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CONGENITAL ADRENAL HYPERPLASIA WITH ASSOCIATED EPISODES RESEMBLING HISTAMINE POISONING

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D.C. (S.M.H. l03781). This white male

child WdS found to have a large ileIls and

some Ul)iC hair tt the age of 5 sears, when examined I)y 1 sCl)(Ol physician. He was then referred to another hospital where the

diag-110515 of congenital a(lrenal hyperplasis was

macic. An increasc(l urinary excretion of

17-ketosteroids \‘as found aiul short courses of

cortisone and 17-methyl-androstenediol were

given. .At the age of 72 ‘ears he was

ad-mitted to Syracuse Memorial Hospital for

sttl(lV prior to re-institution of cortisone therapy.

Family history revealed no evidence of

endocrine (lisor(ler. However a male half-first cousin was exl)lore(l surgically in this hospital at 14 years of age and found to have a per-forated duoclenal ulcer. His chief complaint

This study was supported in part by a research Health, Public Health Service.

l)r. Gonzales is recipient of a fellowship from the New York State Division, American Cancer Society.

ADDRESS: (L.I.G.) Upstate Medical Center, 766 Irving Avenue, Syracuse 10, New York.

524

By Romulo F. Gonzales, M.D., and Lytt I. Gardner, M.D.

Department of Pediatrics, Upstate Medical Center, State University of New York,

Syracuse, New York

T

HIS I)h1)er describes a case of

congeni-tat adrenal hyperplasia in a boy,

corn-plicated by episodes of flushing,

hyper-thermia, )aiii in head and/or abdomen and

prostration. Rare reports exist of patients

with congeiu tal adrenal hvperplasia who

ha-’e hv1)ertensioll’ ai-icl vho lllt\e

hypogly-cemia.2 There appears to l)e no reported

instance of a Pltie1lt with congenital

adrenal hyperplasia showing the symptoms

descril)ed above. Observations on this child have I)een inide over a period of years, and it seems justifiable to report them, both be-cause of the unusual nature of the symptoms and the possibility that the adrenocortical

disease is metabolically related to the

)arOXysIl1al episodes.

History

CASE REPORT

had been nocturnal abdominal pains.

The parents’ history of the patient stated

that he had been born normally, and that they

considered his development to be normal up

to 3 years of age when he manifested

ab-normally large musculature. After the age of

4 years he began to have bouts of headache

and/or abdominal pain and fever. Two of

these episodes were diagnosed as

“pneu-monia” but did not respond to antibiotic

therapy. These episodes occurred as frequently

as 3 times a month. There had been no

convul-SiOns or epileptiform seizures prior to

admis-sion here.

Physical Examination

On physical examination, he had the same

findings as previously mentioned. His

chrono-logical age was 79’i2 years, height-age 133k

years, weight-age 14 years and bone-age be-tween 14 and 15 years.

Laboratory Findings

(

See Appendix for methods.) Serum sodium

concentration was 150 mEq./1. Urinary excre-tion of 17-ketosteroids averaged 25 mg./24 hours. He was given 50 rng. of cortisone

intra-muscularly daily for 3 days and then

main-tamed on 25 mg. orally twice daily. He was

observed as an outpatient, and the excretion of

17-ketosteroids fell to values of 12 and 6 mg./ 24 hours, as shown in Figure 1. The figure also shows a fall in the 17-ketosteroid level in the plasma from a mean value of 82 i.g./1O0 ml. before cortisone therapy to 17 p.g./lOO ml.,

1 1 days after treatment was begun. After 43 days of therapy the level of 17-ketosteroids in the plasma was too low to estimate by the

method used.

(2)

D C.

