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Blackwell Science, Ltd

Letters

Letters Letters Letters

Feline diabetespersonal experience

Recently Neuvians and Berger reported on the nature and
standard of diabetes care in cats and dogs in veterinarian
practices in the city of Dsseldorf [1]. The estimated prevalence
of diabetes is 0.31.0% in dogs and 0.10.3% in cats. Similar
to human diabetes, the incidence of diabetes in pets is expected
to rise due to lifestyle changes of the animals with increasing
body weight, lack of exercise and longer life expectancy. Their
cross-sectional study suggests that much of the current practice
in diabetes care for cats and dogs is neither directed to patient-
orientated goals nor based on adequate evidence with regard
to the efficacy and safety of diagnostic and therapeutic inter-
ventions. As the owner of two geriatric diabetic cats, I strongly
agree with their findings. Being a diabetologist working in a
teaching hospital myself, I also have had ample opportunities
over the years to compare the different aspects of human and
feline diabetes.
My first cat, Max, developed diabetes at the age of 11 and
presented with the classical symptoms of hyperglycaemia
polyuria, polydypsia and weight loss. Diabetes was confirmed
by blood glucose measurement at the vet and he was com-
menced on twice daily insulin therapy. My cat did not object
to the injections at all. Although his polyuria and polydypsia
improved, he failed to gain weight and urine test persistently
showed heavy glycosuria. I tried changing to a different pre-
paration of insulin with no improvement and attempts to adjust
insulin dosage based on urine tests proved extremely difficult
and resulted in two episodes of severe hypoglycaemia. Glucose
profile at the vet was not informative because cats are notori-
ously prone to stress-induced hyperglycaemia. In desperation,
I resorted to trying home blood glucose monitoring myself.
With the help of my diabetes nurse specialists, we chose a
glucose meter that required the smallest volume of blood and
we attempted to do footpad pricks using a spring-loaded penlet
device. Much to our surprise, my cat neither cried nor flinched
with this method. Life was revolutionalized by the availability
of home blood glucose measurement. What I noticed was that
the duration of effect of both intermediate and long-acting
insulin preparations was considerably shorter than expected.
Even with ultralente, the duration of action was only around
69 h and there was not much difference between human and
bovine insulin preparations. I eventually discovered why my
cat did not gain weight despite improvement of his glycaemic
controlhe also had thyrotoxicosis! Once we rendered him
euthyroid with medical treatment, he put on weight and his
diabetes also became a lot easier to control.
When my second cat Macavity developed diabetes recently,
I was able to see whether some of the observations I made
from my first cat applied to other diabetic cats. My second cat
developed diabetes after he was given a steroid injection by
the vet for his eosinophilic dermatitis. He developed severe
symptoms of polyuria and polydypsia 3 days after the steroid
injection and he decided to sleep right next to his water bowl
rather than in his bed! I did a footpad prick and his blood
glucose was well above 20 mmol / l. I started him on insulin
therapy and found that the duration of action of long-acting
insulin preparations was again much shorter. As a result, he
needed multiple daily injections with a mixture of short-acting
and long-acting insulin for a few days to keep his blood glucose
down when the steroid effect was at its peak. Unfortunately,
his diabetes did not appear to be transient. He needed to stay on
insulin therapy even when all the steroid effect had worn off.
My first cat has had diabetes for over 5 years now and is still
going strong, and the other cat is also doing well. According to
my vet, I am lucky in that both my cats are very friendly in
nature and easy to handle. It would appear that both the insulin
injections and the footpad pricks are not painful as neither of
my cats seem to mind at all. Dietary manipulations have
proved to be more difficult as both my cats are nibblers and
it has not been easy to train them to eat after insulin injections.
Looking after my diabetic cats has been a unique and interest-
ing experience. Throughout the years, my vet and I have learnt
much from each other. I have introduced home blood glucose
monitoring to his practice and we have had many discussions
comparing human and feline diabetes. My diabetic patients,
my medical and nursing colleagues have all shown great
interest in my cats. Many of my colleagues and friends have
been very helpful and supportive and are willing to step in to
give the insulin injections when I am on-call or away on holiday.
My two diabetic cats have become the mascots of our diabetes
centre.

