R EVIEW

Hypoglycaemia: accidents, violence and

murder. Part 2
V Marks*
Death from insulin-induced
hypoglycaemia
Murder by insulin (and sulphonylureas) is rare and can be classified
as shown in Table 1. It can be
extremely difficult to recognise and
even more difficult to confirm.
Mrs ER, a 75-year-old insulin
dependent woman paralysed by
dementia, was found dead in bed in
the nursing home where she lived.
She was last seen alive sitting up in
bed at 4pm in the afternoon of her
death. When next observed at
4.30pm she was dead. No anatomical cause for her sudden death was
found at autopsy and a sample of
serum collected from a peripheral
blood vessel was sent to a clinical
laboratory with a request for an
insulin analysis. The insulin concentration
was
reported
as
150mU/L (1050pmol/L) and was
described as being more than three
times the expected level. Her husband, who had visited her that afternoon, immediately came under suspicion and police investigations
were begun. When I was consulted I
noticed that the patients prescription specified porcine insulin.
Suspecting that the insulin assay
used had been standardised for
human insulin, enquiries were made
of the analyst who confirmed that
the assay used was for human insulin
and that the antiserum used had a
marked preference for porcine
insulin (Figure 1). Re-assay of the
sample using appropriate standards
revealed that the insulin concentration was 30mU/L (210pmol/L)
which is exactly what was expected.
The coroner returned a verdict
of death from natural causes and
the husband was exonerated from
all blame.
Vincent Marks, MA, DM, FRCP, FRCPath,
MAE, Professor of Clinical Biochemistry
Emeritus, Post-Graduate Medical School,
University of Surrey, Guildford, UK

ABSTRACT
The second of the two articles in this series deals with the malicious administration of
insulin to adults and the problems associated with detecting and proving it as the murder
weapon. Differences between the use of insulin as a murder weapon in fiction and in real
life are emphasised. Insulin emerges as a poor and unpredictable weapon that is,
providing the right samples are collected and analysed appropriately, comparatively easy
to detect. Pathologists and clinicians need to be aware what these conditions are and
observe them if miscarriages of justice are to be avoided. Copyright 2005 John Wiley &
Sons, Ltd.
Practical Diabetes Int 2005; 22(9): xxxxxx

KEY WORDS
murder; homicide; pathology; forensic insulin assay; pathology

This case highlights one of the

difficulties of confirming death
from insulin-induced hypoglycaemia after death when blood (and
even vitreous) glucose measurements are worthless for confirming
a diagnosis of hypoglycaemia but
may help exclude it. Diagnosis of
hypoglycaemia is simpler, but still
fraught, if the victim is still alive
when discovered usually in coma
and their blood glucose concentration can be measured meaningfully.
This can only be inferred in a corpse
and then usually only from discrepant plasma insulin and C-peptide results.
Methods for measuring insulin
have evolved enormously since they
were first introduced for the standardisation of pharmaceutical
insulin some 85 years ago. Assays
suitable for clinical use did not
become available, however, until the
early 1950s and were of limited sensitivity and specificity. Nevertheless,
they were sufficiently sensitive and
specific to lead to the first conviction for murder by insulin in 1957.
The situation changed radically with
the invention by Berson and Yalow
of radioimmunoassay in 1960. The

Table 1. Classification of murder

by insulin

*Correspondence to: Professor Vincent

Marks, Oriel House, Derby Road,
Haslemere GU27 1BP, UK;
e-mail: vincentmarks@bigfoot.com

Received: 25 July 2005

Accepted: 16 August 2005

Pract Diab Int November/December 2005 Vol. 22 No. 9

Mass murderers usually of

elderly inmates in nursing
homes and hospitals
Murder of infants and
helpless people including
Munchausen by Proxy
Murder of sentient adults
Motivated
No recognisable motive
Suicide pact

exquisite sensitivity and specificity of

the technique led to major advances
in our understanding of glucose
homeostasis. Although it proved to
be of limited value to clinicians
except for the differential diagnosis
of hypoglycaemia, it set the scene
for the development of assays for
other substances, especially hormones, and is now in one of its various guises among the most popular
techniques used in clinical laboratories throughout the world. The
value of insulin measurements
themselves
are
enormously
increased when combined with
simultaneous C-peptide and sulphonylurea assays.1

Copyright 2005 John Wiley & Sons, Ltd.