URINE

7-KS

MG.PER DA

THERAPY

Course, with Comments

Subsequent developmental progress on a

maintenance dose of 20 mg. of hydrocortisone

Orally twice daily is shown ill Figure 2. In

this figure the oblique dotted line indicates the normal mean for bone-age, height-age and

A- CORTISOW[ ‘1 BEGUN

B- AXILLARY HAIR NOCTURNAL EMISSIONS

Fic. 2. Developmental pattern of patient before and during cortisone therapy.

Average normal growth is indicated by the oblique dotted line.

0 5 10

CHRONOLOGIC AGE

MALE

PLASM A

7- KS

.JJG. PER

CENT

CLINICAL NOTES

CONGENITAL ADRENAL HYPERPLASIA

DAY OFEXPT. 5

7

34 49

CONTROL CORTISONE5OMG. P.O. Q.D.

Fi;. 1. Reduction of 17-ketosteroids in plasma an(l urine when patient was treated with cortisone. The dotted column at the upper right indicates that tile plasma concentration of 17-ketosteroids of the

sample was less than 16 tg./ 100 ml.

(1)

L’J

0

-J

z LU

0

0

-J

LU

>

LU

(3)

Fic. 3. Temperature, blood pressure and sodium and potassium in serum during an episode. The data at

the extreme right of the chart were recorded when the patient was symptom-free. The bone-age curve may be seen considerably

above and approximately parallel to the

isodevelopmentat level before and during the

course of treatment. This chart also shows a

rise in 17-ketosteroids in the plasma at the

onset of “puberty,” while the patient was on

suppressive doses of hydrocortisone. It is

sug-gested that this is due to the elaboration of

normal testicular androgens as a result of

maturation of tile pituitary-gonadal axis.

Wil-kins and Cara have described the relationship between osseous maturation and the onset of gonadal maturation in boys with congenital adrenal hyperplasia who are treated with

corti-sone.3 These authors found that the effects of

cortisone therapy on sexual development

de-pend upon the level of general somatic

de-velopment attained before treatment is begun.

In addition to this typical picture of

con-genital adrenal hyperplasia in a male there

occurred, during our period of observation of

this patient, more than a dozen episodes of

headache and/or abdominal pain, fever,

only once. Their duration was from 1 day to

2 weeks.

In one instance an episode was clearly

re-lated to bilateral otitis media, and in another instance an episode directly followed a blow

on the head from a basketball. No such

obvi-ous stimuli could be incriminated for the great majority of this patient’s episodes. It was the

impression of some observers that the patient

was more likely to have an episode following

emotional excitement. On 1 occasion his

mother mentioned that the patient’s younger

brother had been pestering him a great deal

just before an episode. In 1954 an episode

began on December 23 and progressively

be-came worse, culminating in hospital admission

on Christmas morning.

Such an episode is depicted in Figure 3,

which shows subnormal diastolic pressures

during the febrile period. This was noted on

2 occasions. During an attack the patient

showed generalized muscular contracture,

(4)

527

No abnormal funduscopic or localizing

neuro-logical findings were made at any time. The

face of the patient became suffused with

blood, especially the malar eminences and the

ears. The ears were reminiscent of the “rose-petal” ears of magnesium-deficient rats. There

was marked flushing of the conjunctivae, and

a sensation of irritation and itching was de-scribed there by the patient. There was

some-times vomiting. At the height of such an

attack the patient complained of dizziness if

he sat up. On 1 occasion the patient turned

pate and became unresponsive when placed

in the erect position, and at another time

stopped breathing when placed in the erect

position during general anesthesia for a

pneu-moencephatogram. It is very possible that

postural hypotension was the cause of these

2 spells but no blood pressure data are

availa-ble to confirm this.

Additional Laboratory Findings

Hematological studies were normal. The

urine was negative on routine examination.

Concentrations of sodium, potassium and

chloride in the serum were normal on several occasions. No coproporphyrin, uroporphyrin,

porphobilinogen or 5-hydroxy-indoles could

be detected in the urine. Blood sugar

de-terminations, repeated 6 times in a period of

16 hours during an attack, ranged between 78

and 115 mg./100 ml. Serum amylase activity was normal. A gastrointestinal series revealed

no roentgenotogic evidence of ulcer. Skull

roentgenograms were normal.

