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Medical Forum / Diseases and Disorders / Lupus / October 2007

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Rheumatoid Hyperviscosity Syndrome Spontaneous Lingual Necrosis

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ironjustice@aol.com - 27 Oct 2007 07:07 GMT
This is where your tongue rots off from lack of blood flow due to
thick blood / hyperviscous .. blood ..
You know that hyperviscous blood that .. "doesn't happen" .. in
arthritis ..

Laryngorhinootologie. 2007 Aug 23; [Epub ahead of print] Links
[Spontaneous Tongue Necrosis Consecutive to Rheumatoid Hyperviscosity
Syndrome. A Case Report and Literature Review.][Article in German]

Pfeiffer J, Ridder GJ.
Universitätsklinik für Hals-, Nasen- und Ohrenheilkunde und Poliklinik
(Direktor: Prof. Dr. med. Dr. h. c. R. Laszig), Universitätsklinikum
Freiburg.

BACKGROUND:
Because the tongue is an organ known for its excellent blood supply,
ischaemic lingual necrosis is extremely rare within clinical everyday
life. Acute lingual circulatory disturbances can result from
impairment of venous drainage or more often from ischaemic arterial
occlusion. Due to permanent function loss of the tongue, apparent
lingual necrosis may lead to severe mutilation of the patient. While
vasculitis of the lingual arteries in temporal arteritis is said to be
the most frequent causation of tongue necrosis, diagnosing the
underlying disease of lingual ischaemia may sometimes be challenging
for the clinician.
PATIENTS AND METHODS:
We present the first reported case of a spontaneous lingual necrosis
in a patient with rheumatoid arthritis, due to polyclonal gammopathy
with extensive hyperviscosity syndrome and local vasculitis.
RESULTS:
Clinical symptoms, diagnosis and therapy of tongue necrosis are
presented in a case report. Besides an overview on the disorder of
hyperviscosity syndrome, the discussion will illustrate pathogenetic,
diagnostic and therapeutic considerations of lingual ischaemia. The
international medical literature is reviewed to summarize the causes
of tongue necroses that are described up to now. The particular
importance of temporal arteritis Horton for the otolaryngologist in
general and for the development of lingual necrosis in particular is
highlighted.
CONCLUSIONS:
Apart from the presentation of the first reported case of lingual
necrosis in rheumatoid hyperviscosity syndrome, the intention of this
article is to draw the clinician's attention on the fundamental
aspects of lingual ischaemia and of temporal arteritis.

PMID: 17713879 [PubMed - as supplied by publisher]

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ironjustice@aol.com - 27 Oct 2007 17:51 GMT
On Oct 26, 11:07 pm, "ironjust...@aol.com" <ironjust...@aol.com>
wrote:
This is where your tongue rots off from lack of blood flow due to
thick blood / hyperviscous .. blood .. <<

Does anyone find it curious .. when one goes to altitude .. the
arthritis gets worse and worse UNTIL there are rheumatoid .. nodules.
Down here at sea levels .. when one manifests .. nodules one ALSO
manifests .. hyperviscosity / thick blood.

NOW .. it is VERY curious that when we go to altitude .. the blood
gets hyperviscous.

The REALLY curious thing .. is .. the RF factor .. the **genetic**
marker .. ? .. also rises.

PROVING in MHO .. RF factor is not a **genetic** marker .. at ..
all ..

Now .. smoke that ..

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> Laryngorhinootologie. 2007 Aug 23; [Epub ahead of print] Links
> [Spontaneous Tongue Necrosis Consecutive to Rheumatoid Hyperviscosity
[quoted text clipped - 46 lines]
>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk
ironjustice@aol.com - 27 Oct 2007 18:24 GMT
Hmmm .. so the ace inhibitors "just so happen" / coincidentally ..
WORK .. in arthritis , lupus and high altitude sickness .. all seem to
be connected to the .. high altitude .. dealy ..

ACE inhibitor effective for high-altitude blood disorder

22 February 2002
Lancet 2002; 359: 663-666
ACE inhibitors may reduce cardiovascular complications of a blood
disorder affecting up to 15% of people living at high altitudes,
claims a European team of researchers.

People suffering from altitude polycythemia produce increased levels
of the hormone erythropoitin at high altitudes, which may lead to an
excess of erythrocytes, a high frequency of persistent proteinuria,
chronic renal dysfunction, hypertension, and other cardiovascular
complications.

Previous research has already demonstrated the efficacy of ACE
inhibitors in another form of polycythemia, through inhibition of the
renin-angiotensin system. Therefore, Raul Plata (Renal Disease
Project, La Paz, Bolivia) and colleagues investigated ACE inhibitor
treatment on people with altitude polycythemia using a small,
randomized trial.

All 26 participants had been born at 3200-4000m and had lived in La
Paz, at 3600m, for at least a year.

