This discussion is a prime example of what EVERY patient who suffers
an adverse reaction to these drugs has to endure while seeking
competent medical care to treat such injuries.  After eight years of
putting up with such nonsense I am pretty much immune to this type of
treatment.  Just another day at the office.  I guess when they
graduate from medical school they believe themselves to be
infallible.  Incapable of making either a mistake in judgment or an
error of any kind.  They are now to be considered "GODS" and we are
all expected to bow down to their superior intellect.  Bullshit.  They
are nothing more than glorified mechanics that instead of working on
Porches they now spend fifteen minutes working on a human body.

And a backyard mechanic who has been working on cars themselves is of
no interest to them whatsoever.  Beneath their dignity I would
imagine.  And as direct result of such egotism my life has been
destroyed.  Does this guy care?  Not in the least.

I try to warn him that these drugs have serious side effects that are
non-abating and can last a lifetime.  I try to relate my own
experiences regarding this.  First I tell him that my whole ordeal
began when I developed a kidney stone as a result of being on cipro
and a medrol dose pak.  Bullshit he says, quinolones do not cause
kidney stones.   Ok, I pull up a citation that states exactly that.
Not good enough.

Let's take a moment and look at some of skeptic's statements regarding
kidney stones.  First he states that cipro induced kidney stone is
possible but there had been only ONE reported event (citing to CHOPRA
et al which he was totally unaware of till I brought this to his
attention):

"So while the very very occasional odd side effect is possible, it by
no means should be considered a standard side effect - especially that
is the only ever reported event of that phenomenon."

Then he goes on to state that cipro DOES NOT cause kidney stones.
Even though he just read a report that clearly contradicts him and had
already admitted that fact that this was possible.

"Cipro does not "cause kidney stones". That would be a very misleading
statement. There is one known case of cipro causing stones resulting
in obstruction."

Yet when we look at the package inserts for all the various forms of
cipro what do we find being reported?  FRICKIN KIDNEY STONES:

First Citation:
Ciprofloxacin Injection
Adverse Reactions in Adult Patients
RENAL/UROGENITAL: renal failure, interstitial nephritis, nephritis,
hemorrhagic cystitis, RENAL CALCULI, frequent urination, acidosis,
urethral bleeding, polyuria, urinary retention, gynecomastia,
candiduria, vaginitis, breast pain. Crystalluria, cylindruria,
hematuria and albuminuria have also been reported.

Second Citation:
Cipro:
RENAL CALCULI, serum sickness like reaction, Stevens-Johnson syndrome,
taste loss,

Third Citation:
Cipro IV
RENAL/UROGENITAL:   renal failure, interstitial nephritis, nephritis,
hemorrhagic cystitis, RENAL CALCULI, frequent urination, acidosis,
urethral bleeding, polyuria, urinary retention, gynecomastia,
candiduria, vaginitis, breast pain. Crystalluria, cylindruria,
hematuria and albuminuria have also been reported.

Fourth Citation:
And what does the material safety data sheet regarding Ciprofloxacin
Hydrochloride MSDS state?
May also affect the kidneys and cause nephritis, hematuria,
cylindruria, renal failure,
urinary retention, polyuria, urethral bleeding, RENAL CALCULI,
interstitial nephritis.

Review of the literature also points to this side effect:

First Citation:
Efficacy and safety of ciprofloxacin in the treatment of UTIs and RTIs
in patients affected by liver diseases
"In which it is reported that nephrosis followed cipro induced RENAL
CALCULI"
$32.00 (this may be yet another additional report but I was not
willing to spend  $32 to find out)

Second Citation:
Ciprofloxacin Use in Children: A Review of Recent Findings
from Pediatric Pharmacotherapy it is stated that:
"Renal disease, including interstitial nephritis and RENAL CALCULI,
has been reported in adults taking ciprofloxacin"

Third Citation:
Rev Urol. 2003 Fall; 5(4): 227-231.  PMCID: PMC1508366
Copyright (c) 2003 MedReviews, LLC
Drug-Induced Urinary Calculi
Brian R Matlaga, MD, MPH, Ojas D Shah, MD, and Dean G Assimos, MD
Department of Urology, Wake Forest University School of Medicine,
Winston-Salem, NC
"Urinary calculi can also be induced by medications when the drugs
crystallize and become the primary component of the stones. In this
case, urinary supersaturation of the agent may promote formation of
the calculi. Drugs that INDUCE CALCULI via this process include
magnesium trisilicate; CIPROFLOXACIN; sulfa medications; triamterene;
indinavir; and ephedrine, alone or in combination with guaifenesin.
When this situation occurs, discontinuation of the medication is
usually necessary."

