Negro Boy Research Articles

Constrictive Pericarditis

Constrictive pericarditis is an uncommon disease, particularly in childhood. Approximately 25 cases have been reported in children below 10 years, the youngest at 2½ years of age. 1-12 In approximately twothirds of cases the etiologic agent or mechanism of pericardial constriction is unknown. The interval of time between the original insult to the pericardium and the onset of the constrictive process is rather variable and difficult to determine. 2,9 Similarly, the interval of time between the onset of evidence of constriction and surgical therapy or death varies widely. 10,13 It is the purpose of this report to describe a 7-year-old Negro boy who developed severe constrictive pericarditis within 30 days following an episode of acute pericarditis with effusion. Surgical relief was accomplished 13 days later. The rapid conversion of acute pericarditis with effusion to constrictive pericarditis is unusual. Report of a Case A 7-year-old Negro boy was admitted to the

Systemic deposition of metallic mercury

Case 1. A 4-year-old Negro boy was seen at The Johns Hopkins Hospital with a chief complaint of falling, unconsciousness, and jerking of the extremities of 1 day's duration. Except for 5 days of oxygen therapy during the neonatal period, the past history was unrevealing. Careful inquiry elicited no information which would suggest the entrance of metallic mercury into the body. Physical examination was unremarkable. Laboratory studies, which included lumbar puncture, blood calcium, phosphorus, urea nitrogen, and fasting glucose determinations, were within normal limits. Mercury excretion during a 24-hour period, as determined by the polarographic method, was not significant. X-ray examination of the skull, neck, and trunk (Figs. 1, 2, 3) revealed the presence of many small round shadows of

Congenital asymmetry, short stature, and elevated urinary gonadotropin.

In 1953 we 1 first described the Syndrome of Congenital Hemihypertrophy, Shortness of Stature, and Elevated Urinary Gonadotropins in two children, a girl aged 5½ years and a boy 6 years old. Subsequently Silver and Gruskay 2 reported a case of hemihypertrophy and elevated urinary gonadotropin in a 7-year-old boy with normal height. In none of these cases was there any other evidence of apparent endocrine disturbance. The purpose of this paper is to report two additional cases of this syndrome: the first in an 8½-year-old Negro boy with shortness of stature and elevated urinary gonadotropins in whom the difference in the two sides of the body was limited to the spine, and the other in an 8-month-old white boy with shortness of stature, a difference in size of the legs, and swelling of the dorsa of the hands and feet. A tabulation of the findings in these five cases

Probable acrodermatitis enteropathica treated with nystatin (mycostain).

A 3-month-old Negro boy was first seen, on June 3, 1958, several weeks after a hospitalization by his pediatrician for diarrhea which had been difficult to control. The child continued to have four to five loose stools a day at the time he was seen. The pediatrician had not noted significant dermatitis during the hospitalization. A generalized dermatitis bearing some resemblance to atopic dermatitis was present. Loss of hair in the frontal region of the scalp was very marked. The child was irritable and did not eat or sleep well. A tentative diagnosis of acrodermatitis enteropathica was made at the time of the first visit. Scrapings from the skin and fecal material were both cultured on Nickerson's medium. Both cultures were positive for candida albicans. Because therapy with diiodohydroxyquin (Diodoquin) in acrodermatitis enteropathica has tended to be prolonged, although apparently successful, it was decided to treat

The nephropathies of sickle-cell disease.

Many of the complications of sickle-cell anemia have been well described and may be readily diagnosed, e. g., the pulmonary and cardiac manifestations. 1,2 In contrast, the functional and morphological renal changes associated with hemoglobin S have received little intensive study until the past few years. Margolies, in a clinical and pathologic review of the subject in 1951, mentioned albuminuria, hematuria, cylindruria, frequent urinary infections, fixed specific gravities, uremia and renal thromboses, and infarctions as complications of sicklecell disease and trait. 3 The nephropathies thus far described in detail include gross hematuria, 4 hyposthenuria, 5 fat embolism, 6 and the nephrotic syndrome. 7 The referral of a patient with homozygous hemoglobin S and massive proteinuria provided the opportunity to observe many of these renal defects in the same subject and to study their response to corticotropin (ACTH). Report of Case The patient was a 9-year-old Negro boy with eight hospital admissions preceding the present one.

Calcification of intervertebral disks in children.

