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| I've been on Nexium for years and was getting gradually worse to the
point that I nearly always had heartburn pain. My doctor had me go to
2x/day on Nexium, and I actually felt worse.
I decided to be ruthless about my diet and excluded everything that
caused me problems (coffee, tea, fruit juice, garlic, onions, colas,
chocolate), started eating very small meals especially dinner. Also
started propping my upper body in bed with a long wedge of firm foam
(from waist to head tapers about 8"). At first, it didn't really seem
like it was helping, but after about a month, my heartburn has
disappeared (I'm still on Nexium 1x/day, though).
I don't know if it is a coincidence or not, but last week I went on an
antibiotic for an infection, and that's when my heartburn went away.
In reading a recent article in Scientific American, they mentioned that
some strains of H. Pylori actually may protect against heartburn by
regulating the acid level in the stomach. If that's the case, then the
antibiotic is probably a concidence.
I believe it took that full month for my esophagus to heal. I'm
thinking about taking the next step now--to go off Nexium completely,
though I'll probably try to taper to 20mg/day first.
| |
| John Que 2005-03-19, 1:56 pm |
|
"Grant" <Grant_196@hotmail.com> wrote in message
news:1110905055.683018.263890@l41g2000cwc.googlegroups.com...
> I've been on Nexium for years and was getting gradually worse to the
> point that I nearly always had heartburn pain. My doctor had me go to
> 2x/day on Nexium, and I actually felt worse.
>
> I decided to be ruthless about my diet and excluded everything that
> caused me problems (coffee, tea, fruit juice, garlic, onions, colas,
> chocolate), started eating very small meals especially dinner. Also
> started propping my upper body in bed with a long wedge of firm foam
> (from waist to head tapers about 8"). At first, it didn't really seem
> like it was helping, but after about a month, my heartburn has
> disappeared (I'm still on Nexium 1x/day, though).
For me, meals with lots of quickly release fats tend
to trigger heartburn. I'll also add my standard suggestion,
that you should try sleeping in a recliner with back
propped up at 30 to 40 degrees with a huge pad
placed on the rasied leg rest to prevent excess
pressure on the back of the legs. When I sleep
in the recliner I can snack at bed time.
When I do sleep on the level or in lesser
incline, I take a dose of sucralfate (a prescription item)
or OTC such as Gaviscon or a like "clone" house brand.
Sometime sleeping in recliner make the butt sore from
the pressure so a change in sleeping becomes
vital for me.
>
> I don't know if it is a coincidence or not, but last week I went on an
> antibiotic for an infection, and that's when my heartburn went away.
> In reading a recent article in Scientific American, they mentioned that
> some strains of H. Pylori actually may protect against heartburn by
> regulating the acid level in the stomach. If that's the case, then the
> antibiotic is probably a concidence.
I do not think it was a coincidence. When one suppresses their
stomach acid, the stomach can be colonized by microflora of all
sorts. This is one of the reason that PPI med use increases
the chances of pneumonia. This flora is microaspirated
into the throat and lungs and patient then finds themselves
taking an antibiotic to treat an infection of the throat, upper
respiratory region and or the lungs themselves.
>
> I believe it took that full month for my esophagus to heal. I'm
> thinking about taking the next step now--to go off Nexium completely,
> though I'll probably try to taper to 20mg/day first.
It may take two or three months.
PPI meds taken long term have a range of adverse
effects. And the more and longer, the more
likely they become apparent. They suppress
the levels of testosterone in both genders,
and they slow the breakdown of estradiol
the most potent form of estrogen. They
impair balance and seem to cause some
lasting nervous system damage, IMO.
| |
|
|
John Que wrote:
[stuff snipped]
completely,[vbcol=seagreen]
>
> It may take two or three months.
>
> PPI meds taken long term have a range of adverse
> effects. And the more and longer, the more
> likely they become apparent. They suppress
> the levels of testosterone in both genders,
> and they slow the breakdown of estradiol
> the most potent form of estrogen. They
> impair balance and seem to cause some
> lasting nervous system damage, IMO.
What evidence do you have of this? Any papers to cite?
| |
| John Que 2005-03-19, 1:56 pm |
|
"Grant" <Grant_196@hotmail.com> wrote in message
news:1111073396.468654.189200@z14g2000cwz.googlegroups.com...
