Posted by Larry Hoover on July 29, 2007, at 12:00:52
In reply to Re: Should all drugs be generic? » Larry Hoover, posted by Squiggles on July 29, 2007, at 10:49:58
> > I presented empirical evidence of kidney function disturbance by lithium, which took me less than 10 seconds to find. It is irrelevant that others exclude data to reach contrary conclusions.
> >
> > Moreover, I showed one of many kidney disturbances from lithium intake. I've already shown your supposition to be false.
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> REPLY:
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> Is it "disturbance" or is it "toxicity" or both--
> you seem to be wavering.I am not wavering in the least.
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> http://www.emedicine.com/med/topic1313.htm
>
> "The role of lithium in the production of acute renal failure is well accepted...."Let's stop right there. For a moment, and let that sink in. Your reference, right?
As I stated in the quoted portion of my prior post, above, "It is irrelevant that others exclude data to reach contrary conclusions."
The segment of the article you reference was cherry-picked, and it thus is out of context. It is common in the introduction to a review article to lay out the pros and cons of an argument. You have quoted only one side of the story.
If you were to only review the referenced articles for this one piece (rather than the entire body of medical literature), this, in part, is what you would find:
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=3314489
Am J Kidney Dis. 1987 Nov;10(5):329-45.
Prevalence, pathogenesis, and treatment of renal dysfunction associated with chronic lithium therapy.
Boton R, Gaviria M, Batlle DC.
Department of Psychiatry, University of Illinois at Chicago."...The most prevalent renal effect of lithium is impairment of concentrating ability, which we estimated to be present in at least 54% of 1,105 unselected patients on chronic lithium therapy. This defect translated into overt polyuria in only 19% of unselected cases. A renal lesion confined to the collecting tubule has been described in humans who have taken lithium for short periods of time. This lesion may represent the collecting tubule's response to the intracellular accumulation of lithium, which interferes with cAMP formation and results in an early and probably reversible inhibition of antidiuretic hormone (ADH)-mediated water transport. However, long-term lithium therapy may induce a progressive and partly irreversible defect in concentrating ability...."
So, in 1987, they presume a partly irreversible defect, but by 2005, that changes to "CONCLUSION: ...Long-term treatment with lithium seemed to result in irreversible NDI."
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=15806465
Am J Kidney Dis. 2005 Apr;45(4):626-37.
Causes of reversible nephrogenic diabetes insipidus: a systematic review.
Garofeanu CG, Weir M, Rosas-Arellano MP, Henson G, Garg AX, Clark WF.
Division of Nephrology, Walkerton Health Study, London Health Science Centre, Westminster Campus, Canada.BACKGROUND: In nephrogenic diabetes insipidus (NDI), the kidney is unable to produce concentrated urine because of the insensitivity of the distal nephron to antidiuretic hormone (arginine vasopressin). In settings in which fluid intake cannot be maintained, this may result in severe dehydration and electrolyte imbalances. The risk for conversion of reversible to irreversible NDI seems to be a potential complication. This review summarizes the reversible causes of acquired NDI to facilitate earlier recognition and more effective treatment by clinicians. METHODS: Two reviewers independently searched MEDLINE, Experta Medica (EMBASE), and ISI bibliographic databases. Human studies that described NDI caused by drugs, substances, or metabolic disturbances were included. To evaluate the causal role of the risk factor, data were abstracted according to Koch's postulates. RESULTS: One hundred fifty-five studies published between 1957 and March 2004 described 30 risk factors. Of 155 studies, 58 studies provided a "definite" diagnosis of NDI; 83 studies, a "probable" diagnosis; and 14 studies, a "possible" diagnosis. Nine factors were considered "definite" causes of NDI; 15 factors, "probable" causes; and 6 factors, "possible" causes. The most reported risk factors were lithium (84 studies), antibiotics (16 studies), antifungals (11 studies), antineoplastic agents (9 studies), antivirals (8 studies), and metabolic disturbances (8 studies). Duration of NDI reversal, as well as conversion to irreversible symptoms, seemed to depend on the duration of exposure. CONCLUSION: Most risk factors for reversible NDI were medications, and their identification and removal resulted in resolution of the condition. Long-term treatment with lithium seemed to result in irreversible NDI.
Nota bene that last sentence. Remember, this was your reference. I didn't even have to show you the ones I found.
And about thyrotoxicosis, there is a significant increase over baseline in lithium-exposed patients:
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=11678833
Clin Endocrinol (Oxf). 2001 Oct;55(4):501-8.
Association between lithium use and thyrotoxicosis caused by silent thyroiditis.
Miller KK, Daniels GH.
Neuroendocrine Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.OBJECTIVE: To determine the incidence of silent thyroiditis in lithium users and characterize lithium-associated thyrotoxicosis. DESIGN: Retrospective record review. PATIENTS: 400 consecutive patients (300 with Graves' disease and 100 with silent thyroiditis) who underwent radioiodine scanning of the thyroid. MEASUREMENTS: Odds of lithium exposure. RESULTS: The odds of lithium exposure were increased 4.7-fold in patients with silent thyroiditis compared with those with Graves' disease (95% CI: 1.3, 17). Lithium-associated silent thyroiditis occurred with an incidence rate of approximately 1.3 cases per 1000 person-years, and lithium-associated thyrotoxicosis occurred with an incidence rate of approximately 2.7 cases per 1000 person-years, higher than the reported incidence rates of silent thyroiditis (< 0.03-0.28 cases per 1000 person-years) and of thyrotoxicosis (0.8-1.2 cases per 1000 person-years) in the general population. CONCLUSION: Thyrotoxicosis caused by silent thyroiditis might be associated with lithium use.
The thing is, Squiggles, a valid theory must account for all empirical findings. I'm trying to account for the evidence that is available for consideration. The Garofeanu et al study is a meta-analysis. That's not cherry-picking. Although the title of the review is about reversible NDI, they yet conclude that lithium causes irreversible NDI.Lar
poster:Larry Hoover
thread:772306
URL: http://www.dr-bob.org/babble/20070719/msgs/772704.html