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Iron deficiency anemia.Am
Fam Physician. 2007 Mar 1;75(5):671-8.
The prevalence of
iron deficiency anemia is 2 percent in adult men, 9 to 12 percent in
non-Hispanic white women, and nearly 20 percent in black and
Mexican-American women. Nine percent of patients older than 65 years
with iron deficiency anemia have a gastrointestinal cancer when
evaluated. The U.S. Preventive Services Task Force currently
recommends screening for iron deficiency anemia in pregnant women but
not in other groups. Routine iron supplementation is recommended for
high-risk infants six to 12 months of age. Iron deficiency anemia is
classically described as a microcytic anemia. The differential
diagnosis includes thalassemia, sideroblastic anemias, some types of
anemia of chronic disease, and lead poisoning. Serum ferritin is the
preferred initial diagnostic test. Total iron-binding capacity,
transferrin saturation, serum iron, and serum transferrin receptor
levels may be helpful if the ferritin level is between 46 and 99 ng
per mL (46 and 99 mcg per L); bone marrow biopsy may be necessary in
these patients for a definitive diagnosis. In children, adolescents,
and women of reproductive age, a trial of iron is a reasonable
approach if the review of symptoms, history, and physical examination
are negative; however, the hemoglobin should be checked at one month.
If there is not a 1 to 2 g per dL (10 to 20 g per L) increase in the
hemoglobin level in that time, possibilities include malabsorption of
oral iron, continued bleeding, or unknown lesion. For other patients,
an endoscopic evaluation is recommended beginning with colonoscopy if
the patient is older than 50.
Universal
versus selective iron supplementation for infants and the risk of
unintentional poisoning in young children: a comparative study of two
populations.
Ann
Pharmacother. 2007 Mar;41(3):414-9.
BACKGROUND:
Iron continues to be a common cause of poisoning in young children, in
part due to its widespread use and easy accessibility. OBJECTIVE: To
determine differences in the epidemiology and outcome of unintentional
iron ingestion by young children in populations practicing selective (eg,
US) versus universal (eg, Israel) iron supplementation to infants.
METHODS: All cases of unintentional iron ingestion in children younger
than 7 years in a one year period were identified through the poison
control center databases of 2 sites (Illinois and Israel). Parameters
compared include patient sex and age; type, form, and dose of iron
preparation; circumstances and clinical manifestations; management;
and outcome. RESULTS: A total of 602 children were identified: 459 in
Illinois and 143 in Israel. The majority of Illinois children ingested
multivitamin preparations (94%), whereas Israeli children ingested
single-ingredient iron preparations (78%) (p < 0.001). Iron doses
ingested were higher in Israel (median 14.5 vs 6.6 mg/kg; p < 0.001)
but remained within the nontoxic range for most children. No deaths or
severe poisonings were reported, and 93% of children in both groups
were asymptomatic. The majority of ingestions in both locations were
due to unintentional self-ingestion. However, parental miscalculation
occurred more frequently in Israel (16%) than in Illinois (1%).
CONCLUSIONS: Universal iron supplementation to infants was not
associated with a negative impact on the outcome of pediatric
unintentional ingestions. Low-dose exposures were safely managed by
on-site observation.
Iron: not
a benign therapeutic drug.Curr
Opin Pediatr. 2006 Apr;18(2):174-9.
PURPOSE OF
REVIEW: This article reviews the pathophysiology and clinical
presentation of iron poisoning. Recently proposed guidelines for
triage of children with iron ingestion will be discussed as well as
diagnostic and treatment modalities. Finally, the potential impact of
unit-dose packaging as a primary preventative measure will be
discussed. RECENT FINDINGS: Carbonyl iron has a greater safety margin
than the iron salts. There have been no published reports of serious
or fatal poisoning from the ingestion of carbonyl iron products.
Evidence-based consensus guidelines have determined that the threshold
for referral to a healthcare facility is 40 mg/kg of elemental iron in
the form of adult iron formulations. Unit-dose packaging of iron
preparations appeared to decrease the number of exposures to iron and
deaths in the United States during the period they were instituted.
SUMMARY: Iron poisoning remains primarily a clinical diagnosis,
although certain laboratory and radiological testing may provide
helpful evidence to guide evaluation and management. Primary
prevention is the best modality for decreasing morbidity and mortality
for all poisonings including iron.
Hepatotoxicity
in acute iron poisoning.Hum
Exp Toxicol. 2005 Nov;24(11):559-62.
Although liver
injury is a recognized consequence of acute iron poisoning, its
description is limited to several case reports. It appears to be
dose-related, however, there are published reports of severe iron
poisoning without liver injury. The purpose of this study is to
examine the hypothesis that this is a dose-related phenomenon and to
identify the serum iron concentration of risk for this outcome. The
design of this study is a retrospective review of our hospital's
experience over 20 years. Extracted data included demographics, time
of ingestion, highest serum iron concentration and highest hepatic
transaminase activity. Iron poisoning was defined as a serum iron
concentration >300 microg/dL (55 micromol/L) within 12 hours of
ingestion. Hepatotoxicity was defined as a serum transaminase (either
ALT or AST) >150 U/L. Severe hepatotoxicity was defined >1000U/L.
