saturnine gout, redux: a review

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REVIEW

Saturnine Gout, Redux: A ReviewSam R. Dalvi, MD,a,b,c Michael H. Pillinger, MDa,b

aDepartment of Medicine, Division of Rheumatology, NYU Hospital for Joint Diseases, New York; bDepartment of Medicine,ection of Rheumatology, New York Harbor Health Care System of the Department of Veterans Affairs, New York Campus,
ew York; cDivision of Rheumatology and Immunology, Duke University Health System, Durham, NC.
E-mail address

0002-9343/$ -see fhttp://dx.doi.org/10

ABSTRACT

Illicitly distilled beverages (colloquially referred to as moonshine) account for approximately one third ofalcohol consumption worldwide. Moonshine is often produced in makeshift distilling units composed ofold, repurposed parts, whose component elements can leach into the distillate. Consequently, the resultantbeverages may inadvertently contain harmful toxins, one of which is the metal lead. One manifestation ofchronic lead toxicity—from moonshine or other forms of chronic lead poisoning—is the rheumatologicentity known as saturnine gout. With the increasing prevalence of gout over the past few decades,physicians should be aware of the association of moonshine consumption or lead toxicity with goutyarthritis. In this article, we present an overview of saturnine gout, beginning with a discussion of leadpoisoning in antiquity and tracing its path to modern times. The contribution of lead to human disease andthe clinical features of saturnine gout are outlined. After describing the role of lead in renal insufficiencyand purine metabolism, we conclude with a discussion of specific strategies to manage this clinicallyimportant form of secondary gout.© 2013 Elsevier Inc. All rights reserved. • The American Journal of Medicine (2013) 126, 450.e1-450.e8

KEYWORDS: Gout; Lead toxicity; Nephropathy; Plumbism

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Tharra in India, Chang’aa in Kenya, and White Lightning inFranklin County, Virginia. These monikers all refer to anillicit, homemade spirit known more commonly in theUnited States as moonshine. According to the World HealthOrganization, illicitly distilled beverages account for 28.6%of alcohol consumption worldwide.1 Moonshine is oftenproduced in makeshift distilling units composed of usedrepurposed parts, whose component elements can leach intothe distillate. As a result, the distilled end products maycontain toxic substances that are harmful to humans, one ofwhich is the heavy metal lead. One manifestation of chroniclead toxicity is a rheumatologic entity known as saturninegout. Although the phenomenon of saturnine gout is wellappreciated, scant attention has been given to this disease in

Funding: Dr Pillinger is the recipient of an investigator-initiated grantfrom URL Pharma/Takeda to study the effects of colchicine on cardiacdisease in patients with gout.

Conflict of Interest: None.Authorship: Both authors had access to the data and played a role in

writing this manuscript.Requests for reprints should be addressed to Sam R. Dalvi, MD,

Division of Rheumatology and Immunology, Duke University Health Sys-tem, Box 3535 DUMC, Durham, NC 27710.

h: [email protected]

ront matter © 2013 Elsevier Inc. All rights reserved..1016/j.amjmed.2012.09.015

recent years, at least outside of the southeastern UnitedStates. However, it is important to note that moonshineingestion is not merely a regional phenomenon.2

With the increasing prevalence of gout,3 physicianshould be aware of the role that homemade alcohol and leadoxicity can play in gouty arthritis, and should inquire rou-inely about illicit alcohol use among patients with gout.he purpose of this article, then, is to present an overviewf the entity known as saturnine gout, beginning with aiscussion of lead poisoning in antiquity and tracing its patho modern times. The contribution of lead to human diseasend the clinical features of saturnine gout are outlined. Afterescribing lead’s role as a contributor to nephropathy and itsffect on purine metabolism, we conclude with a discussionf therapeutic strategies to manage saturnine gout.

