FAMILIAL PITUITARY DWARFISM ASSOCIATED WITH AN ABNORMAL SELLA TURCICA

(1)

( Received

August 26; revision accepted for publication December 10, 1968.)

This study was supported in part by a Research Grant from the National Institute of Child Health and

Human

Development

(

USPHS 2-R01-HD-00999-04).

P.E.F. is the recipient of Research Career Development Award

# 1K3-HD-34,

547-02

from the National Institute of Child Health and Human Development.

ADDRESS: 4800 Sand Point Way N.E., Seattle, Washington 98105.

PEDIATRICS, Vol. 43, No. 5, May 1969

FAMILIAL

PITUITARY

DWARFISM

ASSOCIATED

WITH

AN

ABNORMAL

SELLA

TURCICA

Pierre

E. Ferrier,

M.D.,

and

E. Franklin

Stone,

Jr., M.D.

From the Departnent of Pediatrics, University of Washington, and the Children’s Orthopedic Hospital

and Medical Center (Joan Judson Research Laboratory and Retarded Children’s Clinic),

Seattle, Washington

ABSTRACT. Two non-twin sisters issued from healthy non-consanguineous parents of normal stat-ure demonstrated severe growth failure,

hypoglyce-mia, and evidence of deficiency of growth

hor-monc, thyroid stimulating hormone

( TSH

), and

adrenocorticotropic hormone (ACTH

)

; in addition,

they both had a very slnall sella turcica located in

a sphenoid bone of abnormal morphology. This

form of familial pituitary dwarfism is different from the genetic forms previously described. Pediatrics,

43:858, 1969, FAMILIAL PITUITARY DWARFISM,

SELLA TURCICA, HYPOPITUITARISM.

S

EVERAL FORMS

of

familial

or

genetic

pi-tuitary

dwarfism

now

have

been

recognized.’ They are characterized by

var-ious

pituitary

hormone

deficiencies,

but

in

none

of

them

is the

sella

turcica

strikingly

abnormal.

The

object

of

this

paper

is to

re-port

the

association

of

severe

growth

fail-ure,

inadequate

pituitary

functions,

and

ex-treme

hypoplasia

of the

sella

turcica

in

two

sisters. The familial nature of this

associa-tion

is thought

to be

unique.

METHODS

The

charts

of

the

Harvard

School

of

Public

Health

were

used

for

plotting

growth.’

Bone

maturation

was

estimated

by

use

of

the

tables

of

Greulich

and

Pyle’

and

Wilkins

and

co-workers.4

Urinary

17-hydroxvcorticosteroids were measured

according

to

the

method

of Glenn

and

Nel-son.’

The

semiquantitative

method

of

Dorfman

and

Steiness7

was

utilized

for

the

detection

of

acid

mucopolysaccharides

in

the

urine.

Plasma

growth

hormone

was

mea-sured

by

the

radioimmunoassay

technique

of

Schalch

and

Parker.8

Blood

sugar

was

de-termined

by

means

of

a

glucose-oxidase

method.’

Chromosomal

analyses

of

periph-eral

blood

leukocytes

were

performed

by

a

modification

of

the

technique

of

Moorhead

and co-workers.’#{176}

Patient 1

CASE

REPORTS

This 11-year-old, white girl was initially re-ferred to the Retarded Children’s Clinic at 6 years of age because of her slow development. She

was

the

oldest

child

of

the family, which

con-sisted of the 35-year-old mother, the 39-year-old father, a 10-year-old sister

(

Patient 2) and a

3-year-old sister. Parents were third generation

Americans, and unrelated; the father’s ancestors

were French, and the mother’s were Flemish

( Belgium).

There

was no family history of

ex-cessively short stature. The mother was 5 ft, 3 in. and the father was 5 ft, 10 in. The youngest sister was growing along the 25th percentile according to the Vickers and Stuart chart.’ The patient was

born at 42 weeks of gestation with a weight of

8 lb, ii oz and a length of 21 in. Labor, delivery,

and immediate neonatal period were

uncompli-cated. However, at 10 weeks of age a physician

suspected a thyroid deficiency because she was

“sleepy” and she was treated with dessicated

thyroid for 8 months. This then was discontinued because she was thought to have received

“maxi-mum

benefit

from

the

treatment.”

She

rolled

over

at 5 months, sat at 6 months, and crawled at 11

months. From about 12 months of age her rate of

growth and development was noted to slow down.

