son admission, un traitement à l’azathioprine avait été débuté pour sa
colite ulcéreuse. À l’admission, l’azathioprine a été temporairement
cessée, ce qui a permis la résolution des signes et symptômes. Les
symptômes sont réapparus lorsque l’azathioprine a été reprise. Les
signes et symptômes présentés par le patient étant compatibles avec une
réaction d’hypersensibilité à l’azathioprine, il fut décidé de cesser
définitivement l’azathioprine.
DISCUSSION: Selon les auteurs, il s’agirait du premier cas
d’hypersensibilité à l’azathioprine rapporté chez un patient atteint de
colite ulcéreuse. L’évolution de la réaction dans le temps, les signes et
symptômes de même que la réapparition des symptômes lors de la
réadministration du médicament tendent à incriminer l’azathioprine. Le
Chromium Picolinate Toxicity
Jennifer Cerulli, Darren W Grabe, Isabelle Gauthier, Margaret Malone, and M Donald McGoldrick
OBJECTIVE: To describe a case of toxicity secondary to chronic
ingestion of 6–12 times the recommended daily allowance of over-
the-counter (OTC) chromium picolinate.
CASE SUMMARY: A 33-year-old white woman presented with weight
loss, anemia, thrombocytopenia, hemolysis, liver dysfunction
(aminotransferase enzymes 15–20 times normal, total bilirubin 3
times normal), and renal failure (serum creatinine 5.3 mg/dL; blood
urea nitrogen 152 mg/dL). She had ingested chromium picolinate
1200–2400 µg/d for the previous 4–5 months to enhance weight
loss. The patient had chromium plasma concentrations 2–3 times
normal. Thrombotic thrombocytopenic purpura and hemolytic
uremic syndrome were ruled out by clinical findings, peripheral
blood smears, and a bone marrow biopsy. The patient was managed
with supportive measures and received blood product transfusions
and hemodialysis. Hemolysis stabilized and liver function improved
over 6 days. Liver function returned to normal prior to discharge.
Renal function began to return on day 12 and her serum creatinine
on discharge was 1.3 mg/dL. One year later, all laboratory values
were within normal limits.
DISCUSSION: Trivalent chromium is an essential trace element that is
considered safe when ingested in normal quantities. Trivalent
chromium compounds are used by patients to enhance weight loss,
Jennifer Cerulli PharmD BCPS, Fellow, Nutrition Support, Division of Pharmacy Practice,
Albany College of Pharmacy, Albany, NY
Darren W Grabe PharmD, Fellow, Nephrology, Division of Pharmacy Practice, Albany
College of Pharmacy
Isabelle Gauthier PharmD BCPS, at time of writing, Resident, Oncology, Department of
Pharmacy, Albany Medical Center, Albany, NY, and Division of Pharmacy Practice,
Albany College of Pharmacy; now, Assistant Clinical Professor, Faculty of Pharma-
cy, University of Montreal, Montreal, Canada
Margaret Malone PhD FCCP BCNSP, Professor, Division of Pharmacy Practice, Albany Col-
lege of Pharmacy
M Donald McGoldrick MB FRCP(C), Professor, Department of Medicine, Division of
Nephrology, Albany Medical College, Albany, NY
Reprints: Jennifer Cerulli PharmD BCPS, Division of Pharmacy Practice, Albany College
of Pharmacy, 106 New Scotland Ave., Albany, NY 12208, FAX 518/445-7202
428 ■ The Annals of Pharmacotherapy ■ 1998 April, Volume 32
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mécanisme de cette réaction d’hypersensibilité n’est pas clairement
défini mais pourrait impliquer la portion nitroimidazole de la molécule
d’azathioprine.
CONCLUSIONS: L’hypersensibilité à l’azathioprine se manifeste
fréquemment par des signes et symptômes ressemblant à une infection
systémique tels que fièvre, leucocytose, et évidence de dysfonction d’un
organe. Le diagnostic d’hypersensibilité à l’azathioprine devrait être
considéré chez les patients qui reçoivent depuis peu de l’azathioprine ou
chez qui la dose d’azathioprine a été augmentée.
ALAIN MARCOTTE
increase lean body mass, and/or improve glycemic control.
Information regarding the toxicity of chromium picolinate is limited.
CONCLUSIONS: Chromium supplements may cause serious renal
impairment when ingested in excess. Medication histories should
include attention to the use of OTC nutritional supplements often
regarded as harmless by the public and lay media.