HISTORICAL PERSPECTIVE ON THE“MOONSHINE MALADY”The earliest historical records of lead poisoning can betraced back to antiquity. Hernberg4 notes that lead-basedompounds may have been used in ancient Egypt to commiturder.4 Unknowingly, Hippocrates, in his Epidemics, may

ave described the first case of lead toxicity, also known as

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plumbism:* “The man from the mines; right hypochondriumstrained; enlarged spleen; stomach tense. . .the illness wentto the left knee, recurrence; he was completely exam-ined.”5 (Plumbism, from the Latin plumbum, means lead;

ote that the periodic table symbol for lead is Pb. Al-hough plumbism may be defineds any lead toxicity, it is mostommonly used to denote leadoxicity resulting from chronic,ather than acute exposure.)

Waldron6 notes that propercredit should be given to Nicander(Greek, second century BCE) forhe first explicit documentation ofead poisoning. In any case, iteems that the deleterious effectsf lead were both common andell recognized during Roman

imes. Lead at that time was usedn a variety of ways: shipbuilding,ottery glazing, creation of cook-ng utensils and water pipes, andhe storage of alcoholic bever-ges.4 This last example deservesurther mention, given the focus ofhis article. Roman must (grapeuice) was often boiled in leadontainers to make the resultant elixir more sweet, to makeine and other spirits more visually appealing, and to pre-ent spoilage.7 The increased sweetness of this liquidknown in antiquity as sapa and defrutum) resulted fromead acetate production during the boiling process. Al-hough gout was well known to the Roman empire, and theelationship between alcohol and gout was well appreciated,t seems that the connection between lead exposure and goutas not recognized.“Sugar of lead” continued in use until well into the 16th

entury. With the recognition of a possible relationship betweenead acetate and illness, laws were passed in certain regions of5th and 16th century Europe, whereby persons found to havedulterated wine with lead acetate were sentenced to death.4

The relationship between lead toxicity and gout wasreestablished in the 18th and 19th centuries. In the midst ofthe War of Spanish Succession (1701-1714), an accord wassigned between England and Portugal, known as the Treatyof Methuen. Under its terms, England would export wool toPortugal in exchange for importing Portuguese wines at adiscount relative to French varietals.8,9 These cheaper, “for-tified” (with lead acetate) wines were consumed enthusias-tically by the English, thus ushering in the next plague oflead-associated gout.9

In 1703, the same year as the Methuen treaty, Musgravecoined the term saturnine gout to describe the associationbetween lead poisoning and gout. The term saturnine hastraditionally carried at least 2 meanings, both relevant to the

CLINICAL SIGNIF

● Moonshine accoworldwide alcohmay contain toxilead.

● One manifestatiosoning is saturn

● Clinicians carinshould bear in mroutinely inquiremoonshine.

● Other forms of osure can contribuof saturnine gou

gouty patient. In one sense, saturnine refers to the Roman

God Saturn, and to his torpid personality. In that sense,saturnine may refer to the mopish emotional state of thechronic drinker, an individual strongly predisposed to gout.However, it would seem more likely (although not mutuallyexclusive) that the coinage saturnine more specifically re-

fers to the planet Saturn, the al-chemical symbol for lead.10,11

Thus, saturnine gout may be aconsequence of lead poisoning nomatter how obtained, althoughperhaps most commonly in thecontext of adulterated alcohol. AsWedeen12 notes, Swiss physicianJohann Wepfer deserves credit forinitiating the investigations thatwould implicate lead in exacerbat-ing gouty arthritis. In 1671, Wep-fer conducted chemical experi-ments using sulfuric acid todemonstrate that lead was a con-taminant of wine. Nearly a centurylater, the Englishman GeorgeBaker identified lead as the culpritin the Devonshire colic, an epi-demic of lead poisoning in Britainthat resulted from the consump-tion of adulterated cider.12

In the mid-19th century, the associations among alcohol,lead poisoning, and gout became more firmly established. In1859, Alfred Baring Garrod noted that, “. . . no truth inmedicine is better established than the fact that the use offermented. . .liquors is the most powerful of all the predis-posing causes of gout.”8,13 Conclusive evidence for a “gout-inducing property” of the Portuguese imports came in 1971,when Halla and Ball14 analyzed concentrations of lead in9th century wines. They found that lead levels in theseamples varied from 320 to 1900 �g/L. Current-day winesere sampled simultaneously and found to have lead levelsf only 100 to 200 �g/L.