Fourth Citation:
Within Antimicrobial Therapy in Veterinary Medicine, Fourth Edition,
it stated the following in regards to cipro:
"Crystalluria leading to obstructive uropathy has been reported in
human studies.  Other renal toxciities include acutre renal failure
associated with interstitial nerphritis."
Notice here how the authors cited to "human studies" which means MORE
THAN ONE STUDY.

The fact that quinolones can induce renal calculus has been well known
since 1983.  For example in this article this association is reported
with flumequine.  A quinolone drug:

First Citation:
Ann Biol Clin (Paris). 1983;41(4):239-49.Links
[Detection and diagnosis of drug induced lithiasis][Article in French]
Daudon M, Protat MF, Réveillaud RJ.
DRUG-INDUCED CALCULI are often mis-diagnosed because of inadequate
analysis of the urinary calculi. These stones can only be
characterized unambiguously by global physical methods like infra-red
spectrophotometry. From a series of 2,000 calculi analysed under infra-
red, we identified 22, i.e. 1.1% of cases, which contained, partly or
entirely, drug products. Ten other cases are still being studied.
Amongst the products identified we found metabolites of glafenine
(Glifanan) in 7 cases, triamterene and its derivatives (Cycloteriam)
in 7 cases, metabolites of phenazopyridine (Pyridium) in 4 cases,
sulphonamides in 2 cases : N-acetylsulphamethoxazole hydrochloride
(Bactrim) and N-acetylsulphaguanidine (Guanidan), FLUMEQUINE (Apurone)
in 1 case and calcite (Cal-Mag-Na) in 1 case. The authors estimate
that about 100,000 calculi are excreted in France each year and that
at least 1,000 of these potentially contain drugs and are not
diagnosed. Early recognition of drug induced stones is essential in
order to protect the patient from recurrences, the risks of renal
complications or, more simply, from useless therapeutic or dietetic
regimes.

Second Citation:
Kidney stone
1: J Clin Chem Clin Biochem. 1987 May;25(5):313-4.Links
IDENTIFICATION OF FLUMEQUINE IN A URINARY CALCULUS.Rincé C, Daudon M,
Moesch C, Rincé M, Leroux-Robert C.
Various analytical methods are available to help identify the presence
of drugs in urinary calculi. Using infrared spectrophotometric
analysis, nonmetabolized flumequine was identified in a protein
calculus from a patient who had taken the drug for a urinary tract
infection. Free flumequine can precipitate in an acidic environment.

Third Citation:
1: Presse Med. 1983 Oct 29;12(38):2389-92.Links
[Drug-induced urinary lithiasis][Article in French]
Reveillaud RJ, Daudon M.
All urinary calculi should be thoroughly examined. Among 2 000 calculi
analyzed by infra-red spectrophotometry, some were found to contain
rare constituants and drugs which might be held responsible for
urinary stone formation. These included glafenine, triamterene, co-
trimoxazole, sulphaguanidine, allopurinol, phenazopyridine, FLUMEQUINE
and anti-acid powders containing aluminium, calcium and magnesium
trisilicates and/or carbonates or bicarbonates.

So basically our good doctor is full of it.  More than one case of
cipro induced renal colic has been reported or we would not see this
listed as a side effect in all the package inserts.  I rather doubt
that the various manufacturers (cipro has gone generic) would include
this side effect based upon ONE report.

He also blows off the significance of crystalluria:

"The fact that there may or may not be crystalluria at an increased
incidence is cute but of no clinical consequence."

Which once again is not true. Why is this of any clinical
consequence?  Because nephrolithiasis (kidney stones) is PRECEDED by
Crystalluria, that is why. Crystal precipitation is the necessary
initial step in kidney stone formation. But once again we find that
the literature does NOT support his opinions in this matter:

First Citation:
"Crystalluria examination is an essential laboratory test for
detecting and following pathological conditions, which may induce
renal stone disease or alter kidney function due to urine crystals."
Ann Biol Clin (Paris). 2004 Jul-Aug;62(4):379-93. Links
[Clinical value of crystalluria study][Article in French]
Daudon M, Jungers P, Lacour B.
Laboratoire de Biochimie A, Groupe hospitalier Necker-enfants malades,
Paris. michel.daudon@nck.ap-hop-paris.fr

Second Citation:
Scand J Urol Nephrol. 1993;27(2):145-9.Links
Crystalluria and its possible significance. A patient-control
study.Abdel-Halim RE.
The significance of crystalluria in the diagnosis and prognosis of
urolithiasis remains a controversial subject in the current urological
literature. In this study, in addition to the standard urolithiasis
clinical and biochemical work-up, routine urine microscopy was
performed to study crystals in 1 fresh and 2 stored morning urine
samples from 140 urinary stone patients and 42 controls. Crystalluria
was more frequently detected in patients (9.3% of the fresh samples)
than in controls (2%). Storing the samples for 6 hours did not
increase the frequency percent of detected crystalluria either in
patients or controls. However, in the samples stored for 24 hours, the
frequency of crystalluria increased to 27.1% in patients and only to
12% in controls, though the pH did not change from that of the fresh
sample. In addition, while calcium oxalate crystals in patients formed
aggregates whether in fresh or 24 hour samples, those of controls did
not. This denotes a characteristic change in the physico-chemical
properties of the urine of stone formers from that of controls.
Accordingly, the study of crystalluria in patients with urolithiasis
seems to help in the proper evaluation and, maybe, treatment of the
disease.