KEY WORDS: chromium picolinate, toxicity.
Ann Pharmacother 1998;32:428-31.
THERE IS INCREASING INTEREST in the use of nutritional sup-
plements to promote or improve health status. Individuals
can gain information on nutritional supplements from the
lay press or on the Internet, and purchase them at pharma-
cies and health food stores. Often, information regarding
the efficacy and toxicity of these products is lacking in the
medical literature. Clinicians should be aware of their pa-
tients’ use of over-the-counter (OTC) nutritional supple-
ments. OTC chromium compounds are used to enhance
weight loss and improve glycemic control. Currently, there
is little information available regarding the toxicity of
trivalent chromium (III), a naturally occurring essential el-
ement, which is considered safe when consumed in normal
amounts.1 The current recommended daily allowance
(RDA) is 50 –200 µg/d.2 Recently, a trivalent chromium
compound, chromium picolinate, was indicated as the
cause of chronic renal failure in a 49-year-old woman who
ingested 600 µg/d for 6 weeks.3 We describe a patient who
developed thrombocytopenia, hemolysis, hepatic dysfunc-
tion, and acute renal failure after chronic ingestion of 6–12
times the maximum RDA of chromium picolinate.
 Case Reports

CASE REPORT
A 33-year-old white woman presented to the emergency depart-
ment after a 1–2 week history of severe fatigue and malaise that
had worsened over the past 3 days. She reported fever and chills
without diaphoresis, abdominal pain, nausea, or vomiting. Her
medical history was significant for schizophrenia and depression,
which were diagnosed approximately 6 months prior. She had re-
ceived paroxetine and monthly fluphenazine injections until 2
weeks prior to admission. The patient reported currently taking
no OTC or prescription medications other than 6–12 chromium
picolinate 200-µg tablets per day for the past 4–5 months to in-
duce weight loss. She had intentionally lost 4.5 kg in the previous
2 weeks and a total of 11.4 kg over 3 months. She was subse-
quently diagnosed with an eating disorder, for which dietary and
psychiatric counseling were provided.
Physical examination revealed a 157-cm, 41-kg, cachetic,
jaundiced woman. Her BP was 94/62 mm Hg, HR 97 beats/min,
and T 36.4 ˚C. Her sclera were icteric and her abdomen was
scaphoid, nontender, and nondistended, with bowel sounds. The
examination was negative for hepatosplenomegaly, edema, and
petechiae. She was alert and oriented.
The patient presented with anemia, hemolysis, thrombocy-
topenia, hepatic dysfunction, and acute renal failure. Pertinent
laboratory results are presented in Table 1. A Coombs test was
negative, and the haptoglobin concentration was less than 50
mg/dL (normal 50–220). Wilson’s disease was ruled out as a
cause of hemolysis because of normal ceruloplasmin and copper
concentrations, and no Kayser–Fleischer ring was observed on
ophthalmologic examination. A preliminary diagnosis of severe
hemolysis secondary to thrombotic thrombocytopenic purpura or
hemolytic uremic syndrome (TTP/HUS) was made on the basis
of initial peripheral blood smear, which revealed schistocytes.
However, subsequent peripheral blood smears and a bone mar-
row biopsy revealed no evidence of microangiopathic hemolytic
anemia, despite continued hemolysis. In addition, the patient was
afebrile on admission and without mental status changes. There-
fore, TTP/HUS was considered unlikely, and plasmapheresis was
Table 1. Laboratory Results
HOSPITAL DAY
3 3
PARAMETER 1 2 (pre-HD) (post-HD) 11
not performed. The patient received transfusions of packed red
blood cells and platelets. By day 6 the intravascular hemolysis
stabilized, and her platelet count began to rise.
On admission the patient’s liver function enzymes and bilirubin
were elevated; however, they immediately began to decrease af-
ter admission and normalized prior to discharge. Initial prothrom-
bin time and partial thromboplastin time values were slightly ele-
vated, but returned to normal by week 2 of hospitalization. The
results of a hepatitis panel were negative.