Seventy-three patients (1-48 years old) participated in the study and
of these patients 60 (47 female) did not have hepatotoxicity. Their
serum iron concentrations were 300-704 microg/dL (55-128 micromol/L).
Thirteen patients had hepatotoxicity and of these patients, nine had
severe liver injury. Severe injury was associated with serum iron
concentrations well in excess of 1000 microg/dL (182 micromol/L). Our
data support hepatotoxicity due to iron poisoning as a dose-related
phenomenon with clinically important cases unlikely with a serum iron
concentration of < 700 microg/dL (128 micromol/L) within the first 12
hours. Clinically important hepatotoxicity occurs with values in
excess of 1000 microg/dL (182 micromol/L).
Iron
ingestion: an evidence-based consensus guideline for out-of-hospital
management.
Clin Toxicol (Phila). 2005;43(6):553-70.
From 1983 to
1991, iron caused over 30% of the deaths from accidental ingestion of
drug products by children. An evidence-based expert consensus process
was used to create this guideline. Relevant articles were abstracted
by a trained physician researcher. The first draft of the guideline
was created by the primary author. The entire panel discussed and
refined the guideline before its distribution to secondary reviewers
for comment. The panel then made changes in response to comments
received. The objective of this guideline is to assist poison center
personnel in the appropriate out-of-hospital triage and initial
management of patients with suspected ingestions of iron by 1)
describing the manner in which an ingestion of iron might be managed,
2) identifying the key decision elements in managing cases of iron
ingestion, 3) providing clear and practical recommendations that
reflect the current state of knowledge, and 4) identifying needs for
research. This guideline applies to ingestion of iron alone and is
based on an assessment of current scientific and clinical information.
The expert consensus panel recognizes that specific patient care
decisions may be at variance with this guideline and are the
prerogative of the patient and the health professionals providing
care, considering all of the circumstances involved. The panel's
recommendations follow; the grade of recommendation is in parentheses.
1) Patients with stated or suspected self-harm or who are victims of
malicious administration of an iron product should be referred to an
acute care medical facility immediately. This activity should be
guided by local poison center procedures. In general, this should
occur regardless of the amount ingested (Grade D). 2) Pediatric or
adult patients with a known ingestion of 40 mg/kg or greater of
elemental iron in the form of adult ferrous salt formulations or who
have severe or persistent symptoms related to iron ingestion should be
referred to a healthcare facility for medical evaluation. Patients who
have ingested less than 40 mg/kg of elemental iron and who are having
mild symptoms can be observed at home. Mild symptoms such as vomiting
and diarrhea occur frequently. These mild symptoms should not
necessarily prompt referral to a healthcare facility. Patients with
more serious symptoms, such as persistent vomiting and diarrhea,
alterations in level of consciousness, hematemesis, and bloody
diarrhea require referral. The same dose threshold should be used for
pregnant women, however, when calculating the mg/kg dose ingested, the
pre-pregnancy weight of the woman should be used (Grade C). 3)
Patients with ingestions of children's chewable vitamins plus iron
should be observed at home with appropriate follow-up. The presence of
diarrhea should not be the sole indicator for referral as these
products are often sweetened with sorbitol. Children may need referral
for the management of dehydration if vomiting or diarrhea is severe or
prolonged (Grade C). 4) Patients with unintentional ingestions of
carbonyl iron or polysaccharide-iron complex formulations should be
observed at home with appropriate follow-up (Grade C). 5) Ipecac
syrup, activated charcoal, cathartics, or oral complexing agents, such
as bicarbonate or phosphate solutions, should not be used in the
out-of-hospital management of iron ingestions (Grade C). 6)
Asymptomatic patients are unlikely to develop symptoms if the interval
between ingestion and the call to the poison center is greater than 6
hours. These patients should not need referral or prolonged
observation. Depending on the specific circumstances, follow-up calls
might be indicated (Grade C).
Unit-dose
packaging of iron supplements and reduction of iron poisoning in young
children.
Arch Pediatr Adolesc Med. 2005
Jun;159(6):557-60.
BACKGROUND:
Iron poisoning is a major cause of unintentional poisoning death in
young children. The US Food and Drug Administration proclaimed a
regulation for unit-dose packaging of iron supplements in 1997.
