the children of affected parents had goiters while 27.6 per cent of the children of normal parents were goitrous. The records of cases from Chicago show 46 per cent of the children of affected parents and 43 per cent of the children of normal parents had goiters.

The family records from goiter cases in Chicago would represent instances of dominate Mendelian inheritance of a predisposition for the disease. The large per cent of cases which do indicate familial tendency would have considerable influence on the incidence of goiter in a goitrous region.

FAMILY PEDIGREES

Two family pedigrees and histories inheritance. Chart 1 illustrates an are given here to show cases of actual example of inherited goiter which was present at birth and disappeared during early childhood only to reappear at puberty or later in life. The mother II had a goiter, noticeable since she was sixteen years old which increased in severity at the birth of each child. Her sister II, had similar symptoms but her gland enlarged at an earlier age than II. The grandmother I, who had been dead several years did not have a noticeable. goiter so far as was known. IIg has six children, four girls and two boys. These four girls all developed goiters between eight and nine years of age, which have gradually enlarged and at the time of interview the mother and the two oldest daughters were receiving treatment. The aunt II had been operated on for goiter. The two daughters were sixteen and eighteen years of age. It would seem reasonable to suspect that these might represent typical congenital cases since their mother had a goiter at their birth and those in the children were developing at the expected time and similar to their mother's. This type of goiter is known to either disappear a few days after birth or develop and cause the death of the child. This family would represent a good example of the hypothesis that "goitrous mothers in a goitrous region bear children with goiters."

Chart 2 represents a similar family history except as to the severity of the disease in the individuals. Those affected had noticeable enlargements of the gland and symptoms but only

when aggravated by these factors, develops serious goiter symptoms.

These secondary causes such as childbirth and puberty are conducive to the development of goiters which vary a great deal in intensity and in response to treatment. Some of the patients who came in complaining of goiter, which seemed to have developed at puberty, were found to have noticed the enlargement since they were seven or eight years old. This might suggest that in such cases the goiter may have been present at birth but disappeared when the child was only a few months old only to reappear at puberty.

Cases in the group attributed to infection were quite rare but among these so designated one developed after severe illness from tonsillitis, another followed diphtheria and a more serious case developed rapidly during the time the patient had a badly infected tooth.

The part that seemed to be played by infected tonsils in the development of goiter was shown by the number of cases in which chronic tonsillitis accompanied goiter and reports of improvement in the goitrous condition after tonsillectomy.

Forty and eight-tenths per cent in the series of 100 cases in their histories

showed the complaint of seasonal sore throat. The complaints of severity of goiter symptoms also show seasonal variation.

These causes for goiter in cases which appear to be hereditary are reported for a temporary record of the cases at the time of treatment.

The per cent of cases which may be due to possible inheritance of a predisposition to goiter among a people in a goitrous region must augment the incidence in that region and offers a cause which cannot be disregarded.

The strength of transmission of a goitrous condition which results in a congenital goiter does not seem to be as great in these cases as has been found in foreign countries (Baillarger, 1873). The familial influence seemed to be great between mother and child but showed very slight affects on the grandchildren or the fourth generation, as indicated in table 19. Reports from foreign goitrous regions indicate that the persons of generation four, in terms of table 19 would show a high incidence of cretins. A comparison of the cases in this region would draw attention to the familial influence as a cause for a greater incidence in these regions. There may be several causes for this, such as decrease in the influence by generations, greater environmental influences or a difference in the constitutional conditions of the people.

There can be no doubt but that the predisposition to goiters is inherited but the method of inheritance has not been definitely established although several instances have shown typical dominate Mendelian characteristics. There seems to be a regularity in some families by which the same type of

goiter occurs as in the parent with similar degrees of severity but often with different symptoms which may be due to individual variation.

SUMMARY

A study of family histories for as many as four generations showed the familial tendency to the disease to be most noticeable in the second and third generation, which were equally affected, in the cases from St. Louis and a gradual increase in the number of affected individuals from the first

to the third generations in the cases from Chicago.

The recorded family histories from St. Louis showed 20 per cent of the children of goitrous mothers were affected. Similar data from Chicago showed 46 per cent of the children of affected parents were goitrous. No cretins were reported.