On presentation to the emergency department, the patient’s
blood urea nitrogen (BUN) was 152 mg/dL, serum creatinine
was 5.3 mg/dL, and urine output was estimated to be less than
200 mL/d. A urinalysis revealed brown cloudy urine containing
muddy brown casts and the following data: pH 5, protein more
than 300 mg/dL, glucose 100 mg/dL, urobilinogen = 1 EU/L,
2–5 white blood cells/high power field (hpf), 40–50 red blood
cells/hpf, and 2+ bacteria/hpf. The urine was positive for nitrate
and leukocyte esterase, but contained no ketones or squamous
epithelial cells. The urine culture grew more than 100 000 Cit-
robacter koseri and the patient was treated with a 7-day course of
ofloxacin. Her serum creatinine continued to rise to 6.1 mg/dL on
day 3, at which time she became encephalopathic. Hemodialysis
was undertaken on days 3, 4, 6, 7, 9, 10, 11, and 13. An abdomi-
nal/renal ultrasound performed on day 8 revealed enlarged kid-
neys (14 cm) consistent with an acute infiltrative process. On day
11, the urine output began to increase and by day 12 had in-
creased to 2 L/24 hours. Her serum creatinine on discharge on
day 26 was 1.3 mg/dL.
Due to the patient’s chronic consumption of chromium picoli-
nate, chromium toxicity was suspected. A plasma chromium
concentration obtained on day 2 was elevated at 4.6 µg/mL (nor-
mal 0.1–2.1). Additional chromium concentrations were obtained
before and after hemodialysis on day 3 (4.3 and 6.5 µg/mL, re-
spectively) and repeated on day 12 (5.3 µg/mL).
After 26 days of hospitalization, the patient was discharged
with a final diagnosis of hemolysis, as well as acute liver and re-
nal failure secondary to chromium toxicity. One year later, on ad-
mission to the mental health unit, her serum crea-
tinine was 0.4 mg/dL, and her liver enzymes and
hematologic laboratory values were within normal
limits. No additional chromium concentrations
were obtained.
Discussion
12 26

WBC (103/mm3) 22.5 9.5 13.0 6.4 13.1 11.9 13.9 Chromium is an essential trace element that
Hct (%) 15.3 26.8 25 27.9 33.8 38.2 36.7 can occur in several oxidative states from 2– to
Plt (103/mm3) 15 95 62 28 325 6+.1 The most commonly occurring forms of
Alkaline 131 146 135 116 chromium are hexavalent (VI) and trivalent
phosphatase (III). Hexavalent chromium is used for dyes,
(IU/mL) leather tanning, and chrome plating. Chronic
AST (IU/L) 1274 549 370 223 17 exposure to hexavalent chromium compounds
ALT (IU/L) 992 891 is responsible for industrial health problems
Total bilirubin 3.7 1.3 0.6
(mg/dL)
such as skin ulcerations, nasal septum perfora-
LDH (IU/L) 7879a a
1396 1154 420 220 tion, chromate dermatitis, and lung cancer,4
CK (IU/L) 981 a
361 190 23 and is considered 100 times more toxic than
BUN (mg/dL) 152 140 144 36 38 32 40 trivalent chromium.4
SCr (mg/dL) 5.3 6.0 6.1 1.8 4.5 3.8 1.3 Cases of acute ingestion of industrial hex-
Urine output 100–200 200 120 700+ 2100 4000 avalent chromium have been reported.5,6 A
(mL/d) worker developed thrombocytopenia, hemor-
Chromium 4.6 4.3 6.5 5.3 rhage, gastroenteritis, toxic hepatitis, and tubu-
concentration lar nephritis after accidental oral ingestion of
(µg/mL)
(normal 0.1–2.1) chromic acid (a hexavalent chromium com-
pound).5 The patient received three hemodial-
ALT = alanine aminotransferase; AST = aspartate aminotransferase; BUN = blood urea ysis sessions and made a complete recovery.
nitrogen; CK = creatine kinase; Hct = hematocrit; HD = hemodialysis; LDH = lactate de-
hydrogenase; Plt = platelets; SCr = serum creatinine; WBC = white blood cell count. Chromium concentrations were obtained from
a
Hemolyzed specimen. the blood, the urine, and the dialysis fluid; this

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demonstrated that hemodialysis was an effective means of
removing chromium during acute toxicity.
Another case of acute toxicity involved an oral ingestion
of chromium sulfate, a hexavalent compound used as a
leather-tanning solution.6 The patient developed coagu-
lopathy, erosive gastroenteritis, pancreatitis, pulmonary
edema, and renal failure after oral ingestion of chromium
sulfate. Hemodialysis was performed; however, further re-
suscitation measures were not undertaken and the patient
died. Based on the evaluation of serum concentrations,
hemodialysis was efficacious in removing hexavalent
chromium in acute toxicity.