During the 20th century, heavy consumption of moon-hine, particularly in the southeastern United States, con-ributed to a redux in saturnine gout. Although moonshineroduction may have reached its apogee during prohibition,he practice did not end with the repeal of the 18th Amend-ent. Halla and Ball14 noted that production of moonshine

n the 1960s was more than 55 million gallons. Becauseoonshine production is illegal, moonshiners would cre-

te distilleries in clandestine locations using readilyvailable materials. As Halla and Ball note, “an automo-ile radiator, with its many lead-soldered connections of-en serves as a condenser.”14 A 1965 study demonstratedhat lead was present in approximately 90% of samples oflabama moonshine analyzed at the Atlanta Regional Lab-ratory; 40% of such samples contained what were consid-red to be toxic amounts of the metal.10,14 Over the next

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because of several factors: increased activity by law en-forcement, increasing costs, and dissemination to the publicregarding lead contamination in moonshine. As a result, by1982, cases of saturnine gout comprised less than 5% of alldiagnoses of gout at the Birmingham Veterans Affairs Med-ical Center.14

However, recent studies suggest that the decline in leadtoxicity among moonshine drinkers may have been exag-gerated. A 2001 study at Grady Memorial Hospital in At-lanta, Georgia, evaluated 49 patients reporting moonshineconsumption within the previous 5 years. Of these, approx-imately 50% were found to have abnormal serum lead levels(�15 �g/dL) and 30% of the cohort had markedly elevated�50 �g/dL) lead levels.15 To validate the hypothesis thatlevated lead levels result from moonshine ingestion, morehan 100 moonshine samples were confiscated by law en-orcement officials between 1995 and 2001. The samplesere obtained from 5 southeastern states, as well as Mis-

ouri, Ohio, Wisconsin, and West Virginia. Approximately0% of the samples contained lead levels greater than 300

�g/dL, suggesting that lead-contaminated “firewater” con-tinues to be a significant problem, and not only in thesoutheastern United States.16 Another study analyzing 48moonshine samples obtained by law officials showed sim-ilarly impressive findings: Measureable lead levels weredetected in 90% of the samples, of which 60% had leadconcentrations greater than or equal to the EnvironmentalProtection Agency’s action level of 15 ppb.17 A 2003 studystimated the prevalence of moonshine consumption (withinhe previous 5 years) among patients admitted to an emer-ency department in a large metropolitan county hospital atpproximately 9%.18 Taken together, these studies suggest

that moonshine consumption remains a common practiceand that lead contamination remains a serious concern.

LEAD TOXICOLOGY AND CONTRIBUTIONTO DISEASEIn addition to moonshine, lead exposure worldwide can be attrib-uted to 6 groups of products, including ceramic glazes, solder,gasoline additives, certain paint products, drinking water systems,and natural remedies.19,20 Although moonshine consumption addshe risk of alcohol to that of lead, the promotion of gout throughead exposure and toxicity is not likely to differ whether the sources moonshine or other products.

In adults, non-moonshine lead poisoning is usually aesult of inhalational exposure or inadvertent ingestion ofead particles at the workplace, whereas in children expo-ure occurs via ingestion of lead-based paint chips in olderomes and apartments, often in the setting of poverty.21 Inddition to chipping, lead-based paint aerosolizes as it de-eriorates, and domestic lead inhalation is another mecha-ism for pediatric lead poisoning. After a period of time,ead particles settle and contaminate soil around homes.21

Over the last century, effective public health policy initia-tives in the United States have reduced the incidence of
environmentally based lead toxicity. However, recent stud-
ies suggest that even blood lead levels previously consideredacceptable have been associated with neurologic disorders,cognitive impairment, and hypertension.19 Moreover, a cross-sectional study by Krishnan et al22 suggests that subtoxic bloodead levels also are associated with increased prevalences ofyperuricemia and gout.

