Chemistry Reference
In-Depth Information
give rise to a variety of effects. The presenting features
may be entirely nonspecifi c, the clinical examination
giving no lead on the cause of the illness. The principal
features that should be considered in arriving at a cor-
rect diagnosis are elaborated in the following.
with possible side effects is stressful to patients, and an
orally effective iron chelator, deferiprone, is suited for
long-term in-home treatment. This can be combined
with desferrioxamine and be effective at lower doses
(Kontogiorghes
et al.,
2000).
Primary or idiopathic hemochromatosis is an auto-
somal-recessive disorder caused by excessive absorp-
tion and storage of iron. Deposition of iron in organs
and tissues causes fi brotic changes and functional
impairment, in particular arthropathy, cirrhosis with
hepatomegaly, diabetic mellitus, hypogonadism, car-
diac arrhythmias, heart failure, and skin pigmentation
caused by melanin and hemosiderin deposition (Bacon,
2001; Niederau
et al
., 1994). Repeated phlebotomus has
been effective in reducing serum ferritin, and in cases
with excessive iron deposits, this has been combined
with an iron-chelating agent, in particular desferriox-
amine. Because early diagnosis is essential for the suc-
cessful treatment of this condition, relatives of patients
with primary hemochromatosis are candidates for
genetic screening (Tavill, 1999).
In Wilson's disease, hepatolenticular degeneration,
a recessively inherited metabolic disorder, there is
a failure to excrete copper into bile, resulting in copper
accumulation fi rst in the liver, then in the brain, cornea,
and kidneys (Walshe, 1984). The age of onset may be as
early as 5 years up to the fi fth decade. Hepatic necrosis
releases copper into the circulation, causing damage to
erythrocyte membranes leading to hemolytic anaemia.
Copper accumulation results in widespread neurologi-
cal disturbances with tremor, slurred speech, muscu-
lar rigidity, mental deterioration, and pigmented rings
at the corneal rims of the eye, this being a diagnostic
marker. Diagnosis depends on an accurate estimation
of copper in an uncontaminated 24-hour urine sam-
ple, in Wilson's disease usually more than 100
2.1 History of Exposure
In most cases, a history of exposure to a toxic metal
will give the necessary clue. In an industrial situation,
there may be a clear history of exposure that may be
obtained from the patient, a relative, or a coworker.
The clinician should not fail to take a full and accu-
rate occupational history when a poisoning of occupa-
tional origin is suspected. It may be necessary to seek
additional information from the employer or his agent,
from an occupational hygienist, or from a health and
safety representative. Exposure to a toxic metal may,
however, occur without this being suspected by any of
the persons questioned, and this can only be inferred
by an adequate knowledge of the work processes
involved. A good example may be given with expo-
sure to arsine gas, which usually presents as an acute
medical emergency. Arsenic may be a contaminant in
scrap metals, fl ue dusts, etc., and arsine may be formed
in any reducing situation, or when a metallic dross
containing arsenic comes into contact with water. The
condition should, therefore, be suspected in a scrap-
metal worker presenting with the appropriate clinical
features.
In the domestic environment, an appropriate his-
tory may give an exposure inferred from medicaments
such as iron pills or household chemicals. Unla-
beled pills or chemicals should, of course, be kept for
analysis. In a homicidal instance, a psychotic factory
worker succeeded in poisoning three fellow workers in
succession by adding a thallium salt to tea, causing the
deaths of two men before the poisoning was suspected
(Cavanagh
et al
., 1974). In the general environment,
diagnosis of metal poisoning, especially if caused by
long-term absorption of cumulative metals in the body,
can be very diffi cult. Methylmercury poisoning after
the eating of contaminated bread in Iraq was diagnosed
at the beginning of the outbreak, because the medical
offi cers had previous experience of the condition.
Metal accumulation may also occur in the absence
of environmental exposure. The thalassemias are
a heterogenous group of genetic disorders of hemo-
globin synthesis. Symptomatic treatment of anemia
requires regular blood transfusion from childhood.
For the prevention and treatment of resulting iron
overload, transfusional siderosis, a chelating agent is
required, desferrioxamine being the best choice. How-
ever, repeated intravenous or subcutaneous injection
g/24
hours. Treatment to produce a negative copper balance
is effective with the chelating agents penicillamine,
triethylene tetramine, and with zinc, which inhibits
copper absorption from food and increases fecal cop-
per excretion. In particular, treatment is more effective
in those diagnosed in the presymptomatic phases of
the disease (Sarkar, 1999).
µ
2.2 Clinical Features
The presenting clinical features, especially in acute
poisoning, may be entirely nonspecifi c. Lead colic has
been mistaken for the acute surgical abdomen, and
craniotomy has been performed after encephalopathy
caused by lead. Such mistakes would not have been
made if a careful history had been taken. Certain clini-
cal sequences should alert the physician to the possi-
bility of metal poisoning. Gastroenteritis followed by