(2)

TABLE I

BLOOD SUGAR AND GRowTH HORMONE DATA

Blood Sugar (my, 100 nil). 36-hr Fast

Pa-lent

8 lg:3O 4

,

n 4 8

AM. P.M. P.M. P.M. AM. AM. AM.

71 68 51 47 45 36 19

10 30 45 60 90 110 3.1

I.9 3.0 6.0

9.7

1.5

ii

I

MONTHS

liii

LNTI1 ‘rri , 1 I ‘* Is 1* C70 Coo LINTH HIIHT C5O I

I

_h

,

j

#{174}OLDU SIlTU

346

8

‘1

Fic. 1. Growth curves of the

two

patients.

years of age she had fallen below the third

per-centile for height. At the age of 6 years psycho-logical testing with the Wechsler Intelligence Scale for Children ( WISC) revealed a verbal scale

I.Q. of 65, a performance scale I.Q. of 54, and a full

scale I.Q. of 56. At this time the value of the serum

PBI was 3.1 eg/100 ml, the bone age was read as

2 years, and an electroencephalogram was con-sidered slightly abnormal in view of the predomi-nant frequency of 4 cycles per second ( slow for

this age). The excretion of aminoacids in this

urine was not excessive. A buccal smear showed a normal female pattern.

Her growth pattern continued to follow a curve below the third percentile, as shown in Figure 1.

At 72 years of age, she had a 4 month history of

repeated episodes of fatigue, vomiting, abdominal pains, and headaches at 1- to 2-week intervals. This was not explored further at the time. Repeat

psychological evaluation at 82 years, with

the

WISC,

revealed

a verbal

scale

I.Q. of 57, a

perform-ance scale I.Q. of 39, and a full scale I.Q. of 43, consistent with functioning in the moderately re-tarded range. At 1 1 years of age she was still enu-retic; she was reading at a pre-primer level and

doing

some simple counting. She also was reported

to have experienced several episodes of motor

weakness during the previous 4 months, usually in the afternoon, characterized by an initial pallor

fol-lowed by poor coordination and staggering gait.

Occasionally there were complaints of associated headache and poorly’ localized pain elsewhere. The episodes usually subsided after a brief nap or rest, following which she usually manifested a ravenous hunger. Feeding during the initial stages of an epi-sode often seemed to abort completion of the full cycle.

Physical examination revealed a very small, well

proportioned, well nourished 11-year-old girl with

a height ( 106 cm) and weight ( 17.2 kg)

corre-sponding to the 50th percentile for 4 years ( Fig. 2 )

.

Span was 97 cm and the lower segment was 55

cm. Head circumference was 50 cm. Variable left

internal strabismus, slight epicanthal folds, and clinodactyly of the fifth fingers were noted. There

was no evidence of pubertal development, and the

rest of the physical examination was not remark-able. The following laboratory studies were ob-tamed.

Blood Sugar Plasma Growth

(mg,’lO() ml) Hormone (mzg/ml)

Control 61 3.9

18-hrfast 38 3.5

Arginine Stirnul.olion Test

Time Pla:nza Growth B1o4 Sugar

(mm) Hormone (mig/ml) (mg/100 ml)

0 4.1 .5.5

(3)

860

‘l’;flLE II

tTulNAuv 17-uI’n1IcxveoltTIcosr:lioIDs (sio/4 iiit)

Metyrajx)ne

. Pre- ,

Post-I atient (.O iiig/kg

iiieti/raJx)ne

j

j.

)

metyrapune

1 1.47 1.61 1.15

‘z (1.66 1.3’2 1.16

RADIOGRAPHS : Examination of multiple ossifica-tim centers revealed a bone age of 3 to 4 years,

and examination of dental radiographs revealed a

tlental age of 8 to 9 years. Lateral views of the spine showed slight ballooning of most of the in-tervertebral spaces, with some increase in the

ks’-1)hOSi5 of the thoracic region and in the lordosis of

the cervical region. Examination of the skull by

conventional views showed no depression in the

usual location of the sella turcica and an exces-sively thick and prominent dorsum sellae

( Fig.

3).

Sagittal tomograms of the skull revealed a very

small, round, radiolucent area

(

5 mm in diameter) within tile sphenoid bone, anterior to the bulky (lorsunl sellae

( Fig.

4

)

. The anterior chinoids only could be identified. A series of frontal plane

tomo-grams through the sphenoid bone were obtained at

1 mm intervals, using a Massiot-Phillips “poly-tome.” The floor of the sella was demonstrated this way to be very shallow

( Fig.

5),

in keeping with the depth observed on lateral tomograms ( Fig. 4).