Calcification of intervertebral disks in children is a curious clinical and radiological entity. The purpose of this paper is to report two children with intervertebral disk calcification. The clinical manifestation, etiology, and pathological physiology are discussed, including differences in children as compared with adults. Nineteen cases have been reported in children. The first, in 1924, was by Baron.1Later, in 1954, Silverman reviewed eight and reported seven other cases.13In 1954 two more cases were reported,12,17and in 1957, two additional cases.6,18 Report of Cases Case1.—An 8-year-old Negro boy was admitted to Duke University Hospital. He had been born at this hospital of an uncomplicated term pregnancy, weighing 1,855 gm. Labor was short; low forceps were used in delivery. He remained in the premature nursery for three weeks and weighed 2,240 gm. on discharge, at which time the physical examination was negative. Blood from the

Varicella gangrenosa

A case of varicella gangrenosa ina 3-year-old Negro boy is presented. The gangrene, involving the skin of both lower extremities and the left foot, required skin grafting of these areas and amputation of the toes of the left foot. No specific hematological cause for the development of gangrene was found. A discussion of theories regarding the etiology and pathogenesis of varicella gangrenosa is presented. It is difficult to place this child in any of these specific categories with the possible exception of individual susceptibility. A case of varicella gangrenosa ina 3-year-old Negro boy is presented. The gangrene, involving the skin of both lower extremities and the left foot, required skin grafting of these areas and amputation of the toes of the left foot. No specific hematological cause for the development of gangrene was found. A discussion of theories regarding the etiology and pathogenesis of varicella gangrenosa is presented. It is difficult to place this child in any of these specific categories with the possible exception of individual susceptibility.

Congenital choledochal cyst; demonstration by oral cholecystography.

Demonstration of a choledochal cyst by means of oral cholecystography has not been reported in the American medical literature until recently. Moseley1presented the first case so demonstrated. The patient was a 5-year-old white girl. More recently, Paulino,2of Rio de Janeiro, reported a case in a 22-year-old woman. To my knowledge, the case herein presented is the third to appear in the American literature. As in the original case, the patient is a child. Report of Case A 13-year-old Negro boy was admitted to St. Joseph Mercy Hospital on June 8, 1957, as a patient of Dr. Richard W. Deatrick. For the preceding six days he had been having colicky epigastric and periumbilical pain. He had vomited intermittenly during this period. The urine was described as dark yellow. Enemas had revealed gray stools. The past history revealed similar attacks of abdominal pain since the age of 5

CLEVELAND DERMATOLOGICAL SOCIETY

<b>Congenital Ichthyosiform Erythroderma.</b>Presented byDrs. W. P. Lascheid, L. W. Potts, andW. E. Clendenning. A 6-month-old Negro boy, presented at birth a generalized erythema and a marked thickening of the horny layer, which gave the skin a parchmentlike appearance. The skin of the face appeared taut, and there was a bilateral ectropion. The baby was immediately transferred to Babies and Childrens Hospital, where he was placed in an incubator with high humidity, and Aquaphor was applied locally several times a day. Vitamin A was administered in high doses. After about two weeks, the outer horny layer began to shed in various areas, leaving shield-like areas of keratin attached to fingers, toes, and several other areas on the extremities. These shields of keratin had to be cut from the fingers and toes to allow normal growth. After several weeks in the constant humid atmosphere, the erythema

Jaundice due to Ascaris obstruction of the common bile duct in an infant.

Jaundice in a 2-year-old infant in this country, secondary to an obstruction of the common bile duct by Ascaris lumbricoides, is so unusual that the following case is reported. <h3>Report of a Case</h3> A 2-year-old Negro boy had been in good health until 10 days prior to admission, when he developed severe watery diarrhea, associated with anorexia and weakness. Three days before admission he vomited an adult ascarid, and the very next day the mother observed that the child's urine was very dark and that his eyes had a yellow tint. The day before admission he vomited 20 more worms, but there was no history of his having passed any worms in the stools. In his earlier history, the child had had no severe illnesses other than upper respiratory infections. At the age of 8 months he had been treated for an Ascaris infestation, after which he passed 50 worms;

Cutaneous papillomatosis; nummular and confluent variety.

Reports of cutaneous papillomatosis are rarely found in the American literature. Wise and Sachs^1,2described the first case of the disorder (confluent and reticulated variety)³to appear in this country in 1937, and Young^4,5recorded the second. Leavitt⁶presented a possible example in 1956. The patient reported herein exhibited an eruption which clinically suggested the nummular and confluent variety of cutaneous papillomatosis and histologically coincided with earlier observations of this disorder. This form of cutaneous papillomatosis has not hitherto been presented in our literature. Report of a Case The patient is a 9½-year-old Negro boy. He was first observed in August, 1956, at which time he presented an asymptomatic eruption located upon the extremities, trunk, and face. The dermatosis had first appeared in 1954 on the face (about the eyes and mouth) and spread to its present confines within a period of several

Acute suppurative dacryoadenitis as a sequel to mumps.