Chromium in the trivalent form occurs naturally in food
sources such as Brewer’s yeast, animal meats, and whole
grains.1 It is considered safe when consumed in normal
quantities and is available for intravenous use as chromium
chloride or OTC as chromium picolinate. Chromium is be-
lieved to be essential for normal glucose metabolism as
chromium deficiency reported in patients receiving long-
term total parenteral nutrition was associated with insulin
resistance, impaired glucose tolerance, and hyperglycemia
with glycosuria.7--9 These symptoms were reversed rapidly
with intravenous chromium chloride supplementation.
The increasing interest in the use of chromium picoli-
nate is due to its proposed benefits for improving both fast-
ing blood glucose and glycosylated hemoglobin, promoting
the development of lean body mass, and having beneficial
effects on cholesterol profiles.10,11 Chromium supplementa-
tion is rarely recommended, as the data substantiating its
benefits are limited.
Little information is available regarding the toxicity of
trivalent chromium. The only case in the literature regard-
ing a significant adverse effect in humans attributed to
chromium picolinate involves a 49-year-old woman who
ingested 600 µg/d for 6 weeks to lose weight.3,12 Other
medications included terazosin, hydrochlorothiazide, and
verapamil. Five months after the ingestion of chromium,
the patient presented with a BUN of 74 mg/dL and a se-
rum creatinine of 5.9 mg/dL. A renal biopsy revealed se-
vere chronic active interstitial nephritis consistent with
heavy-metal exposure. After 2 months of prednisone thera-
py, her serum creatinine decreased to 3.8 mg/dL. No
chromium plasma concentrations were reported, and no
hypothesis for the delayed toxic effect was given. Al-
though there is limited documentation, thiazide diuretics
have been implicated in causing allergic interstitial nephri-
tis (AIN).13 However, in these cases, AIN developed with-
in several weeks of initiating therapy and was accompa-
nied by at least one sign of hypersensitivity (i.e., rash,
eosinophilia, fever). In contrast, this patient has received
hydrochlorothiazide for approximately 3 years with no
signs of hypersensitivity. Hypertensive nephrosclerosis
was also ruled out due to the rapid regression to renal fail-
ure in a patient well controlled on antihypertensive agents.
Our patient developed toxicities similar to those de-
scribed with hexavalent chromium toxicity (i.e., thrombo-
cytopenia, toxic hepatitis, renal failure).5,6 However, our
case differs from the previously reported toxicity sec-
ondary to chromium picolinate.3 Although a renal biopsy
was not performed on our patient, muddy brown casts ob-
430 ■ The Annals of Pharmacotherapy ■ 1998 April, Volume 32
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served in the urinalysis suggest acute tubular necrosis rath-
er than interstitial nephritis, as occurred in the first reported
case3 of renal failure caused by chromium picolinate. In
addition, our patient’s renal function improved rapidly and
returned to normal. In the previously reported case, the pa-
tient experienced residual renal dysfunction. We cannot
explain the differences in renal toxicity seen in these pa-
tients; however, they may be related to the different de-
grees of exposure to chromium picolinate. The first patient
was exposed to chromium 600 µg/d for 6 weeks and pre-
sented with renal failure 5 months later. Our patient was
exposed to chromium 1200 –2400 µg/d for 4 –5 months
and presented during her consumption of chromium. She
was not taking thiazide diuretics, and had no other comor-
bidities such as hypertension that could contribute to renal
failure.
In our case TTP/HUS was initially suspected. TTP/HUS
is commonly recognized by the pentad of microangiopa-
thic hemolytic anemia, thrombocytopenia, fever, neurolog-
ic abnormalities, and renal abnormalities.14 Although the
patient had evidence of hemolysis, thrombocytopenia, and
renal dysfunction, no fever or neurologic abnormalities
were present. Peripheral blood smears and a bone marrow
biopsy revealed no evidence of microangiopathic hemolytic
anemia.
