Relation Between Regular Intake of Phenacetin-Containing Analgesics and Laboratory Evidence for Urorenal Disorders in a Working Female Population of Switzerland

Dubach, U. C.; Rosner, Bernard; Muller, A.; Levy, Paul S.; Baumeler, H. R.; Peier, Andrea; Ehrensperger, T.

doi:10.1016/s0140-6736(75)91557-3

Cited by 40 publications

(7 citation statements)

References 13 publications

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“…Table I summarizes all statements from the original publications referring to caffeine in these studies [31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46][47][48]. Among the nine epidemiological studies, five do not even mention caffeine at all, only three provide data (Elseviers [2], Pommer [4] and Sandler et al [6]) and a fourth addresses possible abuse (Dubach [3]).…”

Section: Resultsmentioning

confidence: 99%

Caffeine as a promoter of analgesic‐associated nephropathy – where is the evidence?

Fox

Siebers²

2003

Fundamemntal Clinical Pharma

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Individual groups of nephrologists - in their responsibility for their patients - initiated a most controversial discussion whether or not caffeine - coformulated to analgesics - might initiate or sustain analgesic overdosing. The original sources (data) of such suspicion have got lost during the debate of the last two decades. Therefore, it seemed to be appropriate to investigate the original data background and the reasons why nephrologists started to suspect caffeine as a stimulant of analgesic overdosing by employing a systematic and exhaustive review of primary nephrological publications. Their selection followed a precise selection plan, including all epidemiological studies on analgesic-associated nephropathy, the original papers of all groups having been involved in those studies, further originals from the mainly involved countries (academically, politically), and any literature thereof cited as a proof. The following results emerged from the investigation: (i) The epidemiological studies warranted no conclusion about a role of caffeine in prompting excessive analgesic use. (ii) The identified groups of nephrologists provided not substantial data to advocate the said suspicion, except for the observation of a preferential choice of phenacetin-containing combinations, especially powder preparations. (iii) Only two cited original data sources revealed drug-seeking behaviour with phenacetin-containing preparations which subsided, after phenacetin was banned from the respective markets. Conclusively, it appears that there is no substantial data to support a pivotal role of caffeine in initiating or sustaining analgesic overdosing. However, there is strong data that phenacetin, by its psychotropic properties, may have caused drug-seeking behaviour and thus led to analgesic overdosing. This conclusion is convincingly supported by thorough pharmacokinetic investigations. Note: All caffeine-related statements within the reviewed literature have been collected in tables (referred to as Table SX) which are provided in full text for check on the following website: http://www.blackwellpublishing.com/products/journals/suppmat/FCP/FCP174/FCP174sm.htm

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Section: Resultsmentioning

confidence: 99%

Caffeine as a promoter of analgesic‐associated nephropathy – where is the evidence?

Fox

Siebers²

2003

Fundamemntal Clinical Pharma

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“…Inadequate prostaglandin production plus NAPQI adducts in the kidney may conjointly lead to nephropathy causing hypertension, cardiovascular events including cardiac infarction and stroke, i.e., all symptoms that had already been observed by Spühler and Zollinger (), Moeschlin () and Dubach et al. () and which are regarded typical for NSAIDs. In the liver, NAPQI alone may do the job.…”

Section: Paracetamol In the Futurementioning

confidence: 96%

“…In addition, some combinations -and regrettably, these are the ones used most widely -contain paracetamol (or formerly phenacetin), which are both transformed into the toxic metabolite, NAPQI, in the kidney. Inadequate prostaglandin production plus NAPQI adducts in the kidney may conjointly lead to nephropathy causing hypertension, cardiovascular events including cardiac infarction and stroke, i.e., all symptoms that had already been observed by Spühler and Zollinger (1953), Moeschlin (1957) and Dubach et al (1975) and which are regarded typical for NSAIDs. In the liver, NAPQI alone may do the job.…”

Section: Alternativesmentioning

confidence: 98%

Acetaminophen/paracetamol: A history of errors, failures and false decisions

Brune

Renner

Tiegs

2014

European Journal of Pain

174

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Acetaminophen/paracetamol is the most widely used drug of the world. At the same time, it is probably one of the most dangerous compounds in medical use, causing hundreds of deaths in all industrialized countries due to acute liver failure (ALF). Publications of the last 130 years found in the usual databases were analyzed. Personal contacts existed to renowned researchers having contributed to the medical use of paracetamol and its precursors as H.U. Zollinger, S. Moeschlin, U. Dubach, J. Axelrod and others. Further information is found in earlier reviews by Eichengrün, Rodnan and Benedek, Sneader, Brune; comp. references. The history of the discovery of paracetamol starts with an error (active against worms), continues with a false assumption (paracetamol is safer than phenacetin), describes the first side-effect 'epidemy' (phenacetin nephropathy, drug-induced interstitial nephritis) and ends with the discovery of second-generation problems due to the unavoidable production of a highly toxic metabolite of paracetamol N-acetyl-p-benzoquinone imine (NAPQI) that may cause not only ALF and kidney damage but also impaired development of the fetus and the newborn child. It appears timely to reassess the risk/benefit ratio of this compound.

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“…Gastrointestinal distress , often including hematemesis and peptic ulcer, may have led to gastrectomy and iron-deficiency anemia , before hypertension , uremia , urinary infection, hematuria , or renal colic focus attention on the kidney (209)(210)(211)(212)(213). The earliest manifestation of renal dysfunction is usually impaired urinary concentration (217) . Renal failure occurs late in the course and correlates with the quantity of analgesics ingested.…”

Section: Toxic Nephropathies 627mentioning

confidence: 99%

“…Glomerular filtration decreases and with continued analgesic abuse the course progresses downhill with death in renal failure. When analgesic intake is discontinued , acetaminophen excretion should cease (217) and renal function should improve in about half of the patients (2 , 211) . Once severe renal failure has occurred , appropriate management , including discontinuation of analgesics, should improve function in about one sixth of the patients, more than half should stabilize , and about one fourth will deteriorate, nevertheless (209) .…”

Section: Toxic Nephropathies 627mentioning

confidence: 99%

Toxic Nephropathies

Maher¹

1991

Therapy of Renal Diseases and Related Disorders

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Relation Between Regular Intake of Phenacetin-Containing Analgesics and Laboratory Evidence for Urorenal Disorders in a Working Female Population of Switzerland

Cited by 40 publications

References 13 publications

Caffeine as a promoter of analgesic‐associated nephropathy – where is the evidence?

Caffeine as a promoter of analgesic‐associated nephropathy – where is the evidence?

Acetaminophen/paracetamol: A history of errors, failures and false decisions

Toxic Nephropathies

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