After exposure, up to 40% of inhaled lead is absorbednto the bloodstream, whereas gastrointestinal absorption isariable and dependent on age and overall state of nutri-ion.19 Approximately 99% of lead in the bloodstream is

bound to erythrocytes. The half-life of lead-bound red cellsranges from 35 to 40 days. Lead is then transferred to softtissues before being deposited in bone, where its half-life isestimated at 20 to 30 years. Conditions associated with highbone turnover, such as pregnancy, certain malignancies, andpostmenopausal osteoporosis, can leach lead out of bone,thereby promoting plumbism.18,19 Excretion of lead occursprimarily through the urinary tract (Figure).23,24

SATURNINE GOUT: CHARACTERISTIC FEATURESAND CLINICAL MANIFESTATIONSIn his 1886 description of saturnine gout, Lorimer25 notedcertain unique characteristics in patients with lead-associ-ated gouty arthritis compared with patients with gout with-out plumbism, including signs of lead toxicity, such as anemiaand Burton’s lines (a bluish line on the gums when lead reactswith sulfur compounds produced by bacteria), and a predilec-tion for certain joints. In Halla and Ball’s review,14 the kneewas the most commonly affected joint in saturnine gout (83%)(in contrast to the first metatarsophalangeal joint in primarygout), and polyarticular involvement was observed in 36% ofcases.14 In 1969, Ball and Sorensen10 identified the followingcommon features among 37 patients with saturnine gout: lowsocioeconomic status, chronic moonshine exposure, hyperten-sion, mild anemia, slowly progressive kidney disease, elevatedurine lead levels, and absence of family history of gout. A 1968study by Emmerson26 comparing patients with primary versussaturnine gout highlighted differences in the 2 groups. Thesaturnine gout group consisted of patients whose lead burdenderived from childhood exposure, supporting that plumbismfrom any source can contribute to gouty arthropathy. The malepredominance typical of patients with primary gout was lesspronounced in the saturnine gout group (male/female ratios of15:1 and 9:8, respectively). In addition, patients in the satur-nine gout group had fewer and less severe (34%) gouty ar-thritic flares relative to the primary gout group (66%), despitethe fact that all patients in the saturnine gout group had renalfailure, an established risk factor for hyperuricemia and goutincidence/severity (Tables 1 and 2).26

MECHANISMS OF SATURNINE GOUT: ROLE OFLEAD IN RENAL INSUFFICIENCY, PURINEMETABOLISM, AND URATE OVERPRODUCTIONOur understanding of the relationships among chronic lead
poisoning, renal disease, and hyperuricemia has advanced

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considerably over the past 100 years. Hyperuricemia is aconsequence of systemic overproduction of uric acid, renalunderexcretion of urate, or a combination of both. Much ofthe literature on lead nephropathy and urate handling im-

Figure Lead handling in the body. GI �either inhalation or ingestion. Up to 40%gastrointestinal absorption depends on selead absorption within the GI tract appeainvolve both divalent metal transport 1 (DMFollowing absorption, most lead is then boorgans such as bone and the kidneys. TExcretion of lead occurs mostly through t

Table 1 Distinguishing Features of Saturnine and Nonsaturnin

Saturnine Gout

Moonshine consumption CommonSex incidence Equal penetrance after lead ex

Age 40-60 y for moonshine consumfor childhood lead exposure

Presence of CKD at diagnosis CommonAnemia Common

Proteinuria CommonFrequency of attacks Less

CKD � chronic kidney disease.*Excludes secondary gout resulting from hyperuricemia due to other†For example, chronic kidney disease, diuretic use, and drug-induced‡Note that sex incidence is likely similar to primary gout when sourc

by males.