Acute dacryoadenitis is a relatively rare condition usually caused by the mumps virus. According to Duke-Elder1the dacryoadenitis of mumps is always bilateral and nonsuppurative. The case we are presenting is somewhat unusual in that the dacryoadenitis occurred as the symptoms of mumps were subsiding and it was unilateral and suppurative. Duke-Elder1feels that suppurative dacryoadenitis occurs only with systemic infection, presumably bacterial. In this patient there was no positive systemic finding except a positive complement-fixation test to the virus of mumps. Report of a Case A 6-year-old Negro boy was admitted to King County Hospital, Seattle, Nov. 7, 1955. The chief complaint was of an increasing pain, tenderness, and swelling of the lateral portion of the left upper eye lid for three days. Two weeks prior to admission the patient had been sent home from school, where the incidence of mumps had been high, with malaise, nausea,

Studies in Sickle-Cell Anemia

Sickle-cell anemia (SCA) was first described in 1910,1but involvement of osseous tissue in this disease was not reported until 1924, when Graham2autopsied a 30-year-old man and found the marrow cavity reduced in size and at one point obliterated. In 1927, Cooley3described a skull which on roentgenography showed widening of the diploic spaces, a thin or absent outer table, and parallel lines radiating from the inner table. Similar roentgenograms have subsequently been reported in other patients with SCA. More recently, there have been additional publications4-32on bone involvement in SCA, but few of these report aseptic necrosis of the femur or the humerus. This paper presents two additional cases of aseptic necrosis of the femur in children with SCA. One of these cases also showed aseptic necrosis of the head of the humerus. Report of Cases Case1.—A 14-year-old Negro boy was hospitalized on

Hereditary spherocytosis in the Negro.

Congenital spherocytosis is a disease characterized by a varying degree of anemia, microspherocytes in the peripheral blood smear, splenomegaly, and increased hemolysis in hypotonic saline solutions. Although probably recognized1and treated2in the latter part of the 19th century, it was first accurately described as a clinical entity by Minkowski3in 1900, and in 1907 Chauffard4first described the increased fragility of the erythrocytes in hypotonic saline. Since that time the disease has been thoroughly studied and reviewed by many workers.5-7 The purpose of this paper is to report a genetic study in a Negro family in which there are members with evidence of congenital spherocytosis. The literature pertinent to the Negro race is reviewed, and some conclusions are drawn as to hereditary factors involved. Report of Cases Case1.—A 10-year-old Negro boy (Fig. 1) was admitted to the Harriet Lane Home June 2, 1956,

Bone infarcts in sickle-cell anemia.

Bone infarcts in children with sickle-cell anemia may produce a striking radiographic picture of extreme bone destruction and rapid rebuilding. We have recently seen a case which we believe to be an excellent example of this process; in a second case, in which an initial diagnosis of osteomyelitis was entertained, the subsequent course was more suggestive of bone infarct. The phenomenon of infarction in sickle-cell anemia has long been recognized, and aseptic necrosis resembling infarction pathologically has been described in virtually every organ and tissue of the body (6). Bone infarcts have received less attention in the literature than other features of this disease, and it is not at all certain that there is uniformity in the interpretation of certain of the bone changes, especially with regard to infarcts and osteomyelitis. Four cases, for example, similar to Case I of the present study have been reported as bone infarcts (1, 4, 9, 11), while comparable cases have been described merely as “unusual bone changes” (2, 3, 7). One of the first accounts of bone infarcts in sickle-cell anemia was published in 1937, by Diggs, Pulliam, and King (4), who stated that patients with this disease were subject to attacks of severe bone pain with localized tenderness, fever, and leukocytosis, leading to a diagnosis of osteomyelitis and subsequent surgery; on opening the bone, however, no exudate was encountered and cultures were sterile. The authors concluded that the lesions represented bone infarcts. One patient in their series actually had a proved staphylococcal osteomyelitis in addition to sickle-cell anemia. In 1948, a series of 48 cases of sickle-cell anemia was published by Macht and Roman (9). They found bone destruction, which they called infarction, in 5 cases, involving the long bones and the metatarsals. In 1954, Tori (11) reported 102 cases of sickle-cell anemia; in 1 of these, areas of destruction in the metacarpals were believed to be infarcts. It is our contention that many cases of bone infarction in individuals with sickle-cell anemia go unrecognized either because no films are made, or because of an insufficient interval between the onset of symptoms and roentgen examination. Cases in which bone lesions are discovered, on the other hand, may be mistakenly diagnosed as osteomyelitis when the lesions are in reality uncomplicated bone infarcts. Case Reports Case I: J. R. F., a 22-month-old Negro boy, was admitted to the hospital on Nov. 22, 1955, because of a “swollen arm.” At eight months of age, he had been seen by a physician because of irritability and at that time a diagnosis of anemia was made. Swelling of the hands and feet subsequently developed, and since September 1955 the child had refused to walk. The swelling was associated with pain and tenderness and often accompanied by fever.