>
> John Que wrote:
>
> [stuff snipped]
>
> completely,
>
> What evidence do you have of this? Any papers to cite?
Excellent question.
My comments are based in part in personal experience.
So my selection of the following citations
and studies was driven by that experience.
Even the drug studies that seem to support the
safety of members of this drug class,
suggests to me that "someone" was concerned and
I'll further suggest the drug companies MAY have only
published the small short term studies that went their
way. Next compare the case reports which support
my view. The drug studies are at
the end of this posting. Drug studies are likely the product
of drug company sponsored research and case
reports are likely the product of actual medical practitioners.
Who has more vested interest or bias?
_______________________________________
The cut and paste begins with a few comments of my
own.
_______________________________________
PPI meds are listed as drugs that can cause
gynecomastia in men.
1: Med Clin (Barc). 2001 Mar 24;116(11):437-8.
[Gynecomastia associated with the simultaneous use of cisapride and
lansoprazole]
[Article in Spanish]
Cuervo Martin JR, Garcia Ortega P,
Sanchez Sanchez A,
Carvajal Garcia-Pando A.
Publication Types:
Case Reports
Letter
PMID: 11333695 [PubMed - indexed for MEDLINE]
2: Med Clin (Barc). 2000 Mar 18;114(10):397.
[Lansoprazole-induced gynecomastia]
[Article in Spanish]
Comas A, Salgueiro E, Hidalgo A.
Publication Types:
Case Reports
Letter
PMID: 10786353 [PubMed - indexed for MEDLINE]
1: Biol Pharm Bull. 2003 May;26(5):695-700.
Studies on the interactions between drug and estrogen. II.
On the inhibitory effect of 29 drugs reported to
induce gynecomastia on the oxidation of estradiol
at C-2 or C-17.
Satoh T, Munakata H, Fujita K, Itoh S,
Itoh S, Kamataki T, Yoshizawa I.
Hokkaido college of Pharmacy,
Otaru, Hokkaido,
Japan.
A study was investigated on the inhibitory effect of 29
drugs that have been reported to induce gynecomastia
on the 2-hydroxylation of estradiol (E2) by
recombinant P450 CYP3A4 and on the 17-oxidation
of E2 by hepatic microsomal type II 17beta-hydroxysteroid
dehydrogenase (17beta-HSD) of human male. The IC(50)
values were determined for each drug relative to
the 2-hydroxylation of E2 (catalytic activity:
1.54 nmol/nmol P450/min), and the inhibition constants
(K(i)) were determined for 13 drugs of which IC(50) values
were 100 microM or less. Ketoconazole exhibited
the lowest inhibitory concentration, and IC(50) and
K(i) values of 0.007 and 0.01 microM, respectively,
were obtained. The IC(50) and K(i) values for each
of the 12 remaining drugs were as follows: cyclosporin
A (IC(50): 0.064, K(i): 0.30), nicardipine
hydrochloride (0.55, 0.29), tacrolimus (0.64, 0.88),
mandipine hydrochloride (3.9, 2.6), nisoldipine (10,
3.3), verapamil hydrochloride (10, 20), domperidone (13, 7.2),
haloperidol (14, 55), nitrendipine (14, 2.5),
chlormadinone acetate (16, 10), flutamide (30, 39)
and omeprazole (49, 47). With the exception of
cyclosporin A that exhibited a competitive inhibition,
the inhibition mechanisms of these drugs were all
non-competitive. Next, the percentage inhibition
of the above 29 drugs relative to the 17-oxidation
of E2 (catalytic activity: 0.47 nmol/mg protein/min) was
investigated at the approximate therapeutic concentration
(1 microM) and at the non-clinical overdose concentration
(100 microM). Although none of the drugs
investigated exhibited inhibitory effects at a concentration
of 1 microM, spironolactone and ketoconazole at
100 microM demonstrated percentage
inhibitions of 96% and 77%, respectively.
When the K(i) values were determined
for these two drugs, the former had a K(i) value
of 2.4 microM and the latter,
41 microM, and both of their inhibition mechanisms
were non-competitive. On the basis of the above
results, a total of 14 drugs consisting of the
above 13 drugs plus spironolactone were
found to inhibit the 2-hydroxylation or 17-oxidation of
E2 in the liver, and this is presumed to act as a trigger
that causes as increase in the estradiol pool,
followed by induction of gynecomastia.