plicates lead as contributing both to intrinsic kidney diseaseand to underexcretion of urate (Table 3), whereas a smallerbody of research proposes a role for lead in promotingincreased urate synthesis.

ointestinal. Lead enters the body throughaled lead is absorbed systemically, whileactors. Though incompletely understood,ccur within the small intestine, and mayependent and -independent pathways.23,24

erythrocytes, before being sequestered in-life of lead in bone is about 25 years.itourinary tract.21

Nonsaturnine Gout

Primary Gout*Non–Lead-relatedSecondary Gout†

Uncommon Intermediate‡ Overwhelmingly male, less

so after menopauseVariable

; �40 y �50 y 60-70 y

Uncommon VariableUncommon (unless

chronic tophaceous)Variable

Uncommon VariableMore Variable

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Lead and the KidneyLanceraux made the connection between lead toxicity andrenal pathology in 1863 when he described an atrophic,fibrotic kidney of an artist who used his mouth to hold apaintbrush (in an era when paints frequently includedlead).30 In 1914, Sir Thomas Oliver further promoted therelationship between lead exposure and kidney disease: “In-terstitial nephritis or contracted kidney is the most commonpathological event in chronic plumbism.”31

Table 2 Relevant Publications Detailing the Pathophysiology a

Author (Year) Type of Study

Emmerson (1968) Observational 67 patients

Ball and Sorensen (1969) Nonrandomized 3 patients

Inglis et al (1978) Retrospective 53 patients

Halla and Ball (1982) Retrospective 42 patients

Reynolds et al (1983) Case-control 60 patients

Nolan and Shaikh (1992) ReviewPatrick (2006) Review

EDTA � ethylenediaminetetraacetic acid.

Table 3 Relevant Publications Examining the Association of L

Author(s) Journal References Typ

organ et al Arch Intern Med. 1966;118:17-29 No

edeen et al Arch Intern Med. 1979;139:53-57 No

atuman et al N Engl J Med. 1981;304:520-523 No

taessen et al27

Cadmibel study groupN Engl J Med. 1992;327:151-156 Cro

Lin et al Kidney Int. 2001;60:266-271 CroR

Brewster and Perazella Am J Med Sci. 2004;327:341-347 Re

in et al28 Am J Med. 2006;119:707.e1-9 Ob

kong et al29 Kidney Int. 2006;70:2074-2084 Re

CI � confidence interval; CKD � chronic kidney disease; EDTA � ethy
controlled trial.
Studies conducted by Inglis et al32,33 during the first halfof the 20th century argued convincingly for lead as theetiologic agent of chronic kidney disease and saturnine goutin patients with childhood lead exposure. To better under-stand the role of lead toxicity in nephropathy, Morgan etal31 evaluated 13 patients seen at the University of Alabama

edical Center between 1959 and 1965. All of the patientsad known diagnoses of lead poisoning, and all underwentenal biopsies. Nearly all of the patients had chronic renal

enotypic Profile of Saturnine Gout

gs/Summary

tion of clinical features of gout among patients with childhoodexposure vs those withoutstrates role of impaired renal function contributing toruricemia in patients with saturnine goutthe clinical features and renal histopathologic findings of

ents with childhood lead poisoning in Queensland, Australiaew of clinical features of a cohort of saturnine gout patients atBirmingham, Alabama, Veterans Affairs Medical Centerrelation between creatinine clearance and urinary leadetion after EDTA administrationrizes the biochemical effects of lead on the kidney

sion of characteristic features of lead poisoning and the role ofradicals in the pathogenesis of lead exposure–related organage

vels and Renal Function

tudy Findings/Summary

mized Demonstrated association between renal impairmentand chronic lead toxicity.

mized Suggested that reduced GFR in patients withoccupational lead exposure may be reversibleafter chelation therapy.

mized Among patients with gout, the amount ofmobilizable lead after EDTA testing correlatedwith the degree of renal insufficiency.

tional Creatinine clearance rate was inversely associatedwith blood lead values (95% CI, 1.37-10.4;P � .01).

tional/ Chronic low-level environmental lead exposure mayinterfere with urate excretion in patients withCKD.