R EVIEW
Hypoglycaemia: accidents, violence and murder

Figure 1. Cross reactivity with pig insulin, human proinsulin and lispro
(human insulin =100%) of 4 different immunoassay kits selected from data
presented by Sapin2
500

400

Percent

Radioimmunoassay, the first of

the genre, was the progenitor of all
subsequent types of immunoassay
which, like radioimmunoassay itself,
rely upon the specificity and binding
characteristics of one or more antibodies. They are the key reagents
whether produced in an animal
(polyclonal antibodies) or in a fermenter (monoclonal antibodies).
The two others key reagents are a
label and a standard identical to the
substance being measured. Some of
the different types of assay currently
available in Europe2 for the measurement of insulin in blood plasma
(serum) are shown in Table 2.
Once assays sufficiently sensitive
to detect insulin in post-mortem blood
serum became available, the number of cases of murder brought to
court following the Barlow case in
1957 increased though not as
rapidly as some novelists would have
us believe. The evidence in most
cases rests on the results of simultaneous insulin and C-peptide measurement showing inappropriately
high insulin in the presence of
undetectable, or extremely low, Cpeptide levels. This combination
has, however, been accepted too
uncritically as conclusive proof of
exogenous insulin administration
even when there was no supporting
evidence, such as an insulin injection site, and has led to several miscarriages of justice, only some of
which have been rectified.
One of the reasons for this lies in
the fact that despite their immense
value in research and clinical practice, immunoassays do not, unless
combined with other laboratory procedures such as gel filtration or high
performance liquid chromatography (HPLC),3,4 meet the criteria of
specificity required for forensic purposes (Figure 2). This is partly due
to an inherent disadvantage of
immunoassay procedures, which are
subject to both specific and non-specific interference by substances
uniquely present in the patients
serum, but not the comparators,5
and partly to the fact that insulin is
not a single chemical entity.
Once the molecular structure of
insulin from various animal species
had been elucidated it became clear
that insulin was a generic rather

300

200

100

RIA

Proinsulin

ELISA
IRMA
IBCMA
Selected commercial immunoassay kits
Pig insulin

Lispro

Insulin

Table 2. Types of Immunoassay (for measuring insulin in human

plasma/serum). The numbers in parenthesis refer to the number of different
assay kits on the market in Europe

Competitive

Non-competitive

RIA (9)
(radioimmunoassay)

IRMA (5)
Immunoradiometric-assay
IEMA (8)
Immunoenzymometric-assay
ICMA (2)
Immunochemilumino-assay
IFMA (1)
Immunofluorimetric-assay
IECMA (1)
Immunoelectrochemi-luminometric-assay

than a specific term. Subtle differences between insulins from different species have comparatively little
effect upon their biological properties but can, and sometimes do, profoundly alter their immunological
properties (Table 3). This can, as in
the case of ER described above,
have unfortunate effects or, as in
others, convert a suspicion of
exogenous insulin administration
to a certainty. It must never be forgotten that despite what their manufacturers may say immunoassays
are never quite as specific as they
are claimed to be: they almost
invariably interact, for example,

Pract Diab Int November/December 2005 Vol. 22 No. 9

with glycated insulin6 whose

importance is still largely unrecognised as well as to a greater or
lesser extent with pro-insulin and its
partially split products.2
Cross reactivity and either its
presence or absence in immunoassay procedures is likely to become
increasingly important in forensic
work with the introduction of synthetic insulin analogues such as
lispro, aspart, detemir and glargine.
All possess insulins ability to lower
blood glucose levels to dangerous
levels and may, or may not, react
with the antibodies used in any particular insulin assay kit. This prob-

Copyright 2005 John Wiley & Sons, Ltd.