The aplastic crisis of sickle-cell disease; occurrence in several members of families within a short period of time.

The crisis of congenital spherocytic anemia is a well-documented syndrome.1,2It is known that these erythroblastopenic states may occur in several members of a family within a short period of time. Recently these crises have been also described in sickle-cell anemia.3,4The purpose of this article is to report on members of two families with sickle-cell anemia in which aplastic crises developed within a short period of time. Report of Cases Family A Case1A.—This 5-year-old Negro boy was admitted to the hospital on Nov. 28, 1955. He had been known to have sickle-cell anemia since the age of 5 months. In November and December, 1954, he had had two attacks of cerebral thrombosis leaving him with aphasia and inability to properly handle his oral secretion and a paresis of his left upper extremity. One day prior to admission he was noted to be pale and weak.

An unusual complication of otitis media; extrusion of the incus into the external auditory canal.

Extrusion of the incus into the external auditory canal as a complication of otitis media has not recently been described. The literature from 1945 to 1956 1-3 was carefully reviewed and several texts 4-11 were consulted without this or a similar situation being noted. Degeneration and destruction of the ossicles by a purulent process in the middle ear is apparently not uncommon, 12-16 but only in several of the older texts 15,16 was the possibility of the extrusion of a nearly intact ossicle discussed. Report of Case The patient, a 2-year-old Negro boy, first complained of pain and discharge in the right ear about a month prior to admission. The process subsided after several days, but within a week the patient began to complain of discomfort again and the sensation of a foreign body in his ear. His mother removed a small hard object from the right external canal, and

Parathyroid adenoma in a child; report of a case presenting as central nervous system disease and complicated by magnesium deficiency.

Parathyroid adenomas are exceedingly rare in childhood. Primary hyperplasia of the parathyroid gland has been reported in infants and young children, but the parathyroid adenoma seems to be almost exclusively a disease of the older age group. Of 140 cases in a recent Mayo Clinic series, the youngest was 14 years old.1The case to be presented, at 7 years of age, represents the youngest child with a functioning adenoma, surgically removed and proved pathologically. It is the purpose of this report to review primary hyperparathyroidism as it is seen in children and to stress two unusual features of this case, namely, permanent neurological damage and an unusual serum magnesium deficit. REPORT OF A CASE A 6-year-old Negro boy was first admitted to the Cincinnati General Hospital on Nov. 11, 1953, with the following history. Five days prior to admission he was listless and complained of headache and aching

Cancer of the thyroid with metastases to the lungs; condition shown by scintigram in absence of definite x-ray findings.

There have been several reports on the use of radioactive iodine (I 131 ) in the treatment of lung metastases from cancer of the thyroid gland. In these reports collection of I 131 in the chest was detected in sites corresponding to the observable metastases in the x-ray films. Our purpose in presenting the case that follows is to show that the presence of metastases in the lungs may be demonstrated by the use of the scintigram in instances in which roentgenograms fail to show them. The following observations in a boy 11 years of age make this case an important one for future studies in the detection of chest metastases in children. Report of a Case The patient, an 11-year-old Negro boy, came to the ear, nose, and throat clinic on Aug. 27, 1953, with acute tonsillitis. He had been told one year previously that he had two masses in the right

Spontaneous rupture of the stomach in the newborn.

FOUR NEWBORN children were admitted to the surgical service at the Children's Hospital of Philadelphia in a four-year period with the unusual finding of a spontaneous perforation of the stomach. Our interest in the problem was aroused, and it is our purpose here to record briefly the case histories on each of these patients, bring the literature up to date as to the occurrence of this lesion, and discuss possible etiological mechanisms by which it can occur. REPORT OF CASES Case1.—This 5-day-old Negro boy was admitted to the Children's Hospital of Philadelphia with a history that he had had an uneventful birth on Dec. 9, 1949, and had seemed perfectly normal for the first two days of life. On the evening of Dec. 11, 1949, it was noted that the baby was listless, refused his bottle, and became cyanotic, necessitating the use of oxygen. Next morning the respirations were