Thirteen participants were assigned to 5mg/day enalapril, and
thirteen
to no treatment for two years. Urine protein excretion, blood
pressure, body weight, packed cell volume, hemoglobin concentration,
proteinuria, and renal function measurements were taken after 12 and
24 months and compared with those at baseline.

The researchers found that packed cell volume, hemoglobin
concentration, and 24-hour protein urine excretion decreased
significantly in the treatment group, but not in controls.

Systolic and diastolic blood pressure decreased slightly, but not
significantly, in those treated with enalapril, compared with
controls.

'Reductions in both packed cell volume and proteinuria should have an
additive effect in decreasing the cardiovascular and renal
complications of altitude polycythemia, and, in the long term, should
substantially reduce morbidity and mortality,' say the researchers.

-----------------------------------------------

Angiotensin converting enzyme inhibitor-induced angioedema: a report
of two cases
Journal Pediatric Nephrology

Authors
F. K. Assadi, H. E. Wang2, S. Lawless2, C. P. McKay1, L. Hopp1, D.
Fattori1
1Department of Pediatrics, Division of Nephrology, Alfred I. duPont
Hospital for Children, Wilmington, Delaware, USA
2Department of Pediatrics, Division of Anesthesia/Critical Care,
Jefferson Medical College, Philadelphia, Pennsylvania, USA
3Division of Nephrology, A.I. duPont Hospital for Children, 1600
Rockland Road, Wilmington, DE 19899, USA e-mail: fass...@nemours.org
Tel.: +1-302-6514114, Fax: +1-302-6514547

Abstract

Angioedema is a rare but potentially fatal side effect of angiotensin
converting enzyme (ACE) inhibitors. We report for the first time, two
children with systemic lupus erythematosus who developed acute
angioedema after the long-term use of enalapril. Prompt recognition
and appropriate management of ACE-induced angioedema prevented life-
threatening complications. This report highlights the potential risks
of angioedema associated with the use of ACE inhibitors in children.
Patients should be advised to seek medical treatment immediately if
they experience swelling of the face, neck, or tongue, and especially
if they have trouble breathing, speaking, or swallowing.
Publisher Springer Berlin / Heidelberg
ISSN 0931-041X (Print) 1432-198X (Online)
Issue Volume 13, Number 9 / November, 1999
Category Original Article
DOI 10.1007/s004670050727
Pages 917-919
Subject Collection Medicine
SpringerLink Date Thursday, February 19, 2004

Keywords
Key words Angioedema · Angiotensin converting enzyme inhibitor ·
Enalapril

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ironjustice@aol.com - 27 Oct 2007 19:07 GMT
"Resolved after treatment"

I guess that means .. cured .. ?

Am J Ophthalmol. 2002 Jul ;134 (1):130-2 12095825
Rheumatoid hyperviscosity syndrome: reversibility of microvascular
abnormalities after treatment.
[My paper] Kourous A Rezai , Samir C Patel , Dean Eliott , Michael A
Becker
PURPOSE:
To report a case of rheumatoid hyperviscosity syndrome involving both
retinal and choroidal circulation that resolved after treatment.
DESIGN:
Interventional case report.
METHODS:
A 58-year-old woman with clinical and serologic evidence of an
inflammatory connective tissue disease without any visual complaints
was referred for a funduscopic evaluation.
RESULTS:
Funduscopic examination revealed marked dilation and beading of the
venous system, microaneurysms, and telangiectatic capillary beds in
the posterior pole. Fluorescein angiography disclosed delayed
choroidal filling, prolonged arteriovenous transit time, and areas of
capillary nonperfusion. These findings were accompanied by a severe
polyclonal hypergammaglobulinemia and a 10-fold increase in serum
viscosity. The ocular findings were reversible after plasmapheresis
and steroid treatment.
CONCLUSION:
Rheumatoid hyperviscosity syndrome can involve both retinal and
choroidal circulation. The prominent microvasculopathy is reversible
after appropriate treatment.
Mesh-terms: Administration, Oral; Arthritis, Rheumatoid, blood;
Arthritis, Rheumatoid, complications; Arthritis, Rheumatoid, therapy;
Blood Viscosity; Choroid Diseases, blood; Choroid Diseases, etiology;
Choroid Diseases, therapy; Choroid, blood supply; Female; Fluorescein
Angiography; Glucocorticoids, therapeutic use; Human;
Hypergammaglobulinemia, blood; Hypergammaglobulinemia, complications;
Hypergammaglobulinemia, therapy; Infusions, Intravenous;
Methylprednisolone, therapeutic use; Middle Aged; Plasmapheresis,
methods; Prednisolone, therapeutic use; Retinal Diseases, blood;
Retinal Diseases, etiology; Retinal Diseases, therapy; Retinal
Vessels, pathology; Syndrome;

[Pubmed] [Scholar] [EndNote] [BibTex]

---------------------------------------------------------

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com

Man Is A Herbivore!
http://tinyurl.com/a3cc3

DEAD PEOPLE WALKING
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