LABORATORY DATA : Several determinations of

the serum protein-bound iodine gave the following values: 4.6, 3.1, and 3.9 ag/100 ml. Oral

admin-100 cm

1%1

I

Fic. 2. Rig/it, Patient 1 (older sister) at the age of 11 years. Left, Patient 2

(4)

FIG. 3. Skull radiograph of Patient 1. Chronologi-cal age, 1 1 years. Dental age, 8ll years. istration of a test close of 1131 resulted in a 7.7%

uptake by tile thyroid gland, both at 2 and 24

hours.

Following

two

injections

of 10 units of

thyroid-stimulating hormone

(

TSH ) intramuscu-larly at 24-hour intervals, the 1131 uptake by the

thyroid

rose

to 14% at 2 hours and 26% at 24 hours.

Scanning of the neck showed the thyroid gland to

he in its normal location. Following an overnight

fast, the blood sugar at 8 AM. was 72 mg/100 ml.

Fast then was continued for 24 hours and the

blood sugar progressively decreased to reach a

nlinimum level of 29 mg/100 ml at 8 AM. the next morning

(

Table I). The pituitary-adrenal axis was

tested in the following manner: 30 mg/kg of

metyrapone

( Metopirone

)

was given intravenously in a small volume of saline over a 4-hour period.

This did not cause a significant increase in the

urinary excretion of 17-hydroxycorticosteroids

(

Ta-ble II). A test for acid mucopolysaccharides in the urine did not reveal an excessive excretion.

Chro-mosome analysis from peripheral blood

leuko-cytes showed a normal 46,XX constitution.

Patient 2

The 10-year-old sister of Patient 1 was seen mi-tially in the Retarded Children’s Clinic along with her sister, also because of slow development. She was the product of the mother’s second pregnancy. She was born at term, weighed 7 lb, 8 oz, and was 21 in. long. Pregnancy, labor, and delivery were free of complications. The longitudinal growth of

this

child

also is represented in Fig. 1. By 1 year

of age her length was below the third percentile,

and by the age of 10 years her height

corre-sponded to the 50th percentile for a 53i-year-old

girl. Early development appeared normal;

how-ever, she did not walk until 19 months, use spoken words until 2 years, or use sentences until 4 years.

At

the

age of 10 years she was enrolled in a

“trainable” class in the special education program. She continued to experience nocturnal enuresis and constipation. At 10 years her measurements were:

height, 110 cm; span, 106 cm; lower segment, 52

cm; head circumference, 48.5 cm; and weight,

18.3 kg. Except for internal strabismus and mild myopia, there were no other somatic anomalies. None of the secondary sex characteristics was de-veloped ( Fig. 2 ). On psychological testing with

the

Stanford-Binet

intelligence

scale

(form

L-M)

she was attributed an I.Q. of 39. The qualitative

aspects of her performance were thought to

sug-gest “cortical dysfunctioning.”

RADIOGRAPHS : Bone age, as interpreted from

multiple centers, was 4 years. Dental age was 9 to 10 years. Skull radiographs at 43i years and again at 93 years revealed an anomaly similar to that of her older sister: an extremely shallow sella turcica making a slight depression on the upper surface of a sphenoid bone of unusual thickness. The dorsum

sellae was particularly thick and prominent (Fig. 6).

LABORATORY DATA: A buccal smear was

posi-tive for sex chromatin, and chromosome analysis showed a normal 46,XX complement. The serum

protein-bound iodine was 4.5 eg/100 ml on

two

occasions. J131 uptake by the thyroid was 9% at 2

and 11% at 24 hours. After intramuscular admin-istration of 10 units of TSH on two consecutive days, the uptake values were 15% and 21, respec-tively. A scan of the neck showed the gland to be in

its

normal location. Urinary

17-hydroxycorti-FIG. 4. Sagittal tomogram of the skull of Patient 1, Note the very small sella and the massive bony

(5)

862

FIG. 5. Frontal tomograms of skull of Patient 1.

‘fop, section through tile middle of the seila,

sIloss’-ing a slight depression of the floor ( arrows ).