Overview of lead nephropathy with emphasis onchelation therapy and alteration of GFR inpatients with CKD.

onal/RCT Among patients with low–normal body lead burdenand nondiabetic CKD, renal function deterioratedcompared with patients receiving chelationtherapy.

Overview of epidemiologic research involving effectsof lead exposure on renal function.

inetetraacetic acid; GFR � glomerular filtration rate; RCT � randomized

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insufficiency and hypertension, and all but 1 patient regu-larly consumed moonshine. The histopathologic findingsfrom the renal biopsies were nearly invariant and revealedinterstitial fibrosis, adventitial fibrosis of small arteries, andeosinophilic intranuclear inclusion bodies.31 Although theauthors admonished that the frequent presence of comorbidconditions that themselves promote nephropathy (eg, hyper-tension, hyperuricemia) made it difficult to identify specif-ically lead-associated histopathologies, they nonethelessconcluded that lead played an important nephropathic rolein these patients.

To further investigate the hypothesis that lead contrib-utes to renal disease in patients with gout, Batuman et al34

performed the ethylenediaminetetraacetic acid (EDTA)lead-mobilization test in 44 patients with gout from a Vet-erans Affairs Medical Center in New Jersey. The removal ofsystemic lead after chelation by EDTA occurs through renalfiltration and subsequent urinary excretion, the rate of whichwas determined in these studies. The authors demonstratedthat increased excretable urinary lead levels (reflectinghigher lead body burdens) correlated directly with poorerrenal function. Further analysis of control patients with goutand preserved renal function, and patients without goutdespite advanced renal disease, revealed that these 2 controlgroups had markedly less urinary lead excretion (exposure)than the patients with both gout and renal disease. Thesefindings suggest that lead burden may indeed contribute torenal disease in patients with gouty arthritis.33 In contrast,however, a study of patients with gout at Duke MedicalCenter did not find a correlation between lead excretion andcreatinine clearance.35

After systemic absorption, lead accumulates within thekidneys.36 After filtration at the glomerulus, lead ionsre taken up by renal tubular epithelial cells by both activeransport and cotransport with organic anions. Although theole of various organic anionic substrates on urate transport-rs in the kidney has been well characterized, the effects ofnorganic cations (eg, lead) on urate transport have yet to beully delineated.

Lead Toxicity and Urate OverproductionA possible role for lead in altering purine metabolism isintriguing, although less well established. Farkas andStanawitz37 reported that guanine aminohydrolase, an en-yme that catalyzes the conversion of guanine to xanthine,s sensitive to inhibition by lead. Inhibition of this enzymeay then allow for increased production of inosine mono-

hosphate (resulting from accumulation of guanine nucleo-ides), which may, in turn, lead to urate production. Lud-ig38 posited that, in patients with severe lead poisoning

causing hematologic derangements (anemia, basophilicstippling), enhanced nucleoprotein turnover occurs, therebyincreasing uric acid production. Recent investigations sur-rounding the genotoxic effects of lead implicate both directand indirect mechanisms for lead-induced urate production.
These studies suggest that lead may promote genotoxicity
by interfering with enzymes involved in DNA repair and viaproduction of free radicals. In some cases, this may have adirect effect on genes associated with gout. García-Lestón etal39 recently demonstrated that lead acetate induced a dose-dependent increase of mutant frequency within the HGPRTgene of Chinese hamster ovary K1 cells. HGPRT is a purinesalvage enzyme whose partial or complete inactivation haslong been appreciated to promote hyperuricemia and sub-sequent gout.