R EVIEW
Hypoglycaemia: accidents, violence and murder

Figure 2. Comparison of results of plasma insulin assays obtained using a

sandwich type immunoassay and an IDA-MS technique on 10 plasma
samples from otherwise healthy obese non-diabetic subjects. (Redrawn
from the data of Kippen8
350
300

Insulin pmol/L

250
200
150
100
50
0

MEIA

5
6
7
Plasma sample

10

IDA-MS

Table 3. What is insulin?

Specific insulin used

in therapy

Synthetic insulins currently

available for therapy

Human insulin
Porcine insulin
Bovine insulin

Lispro
Aspart
Detemir
Glargine

Each is available in various

formulations but circulates in the
blood as the native hormone
Each is chemically and
immunologically unique

lem first came to our attention in

1997 when we were asked to investigate the cause of seemingly inexplicable hypoglycaemia in a patient with
type 1 diabetes who, despite omitting to take her insulin, suffered
habitual episodes of hypoglycaemia.
None of the causes of spontaneous
hypoglycaemia other than insulin
administration was immediately evident yet both her plasma insulin
and, of course, her C-peptide assays
were negative when her blood glucose concentration was low.
Uncritical acceptance of these
results would have led to a wild
goose chase for other extremely rare
causes of spontaneous hypogly-

Each circulates in its synthetic form

Each is chemically and
immunologically unique

caemia had we not decided to use a

different assay kit. This showed the
expected inappropriately high
plasma insulin concentration
which, in this case, turned out to be
lispro. Although this was the first
case of factitious hypoglycaemia to
be recognised as caused by an
insulin analogue, it will certainly not
be the last.
One of the ways to get round the
non-specificity of immunoassays is to
combine them with another technique such as gel filtration or HPLC,
but even here it cannot be guaranteed. The answer lies in the use of
mass spectrometry (MS)7 preferably
with a stable isotope internal stan-

Pract Diab Int November/December 2005 Vol. 22 No. 9

dard8 but this is neither widely available nor very likely to become routine for many years to come. The use
of MS in forensic cases, and in which
the whole case rests entirely upon
the specificity of the assay result, is,
however, essential if some of the miscarriages of justice that have
occurred in the past are not to be
repeated.
Expert witnesses should also be
aware that even when the insulin
(and C-peptide) results are beyond
reproach their interpretation might
not be. Contrary to dogma an inappropriately high plasma insulin and
a low C-peptide concentration
especially in the presence of hypoglycaemia though highly suggestive, is not pathognomonic of
exogenous insulin administration.
It also occurs, in its most flagrant
form, in the Auto-immune Insulin
Syndrome9 but possibly in other
conditions where there are homologous or heterologous insulin
antibodies present in the circulation but which are entirely unsuspected.10 Inappropriately high
insulinC-peptide ratios can also
occur in conditions in which the
rate of insulin removal from the circulation, but not of that of C-peptide, is reduced. The possibility cannot be dismissed that the C-peptide
but not insulin concentration was
fallaciously low due to its enzymatic
destruction or non-enzymatic
degradation in the sample after its
collection from the body.
I now believe that a mistaken
belief in the specific diagnostic
value11 of the C-peptideinsulin
ratio explains some of the cases of
factitious hypoglycaemia that we
and others have diagnosed in the
past exclusively on the results of
insulin and C-peptide measurements, but which have been vehemently denied by the patient.
Undoubtedly, some of these cases
are genuine, but use of an abnormal
insulinC-peptide ratio as the sole
evidence for making it is an example
of a circular argument which is
illogical.

Murder by insulin
Murder by insulin is more popular
in fiction than in real life. The quotation taken from Dancing is typi-

Copyright 2005 John Wiley & Sons, Ltd.

