the aetiology of AIDS needs to be re-assessed. They point out that in
some contexts HIV/AIDS appears to be quite difficult to transmit. They
cite the lack of evidence for heterosexual transmission of T-cell subset
abnormalities from hemophiliacs to their spouses, (5) as well as the
recognized absence of HIV seroconversion or AIDS among health care workers
with documented percutaneous HIV injuries. (6, 7) Later studies suggest
this phenomenon may in fact represent natural immunity to HIV, as
evidenced by high levels of HIV-specific CD8-bearing cytotoxic T-
lymphocytes. (8-10)

However, in the well-studied male homosexual cohorts in the
industrialised West, AIDS does seem to be overwhelmingly associated with
sexual transmission. This is why most HIV treaters, and even some AIDS
dissidents, (11) while acknowledging gaps in our understanding of
pathogenesis, cannot reconcile the Duesberg/Rasnick non-infectious
aetiology (based on drugs and malnutrition) with the many multi-partner
homosexual men who apparently share only sexual exposure as an AIDS risk.

Aetiologic hypotheses may therefore need to be expanded to include
other immune regulating infectious diseases that could be a co-factor for
the nearly irreversible loss of CD-4 helper cell-driven anamnestic
responses in AIDS. (12-15) The resulting down-regulating cytokines from
such a disease, transmitted through blood products - cytokines which would
escape viral inactivation techniques - could then contribute to the immune
suppression in transfusion cases, in coagulopathies and globinopathies,
(16-19) and in mother-to-child AIDS, given the intimate relationship
between the course of disease in children and the severity of the disease
in their mothers. (20) Chronic exposure to these immuno-regulatory
molecules from infected individuals - whether transmitted during ongoing
haemophilia treatments, breast-feeding, or immune system ontogeny in utero
- may well play as important a role as HIV in the induction of AIDS.

In the industrialised West, the most likely infection that could best
set the stage for the immunology seen in HIV/AIDS, (21-29) often
undetected and untreated (30-33) among homosexual male blood donors
preceding the modern AIDS epidemic, is Osler's Great Masquerader -
syphilis. Both the Olso (34) and Tuskegee (35) natural history studies of
untreated syphilis, as well as many other authors, (36-49) have raised the
likelihood of excess mortality from long-standing untreated syphilis, i.e.
deaths not associated with late lesions but due instead to pneumonia,
consumption and cancer. This idea faded into the background, however,
amidst the euphoria surrounding the efficacy of penicillin in early acute
syphilis.

It is generally accepted today that current syphilis screening
techniques are sufficiently sensitive to diagnose the disease in HIV-
infected persons. It should be noted, however, that the current concept
for detecting syphilis in most of the world is still based on the
Wassermann reaction. This was first developed in 1906 to detect non-
specific auto-antibodies to cardiolipin extracted from liver emulsions of
still-born syphilitic babies. Despite a strong correlation between
reactivity in this non-specific screening assay and symptomatic or acute
early syphilis, this indirect method is not sensitive for assessing
prevalence of the disease as a whole, nor always reliable in detecting the
incidence of the acute infectious stages. (50-52)

To make matters worse, these anti-lipoidal tests (including the
modern reagents used today) have never worked well for re-infection. This
was demonstrated by several experimental investigators in the 1940s and
1950s, using both animal and human subjects. (38, 53-58) In some of these
models, infection and/or re-infection with T. pallidum was symptomless and
often produced no reaction in the Venereal Disease Research Laboratory
(VDRL) test, i.e. the sensitivity could approach zero, despite proven
dissemination of T. pallidum. Patients who no longer react to re-exposure
in the VDRL these days are perhaps "syphilised", to quote a term first
coined by Joseph Auzias-Turenne (1813-1870). He observed that after
catching syphilis a few times, the classical symptoms were never seen
again. (59, 60)

