--- In
fqtoxicity@yahoogro ups.com, Fqresearch@. .. wrote:
>
> My mistake. You are indeed correct. I need to read these emails
more
> carefully.
>
> Diabetes insipidus (DI) is a condition characterized by excretion
of large
> amounts of severely diluted urine, which cannot be reduced when
fluid intake is
> reduced. It denotes inability of the kidney to concentrate urine.
Where as
> Diabetes mellitus is a disorder in which blood sugar (glucose)
levels are
> abnormally high because the body does not produce enough insulin.
>
> DI is caused by a deficiency of antidiuretic hormone (ADH), also
known as
> vasopressin, due to the destruction of the back or "posterior" part
of the
> pituitary gland where vasopressin is normally
released from, or by
an
> insensitivity of the kidneys to that hormone. It can also be
induced iatrogenically by
> various drugs as we see with the fluoroquinolones.
>
> Basically one is a disease of the pancreas where as the other is a
disease
> of the hypothalamus and pituitary gland. Mixing my apples and
oranges I was
> here. But I will find the citations for fluoroquinolne induced
diabetes
> insipidus that I have and post them here as well as separate them
out on the
> research site.
>
> capt' dave
>
>
>
> Hi Dave,
Some of the basics are that basically the vasculitis killed part of
the pituitary which does not repair itself....therefore all the
hormones get out of whack. Key things with NDI is that you can die of
hypernatremia, encephalopathy of the brain if you dont drink enough
water. Apparently the blood is
not diluted enough so basically has
too much sodium in it. Nothing in the kidneys to stop need to
urinate,,,as urine and minerals go out,,,energy depletes and thirst
increases... ..then viscious cycle repeats.
They recommend wearing a medical alert bracelet.
Restricting salt intake, and protein intake.
Urinating every two hours because the excess urine dialates the
ureters and damages them over time.
Drink 3-5 times as much water as a normal person. BUT JUST DRINK
BASICALLY TO THIRST BECAUSE WATER INTOXICATION CAN KILL ALSO.
Replace lost minerals like potassium, magnesium, calcium , zinc. iron.
Also they recommend a potassium sparing diuretic...forr example
spironolactone.
AND DO NOT CROSS A DESERT WITH A CANTEEN :)
YOU ARE GREAT DAVE ! KEEP UP THE HARD WORK AND LETS TAKE THESE @#$%
^&*& DOWN ! My heart breaks with each new victim and also for myself
and the
injury to my body.
THIS SHOULD BE MADE INTO A CONSPIRACY THEORY MOVIE ABOUT KILLING OFF
A PLANET !
I FEEL FOR THE VICTIMS THAT ARE NOT MEDICAL BECAUSE EVEN AS A
MEDICAL PERSON IT TAKES HOURS AND HOURS OF RESEARCH TO FIGURE OUT THE
MECHANICS BEHIND THE DAMAGE.....BUT AT LEAST YOU KNOW WHY YOU ARE
GUZZLING ICE WATER AT 3 AM AND ALL DAY LONG,,,,WHY A LITTLE YAPPING
DOG DRIVES YOU INSANE ( HYPERACUSIS ) .....
Just a good article about a patient:
DIABETES INSPIDUS INDUCED BY OFLOXACIN
Anil Bharani, et al. Department of Medicine, MGM Medical College and
MY Hospital, Indore, India
Nephrogenic diabetes insipidus occurs with agents such as lithium,
methoxyfluorane, vitamin D, and demeclocycline. We report a case of
diabetes insipidus induced by ofloxacin.
A 25 year old man was admitted with fever, a dry cough, and dyspnoea
of three days' duration. He had had an influenza-like illness
in the
preceding week, and his doctor had prescribed ampicillin 2 g daily
for three days. On examination he was febrile, toxic, dyspnoeic, and
had poor oral hygiene. His pulse was 130 beats/min, blood pressure
110/70 mm Hg, and respiration 35 breaths/min. A chest examination
showed signs of bilateral lobar consolidation of the mid zones. His
total white blood cell count was 20×109/l with 90% polymorphs, the
results of blood biochemistry were normal, and he had negative
results for hepatitis B surface antigen, HIV-1, and HIV-2. A chest x
ray film showed bilateral lobar infiltrates, no pleural reaction, and
a normal cardiac silhouette. We diagnosed "typical" bilateral lobar
pneumonia acquired in the community after influenza. He was treated
with multiple antibiotics as sputum and relevant bacteriology results
could not be obtained: penicillin G 2 million units four times daily,
gentamicin 60 mg
every eight hours, clarithromycin 500 mg twice
daily, and metronidazole 400 mg every eight hours. He was also given
a mucolytic, intravenous fluids, vitamins, and intranasal oxygen.
On the third day after admission his response was poor and he was
given ofloxacin 200 mg twice daily. He seemed to improve, but on the
fifth day he developed polyuria (>20 l/day) with excessive thirst
(urine 264 mOsmol/kg with urinary sodium excretion 286 mmol/day).
Ofloxacin induced diabetes insipidus was suspected, and the drug was
stopped. His urine volume gradually decreased and his thirst
normalised within 36 hours while the other drugs were continued. As
he continued to improve we rechallenged him with ofloxacin 400 mg
daily. Again his urine production increased in association with
polydipsia. Ofloxacin was stopped. A chest x ray film showed
resolution of the pneumonic consolidation. Multiple cavity formation
bilaterally suggested infection with Staphylococcus aureus. He was
given ceftriazone 2 g daily and cloxacillin 500 mg four times daily.
His symptoms resolved after two weeks.
That the diabetes insipidus recurred when he was rechallenged with
ofloxacin and resolved after the drug was stopped while other
treatment was continued suggests a causal relation. We could find no
report on ofloxacin induced diabetes insipidus in the published
literature or from the product monograph. We reported this side
effect to the manufacturer and the Central Drug Standard Control
Organisation (west zone), both of which were unaware of any such
report. Similarly, the other drugs the patient took were unlikely to
interact to cause a diabetes insipidus-like syndrome. The mechanism
of this interaction is not clear; it could be similar to that of
lithium or demeclocycline, which interferes with the action of
antidiuretic hormone on the collecting ducts.
You will not find any doctor willing to acknowledge this fact. There
is no wonder that the majority of reports about the toxicity of
quinolones come from abroad the USA, suggesting that in that country,
where the medical arts are more advanced, doctors are usually
hostages of the industry, whereas in Europe, Japan, India, Australia,
there are more independent researchers, that work in their public
health systems, much more powerful than its counterpart in North
America.
Remember that diabetes insipidus is not what people normally know as
diabetes. Diabetes insipidus is caused by the inability of the
kidneys to conserve water, which leads to frequent urination and
pronounced thirst. Diabetes insipidus occurs when the kidneys are
unable to conserve water as they perform their function of filtering
blood. The amount of water conserved is controlled by
antidiuretic
hormone (ADH), also called vasopressin. We have asked to a selected
group of floxed persons to report their ADH levels, to see if there
is a correlation with the symptoms of their floxing, and the results
are pending.
If you want to learn more about the assault that the fluoroquinolone
antibiotics do on the human kidneys, have a look to the database of
reference: www.fqresearch. org
Fluroquinolones also damage the nerves that control the urinary
functions, so there is difficulty to hold urine in many cases, and
the nervous system also send wrong signals of full bladder, with an
insuperable urgency to evacuate.
>
>
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