Previous reports5,6 of acute chromium toxicity used he-
modialysis as an effective mechanism for chromium re-
moval. In contrast, our patient’s chromium concentration
increased after hemodialysis, and the concentration on day
12 (5.3 µg/mL) was greater than that on day 2 (4.6
µg/mL), even after seven hemodialysis sessions. Possible
explanations for this observation could be volume contrac-
tion, persistent covert consumption of chromium picoli-
nate, or a redistribution of chromium from tissues into the
plasma. A family member of the patient provided us with
her current bottle of chromium; it is unlikely that she con-
tinued her consumption. Chromium is widely distributed
throughout the body, and tissue concentrations are 10–100
times higher than those found in the blood.1 Although
hemodialysis was effective in the management of acute
toxicity, chromium would be widely distributed to the tis-
sues after chronic ingestion. Therefore, hemodialysis may
have lowered the concentration of chromium in the blood
acutely, creating a concentration gradient and promoting
redistribution of chromium from the tissues into the blood.
Summary
This case increased our awareness of the potential for
the abuse of OTC nutritional supplements and the toxicity
that can occur with excessive intake. It is important for
clinicians to include nutritional supplements in a medica-
tion history and to evaluate the level of intake and duration
of ingestion. Further investigation into the toxicities and
long-term effects of OTC nutritional products not regulat-
ed by the Food and Drug Administration is warranted.
References
1. Nielsen FH. Chromium. In: Shils ME, Olson JA, Shike M, eds. Modern
nutrition in health and disease. 8th ed. Philadelphia: Lea & Febiger,

1994:264–8.
2. Food and Nutrition Board, National Research Council. Recommended
dietary allowances. 10th ed. Washington, DC: National Academy Press,
1989.
3. Wasser WG, Feldman NS, D’Agati VD. Chronic renal failure after in-
gestion of over-the-counter chromium picolinate (letter). Ann Intern
Med 1997;126:410.
4. Katz SA, Salem H. The toxicology of chromium with respect to its
chemical speciation: a review. J Appl Toxicol 1993;13:217-24.
5. Fristedt B, Lindqvist B, Schütz A, Övrum P. Survival in a case of acute
oral chromic acid poisoning with acute renal failure treated by haemo-
dialysis. Acta Med Scand 1965;177:153-9.
6. van Heerden PV, Jenkins IR, Woods WPD, Rossi E, Cameron PD.
Death by tanning — a case of fatal basic chromium sulphate poisoning.
Intensive Care Med 1994;20:145-7.
7. JeeJeebhoy KN, Chu RC, Marliss EB, Greenberg GR, Bruce-Robertson
A. Chromium deficiency, glucose intolerance, and neuropathy reversed
by chromium supplementation, in a patient receiving long-term total par-
enteral nutrition. Am J Clin Nutr 1977;30:531-8.
8. Freund H, Atamian S, Fischer JEP. Chromium deficiency during total
parenteral nutrition. J Am Med Assoc 1979;241:496-8.
9. Brown RO, Forloines-Lynn S, Cross RE, Heizer WD. Chromium defi-
ciency after long-term total parenteral nutrition. Dig Dis Sci 1986;31:
661-4.
10. McCarty MF. The case for supplemental chromium and a survey of clin-
ical studies with chromium picolinate. J Appl Nutr 1991;43:58-66.
11. Mertz W. Chromium in human nutrition: a review. J Nutr 1993;123:626-
33.
12. Wasser WG, Yusuf SA, D’Agati VD. Over-the-counter chromium and
renal failure (letter). Ann Intern Med 1997;127:656.
13. Lyons H, Pinn VW, Cortell S, Cohen JJ, Harrington JT. Allergic intersti-
tial nephritis causing reversible renal failure in four patients with idio-
pathic nephrotic syndrome. N Engl J Med 1973;288:124-8.
14. Rosse W, Bunn HF. Hemolytic anemias. In: Isselbacher KJ, Braunwald
E, Wilson JD, Martin JB, Fauci AS, Kasper DL, eds. Harrison’s princi-
ples of internal medicine. 13th ed. New York: McGraw-Hill, 1994;1743-
54.
EXTRACTO
OBJETIVO: Describir un caso de toxicidad producida por la ingestión
crónica de picolinato de cromio, producto que no requiere prescripción
médica, en cantidades de 6–12 veces mayores que las recomendadas.