_____________________________________
Note that the full article is available from J Stage.
_____________________________________
_____________________________________
This next one can kill in short order
_______________________________
1: JAMA. 2004 Oct 27;292(16):1955-60.
Comment in:
JAMA. 2004 Oct 27;292(16):2012-3.
JAMA. 2005 Feb 16;293(7):795-6; author reply 796.
Risk of community-acquired pneumonia
and use of gastric acid-suppressive drugs.
Laheij RJ, Sturkenboom MC, Hassing RJ,
Dieleman J, Stricker BH, Jansen JB.
Department of Gastroenterology,
University Medical Center St. Radboud, Nijmegen,
The Netherlands. R.Laheij@mdl.umcn.nl
CONTEXT: Reduction of gastric acid secretion by
acid-suppressive therapy allows
pathogen colonization from the upper
gastrointestinal tract. The bacteria and
viruses in the contaminated stomach
have been identified as species from the
oral cavity.
OBJECTIVE: To examine
the association between the use of
acid-suppressive drugs and occurrence
of community-acquired pneumonia.
DESIGN, SETTING, AND PARTICIPANTS:
Incident acid-suppressive drug users with at least 1
year of valid database history were identified from
the Integrated Primary Care
Information database between
January 1, 1995, and December 31, 2002.
Incidence rates for pneumonia were
calculated for unexposed and exposed
individuals. To
reduce confounding by indication,
a case-control analysis was conducted
nested in a cohort of incident users
of acid-suppressive drugs. Cases were all
individuals with incident pneumonia
during or after stopping use of
acid-suppressive drugs. Up to 10
controls were matched to each case for
practice, year of birth, sex, and index date.
Conditional logistic regression
was used to compare the risk of
community-acquired pneumonia between use of
proton pump inhibitors (PPIs) and H2-receptor antagonists.
MAIN OUTCOME MEASURE:
Community-acquired pneumonia defined as certain
(proven by radiography or sputum culture) or probable
(clinical symptoms consistent with pneumonia).
RESULTS:
The study population comprised 364,683
individuals who developed 5551 first
occurrences of pneumonia during follow-up.
The incidence rates of pneumonia in
non-acid-suppressive drug users and
acid-suppressive drug users were 0.6 and
2.45 per 100 person-years, respectively.
The adjusted relative risk for
pneumonia among persons currently using
PPIs compared with those who stopped
using PPIs was 1.89 (95% confidence interval,
1.36-2.62). Current users of H2-receptor
antagonists had a 1.63-fold increased risk of
pneumonia (95% confidence interval, 1.07-2.48)
compared with those who stopped use. For current
PPI users, a significant positive dose-response
relationship was observed. For
H2-receptor antagonist users, the variation in
dose was restricted.
CONCLUSION:
Current use of gastric acid-suppressive
therapy was associated with an increased
risk of community-acquired pneumonia.
PMID: 15507580 [PubMed - indexed for MEDLINE]
__________________________________________________________
What happens in rats.
__________________________________________________________
: Toxicol Appl Pharmacol. 2003 Oct 15;192(2):154-63.
Lansoprazole increases testosterone metabolism
and clearance in male Sprague-Dawley rats:
implications for Leydig cell carcinogenesis.
Coulson M, Gibson GG, Plant N,
Hammond T, Graham M.
Molecular Toxicology Group,
School of Biomedical & Life Sciences, university of
Surrey, Guildford GU2 7XH, UK.
Leydig cell tumours (LCTs) are frequently observed during rodent
carcinogenicitystudies, however, the
significance of this effect to humans remains a matter
of debate. Many chemicals that produce
LCTs also induce hepatic cytochromes
P450(CYPs), but it is unknown whether
these two phenomena are causally related.
Our aim was to investigate the
existence of a liver-testis axis wherein
microsomal enzyme inducers enhance
testosterone metabolic clearance, resulting in a
drop in circulating hormone levels
and a consequent hypertrophic response from the
hypothalamic-pituitary-testis axis.