Acknowledgements

My sincere thanks to Wendy Lam, Siu-Kuen Leung, Marina
Cheung, Elaine Leung, Karman Yu and Doctors Sidney Tam,
Nelson Wat, Wing-Sun Chow, Annette Tso and Ka-Kui Lee
for their support.

K. C. B. Tan

Department of Medicine, University of Hong Kong,
Queen Mary Hospital, Hong Kong

Reference

1 Neuvians TP, Berger M. Diabetes care in cats and dogs.

Diabet Med

2002;

19

: 7779.

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Is the severity of obstructive sleep apnoea
associated with the degree of insulin
resistance?

Obstructive sleep apnoea is associated with insulin resistance,
the metabolic syndrome (dyslipidaemia, visceral obesity,
hypertension, and glucose intolerance) and cardiovascular
disease [1,2]. Since obesity induces an insulin-resistant state, the
relationship between the severity of obstructive sleep apnoea
and insulin resistance should be carefully evaluated. Previous
studies have reported inconsistent results in terms of an asso-
ciation between sleep apnoea and insulin resistance [1,38].
Therefore, we evaluated whether the severity of obstructive
sleep apnoea is associated with the degree of insulin resistance
in obstructive sleep apnoeic patients.
For this study, 38 obstructive sleep apnoeic patients (29
men and nine women; mean age (mean

SEM

) 53.6

2.2 years;
mean body mass index (BMI) 28.1

1.0 kg/m

2

) were included.
All chiefly complained of excessive daytime sleepiness and
snoring. Throughout the sleep study, which commenced at
22.00 hours and ended at 07.00 hours, the following variables
were monitored: electroencephalogram (C3/A2 and C4/A1
from the 1020 international electrode placement system),
electro-oculogram, chin and leg electromyogram, ECG (one
modified V2 lead) and body position. Arterial oxygen satura-
tion (SaO

2

) was measured with an ear oximeter. Obstructive
sleep apnoea was diagnosed by the polysomnography study:
apnoea and hypopnoea index (AHI), defined as the number of
apnoeas and hypopnoeas per hour of sleep, which was greater
than 5. Apnoea was defined as cessation of airflow of at least
10 s. Hypopnoea was defined as reduction in airflow or thoraco-
abdominal movements lasting at least 10 s and accompanied
by oxygen desaturation of at least 4%. The minimum SaO

2

during apnoeic or hypopnoeic episodes was recorded, and all
values were averaged, giving an index of hypoxaemia severity
during sleep (mean minimum SaO

2

). For data analysis, AHI
and the mean minimum SaO

2

were taken as indices of the
severity of sleep apnoea. All subjects received a 75-g oral glucose
tolerance test (OGTT), and venous blood samples were taken
for the determination of plasma glucose and serum insulin
concentrations at 0, 30, 60, 90 and 120 min. The diagnosis of dia-
betes mellitus (DM) and impaired glucose tolerance (IGT) was
performed using the 1997 American Diabetes Association criteria
[9]. The insulin sensitivity index (ISI) proposed by Matsuda
and DeFronzo [10], i.e. 10 000/square root of (fasting glucose

fasting insulin)

(mean glucose

mean insulin during OGTT),
was used as an index of the severity of insulin resistance.
Six patients had DM, 15 patients had IGT, and 17 patients
had normal glucose tolerance. ISI significantly correlated
with the indices of the severity of obstructive sleep apnoea
(

r

=

0.47;

P

< 0.005 for AHI and

r

= 0.44;

P

< 0.01 for mean
minimum SaO

2

). On the other hand, BMI also significantly
correlated with the indices of the severity of obstructive sleep
apnoea (

r

= 0.47;

P

< 0.005 for AHI and

r

=

0.43;

P

< 0.01
for mean minimum SaO

2

). Therefore, we adjusted the relation-
ship between ISI and AHI or mean minimum SaO