R EVIEW
Hypoglycaemia: accidents, violence and murder

Box 1. Murder by insulin: the fiction. (Taken from Dancing by Chesa Baker)
Rory was murdered the tox screen on her blood indicated high levels of
insulin in her system.
Was she diabetic?
Nope. It was the insulin that killed her. But I dont think that it was meant to.
Why do you say that?
The murderer knew how much insulin would be lethal. He gave Rory just
enough so she would simply pass out but, the insulin hit a blood vein
which Im assuming wasnt the murders intention and the insulin mixed
with her blood, and travelled directly to her heart, killing her instantly.

Box 2. Murder by insulin: the sordid

facts12
Tonica Jenkins, 27, the
defendant in this Cleveland (USA)
trial, sought to kill the victim,
Melissa Latham, by injecting her
with catastrophic levels of insulin
on April 21, 2001. When that
didnt work, she asked her
cousin, Kyle Martin, to beat
Latham to death with a brick.

Figure 3. Insulin and C-peptide

concentrations in two samples of
post-mortem urine measured blind.
Note the very large difference in
insulin and close similarity in
concentration of C-peptide in what
are, ostensibly, identical samples
700
600
500

expert witness. It presents many of

the difficulties confronting the
judge and jury when the only evidence that the victims death was
from hypoglycaemia rather than to
an undetermined cause
EL, a 60-year-old man, was found
dead in his bed by his partner of
many years. She was a nurse who on
her return from night duty found
him dead in bed where he had
apparently
vomited.
Autopsy
revealed no anatomical cause for his
death though his coronary arteries
were partially blocked by atheroma.
The academic pathologist who conducted the post-mortem collected
blood and urine for analysis and
handed them to an assistant for storage prior to sending them to a suitable laboratory for analysis for drugs
possibly taken with suicidal intent.
At a corners inquest a few days
after ELs death his daughter
accused his partner, Maria Whiston,
of murder by injecting him with
insulin. The coroner ordered a further autopsy, this time by a forensic
pathologist, but again no anatomical cause for death was found. Nor
did a thorough search of the body
for injection sites, especially
between the toes, reveal anything
abnormal. A further urine sample
was collected. This, together with
the urine and blood samples col-

Pract Diab Int November/December 2005 Vol. 22 No. 9

400
pmol/L

cal and entirely wrong (Box 1). The

reality is totally different as the case
of Tonica Jenkins12 exemplifies
(Box 2). Her victim, Melissa Latham
was able, between the time she was
injected with insulin and the onset
of severe symptomatic hypoglycaemia, to run away from her captors and seek help in a nearby shop
where she collapsed. Indeed, in
most of the small number of cases in
which a defendant has actually been
convicted of murder by insulin, a
second weapon e.g. drowning, battering or suffocation had to be
used to achieve the desired result.13
There are several reasons for
this. To kill a sentient adult with
insulin requires them to be compliant unless they are physically
restrained. The dose necessary to
produce a predictably fatal outcome is large probably in the
region of 1000 units to judge from
the literature relating to suicide by
insulin14 and does not become
manifest until at least 15 minutes
(and generally much longer) after
the injection, giving the victim
ample time, as in the Tonica Jenkins
case, to escape and obtain help.
Hypoglycaemia takes from six to 12
hours of coma to produce irreversible brain damage and even
longer to kill. There remains always
the possibility, therefore, that the
victim will be discovered within the
first six, and possibly 12, hours of
the injection and be resuscitated by
being given intravenous glucose.
This would enable them to name
their attacker who will almost invariably be known to them. An injection
site is also likely to be visible,13
unless great pains have been taken
to prevent it, and the injection is
unlikely to have been accepted by
the victim unknowingly or without a
struggle. Moreover, anyone sufficiently knowledgeable about the
potential lethal effects of insulin to
use it to kill someone would also
know, contrary to popular belief,
that insulin can be detected in the
body after death and identified as a
murder weapon.
I want to conclude this brief journey into the complexities of the
forensic aspects of hypoglycaemia
with a brief description of one of the
cases in which I was involved as an

300
200
100
0
Sample 1 Sample 2
Insulin

C-peptide

lected at the first autopsy, was sent

for analysis to a clinical laboratory in
a hospital specialising in hormone
assays but not for forensic purposes.
On arrival in the laboratory two
blood samples both from the same
body but labelled, and consequently
treated, as separate from one
another were analysed independently. The C-peptide concentrations were recorded as 270pmol/L
and 380pmol/L and the corresponding insulin concentrations as
35pmol/L and 16pmol/L, respectively. These results were, however,
deemed unacceptable because the
samples were too haemolysed to
make the results reliable.
Each of the two urine samples
collected from the first and second
autopsies were also treated blind in
the laboratory and assayed for their

Copyright 2005 John Wiley & Sons, Ltd.