An elegant summary of this ongoing phenomenon was made a century
later by Evan W. Thomas, one of America's greatest authorities on
syphilis: "Within 2 years after infection, untreated syphilis produces
immune changes in the host which, with rare exceptions, are permanent and
make it impossible for tissues to react to subsequent infection with
development of early syphilitic lesions." (50) Thomas made this assertion
after following over two thousand treated patients in New York City, where
he saw only one exception to this rule. The introduction of penicillin did
not alter this finding. This failure to develop early lesions again upon
re-exposure has important implications for the reliability of the non-
treponemal tests, which have been widely trusted for decades, including in
populations at risk for multiple exposures.

Investigators have repeatedly issued warnings about the very high
rates of syphilis among multi-partner homosexual men. (61-63) Classical
understanding teaches that the specific treponemal antibodies (as measured
by the TPHA, FTA-Abs, and TPI assays) remain for life in virtually all
individuals with secondary or later stage syphilis - treated or not. Given
the overwhelming epidemiologic correlation between syphilis and HIV, (64-
66) it follows that there should be a high rate of treponemal antibody in
this population.

To test this assumption, back in the late 1980s investigators at the
Toronto Hospital began screening HIV-infected men - presumably at great
risk for syphilis - using quantified treponemal tests. They found, much to
their surprise, precipitously falling titres of these specific antibodies
to T. pallidum among many of these men, often in the absence of any
evidence of syphilis diagnosis or treatment. (67, 68) Of the 500 HIV-
positive men ultimately screened, not one reacted in the VDRL test. (69)
The sero-reversion of treponemal antibody, which has been reported by
others, (70-72) is found often among men who never knew they had been
infected with syphilis. This loss of antibody also appears to be selective
within the polyclonal activation associated with progressive HIV
infection, (68, 73) i.e. antibodies to other infections remain at the same
levels. This could be due to chronic persistence of the disease in spite
of treatment, (74) or symptomless reinfection. Whatever the mechanism, it
remains unclear why syphilis never behaves as an opportunistic infection
among HIV-coinfected patients. (75) Or is HIV, as some have suggested, (76
-78) the actual opportunistic infection here?

Some HIV patients who have no history of treated syphilis, nor recent
VDRL reactivity, have been found with T-cell-independent IgM responses to
T. pallidum, suggesting an active infection. (79) This finding was
recently documented again in Toronto. (80) Using recombinant T. pallidum
antigens and SDS-PAGE, investigators here screened 557 random, non-nominal
specimens from clinics serving high-risk homosexual populations. They
found 27 cases of syphilis, i.e., a prevalence of nearly 5%, in stark
contrast to the Ontario annual incident rate of under 0.001%. Furthermore,
56% (15/27) had detectable anti-treponemal IgM. Only 33% (9/27) were
detected by the MHA-Tp (equivalent to the European TPHA) at the standard
cut-off, and none were VDRL-positive. This may suggest defective antigen
processing. Sexual contacts had never been traced for 74% (20/27) of these
newly-identified latent cases, nor likely ever will be.

These diagnostic concerns may well extend beyond the HIV/AIDS
context. The Ontario Public Health Laboratory, as a syphilis serology
reference lab in North America (along with those of James N. Miller at
UCLA and Sandra A. Larsen at the CDC), banked many biologic false-positive
specimens collected during routine screening. In other words, the
specimens reacted in the VDRL, but were non-reactive in the standard MHA-
Tp confirmatory test. However, applying the newer standard described above
to 119 specimens, the Ontario lab flagged 11 as possibly syphilitic. Six
results were equivocal, and five were indubitable positives by Western
Blot. (80) The families, contacts, and individual patients have not had
the benefit of this knowledge. At least one other center has documented
this problem with false-negative treponemal testing in HIV injection drug-
users. (81)