Therapeutic StrategiesThe management of patients with saturnine gout requires,first, the proper management of hyperuricemia and inflam-mation common to any patient with gout. Saturnine gout ismost commonly found in patients who also have other risk

Table 4 Saturnine Gout: Approach to Diagnosis andManagement

A. Suspect lead poisoning in a patient with gout with:Chronic renal failureAnemiaPeripheral neuropathyEncephalopathyBurton’s linesHistory of moonshine consumption or other potential leadexposures

B. If high degree of suspicion:*Obtain serial venous blood lead levelsConsider radiographic imaging of long bonesConsider renal biopsy in patients with chronic kidney diseasewithout identifiable causePerform thorough physical examination with developmentalmonitoring (in children)Notify local public health department for furtherinvestigation

C. Management of saturnine goutTreatment of acute gouty arthritisConsideration of urate-lowering therapyIdentify and avoid possible lead exposuresConsultation with a medical toxicologistChelation therapy

Calcium disodium EDTADimercaprolSuccimer

Use of antioxidantsAscorbic acidZincN-acetylcysteine

EDTA � ethylenediaminetetraacetic acid.*Measurement of blood lead levels seems to be a useful initial

screening test for detection of acute lead exposure/toxicity. Because thehalf-life of lead in circulating erythrocytes is �35 days, obtaining bloodlead levels is generally useful only in patients with recent exposure (�6weeks). For those patients with a remote history of lead exposure, othertests (mentioned above) may aid in diagnosis. For more information,visit the Agency for Toxic Substances and Disease Registry website at:http://www.atsdr.cdc.gov.

factors for hyperuricemia, and identifying and managing

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other hyperuricemic risk factors is a critical first step inmanaging the saturnine version of the disease. Modificationof dietary and pharmacologic risk factors, reduction of over-all alcohol consumption, and potential initiation of urate-lowering drug therapy all have a role. Once lead exposure inthe form of moonshine (or other environmental risk factors)has been demonstrated (Table 4), and gout has been con-firmed by history and diagnostic arthrocentesis, treatmentshould additionally focus both on avoidance of lead-taintedingestions and on removal of lead from the body. The latteris accomplished through use of chelating agents, such ascalcium disodium EDTA, dimercaprol, and succimer.19

Consultation with a medical toxicologist is important toassist in developing a therapeutic protocol (Table 4).

In addition to reducing body lead stores and minimizingthe cumulative toxic effects of lead, Lin et al40 demon-strated that chelation therapy increased urate clearance anddecreased serum urate levels in patients with chronic renalinsufficiency and gout. Moreover, a trend toward improvedcreatinine clearance after therapy also was noted. This resultis similar to a previous study by Wedeen et al,41 in which0% of patients with significant lead exposure and renalisease had a 20% increase in glomerular filtration rate afterreatment with intramuscular EDTA. In addition, recentesearch examining lead’s role in oxidative stress and con-equent tissue damage has led to consideration of the ther-peutic use of antioxidants such as ascorbic acid, zinc, andyridoxine.42,43 These data collectively suggest that there is

a reversible component to lead nephropathy and its resultinghyperuricemia, and that saturnine gout can not only bemanaged but also partly remediated.

CONCLUSIONSSaturnine gout as a manifestation of lead poisoning origi-nated in antiquity and underwent a resurgence in the 20thcentury, especially within rural areas of the southeastern andmidwestern United States. Today, moonshiners can befound throughout the entire United States. Over the last 2decades, the emergence of a growing number of homebrew-ers and their artisanal alcohol beverages has brought with ita renewed concern for lead toxicity.44 Clinicians caring foratients with gout should bear in mind the role of lead andoutinely inquire about consumption of moonshine. Physi-ians also should remain cognizant that other forms of leadxposure can contribute to the development of saturnineout, though without providing the concomitant alcohoload. Identifying and modifying risk factors for hyperurice-ia, initiating pharmacologic therapy, and initiating early

herapeutic intervention with chelating agents may not onlylleviate the articular symptoms of the “shine sickness” butlso avert the other deleterious consequences of chronicead exposure.

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shine: a report of Bureau of Alcohol, Tobacco and Firearms analyzedsamples. Vet Hum Toxicol. 2004;46:89-90.

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