Bot-toni, Se(’tiOll more anteriorly’ tilall top, showing the

elevation of the floor ( arrosvs ). The anterior

clinoicls, ill section, are visible laterally.

costeroi(i excretion \vis 0.66 nig per 24 hrs. Nh’-tvrapolle stillRhlatioll, 5tithS 30 mg/kg of the drug

(t(hluinistered intravenously in a small volume of sahille over a 4-hour period, failed to produce a significailt incredse in this excretion ( Table II). After au overnight fast, the blood sugar value was (ii mg/100 ml; at this time the 1)lasma growth hor-IT1OI1C l(’V(i was 3.9 niag/nli. Fasting then was

prolonged for 18 more hours, at which time the

1)100(1 sugar was 38 mg/100 ml and the plasma

growth hormoiie was 3.1 mug/mi. Thus, there was

110 rise iii tile I)lasna growth hormone despite a renlarkal)iv lOW 1)100(1 sugar. The -apacitv to re-ledsc growth hormone was tested further by argi-ICICle stinuilation i)y’ using 0.5 gm/kg of arginine lllOnoChlOride#{176} as a 10% solution, administered O%P :30 millilteS. The values for blood sugar and plasma growth hormone during and after stimula-tion are shown Ill Table I. A peak growth

hor-mone ‘alue of 9.7 m,zg/ml was observed at 90

minutes. A semiquantitative determination did not

* Kindl’ 5Il)plied for investigative purposes by

11.

J.

Prentice, M.D., Cutter Laboratories, Berkeley, California.

reveal an excess of acid Illtlcopohvsacchlarides ill the urine.

Skull Radiographs of Other Family Members

‘Fhe niother and tile tllird sistcr each had a nor-hid1 ap)earing sella turdca. lhlc father had a nor-Illai-5iZe(l

sella

svith i)riclging of the clinoid pro-((55e5.

DISCUSSION

Evidence of Hypopituitarism

The

tvo

sisters

are

l)elievcd

to

(lemon-strate evidence of hypopituitarism. Their

l)irth weights and lengths were normal, l)ut

growth

failure became evident early in

in-fancy and Persiste(l during the following ‘ears. Lal)oratory CVi(lCflCC of liypoglvcc-cilia OIl fastilig s’as ol)taiIlc(l in 1)0th; ifl

ad-dition, one had symptoms suggestive of

spontaneous

hypoglycemia.

Poor

ability

to

maintain

a normal

blood

sugar level is not

uncommon in pituitary (lwarfism.’1 In the

younger sister, prolonged fasting and

subse-quent hypoglycemia failed to cause an

in-crease in plasma growth hormone

concen-tration.

An

increase

is expected

in

normal

subjects,- and its absence is consi(lcred

by

some investigators as a good criterion for

ppril3

Arginine

stimulation

of

growth hormone release has not been fully

evaluated in

children

vet.

The

highest

plasma value of 9.7 m.g/ml observed after

arginine infusion in the younger sister is

relatively

low,l36

hut it clearly indicates

that some growth hormone could be

re-leased into the circulation following this

I)artic1lar

type

of stimulation.

The

PBI

values

were

within normal

lim-its

or

just

below,

as

they

most

often

are

in

1)ituitary dvarfism. The values for 1131 up_

take

by

the

thyroid

were

low

and

were

cor-rected

by

administration

of

TSH,

a finding

suggestive

of

TSH

deficiency.

The

marked

retardation

in bone

maturation

was

in

keep-ing

with

hypopituitarism.

Finally,

the

low

excretion

of

17-hydroxycorticosteroids

and

the

lack

of

response

to

metyrapone

block-ade

in both

patients

constituted

evidence

of

(6)

Fie. 6. Skull radiograph of Patient 2. Very shal-low sella turcica and thick clorsulll seilae. Chrono-logical age, 10 years. Dental age, 9 to 10 cars.

Small Sella Turcica

The

difficulties

of

estimating

the

volume

of the sella turcica from radiographs have

been

demonstrated

in

the

studies

of

Silverman’8 in children and of Fisher and

Di

Chiro’#{176}in

adults

and

children.

The

pi-tuitary fossae

of tile

twO patients presented here had a sagittal area well below the

nor-mal values established by Silverman’8 for

girls of this age or even of this height age.

On

the

basis

of radiographic

measurements,

Fisher and Di Chiro’#{176} estimated that the sella turcica was small in 18 of 28 hypopi-tuitary children less than 15 years of age.

The

finding

was

thought

to

be

significant,

for

no

example

of

a small

sella

was

found

by

these authors in patients with dwarfism associated with achondroplasia, hypothy-roidism or gonadal dysgenesis. A small sella

was

found

in

10 of 74 patients

with

“dwarf-ism” of unknown etiology. The finding of a

small sella in dwarfed individuals is

there-fore

suggestive,

but

not

specific,

of pituitary

dysfunction. An apparently small sella

tur-cica associated with growth hormone

defi-ciency has been observed in two unrelated patients

by

Frances, et 20 These patients

had

fusion defects of the face

(

cleft

lip-pal-ate

)

.