Electroen-cephalograms were taken on 5 different

oc-casions and all were described as showing cerebral dysrhythmia without focal features. The degree of dysrhythmia was greater in

trac-ings taken during an attack than in those

taken before or after the attack.

Pneu-moencephalography was attempted but was

not successful for the reason previously noted.

Therapy

Treatment during these attacks was

symp-tomatic, antipyretics and sedatives. Dilantin#{174},

0 Bartter et al. have reported electroencephal-ographic studies on 3 females with congenital adrenal hyperptasia.42 Tracings on all 3 showed

asymmetry, elevation of voltages and abnormal

slow waves. The finding was unexplained. No

episodes of flushing, hyperthermia, etc., were

described.

Tridione#{174}, and chlorpromazine have been tried

at different times on a prophylactic basis. It has not yet been possible to assess whether or not any one of these agents has been helpful.

DISCUSSION

The natural history of congenital adrenal

hyperplasia in the male has been

ade-quately described eIsewhere. The patient responded to cortisone therapy by a reduc-tion in urinary excretion of 17-ketosteroids.5

A fall in the level of 17-ketosteroids in the

plasma was also demonstrated when

corti-sone was given. It had been hoped that

long-term cortisone therapy might postpone

the early fusion of epiphyses which

ordi-narily takes place in patients with this disease. Figure 2 shows that this result was

not accomplished, and repeated

measure-ments of height indicate that he has

stopped growing. Because his bone-age was

over 14 years at the onset of therapy, it may

have come too late. Secondly, the oral route

of therapy may not have provided a

suffi-ciently uniform suppression of androgen

production, a disadvantage of oral therapy

which has been pointed out by Wilkins et

al.’

The patient’s episodes bear some

re-semblance to a disturbance in the

hypo-thalamus. Various mechanisms have been

offered to explain periodic massive

dis-charge of hyperactivity from the hypothal-amus. Riley and colleagues have described

48 cases of “familial dysautonomia.

In

these cases, attacks were provoked by

an-tagonizing the child. There was defective lacrimation, ease of perspiration,

erythema-tous blotches on excitement, inadequate temperature control and postural

hpoten-sion. In addition there was interference of

growth, speech defects and neurological

findings such as absent or diminished deep

tendon reflexes. These authors proposed a

vicious cycle starting with a functional

de-rangement of the central nervous system

re-sulting in the autonomic attacks.

.In a study of more than 100 schizophrenic

children Bender noted disturbances in

(5)

manifesta-invasion of the brain. Aring and Engel

have described another variation on this

theme in a hyperphagic dwarf with

tha-lamic lesions who had autonomic attacks.#{176}

In this case attacks were provoked by

emo-tional excitement of any sort or by illness.

The author suggested that the lesions in the

thalamus acted as an interruption to the

higher cortical controt of hypothalamic

functions. By this hypothesis emotional stimuli, thus released from higher control,