It is therefore urgent that clinicians worldwide re-screen all their
patients - including those without HIV - for treponemal antibody using
better tests until revised guidelines are issued. A better understanding
of the treponematoses, such as syphilis, will then likely become an
integral part of AIDS care. An improved detection system should ideally be
based on batched recombinant treponemal antigens. (82) Confirmation of an
inappropriate immune response to syphilis can then be provided by IgM-SDS
PAGE, direct detection by PCR of treponemal DNA, (83) or a strip assay
(84) where individual recombinant antigens bind the antibodies. These
kinds of assays are available, some licensed commercially, and costs are
often comparable to existing VDRL/TPHA technology. The quality and safety
of health care may materially benefit when blood donor lots are
additionally screened with better treponemal tests, and the syphilitic
cases further evaluated. As well, earlier findings of low T-cell levels in
populations with high syphilis rates (85) should be re-assessed.

There is now ample evidence to have another look at the Great
Masquerader. We may learn that syphilis plays a role in AIDS beyond merely
facilitating HIV transmission - and may have done so for centuries, as a
result of the "syphilisation" effect on the Gell and Coombs Type IV
immunologic recall. (86) Is syphilis the "elephant in the room" of AIDS -
to quote Professor Davidoff, "something so big and disturbing that we
don't even see it, despite the fact that we keep bumping into it"? (87)
Our continued reliance on a nearly century-old diagnostic concept for such
a deadly infectious disease may well be seen as a shameful act in years to
come.

John Scythes

Colman Jones

Toronto, Canada

More of these concerns can be found online at
http://cbc.ca/ideas/Aids

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87. Davidoff F. Shame: the elephant in the room. BMJ 2002; 324:623-4.

Editor,

The BMJ editorial titled “Shame: the elephant in the room” (1) examines
the issue of shame mainly from a service provider’s perspective. It
highlights the improvements necessary in order to improve the safety and
quality of medical care. It states “countering shame can motivate health
care providers to learn and improve, bolstering their competence and their
sense of self worth leading to better quality service provision”.

It is also important in our view, to examine the issue of shame from
a patient’s perspective. A topical example is the national strategy for
sexual health and HIV (2).This is a welcome step towards addressing a
worrying increase in both the incidence and prevalence of sexually
transmitted infections (STIs), particularly among young adults and
teenagers. Many still consider STIs a moral issue with the resultant
negative attitudes towards cases persisting even among health care
providers.

This increases the stigma and shame that patients with STIs feel when
having to talk about their problem. Patients have great difficulty talking
about their sexual health and initiatives targeted towards primary care
such as update courses on taking a sexual history are to be applauded.
It is embarrassment and shame that prevents patients from seeking help
from available services, and also leads in many cases to reluctance to
inform their sexual contacts due to the shame of admitting the source of
infection may have been outside of an established relationship.

The message that all services for STIs are confidential needs to be
put across, particularly for school children, teenagers and young adults.
Victims of sexual assault with or without alcohol intoxication are in a
special category. These individuals have been both physically and
emotionally traumatised, and suffer feelings of fear and shame. Emergency
services and law enforcement agencies have mechanisms built into their
systems to deal with these issues, but cases do not always present to them
first. Concerns about STIs need to be dealt with sensitively.

Improvements in communication between parents and their children,
sexual partners, school nurses and students and general practitioners as a
first point of contact between the patients and available services is key
to scaring off this elephant that patients inevitably carry around with
them.

Bolanle Akinosi, Specialist Registrar in Public health Medicine

R. Nicholas Pugh, Consultant in Communicable Disease Control

Walsall Heath Authority, Lichfield House, 27-31 Lichfield Street,
Walsall WS1 1TE

Correspondence to akinosib@ha.walsall-ha.wmids.nhs.uk

References

1. Davidoff, F. Shame: the elephant in the room. Managing shame is
important for improving health care. BMJ 2002; 324: 623-4

2. Department of Health. The national strategy for sexual health and HIV.
London: Department of Health, 2001. www.doh.gov.uk/nshs/index.htm