The

combination

of an

abnormal

sella

with midline facial defects has been

ob-served in cases of D1 trisomy.’1 These

pa-tients had a shallow and ill-formed sella but

a

normal )ituitary. By contrast, ill

other

pa-tielits with fusion defects of the face’

and

in

certain

cases of iioloprosencephal,’ C

the

l)itllitarv gland

was

ai)sent, hut the 1)ituitarv fossa was normally developed.

Familial Pituitary Deficiency

Different sorts of familial or genetic

pi-Rotary dwarfism flOW

have

been

isolated.

Rimoin, et 25

and

Seip,

et a!.’ have

stud-ied a form of familial pituitary dwarfism

characterized I)y isolated growth

hor-Iflolle deficiency

(

sexual ateliosis”

)

. These

dwarfs eventually develop sexually, and re-produce; and, postpartum lactation occurs

in the females. The sella turcica is of nor-ma! size in proportion to the skull.’”

Pedi-gree studies support an autosomal recessive

inheritance.

In

other

instances

of

probably

recessive pituitary dwarfism,’ ‘‘ sexual

de-velopment does not take place and a

defi-ciency of several trophic hormones of the

pituitary seems to IJe llresent.

The

sella

tur-cica appeared normal radiologically in the

members of at least one such family.2

Iii

yet another form of genetic dwarfism, the

affected subjects seem to be able to

pro-duce immunoreactive growth hormone but

either suffer from a peripheral, non-respon-siveness to this product or tile product itself

is devoid

of

growth

promoting

activity,

perhaps due to a molecular mutation.

End-organ non-responsiveness seems to he

responsible for the short stature of

the

African

pygmies.’1

Apituitarism

(

absent

gland

)

has l)ee:1

verified

at

autopsy

in

One patient whose

non-twin sister seemed to be similarly

affected.” Dwarfism and hypoplasia of all

existing endocrine glands were extreme in

this patieiit, who died at 17 years of age.

The sella turcica

vas

of

normal

size

aIl(l

shape, despite the complete absence of tile hypophysis.

CONCLUSION

The

syndrome

exhibited

by

the

two

(7)

one

of the

known

familial

forms

of pituitary

dwarfism

as

listed

here.

It

is characterized

by

an

excessively

small

sella

turcica

located

in

a sphenoid

bone

of

abnormal

morphol-ogy

and

by

deficient

production

of multiple

pituitary

hormones,

including

growth

hor-mone.

Mental

retardation,

perhaps

secon-dary

to

recurrent

hypoglycemia,

is

also

present.

An

autosomal

recessive

inheritance

is possible.

SUMMARY

An

11-year-old

girl

and

her

10-year-old

sister

presented

the

following

characteris-tics: severe growth

failure

since

early

in-fancy;

a

tendency

to

hypoglycemia;

poor

production

of

growth

hormone,

TSH,

and

ACTH;

marked

retardation

in skeletal

mat-uration;

and

an

excessively

small

sella

turcica

with

abnormal

sphenoid

bone

mor-phology.

Mental

retardation,

moderately

se-vere,

was

perhaps

secondary

to

recurrent

hypoglycemia.

This

syndrome

is believed

to

represent

a hitherto

unrecognized

form

of

genetically determined pituitary dwarfism.

REFERENCES

1. Seip, M., Van der Hagen, C. B., and Trygstad,

0. : Hereditary pituitary dwarfism with

spon-taneous puberty. Arch. Dis. Child., 43:47, 1968.

2. Vickers, V. S., and Stuart, H. C. : Anthropome-try in the pediatrician’s office: norms for

se-lected body measurements on studies of

children of North European stock.

J. Pediat.,

22:155, 1943.

3. Creulich, W. W., and Pyle, S. I. : Radiographic Atlas of Skeletal Development of the Hand and Wrist, ed. 2. Stanford, California: Stan-ford University Press, 1959.

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C.

J.

: The Diagnosis and Treatment of Endo-crine Disorders in Childhood and Adoles-cence, ed 3. Springfield, Illinois: Charles C Thomas, 1965.

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PEDIATRICS, 22:576, 1958.

7.

Steiness, I. : Acid mucopolysaccharides in urine in gargoylism. PEDIATRICS, 27:112, 1961.