would! provoke autonomic changes to an

exaggerated extent. Penfield has described

a syndrome of “diencephalic autonomic

epilepsy.” His first case, reported in 1929,

was due to a ball-valve tumor of the third

ventricle. In this patient the severity and

duration of the seizures apparently

de-pended upon the degree and duration of

pressure on the thalamus. Penfield and

Jasper iii subsequent reports of other cases

showed that individual sym)tOmS shown

by the patients could be reproduced by

stimulation of certain cortical areas.’2 It

was thought that these cortical areas had

pathways through the hypothalamus. When

Bauer Surveyed! 60 cases of hypothalamic

disease with various endocrine

manifesta-tions, hypothalamic changes found at

nec-ropsy consisted of 51 neoplasms, 7

inflam-matory lesions and 2 degenerative ones.’3

Several elements of our patient’s

paroxys-mal episodes : headache, facial flushing,

lowered diastolic blood pressure, vomiting

and 1)rostration resellible histamine

poison-ing.’4 The attacks were more generalized

than the syndrome of intense unilateral

headache, lacrimation, salivation and

sweat-ing described! by Horton and theorized by

him as due to histamine.’7 Whether the

symptomatology of our patient is due, in

fact, to the endogenous liberation of

hista-mine or a histamine-like substance must

await further study. Nevertheless this

in-teresting )ossibility perniits the proposal

of an hypothesis interrelating congenital

siderable evidence that histamine metabo-lism is influenced by adrenal corticosteroids.

The adrenalectomized rat is more

suscepti-ble to histamine intoxication, and its tissue

histamine concentration has been found

to be very high.lH The administration of

adrenal cortical extract to adrenalectomized

rats has been found to restore the ability

of the animal to inactivate injected

hista-mine.0 The hypophysectomized rat is also

quite Susce1)tible to histamine intoxication,

and this lowered resistance is brought hack

to normal by treatment with

adrenocorti-cotropin (ACTH).” Following

adrenalec-toniy the rat lung shows a marked

diminu-tion of histaminase activity, which can be

restored by treatment with adrenal cortical

extract.” Urinary excretion of histamine

rises in the normat and allergic human

sub-ject when ACTH or cortisone is

The administration of cortisone to guinea

pigs, dogs and human beings causes a fall

in histamine concentration in the

As most histamine in the blood is in the

formed leukocytes,” changes in

concentra-tion of histamine in the whole blood more

nearly reflect shifts intracellularly than

extracellularly. The foregoing data suggest

that the level of circulating

corticoster-oids profoundty affects the intracellular

con-centration of histamine. Increased levels of

corticosteroids in plasma are associated

with increased renal excretion of histamine

and lower intracellular concentration of

histamine, whereas lower levels of

corti-costeroids in plasma are associated with

higher intracellular concentration of

hista-mine.

(h) Possible relation of histamine to an

error in corticosteroid metabolism in

con-genital adrenal hyperplasia. The relative

inability of patients with congenital adrenal

hyperplasia to maintain adequate levels of

corticosteroids in plasma is now well

docu-2627 Jf intracellular concentration of

(6)

concen-tration of circulating corticosteroids, then

these patients should have chronically

dc-vated levels of histamine in tissues. It is

possible that the mobilization of a

hista-mine-like substance from cells to plasma

during sudden stressful situations would

account for the systemic manifestations

of our patient. Because individuals with

congenital adrenal hyperplasia are unable

to raise their low plasma levels of

corti-costeroids, even when maximally stimulated

by ACTH, their adrenal mechanisms for

promoting urinary excretion of histamine

should be almost nonfunctional. Thus if

stress were to liberate histamine-like

sub-stances from the intracellular compartment,

the lack of an adrenal mechanism to

pro-mote its urinary excretion might result in

signs of histamine poisoning. Furthermore,

despite exogenous cortisone treatment the

patient with congenital adrenal hyperplasia

has little or no endocrine control over his

level of circulating corticosteroids, in

con-trast to the normal individual. It is not

possible for him to meet a sudden metabolic

demand for an increased plasma

concen-tration of corticosteroids. If the patient is

treated with oral cortisone, as was the

present case, another dimension of

non-homeostatic variability is added. Wilkins

has pointed out that the effects of oral

cortisone are transient and probably wear

off during each night.’

Why are there not more patients with

congenital adrenal hyperplasia who show

such episodes? This cannot be answered

at present, but it may be pointed out that

neither has it been explained why there are

not more cases of hypoglycemia in this

group of patients, yet the nature of the

metabolic defect involves chronically low

plasma level of corticosteroids (cf.

discus-sion by Bongiovanni et al.’). The possible

diagnoses of paroxysmal diencephalic

dis-charge versus endogenous liberation cf a

histamine-like substance are not necessarily

mutually exclusive. The relationship of

emo-tional stress to chronic urticaria,

angioneu-rotic edema and asthma is a case in point.