Third Citation
Serial crystalluria determination and the risk of recurrence in
calcium stone formers
MICHEL DAUDON, CAROLE HENNEQUIN, GHAZI BOUJELBEN1, BERNARD LACOUR and
PAUL JUNGERS
Department of Biochemistry A, Necker Hosptial, Paris, France; and
Department of Nephrology, Necker Hospital, Paris, France
Serial crystalluria determination and the risk of recurrence in
calcium stone formers.
Background Urinary crystal precipitation is the necessary initial step
in kidney stone formation. However, clinical relevance of crystalluria
in the evaluation of stone formers is disputed.
Methods We serially determined crystalluria in first-voided morning
urine samples, together with full 24-hour urine biochemistry, in 181
patients with idiopathic calcium nephrolithiasis who had formed at
least one calcium-oxalate stone and were followed for at least 3 years
under our care. All stone events which occurred prior to referral,
then after entry in the study were recorded.
Results As compared with 109 patients who had no evidence of stone
recurrence during follow-up, the 72 patients who experienced  one
recurrent stone event had a lower daily urine volume (1.74  0.06 vs.
2.26  0.05 L/day (mean  SEM) (P < 0.0001), higher urine calcium and
oxalate concentrations, and daily calcium excretion, and they had more
frequent crystalluria (68% vs. 23% of urine samples) (P < 0.0001). By
multivariate Cox regression analysis, the hazard ratio for stone
recurrence was 0.32 (95% CI 0.16-0.62) for 1 L increase in daily urine
volume, 1.12 (1.09-1.24) for 1 mmol/L increase in urine calcium
concentration, 1.24 (1.02-1.50) for 0.1 mmol/L increase in urine
oxalate concentration and 27.8 (10.2-75.6) for crystalluria index.
Conclusion These data provide evidence that crystalluria, when
repeatedly found in early morning urine samples, is highly predictive
of the risk of stone recurrence in calcium stone formers. Serial
search for crystalluria, a simple and cheap method, may be proposed as
a useful tool for the monitoring of calcium stone formers, in addition
to urine biochemistry

Acute renal colic is described as one of the WORST types of pain that
a patient can suffer. Note that the pain is generally due to the
stone's presence in the ureter, and not--as is commonly believed--the
urethra and lower genitals.  So once again common sense would dictate
that if you gave a damn about your patients you would not want to
subject them to the WORSE TYPE OF PAIN THAT A PATIENT CAN SUFFER
needlessly.  Crystalluria is therefore VERY relevant and of course
clinically relevant if you engage in treating patients with kidney
stones.  Especially when your favorite drug has been shown to cause
such stones as a direct result of such Crystalluria.

So what does the good doctor do when I inform him that in humans,
ciprofloxacin crystalluria may be induced when urinary pH is greater
than 7.3?  He says"bullshit" this only applies to animals treated by
enrofloxacin and not humans.  So what exactly is enrofloxacin?  You
may have heard of is as Baytril.  Which is the veterinary form of
what?  CIPROFLOXACIN. Enrofloxacin is an analogue of the human
antibacterial ciprofloxacin.  Ciprofloxacin is a metabolic breakdown
product of enrofloxacin. Ciprofloxacin has been identified as a major
metabolite of enrofloxacin.

Enrofloxacin, its counterpart for human use ciprofloxacin, has toxic
properties in humans yet we find very little difference in its
chemical structure and cipro:

C19H22FN3O3 is the chemical structure of N-Ethylciprofloxacin
(commonly known as Enrofloxacin or Baytril)

C17H18FN3O3 is the chemical structure of Ciprofloxacin.

Most fluoroquinolones possess a nitrogen-containing cyclic substituent
on the quinolone nucleus. Although several ring structures are
possible, the 1-piperazinyl substituent and the 4-methyl-1-piperazinyl
substituent are the most common ones. The only real difference being
the subsitition of 7-(4-ethylpiperazin-1-yl) for  7-piperazin.  Hence
what we see here is Enrofloxacin uses the 4-methyl-1-piperazinyl
substituent where as cipro uses the 1-piperazinyl substituent.  Not a
whole lot of difference. In fact you will find enrofloxacin and
ciprofloxacin used interchangeably within the literature.