Lansoprazole was selected as the model
compound as it induces hepatic
CYPs and produces LCTs in rats. Male
Sprague-Dawley rats were dosed
with lansoprazole (150 mg/kg/day) or vehicle
for 14 days. Lansoprazole treatment
produced effects on the liver consistent
with an enhanced metabolic capacity,
including significant increases in relative
liverweights, total microsomal
CYP content, individual CYP protein levels, and
enhanced CYP-dependent testosterone
metabolism in vitro. Following
intravenous administration of [14C]testosterone,
lansoprazole-treated rats exhibited a
significantly smaller area under the curve and
significantly higher plasma
clearance. Significant reductions in
plasma and testicular testosterone
levels were observed, confirming the
ability of this compound to perturb androgen
homeostasis. No significant changes in
plasma LH, FSH, or prolactin levels
were detected under our experimental
conditions. Lansoprazole treatment exerted
no marked effects on testicular
testosterone metabolism. In summary,
lansoprazole treatment induced hepatic
CYP-dependent testosterone metabolism in vitro and
enhanced plasma clearance of radiolabelled
testosterone in vivo. These
effects may contribute to depletion
of circulating testosterone levels and hence
play a role in the mode of LCT induction
in lansoprazole-treated rats.
PMID: 14550749 [PubMed - indexed for MEDLINE]
________________________________________________
Not all humans are the same
following women has reduced testosteronedue to the
drug.
________________________________________________
1: Am J Med Sci. 2004 May;327(5):289-93.
Induction of testosterone metabolism
by esomeprazole in a CYP2C19*2
heterozygote.
Rosenshein B, Flockhart DA, Ho H.
Division of Clinical Pharmacology,
Department of Medicine, Indiana University
School of Medicine, Indianapolis,
Indiana 46202-2879, USA. heho@iupui.edu
The authors describe a 42-year-old woman with previously normal sexual
function
who gradually developed loss of libido during treatment with esomeprazole.
While
taking esomeprazole, the patient's loss of libido improved with oral
testosterone supplementation and
deteriorated after testosterone withdrawal.
There was steady improvement
in both sexual function and serum free
testosterone concentration after
discontinuation of esomeprazole. Due to the temporal
relationship between esomeprazole
intake and sexual dysfunction, the authors
postulate that esomeprazole causes
induction of testosterone metabolism. The
authors believe this to be the first
case of female sexual dysfunction
associated with esomeprazole
described in the literature. They discuss a
number of possible mechanisms for this effect.
_________________________________________
GYNECOMASTIA
Drugs that grow breasts on men
_________________________________________
1: Ann Med Interne (Paris). 2000 Feb;151(1):10-7.
[Drug-induced gynecomastia]
[Article in French]
Hugues FC, Gourlot C, Le Jeunne C.
Service de Medecine Interne II,
Hopital Laennec, Faculte de Medecine
Necker-Enfants Malades, Paris.
Drugs are a very common cause of gynecomastia and should always be
entertained as the possible causal agent
of such a condition. This drug side-effect is
due to an impaired balance in the
serum estrogen/serum androgen ratio, whatever
the mechanism, or a rise in
prolactin level. Sex hormones, antiandrogens, are
frequently involved as well as spironolactone, cimetidine, verapamil and
cancer chemotherapy (especially alkylating agents).
Diazepam, tricyclic
antidepressants, neuroleptics, calcium channel blockers, captopril,
digitalis glycosides, omeprazole,
some antibiotics and growth hormone are all
possibly, but less often, the
responsible agent. Criteria of the French method for
determining drug causality are discussed.
Publication Types:
Review
Review, Tutorial
PMID: 10761558 [PubMed - indexed for MEDLINE]
2: Am J Gastroenterol. 1995 Jun;90(6):1028-9.
Gynecomastia and sexual disorders
after the administration of omeprazole.
Carvajal A, Martin Arias LH.
Publication Types:
Letter
PMID: 7771409 [PubMed - indexed for MEDLINE]
3: Ann Med Interne (Paris). 1995;146(3):195.
[Gynecomastia and treatment with omeprazole]
[Article in French]
Durand JM, Cretel E, Kaplanski G, Retornaz F, Soubeyrand J.
Publication Types:
Case Reports
Letter
PMID: 7653926 [PubMed - indexed for MEDLINE]
4: Med Clin (Barc). 1994 Mar 26;102(11):435.
