Sudden infant death syndrome and progesterone

Medical Hypotheses

SUDDEN

INFANT

461-463,

8:

1982

DEATH SYNDROME AND PROGESTERONE.

R.T. Ross, Section Winnipeg, Manitoba,

of Neurology, Canada.

Health

Sciences

Centre,

700

William

Ave,

ABSTRACT Some victims of sudden infant chronically defective ventilation

of

victims seems eye

to

family occur

movement

Both

death syndrome have evidence as do some members of the

and the subsequent when the proportion sleep

endogenous

is

and

tory stimulants. appear to have

siblings. of more

increasing

exogenous

and

Furthermore, the vulnerable non-rapid

serum

progesterone

is

progesterone

are

effective

of

three

features

The relationship been studied.

these

death

low. respiradoes

not

INTRODUCTTON The purpose of this report information on the relationship or

possible

years

prevention

A review 1975-80

hormone. follows.

victims is

of the yielded

The

also

good

why

tion

of

sudden

one

(1,2)

evidence in

an

that otherwise

chronic

expired

There

and relating

miqht

the

have

death

tidal

are of

also SlDS

is

healthy

as

a dozen others (1) which culminates

volume hereditary victims

in

death

and have

syndrome

expected

otherwise

the

cause apnea

not

or

(SIDS). for the

the

are

as

majority

the

first seven

described

lack of cause

of There

hypoxia.

The

and only “tissue-

by

Naeye

(3,4,S,b)

suggest a chronic defect Further in a dead baby.

respiratory and impaired some

apparent and the

a Med-line search the disease and

baby.

hypoxia/hypoxemia

of a chronically abnormal alveolar hypoventilation

Some parents

infant

S IDS may have more than one to succumb to inexplicable

and confirmed by half ventilatory mechanisms evidence of sleep

the

literature no citations

reasons

Al though appear

morbid event markers” of

of

is to point out the between progesterone

state is the chemoreceptor

“near-miss”

familial significantly

SIDS

aspects lower

to

finding regul

babies the

in

(7). SIDS.

ventilatory

responses with and without added resistance and significantly lower respiratory drive with and without added resistance (8). Also, adult sleep apnea has been reported in family members of SIDS victims (9). Final ly, the subsequent siblings of SIDS victims have a three to four fold greater risk of sudden death than infants in the general population (10). Clearly, the death occurs with a background of respiratory mal-function and the victim is not the only abnormal family member with respect to respiratory function. 461

a-

There changes at

are the

two unrelated physiological events undergoing major time when SIDS is most likely to occur. Rapid eye movement (REM) sleep is the predominant sleep pattern in the first two months of life (11) and thereafter diminishes. Normal respiration in non-REM sleep resp i ra tory responses tion

of

non-REM

respiratory death

likely

The

other

is the infancy

sleep

reflexes

is

is critically ( 12) . It in

to

with the

chronically amount

of

defective sleep

time

when

occur.

normal

diminishing

(13).

a baby

increases

dependent on normal automatic be that the increasing propor-

may

physiological

serum levels

The

change

that

17 OH-progesterone are high in cord

possibly

contributes

concentration serum in both

during sexes and

then fall rapidly. l’n females the level continues to decline gradually through the first year and remains at the pre-pubertal leve thereafter. In males, however, the level rises in the first two months and then decl ines. The variations in males (in whom SIDS is more common)(l4,15) may be more important than the absolute level. Progesterone probably responsible luteal venti

stage latory

useful high

of in

the

to

hypoxia

disordered

In

saturation of

(16).

menstruation

altitude.

episodes

an effective ventilatory for the hyperventilation

responses

role

oxygen

is

this

and

normals,

sleep

arterial

strikingly

oxygen

It

occurs

it

is

and

the

has

a

enhances (17).

which

environment and

it

hypercapnia

breathing

unique

during

severe

In

It

stimulant. of pregnancy

during

improves

arterial

abolishes

the

sleep transient

(18).

desaturation

CONCLUSION In

conclusion,

progesterone reflexes at sleep

is

there

levels a time

increasing

There

seems

progesterone

on

particularly

their

is

some

evidence

that

in babies with chronically when the proportion of more

to the

could

contribute

be

information

no

near-miss subsequent

to on

babies sib1

or

ings.

changing poor respiratory vulnerable non-REM

St’DS. the

effects

their Surely

of

family

exogenous

members,

thi’s

warrants

investigation. REFERENCES

1.