2

for BMI.
After this adjustment for BMI, ISI did not continue to make an
independent contribution to the indices of the severity of
obstructive sleep apnoea, but tended to correlate with them
(

r

=

0.31;

P

= 0.07 for AHI and

r

= 0.30;

P

= 0.09 for mean
minimum SaO

2

).
Previous studies reported inconsistent results in terms of
the association between obstructive sleep apnoea and insulin
resistance [1,38]. Some reports showed that there is an effect
of obstructive sleep apnoea on insulin resistance apart from the
effects of coexistent central obesity [1,35]. One of the pos-
sible mechanisms of obstructive sleep apnoea-induced insulin
resistance includes increased sympathetic nerve activity by
nocturnal oxygen desaturations [11]. In terms of the relation-
ship between the severity of obstructive sleep apnoea and the
degree of insulin resistance, there are only two reports by
Tiihonen

et al

. [3] and Ip

et al

. [5]. Our results suggest that the
degree of insulin resistance is possibly related to the severity of
obstructive sleep apnoea through the effects of obesity, which
is inconsistent with their results [3, 5]. The discrepancy may be
derived from the two following reasons. The first is the differ-
ence of subject populations: only 18 patients including two
diabetic patients were enrolled in Tiihonens study [3], and Ip

et al

. [5] excluded the subjects with known DM on medica-
tions. In addition, Ip

et al

. [5] did not evaluate the degree of
glucose tolerance. Second, they used different insulin resist-
ance indices: Tiihonen

et al

. [3] used the product of areas
under glucose and insulin curves during OGTT, whereas Ip

et al

. [5] used the estimation of insulin resistance by the home-
ostasis model assessment method [12]. On the other hand, we
did not investigate the relationship between insulin resistance
in obstructive sleep apnoea and body fat distribution. There-
fore, the distribution of fat should be taken into account in
future studies.

Y. Nagai, Y. Nakatsumi*, T. Abe and G. Nomura

Department of Internal Medicine and

*

Department of Respiratory Medicine, Kanazawa
Municipal Hospital, Kanazawa, Ishikawa, Japan

References

1 Grunstein RR, Stenlof K, Hedner J, Sjostrom L. Impact of obstructive
sleep apnea and sleepiness on metabolic and cardiovascular risk
factors in the Swedish Obese Subjects (SOS) Study.

Int J Obesity

1995;

19

: 410418.
2 Wilcox I, McNamara SG, Collins FL, Grunstein RR, Sullivan CE.
Syndrome Z: the interaction of sleep apnoea, vascular risk factors
and heart disease.

Thorax

1998;

53

: S2528.
3 Tiihonen M, Partinen M, Narvanen S. The severity of obstructive
sleep apnoea is associated with insulin resistance.

J Sleep Res

1993;

2

: 5661.
4 Brooks B, Cistulli PA, Borkman M, Ross G, McGhee S, Grunstein RR

et al.

Obstructive sleep apnea in obese non-insulin-dependent
diabetic patients: effect of continuous positive airway pressure
treatment on insulin responsiveness.

J Clin Endocrinol Metab

1994;

79

: 16811685.
2003 Diabetes UK.

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Letters

5 Ip MS, Lam B, Ng MM, Lam WK, Tsang KW, Lam KS. Obstructive
sleep apnea is independently associated with insulin resistance.

Am J
Respir Crit Care Med

2002;

165

: 670676.
6 Stoohs RA, Facchini F, Guilleminault C. Insulin resistance and sleep-
disordered breathing in healthy humans.

Am J Respir Crit Care Med

1996;

154

: 170174.
7 Vgontzas AN, Papanicolaou DA, Bixler EO, Hopper K, Lotsikas A,
Lin H-M

et al.

Sleep apnea and daytime sleepiness and fatigue: relation
to visceral obesity, insulin resistance, and hypercytokinemia.

J Clin
Endocrinol Metab

2000;

85

: 11511158.
8 Smurra M, Philip P, Taillard J, Guilleminault C, Bioulac B, Gin H.
CPAP treatment does not affect glucose-insulin metabolism in sleep
apneic patients.