[Gynecomastia induced by omeprazole]
[Article in Spanish]
Pedrosa M, Sancho A, Benavent J, Casajuana J.
Publication Types:
Case Reports
Letter
PMID: 8183005 [PubMed - indexed for MEDLINE]
______________________________________________
______________________________________________
While the following report sounds postive for omprazole
recall during early 1990's PPI meds were generally
given for only several months especially in the UK.
5: BMJ. 1994 Feb 19;308(6927):503-6.
Erratum in:
BMJ 1994 Mar 26;308(6932):819.
Risk of gynaecomastia associated with cimetidine,
omeprazole, and other antiulcer drugs.
Garcia Rodriguez LA, Jick H.
Boston Collaborative Drug Surveillance Program, Boston university Medical
Center, Lexington, MA 02173-5207.
OBJECTIVE--To study the risk of gynaecomastia associated with cimetidine,
misoprostol, omeprazole and ranitidine.
DESIGN--Open cohort study with
nested case-control analysis.
SETTING--General practices in United Kingdom that had
computerised offices, 1989-92.
SUBJECTS--81,535 men aged 25-84 years who
received at least one prescription for cimetidine, misoprostol, omeprazole,
or ranitidine during the study period.
MAIN OUTCOME MEASURES--
New occurrences
of idiopathic gynaecomastia diagnosed
by general practitioner.
RESULTS--
The relative risk of gynaecomastia for
current users of cimetidine compared with
non-users was 7.2 (95% confidence interval 4.5 to 11.3). Relative risks for
misoprostol, omeprazole, and ranitidine were 2.0 (0.1 to 10.7), 0.6 (0.1 to
3.3), and 1.5 (0.8 to 2.6), respectively. Current users of cimetidine on a
daily dose > or = 1000 mg had
more than 40 times the risk of developing
gynaecomastia than non-users.
The period of highest risk was seven to 12 months after
starting cimetidine treatment.
Spironolactone (relative risk 9.3 (3.3 to 26.1)) and
verapamil (9.7 (2.6 to 36.0)) were associated with a relative risk of
gynaecomastia comparable to one for cimetidine.
CONCLUSIONS--
Use of cimetidine, but not the three other
antiulcer drugs, is associated with a substantially
greater risk of gynaecomastia in men. A strong dose-response relation was
present among cimetidine users.
PMID: 8136667 [PubMed - indexed for MEDLINE]
6: BMJ. 1992 Aug 22;305(6851):451-2.
Endocrine adverse effects of omeprazole.
Lindquist M, Edwards IR.
WHO Collaborating Centre for International Drug Monitoring, Uppsala, Sweden.
PMID: 1392958 [PubMed - indexed for MEDLINE]
7: Lancet. 1991 Nov 2;338(8775):1153.
Painful gynaecomastia during omeprazole therapy.
Convens C, Verhelst J, Mahler C.
Publication Types:
Case Reports
Letter
PMID: 1682578 [PubMed - indexed for MEDLINE]
8: N Engl J Med. 1991 Feb 28;324(9):635.
Gynecomastia during omeprazole therapy.
Santucci L, Farroni F, Fiorucci S, Morelli A.
Publication Types:
Case Reports
Letter
PMID: 1992328 [PubMed - indexed for MEDLINE]
______________________________________________
______________________________________________
______________________________________________
Pantoprazole-induced acute interstitial nephritis
I. Moore1, J.A. Sayer2, A. Nayar3, S. Ahmed1, J.S. Tapson1
1Department of Nephrology, Freeman Hospital,
Newcastle upon Tyne - United Kingdom
2School of Clinical Medical Sciences,
University of Newcastle upon Tyne - United Kingdom
3Department of Histopathology,
Royal Victoria Infirmary,
Newcastle upon Tyne - United Kingdom
ABSTRACT: Pantoprazole is a proton-pump inhibitor (PPI)
that is commonly prescribed for the treatment of
gastroesophageal reflux-related disorders. There are
many documented side effects of PPIs. Here we
report a case of acute interstitial nephritis, which
developed after 6 weeks of treatment with pantoprazole.
A 23-year-old man presented with acute renal failure
requiring renal replacement therapy. Acute interstitial
nephritis was diagnosed by renal biopsy and was
successfully treated with corticosteroids and
withdrawal of pantoprazole. Drug-induced
acute interstitial nephritis can occur with PPIs
such as pantoprazole and vigilance needs to be maintained.