R EVIEW
Hypoglycaemia: accidents, violence and murder

Figure 4. Urine insulin concentration measured in three different clinical

laboratories on 19 samples of urine collected from cadavers as controls for
results obtained on Mr EL. Note the marked and inconsistent variations
between results obtained by the different laboratories
120

Insulin pmol/L

100
80
60
40
20
0
1
GF

9 10 11 12 13 14 15 16 17 18 19
Case number

OF

NC

Figure 5. Comparison of urine insulin concentrations found in Mr EL

with those found in selected cases in the paper by Chamberlain
and Stimmler16
8000

Insulin pmol/L

6000

4000

2000

0
Case 19 Case 18

Case 16

insulin and C-peptide content using

the standard laboratory assay.
Although this had been developed
and validated only for use with
serum or plasma and not for urine,
the results were reported to the
police who consulted an expert on
their interpretation. He considered
the results (Figure 3), despite the
enormous difference between ostensibly the same specimen, diagnostic

Case 5

EL 2

EL1

of exogenous insulin administration. On the basis of these results

and further investigation into the
circumstances of ELs death his partner, Maria Whiston, was charged
with his murder by injecting him
with insulin.
Experts called by the defence
pointed out that not only were the
analytical results suspect, since the
methods used by laboratory were

Pract Diab Int November/December 2005 Vol. 22 No. 9

not validated for use on urine, but

they also showed an unacceptably
large difference between the results
obtained for insulin (but not for Cpeptide) in the two urine samples
which should of course have been
similar or identical having come
from the same body. Moreover,
interpretation of urinary insulin
results is so fraught that Dr Arthur
Rubenstein, the pioneer of urinary
insulin assays and an expert witness
in the trial, described it as valueless
in the context of ELs death. He
pointed out that ordinarily very little insulin gets into the urine,
unlike C-peptide whose assay has
proved useful in clinical research.
Moreover, it is enormously influenced by numerous clinical conditions, especially those affecting the
kidney,15,16 and had never been
shown to correlate closely with
plasma insulin levels or be useful in
assessing insulin production.
In order to validate their conclusion the prosecution arranged, during the actual trial, for urine samples to be collected at autopsy from
a number of patients of comparable
age and dying from a variety of
causes and for these to be analysed.
This was undertaken in three different clinical laboratories, including
the original one, using different
types of immunoassay. The results
on 19 of the age matched post-mortem
specimens from the three laboratories are shown in Figure 4.
Unfortunately, none of the original
sample(s) of urine from EL was
available for analysis by the other
two laboratories. Despite the large
differences between the results
obtained by the three laboratories
none of those obtained on the control samples, of which there were at
least 30, contained as high a concentration of insulin as even the lowest obtained for EL. It is noteworthy
that whereas the three laboratories
obtained excellent agreement for
the results they obtained for urinary
creatinine content in the post-mortem
samples, the insulin results varied
enormously casting serious doubt
on the ability of any of the three to
measure urinary insulin accurately
and with sufficient reliability to have
any clinical, let alone forensic, value.
Examination of the sparse litera-

Copyright 2005 John Wiley & Sons, Ltd.