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J. Med.,

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R. S., and

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15. Parker, M. L., Hammond,

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19. Fisher, R. L., and Di Chiro, G. : The small

sella. Amer.

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20. Frances, j. M., Knorr, D., Martinez, R., and

Neuh#{228}user, G. : Hypophysarer Zwergwuchs bei Lippen-Kiefer-Spalte. Helv. Paediat.

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21:315, 1966.

21. Marin-Padilla, M., Hoefnagel, D., and Be-nirschke, K.: Anatomic and histopathologic study of two cases of D1 ( 13-15) trisomy. Cytogenetics, 3:258, 1964.

22. Tweedie, A. R., and Keith, A. : Ectopia of the pituitary,

with

other

congenital

anomalies

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ARTICLES

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Soc. Med., Part 2, Larvngol. section, 4:47, 1911.

23. Brewer, D. B. : Congenital absence of the

pi-tuitary

gland

and

its

consequences.

J.

Path.

Bact., 73:59, 1957.

24. Hintz, R. L., Menking, M., and Sotos,

J.

F.:

Familial holoprosencephaly with endocrine dysgenesis.

J.

Pediat., 72:81, 1968. 25. Rimoin, D. L., Merimee, T.

J., and

McKusick,

V. A. : Growth-hormone deficiency in man: an isolated, recessively inherited defect. Sci-ence, 152:1635, 1966.

26. McKusick, V. A. : Primordial dwarfism and ec-topia ientis. Amer.

J.

Hum. Genet., 7:189, 1955.

27. Seip, NI. : Personal communication, 1968. 28. Trygstad, 0., and Seip, M. : Hereditary

pitui-tary dwarfism treated with human growth

hormone. Acta Paediat. Scand., 53:527, 1964. 29. Bierich,

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R. : On genetically determined

pitui-tary dwarfism. (Abst. ) Acta Endocr.

(Suppl. 45), 89:27, 1964.

30. 1.aron, Z., Pertselan, A., and Mannlieimer, S.: Genetic pituitary (lWarflsm with high sertlin concentration of growth hormone: a new

in-born error of metabolism? Israel

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31. Merimee, T.

J.,

Rimoin, D. L., Cavalli-Sforza,

L. C., Rabinowitz, D., and McKusick, V. A.:

Metabolic effects of human growth hormone in the African pygmy. Lancet, 2: 194, 1968. 32. Steiner, M. M., and Boggs,

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D. : Absence of

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Acknowledgment

We are indebted to Dr. Charles C. Gale, Dc-partment of Physiology and Biophysics, for the growth hormone immunoassays, and to Dr. Byron H. Ward, Children’s Orthopedic Hospital and Medical Center, and Dr. Paul S. Paulson, Provi-dence Hospital, Seattle, who performed the radio-logical studies.

JACOB

ABBOTF

(

I 803- I 879), AUTHOR

OF THE MOST

FAMOUS

BOOK

ON

CHILD

REARING

OF THE

1870’S, DISCUSSES

CORPORAL

PUNISHMENT

OF

CHILDREN

Jacob Abbott wrote

the

most

widely

read

book

about

child

nurture

in

the

decade

just

after

the

Civil

War.

His

two

principal

themes

were:

the

absolute

need

for

parental

authority

over the child “without violence or anger,” and “right development of the child’s character . .

irs harmony with the structure and characteris-tics of the juvenile mind.” If the child did not bow to parental authority, Abbott advised par-ents of the need for corporal punishment:

The parental authority must, therefore, be es-tablished-by gentle means, if possible-but it must by all means be established, and be firmly main-tamed. If you cannot govern your child without corporal punishment, it is better to resort to it than not to govern him at all. Taking a wide view of the field, I think there may be several cases in which a resort to the infliction of physical pain as

the only available means of establishing authority may be the only alternative.

. . .

Complete,

abso-lute, unquestioned authority can often be obtained

most forcefully by this form of punishment

.

manoeuvre and artifice and reason and affection ( are ) a sandy foundation for establishing parental authority that came from

God

and nature.1

As harsh

as this

advice

may

seem

today,

Ab-bott

was

convinced

that

his

suggestions

about

“gentler” controls offered proof and

strength-ened

belief

in the

child’s

rationality

or

tracta-bility.

NOTED BY T.E.C., JR., M.D.

REFERENCE

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1969;43;858

Pediatrics

Pierre E. Ferrier and E. Franklin Stone, Jr.

SELLA TURCICA

FAMILIAL PITUITARY DWARFISM ASSOCIATED WITH AN ABNORMAL

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