RESUMEN DEL CASO: Una mujer de 33 años presentaba pérdida de peso,
anemia, trombocitopenia, hemólisis, disfunción hepática (aminotranferasas
15–20 veces el valor normal, bilirubina total tres veces el valor normal),
y fallo renal (creatinina sérica = 5.3 mg/dL, nitrógeno ureíco sanguíneo
= 152 mg/dL). Esta paciente había ingerido 1200–2400 µg diarios de
picolinato de cromio durante los pasados 4–5 meses para bajar de peso.
La paciente tenía una concentración de cromio en el plasma 2–3 veces
lo normal. Se descartaron los síndromes de trombocitopenia púrpura
trombótica y uremia hemolítica mediante hallazgos clínicos, cultivo de
sangre, y biopsia de médula ósea. La paciente se manejó con medidas de
apoyo, transfusiones con productos de sangre y hemodiálisis. La
hemólisis se estabilizó y la función hepática mejoró a los 6 días de
tratamiento. La función hepática regresó a los limites normales antes de
The Annals of Pharmacotherapy
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Case Reports
ser dada de alta. La función renal comenzó a normalizarse el día 12 de la
hospitalización y la creatinina sérica disminuyó a 1.3 mg/dL el día que
la paciente fue dada de alta. Un año más tarde, todos los valores de
laboratorio se encontraban dentro de los límites normales.
DISCUSION: El cromio trivalente es un elemento traza esencial que se
considera seguro cuando se ingiere en cantidades recomendadas. En la
actualidad, los compuestos de cromio trivalente son utilizados para
ayudar en la pérdida de peso, aumentar el peso magro y/o mejorar el
control glucémico. La información disponible relacionada con la
toxicidad del picolinato de cromio es aún muy limitada.
CONCLUSIONES: Los suplementos de cromio pueden causar
impedimentos renales serios cuando se ingieren en cantidades excesivas.
Es importante que el historial médico incluya información sobre los
suplementos nutricionales que pueda estar utilizando el paciente. Estos
productos se adquieren sin prescripción médica y muchas veces el
público y los medios de información no especializados los consideran
inofensivos.
RAFAELA MENA
RÉSUMÉ
OBJECTIF: Décrire un cas de toxicité associée à l’ingestion chronique
d’un produit de comptoir, le picolinate de chromium, à une dose de
6–12 fois celle recommandée quotidiennement.
RÉSUMÉ DU CAS: Une femme âgée de 33 ans se présente à l’urgence où
on constate une perte de poids, une anémie, une thrombocytopénie, une
hémolyse, un problème hépatique (le taux des aminotransférases est de
15–20 fois la normale, le taux de la bilirubine totale est de 3 fois la
normale), et une insuffisance rénale (créatinine sérique = 5.3 mg/dL,
azote uréique sanguine = 152 mg/dL). Elle a ingéré 1200–2400 µg par
jour de picolinate de chromium pendant les 4–5 mois précédents pour
stimuler une perte de poids. Les concentrations plasmatiques de
chromium sont de 2–3 fois la normale. Un purpura thrombotique
thrombocytopénique et un syndrome hémolytique urémique ont été
éliminés à l’aide des données cliniques, des prélèvements sanguins et
d’une biopsie de la moëlle épinière. Un traitement de support a été
administré à la patiente; elle a reçu des transfusions sanguines et une
hémodialyse a été réalisée. L’hémolyse s’est stabilisé et la fonction
hépatique s’est améliorée en 6 jours. La fonction hépatique s’est
normalisée avant le départ de la patiente. La fonction rénale a
commencé à s’améliorer au jour 12 et la créatinine sérique était de 1.3
mg/dL à son départ. Un an plus tard, toutes les valeurs de laboratoire
sont à l’intérieur de la limite de la normale.
DISCUSSION: Le chromium trivalent est un oligo-élément essentiel
considéré sécuritaire lorsqu’il est ingéré en quantité normale. Des
produits à base de chromium trivalent sont utilisés couramment par les
patients pour favoriser la perte de poids, pour augmenter la masse
maigre et/ou pour améliorer le contrôle glycémique. Les données
concernant la toxicité du picolinate de chromium sont limitées.
CONCLUSIONS: Les suppléments de chromium peuvent causer une
altération grave de la fonction rénale s’ils sont ingérés en quantité
excessive. Lors des entrevues avec les patients, une attention particulière
devrait être portée à l’utilisation des suppléments nutritionnels disponibles
sans ordonnance et considérés sans danger par le public et la presse.
MARIE LAROUCHE
■ 1998 April, Volume 32 ■ 431