R EVIEW
Hypoglycaemia: accidents, violence and murder

ture on the subject reveals many

examples in which much higher
concentrations of insulin in
urine16,17 were detected than were
found even in the higher of ELs
results, casting still further doubt on
its diagnostic significance (Figures 5
and 6).
As the urine insulin assay results
were the only evidence offered that
EL had died from anything but natural albeit unexplained causes,
the fact that they were demonstrably
unreliable and uninterpretable
might reasonably have been
expected to lead to Maria Whistons
acquittal. In the event, she was
found guilty. This must surely have
been solely on the circumstantial
evidence, which included the fact
that EL had been admitted to hospital with factitious hypoglycaemia on
two occasions just two years before
his death. The prosecution contended that because EL had no
medical knowledge he could not
possibly have injected himself and,
consequently, that Maria Whiston
must have injected him with murderous intent two years earlier but
had been unsuccessful. The fact that
EL vehemently denied to the doctors and psychiatrists who interviewed him that either he or anyone
else had given him insulin was
ignored, as it invariably is in cases in
which a diagnosis of factitious hypoglycaemia rests entirely upon an
unfavourable plasma insulinC-peptide ratio (see above).
Circumstantial evidence of Maria
Whistons guilt was produced at the
trial and included the fact that she
lied about her whereabouts on the
evening/night before ELs death.
She was not on duty at her hospital,
as she had claimed, but with her new
lover with whom she had gone to
register her forthcoming marriage
on the very morning of ELs death
and prior to his discovery. She also
stood to gain financially from ELs
death though not very substantially which she would not have
done had she left him to marry
someone else. Perhaps Marias former husband provided the most
damning piece of evidence. He testified that during their marriage
Maria had threatened to kill him by
injecting him with insulin between

Figure 6. Comparison of insulin (pmol/L), C-peptide (pmol/L) and

C-peptideinsulin ratio (x100) in urine from Mr EL and the two patients with
spontaneous hypoglycaemia reported by Ichikawa et al.17 Note that in a
typically healthy subject urine insulin concentration is too low to
demonstrate on the scale shown
20000

15000

10000

5000

EL 1

C-peptide

EL 2
Insulin

the toes which, she told him, would

never be discovered.
The fact that EL was found in a
pool of vomit an extremely rare
complication of insulin-induced
hypoglycaemia should itself have
aroused suspicion that the diagnosis
of insulin-induced hypoglycaemia
might have been incorrect and was
based, at best, on very poor evidence. The argument presented by
the defence that there was no evidence worthy of the name to suggest
that EL had died from anything but
natural causes failed to convince the
jury who returned a guilty verdict.
Maria Whistons appeal against

Ichikawa
case 1

Ichikawa
case 2

Typical

C-peptide/insulin

conviction was dismissed by the

Court of Appeal18 but remains one
of the few amongst a small number
of murders by insulin in which the
verdict was based on nothing more
than a single and probably erroneous insulin assay result.

Conclusions
It is possible to kill even sentient
adults with insulin, but is very rare
unless they have participated as a
willing victim in a suicide pact.
Direct evidence upon which convictions have been obtained in the
past, including insulin assays in
blood and urine, is suspect and

Key points
Insulin has been used as a murder weapon especially in fiction. In real life
it is extremely rare except in infants and the infirm elderly
The doses required to kill a sentient adult are large and require their
compliance. It kills through causing hypoglycaemia and takes many hours
to do so during which time discovery and reversal by intravenous glucose
is always possible
Most proven cases of insulin poisoning have involved the use of an
additional weapon
Cases that come to court and depend exclusively on the results of a
single insulin assay should always be suspect as the methods of
measurement employed generally do not meet forensic standards and/or
their interpretation is questionable

Pract Diab Int November/December 2005 Vol. 22 No. 9

Copyright 2005 John Wiley & Sons, Ltd.

R EVIEW
Hypoglycaemia: accidents, violence and murder

should be relied upon only when

there is strong supporting evidence
of wrong doing. Further examples
of the problems associated with
establishing murder by insulin are
described in the book Insulin
Murders, by Vincent Marks and
Caroline Richmond, to be published some time in the future.

Conflict of interest statement

None.
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The first of the two articles in this
series was published in the
October 2005 issue (Pract
Diabetes Int 2005; 22: 303306)

Copyright 2005 John Wiley & Sons, Ltd.