Paroxysmal episodes of flushing have

l)een reported

in

certain patients who have metastatic carcinoid. Since these patients

have abnormal indole metabolism and

cx-crete excessive amounts of

5-hydroxy-in-doles in the urine2, 30 the present patient’s

urine was tested for this class of compound.

No measurable amounts were detected. It

would thus seem unlikely that there is any

connection between the present patient’s

episodes of flushing and the syndrome of

paroxysmal flushing, nletastatic carcinoid

and abnorn at 5-hydroxy-inclole metabol iSm.

SUMMARY

Developmental and metabolic 01)5

tions are presented! on a boy with congenital

adrenal hyperplasia who also exhibited

paroxysmal episodes resembling histamine

These attacks were characterized

by hyperthermia, flushing of the head and

ears, abdominal and/or head pain, chilly

sensations, 1)rostratioil and sometimes

vomit-ing. Diastolic hypotension was observed

twice during the episodes. The patieiit corn-1)laiiled of marked dizziness if placed in the erect positioli. There was no eviclepce of cx-cessive toss of sodium.

Two possible explanations for the above

episodes are discussed: (1) that the

epi-sodes were dine to paroxysmal, massive

di-encephalic discharge, and (2) that the epi-sodes were due to the sudden liberation into

plasma of an intracellular histamine-like

substance. The interrelationships between

histamine metabolism and adrenocortical function are reviewed. It is hypothesized that the patient’s defect in corticosteroid

synthesis may be causally related to the

episodes resembling histamine shock.

APPENDIX

OF ANALYTIC

METHODS

The analytic procedures employed were

as follows: (a) Na and K in serum, method

of Wallace et al.;” (b) Cl in serum, method

of Schales and Schales;’2 (c) neutral

17-ketosteroids in plasma, method of Gardner;’’

(

d) blood sugar, method of Folin and Wti as

modified by Folin;’4 serum amylase activity,

method of Somogyi.0 Coproporphyrin,

(7)

tested for 5-hydroxy-indoles by the

tech-nique of Udenfriend et Bone-age was

estimated by the method of Todd.4’

Height-age and weight-age were estimated using

mean values from Englebach’s tables.4’

Twelve-lead electroencephalograms were

obtained using a Grass Ill-B machine.

ACKNOWLEDGMENTS

The authors are indebted to Drs. Stanley

Batkin, Pierre Brodeur, Julius B. Richmond

and Martin Schulman for advice and

assist-ance. The patient was kindly referred to us

by Dr. Thomas H. Shepard,

II. Thanks

are

due to Salty Merrick, Artelissa Tice and

Sylvia Saarnijoki for technical assistance.

Cortisone and hydrocortisone were

pro-vided by Merck and Company.

REFERENCES

1. (a) Shepard, T. H., II, and Clausen, S. W.:

Case of adrenogenital syndrome

. with hypertension treated with

corti-sone. PEDIATRICS, 8:805, 1951. (b) Wilkins, L. and others: Further studies

on the treatment of congenital adrenal hyperplasia with cortisone. I.

J.

Gun. Endocrinol. & Metab., 12:

257, 1952; II. Ibid., 12:277, 1952;

III. ibid., 12:1015, 1952.

(c) Wilkins, L. : The diagnosis of the

adrenogenital syndrome and its

treatment with cortisone.

J.

Pediat., 41:860, 1952.

2. White, F. P., and Sutton, L. E. :

Adreno-genital syndrome with associated

epi-sodes of hypoglycemia.

J.

Clin. Endo-crinol., 11:1395, 1951.

“3. \Vilkins, L., and Cara,

J.

: Further studies on the treatment of congenital adrenal hyperplasia with cortisone. V. Effects of cortisone therapy on testicular develop-ment.