___________________________________________________
___________________________________________________
___________________________________________________
THE FOLLOWING STUDIES
SHOWED NO ADVERSE EFFECTS.
But note the studies are VERY short term and the number
person studied is very small.
Aliment Pharmacol Ther. 1994 Oct;8(5):549-54.
Effects of pantoprazole on endocrine function in healthy male volunteers.
Dammann HG, Bethke T, Burkhardt F, Wolf N, Khalil H, Luehmann R.
Krankenhaus Bethanien, Hamburg, Germany.
METHOD: In a randomized, double-blind, two-period crossover study,
pantoprazole 40 mg or placebo were given orally
to 12 male volunteers for 2 weeks each.
There was a wash-out period of at least
1 week between the two treatment periods.
The effects of pantoprazole or placebo on
cortisol and testosterone (primary
criteria), and tri-iodothyronine,
thyroxine, thyroid-stimulating hormone,
thyronine-binding protein, parathyroid
hormone, insulin, glucagon, renin,
aldosterone, follicle-stimulating hormone,
luteotrophic hormone, prolactin
and somatotrophic hormone were compared.
In addition, intragastric 24-h pH, 24-h
H(+)-activity, and volume of nocturnal
gastric juice were determined by
gastric aspiration technique.
RESULTS:
Pantoprazole did not influence plasma levels
of testosterone, circadian cortisol concentrations
or plasma cortisol levels after exogenous
adrenocorticotropic hormone stimulation, as compared to
placebo (P > 0.05, Koch's test). Furthermore,
there were no clinically relevant changes
with any of the other endocrine parameters.
Pantoprazole significantly increased
the median 24-h pH (group median
4.3 vs. 1.8; P < 0.001) and decreased 24-h
H(+)-activity (4.0 vs. 22.6 mmol/L; P < 0.001).
The volume of nocturnal
gastric juice did not significantly differ between the two treatments.
Pantoprazole was well tolerated and the
frequency of adverse events was similar to placebo.
No drug-related changes in laboratory values were observed.
CONCLUSION:
Pantoprazole did not influence endocrine function in healthy male volunteers
during short-term treatment.
Publication Types:
Clinical Trial
Randomized Controlled Trial
PMID: 7865648 [PubMed - indexed for MEDLINE]
___________________________________________
___________________________________________
They called three weeks of the following med "chronic".
Nonsense, chronic is the many months and years
real patient use these drug for.
: Eur J Gastroenterol Hepatol. 1995 Mar;7(3):211-3.
Chronic oral administration of lansoprazole does not affect the hypothalamic
pituitary gonadal axis in healthy young men.
Gaetani M, De Giorgio R, Buratti P, Pasquali R, Capelli M, Stanghellini V,
Corinaldesi R.
Institute of Clinical Pharmacology and Therapy, St Orsola Hospital,
University of Bologna, Italy.
OBJECTIVE: To assess the effects of chronic oral administration of standard
doses of lansoprazole on the luteinizing hormone pulsatile pattern and on
follicle stimulating hormone (FSH) and testosterone levels in young men.
DESIGN AND METHODS:
Eleven healthy volunteers were studied on three separate
occasions, before and after two 3-week periods
of treatment with lansoprazole (30 mg
every morning) or a placebo, according to a randomized, double-blind,
double-dummy, cross-over design. On each study day,
blood samples were taken every 15 min
for 8 h. The pulsatile pattern of luteinizing hormone,
mean concentrations ofFSH
and total testosterone plasma levels were
determined for each patient using
specific radioimmunoassays.
RESULTS:
Lansoprazole did not significantly
affect mean plasma levels, the pulsatile pattern
of luteinizing hormone, or mean
plasma concentrations of FSH and testosterone
compared with the placebo.
CONCLUSIONS:
This study indicates that chronic oral administration
of standard doses of lansoprazole
does not affect the concentrations of gonadal hypothalamic
pituitary or sex steroid hormones.
Publication Types:
Clinical Trial
Randomized Controlled Trial
PMID: 7743301 [PubMed - indexed for MEDLINE]
Int J Clin Pharmacol Ther. 1997 Jan;35(1):14-8.