OBJECTIVE: To determine whether the requirement for unit-dose
packaging of iron supplements decreases the incidence of iron
ingestion and the incidence of deaths due to iron poisoning in
children younger than 6 years. METHODS: This is a
preintervention-postintervention study of the US federally mandated
requirement for unit-dose packaging of iron supplements. The 10 years
prior to the intervention were compared with the 5 years after its
promulgation. The incidences of iron ingestion and of iron poisoning
deaths for children younger than 6 years were obtained from the annual
reports of the American Association of Poison Control Centers
(Washington, DC). RESULTS: The average number of iron ingestion calls
per 1000 of all calls to poison control centers regarding children
younger than 6 years decreased from 2.99 per 1000 to 1.91 per 1000
(odds ratio, 1.29 [95% confidence interval, 1.27-1.32]; P<.001). The
number of deaths decreased from 29 to 1 (odds ratio, 13.56 [95%
confidence interval, 1.85-99.52]; P = .03). CONCLUSIONS: These are the
first data that show a decrease in the incidence of nonintentional
ingestion of a specific drug by young children and a decrease in
mortality from poisoning by this drug after the introduction of
unit-dose packaging. There was a decrease in the incidence of iron
ingestion and a dramatic decrease in the number of deaths due to iron
poisoning. This validates unit-dose packaging as an effective strategy
for the prevention of iron poisoning and iron poisoning deaths in
young children. This highly effective intervention should be
considered for other medications with a high hazard for morbidity and
mortality when taken as an overdose.
Measurements of iron
status and survival in African iron overload.S
Afr Med J. 1999 Sep;89(9):966-72.
INTRODUCTION:
Dietary iron overload is common in southern Africa and there is a
misconception that the condition is benign. Early descriptions of the
condition relied on autopsy studies, and the use of indirect
measurements of iron status to diagnose this form of iron overload has
not been clarified. METHODS: The study involved 22 black subjects
found to have iron overload on liver biopsy. Fourteen subjects
presented to hospital with liver disease and were found to have iron
overload on percutaneous liver biopsy. Eight subjects, drawn from a
family study, underwent liver biopsy because of elevated serum
ferritin concentrations suggestive of iron overload. Indirect
measurements of iron status (transferrin saturation, serum ferritin)
were performed on all subjects. Histological iron grade and hepatic
iron concentration were used as direct measures of iron status.
RESULTS: There were no significant differences in either direct or
indirect measurements of iron status between the two groups. In 75% of
these subjects the hepatic iron concentration was greater than 350
micrograms/g dry weight, an extreme elevation associated with a high
risk of fibrosis and cirrhosis. Serum ferritin was elevated in all
subjects and the transferrin saturation was greater than 60% in 93% of
the subjects. Hepatomegaly was present in 20 of the 22 cases and there
was only a moderate derangement in liver enzymes except for a tenfold
increase in the median gamma-glutamyl transpeptidase concentration.
There was a strong correlation between serum ferritin and hepatic iron
concentrations (r = 0.71, P = 0.006). After a median follow-up of 19
months, 6 (26%) of the subjects had died. The risk of mortality
correlated significantly with both the hepatic iron concentration and
the serum ferritin concentration. CONCLUSIONS: Indirect measurements
of iron status (serum ferritin concentration and transferrin
saturation) are useful in the diagnosis of African dietary iron
overload. When dietary iron overload becomes symptomatic it has a high
mortality. Measures to prevent and treat this condition are needed.
Dietary iron
overload as a risk factor for hepatocellular carcinoma in Black
Africans.
Hepatology. 1998 Jun;27(6):1563-6.
Although the
iron-loading disease, hereditary hemochromatosis, has a strong causal
association with hepatocellular carcinoma (HCC), the carcinogenic
potential of dietary iron overload in Black Africans is not known. We
investigated this potential by evaluating iron status, alcohol
consumption, markers for hepatitis B (HBV) and C virus (HCV)
infections, and exposure to dietary aflatoxin B1 in 24 rural patients
with this tumor, 48 race-, sex-, and age-matched hospital-based
controls, and 75 related or unrelated close family members of the
cancer patients. Iron overload was defined as a raised serum ferritin
concentration in combination with a transferrin saturation > or = 60%,
and was confirmed histologically when possible. Among 24 patients and
48 hospital controls, the risk of developing HCC in the iron-loaded
subjects was 10.6 (95% confidence limits of 1.5 and 76.8) relative to
individuals with normal iron status, after adjusting for alcohol
consumption, chronic HBV and HBC infections, and exposure to aflatoxin
B1. The risk of HCC in subjects with HBV infection was 33.2 (7.2,
153.4) (odds ratio [95% confidence limits]), HCV infection 6.4 (0.3,
133.5), and alcohol consumption 2.0 (0.5, 8.2). Aflatoxin B1 exposure
did not appear to increase the risk of HCC. The population
attributable risk of iron overload in the development of HCC was
estimated to be 29%. Among 20 cancer patients and 75 family members,
the risk of developing HCC with iron overload was 4.1 (0.5, 32.2). We
conclude that dietary iron overload may contribute to the development
of HCC in Black Africans. |