Sleep Med

2001;

2

: 207213.
9 The Expert Committee on the Diagnosis and Classification of
Diabetes Mellitus. Report of the Expert Committee on the Diagnosis
and Classification of Diabetes Mellitus.

Diabetes Care

1997;

20

:
11831197.
10 Matsuda M, DeFronzo RA. Insulin sensitivity indices obtained from
oral glucose tolerance testing.

Diabetes Care

1999;

22

: 14621470.
11 Fletcher EC, Miller J, Schaaf JW, Fletcher JG. Urinary catecho-
lamines before and after tracheostomy in patients with obstructive
sleep apnea and hypertension.

Sleep

1987;

10

: 3544.
12 Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF,
Turner RC. Homeostasis model assessment: insulin resistance and

-
cell function from fasting plasma glucose and insulin concentrations
in man.

Diabetologia

1985;

28

: 412419.

19 Letter Letters Letters Letters

St Vincents Declaration 10 years on:
outcome of diabetic pregnancies

If no one has put the record straight on the Norwegian data for
the outcome of pregnancy in Norway I should be grateful if
you could publish the following letter.
The article in your March issue St. Vincents Declaration
10 years on: outcome of diabetic pregnancies by Platt

et al

. [1]
reported rather disappointing outcomes in the North-west
of England. In the Discussion the authors quote a paper by
Hawthorne, Irgens and Lie published in the

British Medical
Journal

[2] which states that the outcome of pregnancy for
women in the North-east of England is similar to that in the North-
west, in contrast to the situation in Norway where the outcome
of diabetic pregnancy is similar to that of the general population.
I feel that it is important to set the record straight. As my
colleague, Dr Frank Johnstone, pointed out in his electronic
reply to that paper, there was a huge difference in prevalence
of diabetic pregnancies reported from the North-east of
England (one in 335 pregnant women) compared with Norway
(one in 90 pregnant women). He noted that, in the North-east,
all women were taking insulin before pregnancy, all were
confirmed by clinicians and from examination of the records.
Norwegian data were from a centralized medical birth registry.
When Dr Johnstone and I checked the Scottish register listings
of pregnancy in women with Type 1 diabetes, while preparing
the Scottish Intercollegiate Guidelines (SIGN), we found that
they were seriously flawed. Most, but not all, women with
Type 1 diabetes were included, but also included were some
women with gestational diabetes, some who had had a glucose
tolerance test which was normal, and even some who only had
a relative with diabetes. We wondered if the same thing could
have happened in Norway.
At a meeting of the North-east and the Norwegian groups,
which I attended, in Newcastle a year ago, it became clear, much
to the embarrassment of the Norwegian group, that that was
exactly what had happened. A Norwegian doctor described
how she had cross-checked the register with her patient records,
as we had done, and found, as we had, that some women with
normal glucose tolerance and some with only a relative with
diabetes had been included on the register. The conclusion was that
the results in Norway are probably no better than those in Britain.
It is clear to anyone looking after women with Type 1 dia-
betes in pregnancy that it would be quite impossible to achieve
an outcome as good as that in the general population. It is like
suggesting that those who have had a myocardial infarct
should live as long as the general population. I am, however,
rather more optimistic than the authors about pre-pregnancy
care. I feel that with increased awareness and enthusiasm of all
those looking after women with diabetes in the reproductive age
group it should be possible, without enormous expense, to increase,
as I have done (> 70% in Edinburgh and now > 60% in Fife), the
proportion of women coming for pre-pregnancy care and hence
to reduce the high incidence of congenital malformations.

J. M. Steel

Department of Diabetes, Victoria Hospital,
Kirkcaldy, Fife, UK

References

1 Platt MJ, Stanisstreet M, Casson IF, Howard CV, Walkinshaw S,
Pennycook S

et al.

St. Vincents Declaration 10 years on: outcomes of
diabetic pregnancies.

Diabet Med

2002;

19

: 216220.
2 Hawthorne G, Irgens LM, Lie RT. Outcome of pregnancy in diabetic
women in Northeast England and in Norway, 19947.

BMJ

2000;

321

: 730731.