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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 stronglyagree 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-actinginsulin 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 Leefor 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 apnoeaassociated with the degree of insulinresistance?

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 at22.00 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 bederived 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.

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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 ClinEndocrinol 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.

19LetterLettersLettersLetters

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 thatthe 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.