Urinary 6 beta-hydroxycortisol and
D-glucaric acid excretion rates are not
affected by lansoprazole treatment.
Rost KL, Mansmann U, Roots I.
Institute of Clinical Pharmacology,
Universitatsklinikum Benjamin Franklin,
Free university of Berlin, Germany.
Lansoprazole has been shown to induce
cytochrome P450 1A (CYP1A) and CYP3A
enzymes in human hepatocytes in vitro.
In this study, urinary excretion of 6
beta-hydroxycortisol (6 beta-OHF) and
D-glucaric acid (D-GA) were used to
investigate the potential enzyme-inducing
property of lansoprazole in vivo.
Twenty-four healthy female volunteers
(aged 19-35 years), who were taking
oral contraceptives containing 0.03 mg
ethinylestradiol and 0.15 mg
levonorgestrel, were randomized in a
cross-over design for the treatment with either 60 mg
lansoprazole or placebo once daily
during 2 subsequent menstrual cycles.
Urinary excretion rates of 6 beta-OHF
and D-GA were measured at days 14 and 21 of
the menstrual cycles. Median pretreatment
urinary excretion of 6 beta-OHF (212
and 218 micrograms/d, n = 24) and
D-GA (20.1 and 32.7 mumol/d) did not
significantly differ. Upon treatment median
excretion of 6 beta-OHF was 255 and 241
micrograms/d (n = 23), and that of D-GA
was 25.5 and 33.8 mumol/d,
respectively. Thus, the relatively high dose
of 60 mg/d lansoprazole failed to
statistically significantly alter urinary
excretion of 6 beta-OHF and D-GA, indicating
that therapeutic doses of lansoprazole
might not exhibit a phenobarbital-like
induction in vivo.
Pharmacology. 1993 Jul;47(1):8-12.
Omeprazole fails to alter the cytochrome
P450-dependent 2-hydroxylation of
estradiol in male volunteers.
Galbraith RA, Michnovicz JJ.
Rockefeller university Hospital, New York, NY 10021.
Omeprazole, a proton pump inhibitor, is used in the treatment of
gastrointestinal diseases associated with hyperacidity. It binds to, and
inhibits, some of the activities of hepatic cytochrome P450 resulting in
increased half-lives of certain pharmacologic and endogenous compounds. It
may also increase the activity of
cytochrome P450 under certain conditions.
Oxidative metabolism of endogenous estrogens, particularly the
2-hydroxylation pathway, is P450-dependent,
and is highly sensitive to a variety of dietary and
pharmacologic agents. We therefore studied the
extent of estradiol 2-hydroxylation in
7 normal male volunteers before and during oral treatment
with omeprazole 20 mg twice daily. Using a specific in vivo radiometric
assay, the mean extent (+/- SEM) of estradiol
2-hydroxylation was found to be
unchanged before and after omeprazole treatment
(27.3 +/- 3.0 vs. 27.5 +/- 3.4%,
respectively). The excretion of the endogenous urinary estrogen metabolites,
2-hydroxyestrone, estriol, and estrone was also unaltered by omeprazole.
These results show that omeprazole,
in contradistinction to other medications used
in the treatment of peptic ulcer disease, is without effect on estradiol
metabolism in men.
PMID: 8337235 [PubMed - indexed for MEDLINE]
These drugs (PPI meds) fogged my thinking, impaired my balance,
cause abdominal tenderness, suppressed libido,
and at higher doses stopped noctural erections.
I'll even suggest these drugs may increase the chances
of prostate and breast cancer. Understand I
claim no direct evidence; rather this just my
hypothesis. It will be decades before the
medical community will know for sure.
JQ
"Burn baby burn" (1960's ghetto rioter)
Now do you have any thoughts?
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| Suddenly, without warning, John Que exclaimed (3/18/2005 2:17 AM):
> "Grant" <Grant_196@hotmail.com> wrote in message
> news:1111073396.468654.189200@z14g2000cwz.googlegroups.com...
>
[vbcol=seagreen]
>
> These drugs (PPI meds) fogged my thinking, impaired my balance,
> cause abdominal tenderness, suppressed libido,
> and at higher doses stopped noctural erections.
>
> I'll even suggest these drugs may increase the chances
> of prostate and breast cancer. Understand I
> claim no direct evidence; rather this just my
> hypothesis. It will be decades before the
> medical community will know for sure.