Valdes-Dapena of the Medical

MA. Sudden Literature

l’nfant Death Syndrome: 1974-1979. Pediatrics

A Review

66: 597-614,

1980. 2.

Burmeister P. Sudden Unexpected Search No. 76-17, U.S.Department Welfare, Pub1 ic Health Service,

3.

Naeye Infant

289:

Death in Infants: of Health,Education National Institutes

RL. Pulmonary Arterial Abnormalities Death Syndrome. New England Journal 1167-1170, 1973.

462

in of

Literature and of Health.

the Sudden Medicine

at

4.

Naeye

Brain-stem

RL.

and

sudden-infant-death

adrenal

abnormalities

in the

J Clin

66:

syndrome.

Am

Path01

526-530,

Ryser M et Science

al. Carotid body in the 191: 567-569, 1976.

Ryser

al.

1976.

5.

Naeye

RL,

infant

6.

Fisher

death

Naeye

RL,

Whalen

abnormalities Am J. Path01

7. a.

9.

Schiffman PL, Westlake Control in Parents of Syndrome.

New

Strohl

Saunders

KP,

death

and

J Prev

Sot

Rev

Journal

NA,

of

Medicine

Feldman NT et New England

members.

Med

EA.

Respir

Phillipson ed pp

302:

25:

Control Dis

EA,

119-134,

118:

of

WC

Breathing

909-939,

Sullivan

C Guilleminault, 47-64.

During

in Sleep

CE.

Ireland.

Sleep.

Alan

Dement.

Apnea R Liss

Syndromes Inc.

Jorgensen

T,

Biering-Sdrensen

F, Hilden

Lewak N, syndrome

Van Den Berg risk factors:

Pediatr

18:

III 68:

BJ, Beckwith Prospective

404-411,

J.

of Sudden

Perinatal

11-22, JB. data

and

1978;

New

York

Sudden

infant

Natalino agent

Clin

353A,

Wei JV, 1978; ed New York

death

1979.

Zwillich CW, progestational 23:

Infant perimortal

reviewed.

17.

Res

Age.

1979.

Goodland RL, Reynolds JG, Pommerenke WT. Alveolar dioxide tensi'on levels during pregnancy and early J Clin Endocrinol Metab 14: 522-530, 1954. MR, Weil JV. on the control

The of

influence breathing

carbon puerperium. of

a

in man.

1975.

in Sleep Apnea Syndromes Kryger MH, Scoggin CH. C Guilleminault, WC Dement. Alan R Liss Inc, pp

119-136.

463 B

sudden

1978.

16.

la.

1980.

Winter JSD, Hughes IA, Reyes FI et al. Pituitary-Gonadal Relations in I‘nfancy: 2. Patterns of Serum Gonadal Steroid

Clin

MH-

486-491,

1971.

Death in Copenhagen 1956-1971. factors. Acta Paediatr Stand 15.

1978.

al. Obstructive sleep Journal of Medicine 299:

Concentrations in Man from Birth to Two Years J Clin Endocrinol Metab 42: 679-686, 1976. 14.

other

syndrome.

1978.

Phillipson Am

13.

Cardiac

infant

Epidemiology of Froggatt P, Lynas MA, MacKenzie G. unexpected death in infants (cot death) in Northern Br

12.

M et

sudden

RE, Santiago TV et al. Ventilatory Victims of Sudden-Infant-Death

England

in family

969-973,

11.

P,

in the sudden 82: l-a, 1976.

Abnormal Ventilatory Responses to Shannon DC, Kelly D. CO2 During Quiet Sleep in Aborted SI'DS. Chest 73: 301,

apnea 10.

R,

syndrome.