Baytril if you will recall has been banned. The Committee noted that
the antimicrobial activity of ciprofloxacin against the relevant human
intestinal microflora was about four times greater than that of
enrofloxacin and that consumers may be exposed to residues of
ciprofloxacin in some species of food-producing animals.
(WHO FOOD ADDITIVES SERIES 39 World Health Organization, Geneva
1997)

So basically in plain English Cipro is derived from Enrofloxacin.  So
common sense would again dictate that when we look at the possible
adrs of cipro me must also take into consideration of the adrs of
enrofloxacin.  Not to mention the fact that the entire food chain has
been contaminated with baytril and people have the potential to being
exposed to this drug everytime they sit down to eat.

Bladder stones are quite common with Enrofloxacin.  But the
manufacturers state that this is because of the pH level of the
animal's urine.  Since human pH is different this would not be an
affect seen in humans.  But once again common sense would dictate that
if the human pH were the same as an animal's pH then there is a
possibility that a bladder stone would occur.  So what does the good
doctor say?

"Cipro does not cause bladder stones. That was just a silly comment.
The pH issue is based on either in vitro lab data or animal data and
since we only have one published case of renal stones resulting from
cipro use we can't really say if acidity of the urine played any
role."

Persistent Crystalluria may contribute to formation and growth of
uroliths.  Crystalluria may solidify crystalline-matrix plugs,
resulting in urethral obstruction. Bladder stones, more correctly
called 'uroliths,' are rock-like collections of minerals that form in
the urinary bladder.  Not a whole lot different than kidney stones. As
such a person's pH is a part of the risk of developing a bladder stone
resulting from being on cipro and something that should be monitored
in a patient undergoing therapy.  States the very same thing within
the package insert and advises that the patient remain hydrated to
avoid this complication.

Therefor I have demonstrated the following:

1. Cipro has been reported to cause kidney stones.
2. Enrofloxacin has been reported to cause bladder stones
3. For all practical purposes Enrofloxacin and Ciprofloxacin are one
and the same
4. Crystalluria has been shown to be a contributory factor to both
stones
5. Cipro causes Crystalluria
6. Crystalluria is a definitive marker for the possibility of forming
either stone
7. We have one case report of cipro-induced bladder stone and kidney
stone; hence it has been confirmed that Cipro is capable of causing
both bladder stones and kidney stones due to crystalluria.
8. We have numerous post marketing reports of kidney stones being
caused by cipro
9. Within the AER database, selecting one quarter at random, showed
numerous reports of kidney stones in which cipro was cited as to being
the primary suspect drug.
10. The pain of a kidney stone is the worse pain that a patient could
possibly experience
11. The good doctor does not give a f.ck about any of this. Being
"right" is far more important to him.

As such I don't give a f.ck about the good doctor's frivolous
opinions.  Neither should his patients for that matter.  Like I said
to him before, he simply is not worth the effort that it takes to do
this kind of research to prove him wrong.  First and foremost because
he won't even bother to read it to begin with.  Secondly rather than
examine it for something of value to his patients, he will examine it
for either a typographical error, misspelling of a medical term, bitch
about the lack of full abstracts and text, or simply tell me that all
of these references are in error as they do not agree with his
preconceived notions.  But the question I continue to ask, the one
that is constantly being ignored, is where the hell are HIS citations
that prove me wrong?  I've added a couple of dozen more to my never-
ending list.  I have yet to see ONE of his.  Must be because they do
not exist.

But can you just imagine what the poor patient who is unaware of any
of this research is up against when fighting with his or her doctor
about these issues?  I can. That is why I continue to do battle with
this stubborn a.s.  If I don't who will?

No, a medical degree does not make one infallible.  I am not
infallible either.  I make mistakes just like everybody else.  And
when I am wrong I say I am wrong if you can prove that this indeed is
the case.  But I do know how to read what others a helluva lot smarter
than I have written.  And I tend to believe what they have to say more
so than this quack.  If I am wrong then you would think that he would
be kind enough to show me my errors based upon the literature rather
than being crude, rude and sarcastic.  Rather than just nit pick and
insult me why does he not simply provide his proofs?  Apparently I am
asking too much of the good doctor for he adamantly refuses to do so.

Respect what he has to say JUST because he is a doctor?  Hell no.
Earn my respect first and we will go from there.  He has failed to do
that as well so far.  I find him to be just as amusing as he finds me
to be.  Perhaps even more so.  I only have a High School Diploma.
What's his excuse for such ignorance?  Egotism? Or infatuation with a
set of 40DDs?

You are not my patient.  You are an overboard, melodramatic, quite possibly
lying internet poster.