>
> JQ
>
> "Burn baby burn" (1960's ghetto rioter)
>
> Now do you have any thoughts?
>
Admittedly, I haven't read any word, but I don't see any neurological
effects in any of these studies.
Fogged thinking can be caused my many things - I had the problem when I
had an issue with candidasis (yeast syndrome), and still can have this
problem if I "overdose" on simple carbs. I also had the problem with
higher doses of Atenolol. I've had impaired balance since an inner ear
infection as a teen; I get short attacks of vertigo, and sudden, short
losses of balance. Also, I had Restless Leg Syndrome, which I finally
traced to Aspartame (I have doubts that the FDA should have approved it)
Had these well before starting on PPIs. Couldn't tell you about
erections though, I lack that equipment 
But there are many, many drugs which can reduce libido. I think my
brand of lanparazole might even have it listed in possible side effects.
In short, I'd like to suggest that either you're an unusual/rare case
(quite possible), or you might want to consider looking elsewhere for
the cause of your problems. Have you discussed them with your doctor?
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Suddenly, without warning, jmc exclaimed (3/18/2005 6:33 AM):
> Suddenly, without warning, John Que exclaimed (3/18/2005 2:17 AM):
>
>
>
> Admittedly, I haven't read any word, but I don't see any neurological
> effects in any of these studies.
>
> Fogged thinking can be caused my many things - I had the problem when I
> had an issue with candidasis (yeast syndrome), and still can have this
> problem if I "overdose" on simple carbs. I also had the problem with
> higher doses of Atenolol. I've had impaired balance since an inner ear
> infection as a teen; I get short attacks of vertigo, and sudden, short
> losses of balance. Also, I had Restless Leg Syndrome, which I finally
> traced to Aspartame (I have doubts that the FDA should have approved it)
> Had these well before starting on PPIs. Couldn't tell you about
> erections though, I lack that equipment
>
> But there are many, many drugs which can reduce libido. I think my
> brand of lanparazole might even have it listed in possible side effects.
>
> In short, I'd like to suggest that either you're an unusual/rare case
> (quite possible), or you might want to consider looking elsewhere for
> the cause of your problems. Have you discussed them with your doctor?
>
I've found the insert for my PPI, Zoton (lanparazole). It specifically
states, " As with other proton pump inhibitors, men taking Zoton may
experience breast swelling or impotence"
To cover your other symptoms, there is a whole list of milder side
effects, including dizziness, vertigo, confusion, and many others. So
it does appear you are right, if 'confusion' covers your brain fog.
So, almost everything you mention is a known, listed possible side
effect. I'm in the UK just now. Does the US insert not state this? If
it does, then I'm not sure what your point is. The drug companies
aren't hiding these side effects, they're right on the inserts.
jmc
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| John Que 2005-03-19, 1:56 pm |
|
"jmc" <NOnewsgroupsSPAM@NOjodiBODY.HOMEus> wrote in message
news:39vcdpF677vk3U1@individual.net...
> Suddenly, without warning, jmc exclaimed (3/18/2005 6:33 AM):
> I've found the insert for my PPI, Zoton (lanparazole). It specifically
> states, " As with other proton pump inhibitors, men taking Zoton may
> experience breast swelling or impotence"
>
> To cover your other symptoms, there is a whole list of milder side
> effects, including dizziness, vertigo, confusion, and many others. So
> it does appear you are right, if 'confusion' covers your brain fog.
>
> So, almost everything you mention is a known, listed possible side
> effect. I'm in the UK just now. Does the US insert not state this? If
> it does, then I'm not sure what your point is. The drug companies
> aren't hiding these side effects, they're right on the inserts.
>
> jmc
Valid point.
I will say many of the medical materials I
seen don't say a peep about adverse effects.
Nor has any medical professional
ever even mentioned to the possiblity to me.
Instead, I found myself telling them.
I was going to get one my drug book out
and list the adverse effects. I noticed
one had percentages on the some
adverse effects.
I'd call vertigo and confusion, adverse
effects on some part of the nervous system.
As I would the twitching the 40mg Prilosec
caused. It quit when I quit the drug though
the face still does not quite feel "right" were
the twitch was.
The brain fog can also be the result
of PPI drug induced andropause.
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