Tonsillitis or seasonal sore throat accompanied goiter symptoms in 40.8 per cent of the cases.

It is with pleasure I acknowledge the advice given by Dr. V. E. Emmel,

BAILLARGER, J. G. F. 1873. Le Goitre et Le Cretinisme.

BLANKENSHIP, R. C. 1921. The incidence of goiter in Wisconsin with suggestions as to medical management. Wis. Med. Journ., xix, 561.

CROTTI, A. 1922. Thyroid and Thymus. Lea and Febiger, Phila.

DAVENPORT, C. B. 1911. Heredity in Relation to Eugenics.

DOCK, G. 1895. Goiter in Michigan. Medical News.

GORDON, M. B. 1922. Childhood myxe

dema in America. Endo., vi, 235. GUILDER, R. 1923. Incidence of goiter

among college students. Ann. Clin. Med., i, 248.

Hrdlicka, AlES. 1916. Goiter among the

Indians along the Missouri River.
Science, xliv, 203.

JONES, E. G. 1918. Goiter in the South-
east. Jour. Amer. Med. Assoc., lxxi,
712.
LEVIN, S. 1921. 1146 Goiters in 1783
people. Arch. Int. Med., xxvii, 421.

Love, A. G., and Davenport, C. B. Defects Found in Drafted Men.

MARINE, D. AND KIMBALL, O. P. 1920. Goiter survey work in Ohio. Ohio Med. Jour., xvi, 757.

PORTER, W. B., AND VONDERLEHR, A. A. 1921. Congenital Goiter. Amer. Jour. Dis. Child., xxii, 477.

SUMMERS, J. E. 1915. The incidence of heredity as a factor in the causation of goiter. Ann. Surg., Ixii, 138. TAYLOR, J. G. 1922. Goiter in 1425 girls. Wis. Med. Jour., xxi, 181. VALLERY-RADOT. 1922. The rôle of heredity in thyroid pathology. Lancet, i,

24.

United States Department of Commerce and Labor. Bureau of the Census. 1920.

United States Department of Commerce and Labor. Mortality Statistics. 1920.

Statistical Report of the St. Louis Public Schools. 1919-1921.

Report of the Division of Child Hygiene. 1919-1921. Chicago.

A

NY DISCUSSION of serologic reactions in syphilis necessarily starts with the older test which has taken the name of the worker who first applied it in a practical way. It will be recalled that Wassermann and Brück (1) in 1905, while working with the complement fixation phenomenon of Bordet and Gengou (2) in tuberculosis, conceived the idea that this method might be applied to the serologic diagnosis of syphilis. Impetus had been given to the study of this protean disease by the discovery of the spirocheta pallida by Schaudinn and Hoffman (3). Together with Neisser, Wassermann and Brück (4) in 1906 applied the complement fixation phenomenon to the serum diagnosis of syphilis. At about the same time Detre (5) was engaged in a series of similar experiments and published his work shortly after the report of Wassermann and his his co-workers. These original reports were soon confirmed, the work extended and its adoption as a laboratory method for the diagnosis of syphilis promptly followed.

The Wassermann test, it may be recalled, consists of a hemolytic system

1 Studies and contributions of the Department of Dermatology and Syphilology of the University of Michigan, service of Dr. U. J. Wile.

on one side, with the antigen antibody complex on the other, midway between which is the thermolabile, so-called "complement." If complement is bound to the antigen-antibody complex, hemolysis is prevented and we have a positive test. The precision and technical ability required for the performance of this test are well known. However, even after the necessary titrations have been properly carried out there still remain numerous variants which are potential sources of error. The most common of these sources of error are the deterioration of complement, an extremely variable element, and the occasional anticomplementary action of the serum. In addition, many serums contain natural hemolysins which may obviously lead to false negative results.

Today this complicated and technically difficult laboratory test is being performed in a different manner by a great number of laboratory workers and is labelled by all as the Wassermann test, irrespective of the variations from the original technic which are being employed. Changes and modifications have been made in practically every ingredient and step entering into the performance of the test, so that almost every laboratory worker has a Wassermann system which is peculiar to his laboratory. Probably