J.

Clin. Endocrinol. & Metab., 14: 287, 1954.

4.

Gardner, L. I., and others: Follow-up

studies in a boy with mixed adrenal

cortical disease. PEDIATRICS,

5:808,

1950.

5. Wilkins, L., and others: Cortisone therapy ill congenital adrenat hyperplasia. j. Cliii. Endocrinol., I I : 1, 1951.

7. Riley, C. M., and others: Further

observa-tions on familial dysautonomia.

PEDI-ATRICS, 14:75, 1954.

8. Bender, L. : Childhood schizophrenia. Clinical study of one hundred schizo-phrenic children. Am.

J.

Orthopsychiat.,

17:40, 1947.

9. Ford, F. R. : Diseases of the Nervous Sys-tem in Infancy, Childhood and

Adoles-cence. Springfield, Thomas, 1946, p.

428.

10. Aring, C. D., and Engel, G. L. :

Hypothala-mic attacks with thalarnic lesions. I.

Physiological and psychological

con-siderations. II. Anatomical considera-tions. Arch. Neurol. & Psychiat., 54:37 (I); 54:44 (II), 1945.

1 1. Penfield, W. C. : Diencephalic autonomic

fits. Arch. Neurol. & Psychiat., 22:358, 1929.

12. Penfield, W. G., and Jasper, H. : Epilepsy

and the Functional Anatomy of the

Human Brain. Boston, Little, 1954, p.

412.

13. Bauer, H. G. : Endocrine and other clinical manifestations of hypothalamic disease.

J.

Ctin. Endocrinol. & Metab., 14:13, 1954.

14. Dale, H. H., and Laidlaw, P. P. :

Hista-mine shock.

J.

Physiol., 52:355, 1919. 15. Weiss, S., and others: The systemic effects

of histamine in man; with special refer-ence to the responses of the

cardiovascu-lar system. Arch.

mt.

Med., 49:360,

1932.

16. Pickering, G. W. : Observations on

mechanism of headache produced by

histamine. Clin. Sc., 1:77, 1933.

17. Horton, B. T. : Histamine cephalalgia.

Journal-Lancet, 72:92, 1952.

18. Rose, B., and Browne,

J.

S. L. : The effect of adrenalectomy on the histamine

con-tent of the tissues of the rat. Am.

J.

Phvsiol., 131 :589, 1940-41.

19. Rose: B. : The effect of cortin and desoxy-corticosterone acetate on the ability of the adrenalectomized rat to inactivate histamine. Am.

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Physiol., 127:780,

1939.

20. Noble, R. L., and Collip,

J.

B. : The re-sponse of normal, hypophysectomised and adrenalectomised rats to histamine administration. Am.

J.

Physiol., 133:623,

1941.

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CLINICAL NOTES

Decrease of histaminase in tissue by

adrenalectomy and its restoration by

cortico-adrenal extract. Am.

J.

Physiol.,

130:539, 1940.

22. Rose, B., and others: Observations on the

metabolic changes resulting from the

administration of ACTH to patients with

asthma and allied conditions, in

Pro-ceedings of the Second Clinical ACTH Conference, vol. 1,

J.

R. Mote, editor.

New York, Blakiston, 1951, pp. 515-525.

23. Grob, D. : The renal excretion of histamine and histidine in man, and the effect of

adrenocorticotropic hormone (ACTH)

and cortisone administration. Bull. Johns Hopkins Hosp., 90:341, 1952.

24. Mitchell, R. G., and Code, C. F. : Urinary excretion of histamine after administra-lion of cortisone.

J.

Clin. Endocrinol. & Metab., 14:707, 1954.

25. Graham, H. T., and others: Distribution of histamine among leucocytes and plate-lets. Blood, 10:467, 1955.

26. Kelley, V. C., and others: Hormone

patterns in patients with congenital adrenal hyperplasia. PEDIATRICS, 12:541, 1953.

27. Bongiovanni, A. M., and others: Studies on

the metabolism of adrenal steroids in

the adrenogenital syndrome.

J.

Cliii. Endocrinol. & Metab., 14:409, 1954.

28. Thorson, A., and others: Malignant

car-cinoid of the small intestine with

metastases to the liver, valvular disease of the right side of the heart, peripheral vasomotor symptoms, bronchoconstric-tion and an unusual type of cyanosis. Am. Heart

J.,

47:795, 1954.

29. Lembeck, F. : 5-Hydroxytryptamine in a

carcinoid tumor. Nature, 172:910, 1953. 30. Sjoerdsma, A., and Udenfriend, S. : Studies

on indole metabolism in patients with

malignant carcinoid (argentaffinoma)

(abstract).

J.

Gun. Investigation, 34:914,

1955.

:31. Wallace, W. M., and others: The

applica-tion of the internal standard flame

photometer to the analysis of biologic material.

J.

Lab. & Cliii. Med., 37:621, 1951.

32. Schales, and Schales, Selma S. : Simple

and accurate method for determination of chloride in biological fluids.

J.

Biol. Chem., 140:879, 1941.

33. Gardner, L. I. : Plasma iieii: rat

17-ketosteroids. I. Technique of estimation.

J.

Cliii. Endocrinol. & Metab., 13:941, 1953.

:34. Folin, 0. : The determination of sugar in

blood and in normal urine.

J.

Biol.

Chem., 67:357, 1926.

35. Somogyi, M. : Micromethods for the esti-mation of diastase.

J.

Bfol. Chem., 125: 399, 1938.

36. Watson, C.

J.

: Porphyria, ill Christian,

H. A. : Oxford Medicine, vol. 4. New

York, Oxford, 1938.

37. Watson, C.

J.,

and Schwartz, S. : A simple test for urinary porphobilinogen. Proc. Soc. Exper. Biol. & Med. 47::393, 1941.

:38. Drekter, I.

J.,

and others: A rapid method

for the determination of total urinary

17-ketosteroids.

J.

Clin. Endocrinol., 7:

795, 1947.

:39. Udenfriend, S., Weissbach, H., and Clark,

C. T. : The estimation of 5-hdroxytryp-tamine (serotonin) in biological tissues.

J.

Biol. Chem., 215:337, 1955. 40. Todd, T. W. : Atlas of Skeletal Maturation.

St. Louis, Mosby, 1937.

41. Englebach, W. : Tables as adapted by

Wilkins, L., The Diagnosis and Treat-ment of Endocrine Disorders in

Child-hood and Adolescence. Springfield,

Thomas, 1950, pp. 30-33.

42. Bartter, F. C., Albright, F., Forbes, A. P., Leaf, A., Dempsey, E., and Carroll, E.: The effects of adrenocorticotropic hor-mone and cortisone in the adrenogenital

syndrome associated with congenital

adrenal hvperplasia: An attempt to

cx-1,l,ii,i and correct its disordered hormonal pattern. j. Clin. Investigation, 30:2.37,

(9)

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1956;17;524

Pediatrics

Romulo F. Gonzales and Lytt I. Gardner

RESEMBLING HISTAMINE POISONING

CONGENITAL ADRENAL HYPERPLASIA WITH ASSOCIATED EPISODES

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To evaluate the effect of loop size and penetration depth on the compressive load, the obtained data of compression tests were analyzed, by using the CCD (central

The results of this study indicated that all the six components of health promoting behaviors were positively correlated with health promoting behaviors. The

Based on the results of research at PT ASI Pudjiastuti Marine Product on the company's business strategy through SWOT analysis, it can be concluded that internal factors in the form

Two recent studies have demonstrated an association in preschool children between middle ear disease and later problems with hyperactivity’2 and inattention.’6 Although our study