Infantile Scurvy Research Articles

On the Identity of Imperfect Congenital Osteogenesis and Idiopathic Osteopsathyrosis, and on the Diagnosis of the Latter from Infantile Scurvy

On the Identity of Imperfect Congenital Osteogenesis and Idiopathic Osteopsathyrosis, and on the Diagnosis of the Latter from Infantile Scurvy

On the Identity of Imperfect Congenital Osteogenesis and Idiopathic Osteopsathyrosis, and on the Diagnosis of the Latter from Infantile Scurvy

On the Identity of Imperfect Congenital Osteogenesis and Idiopathic Osteopsathyrosis, and on the Diagnosis of the Latter from Infantile Scurvy

EXOPHTHALMOS IN INFANTILE SCURVY

While it is difficult to state with any certainty earliest description of scurvy, the reference of Hippocrates to a large number of men in army who suffered from pains in legs, and gangrene of gums, which was accompanied by loss of teeth, seems sufficiently definite to be identified as this (Hess 1 ). Its occurrence in infants was first recorded by Glisson in 1668, but not until 1862 was there any mention of exophthalmos as a complication, when Moeller 2 reported its presence in a case of acute rickets which, in view of subsequent knowledge, was undoubtedly one of scurvy. Magnus, 3 in 1878, was next to record exophthalmos in infantile scurvy; however, little was known of disease until 1883 when Barlow 4 published his classic paper giving anatomic proof that this disorder of infants showed pathologic changes characteristic of adult scurvy. This

THE CLINICAL AND ROENTGENOLOGIC MANIFESTATIONS OF SCURVY IN A SEVEN YEAR OLD CHILD

Poupart 1 wrote one of the first descriptions of adult scurvy in 1669. He described crepitus in the epiphyses of bones, and noted that there were separations of the epiphyses from the shafts. Petit described similar cases in 1773. In 1859, Moeller 1 described a disease in infants characterized by swelling of the extremities, pseudoparalysis and bleeding of the gums. He thought that this disease was an acute form of rickets. In 1883, Barlow 1 recognized the scorbutic origin of the disease described by Moeller, and proved his statements anatomically. However, there was still much confusion between rickets and scurvy, probably because the diseases occurred together so frequently. As time went on cases of Moeller-Barlow disease were observed in infants who did not have rickets, and the identity of this disease and adult scurvy was definitely recognized. The German literature still calls infantile scurvy the Moeller-Barlow disease. There have been

HEALING IN INFANTILE SCURVY AS SHOWN BY X-RAY

Any advance in the knowledge of a disease as widely known as scurvy can be achieved only by first studying the results of the painstaking accumulation of facts made by a host of observers. By pyramiding the roentgenologic investigations of others and using this as a base line for further study, the task of amplifying the information concerning the osseous lesions in this disease has been made easier for us. Although numerous contributions to the literature of infantile scurvy have appeared in recent years, and among them several which deal mainly with its roentgenologic manifestations, they have for the most part been concerned largely with some particular phase of the disease. Thus, Pelkan,1Wimberger,2Nechitch,3and Baetjer4have considered the problem of differential diagnosis in acute scurvy. Wimberger,5Frank,6and, more recently, Schwartz,7have stressed the late manifestations and retrospective diagnosis. In his

The Histological and Radiographic of Appearance of Infantile Scurvy (Barlow's Disease)

The Histological and Radiographic of Appearance of Infantile Scurvy (Barlow's Disease)

THE EPIPHYSEAL CHANGES IN THE DIAGNOSIS OF SCURVY

The finer diagnostic features of infantile scurvy have been frequently overlooked, probably due to the fact that students of the disease have been primarily engaged with its hemorrhagic manifestations. Pediatric as well as roentgenologic texts usually exhibit roentgenograms of the femur with the heavy transverse line at its distal end and the subperiosteal hemorrhage as the essential features of scurvy. Though these are indeed unmistakable evidences of the scorbutic state, roentgenologically visible subperiosteal hemorrhage is comparatively infrequent. The heavy transverse line, the so-called "white line" of Fraenkel, has therefore been the deciding element in the roentgenogram. Focusing all our attention on it, we have frequently overlooked conspicuous signs equally characteristic of scurvy. In studying a large series of roentgenograms taken of a group of infants, I was impressed with the great variability of the photographic material. In any given pathologic condition, this may be due as much to the rapidly

Avitaminosen und Verwandte Krankheitszustände

This addition to the Encyclopaedia of Clinical Medicine fulfills its title in that quite as much attention is given to related conditions as to the proven vitamin deficiencies themselves. Thus, a discussion of pellagra is included on the basis of its being due to deficiency in the quality of the proteins of the diet and sprue is considered impartially as being due to any one or several of many factors such as infection, either with monilia or bacteria, composition of the diet as regards fat and protein, and a deficiency in one or more vitamins. The first part of the book is given to the general nature of the vitamins themselves and the methods used in their study, followed by a section on the pathology of the experimental vitamin deficiencies. The major portion is devoted to the clinical complexes of scurvy, beriberi, rickets, sprue and pellagra. The subjects of infantile scurvy, tetany and “ship-beriberi” are considered separately.

The Influence of Malaria Chills on the Trypanocidal Action of the Serum.

During their experiments on the natural immunity of man against the trypanosomes, which are pathogenic to animals, Laveran and Mesnil discovered the trypanocidal action of the human serum. The serum does not destroy the trypanosomes in vitro, but it protects mice for from 1 to 2 weeks against an infection, which otherwise would cause death within a few days. It delays, therefore, only the development of the trypanosomes in the mouse. A complete protection is rare. The trypanocidal substances are scanty in or absent from the serum of the newborn (Rosenthal and Nossen, Platau, Leichtentritt, Neumark and Pogorschelsky). In healthy children they appear after the 11th to 15th week and persist throughout life, although individual differences as to their strength exist. According to Rosenthal and Kleeman the trypanocidal substances are increased in the later part of pregnancy. Under certain abnormal conditions they disappear more or less completely. Leichtentritt and Zielaskowsky found a marked decrease in Barlow's disease, Grunwald and Leichtentritt in xerophthalmia and infantile scurvy. Much, attention has been given to the fact that diffuse diseases of the liver cause a very distinct reduction of the trypanocidal power of the serum (Ehrlich and Wechsberg, Rosenthal and Krueger, Mignoli, Peutz, Platau, Munter). Since the accumulation of the bile pigment and the bile acids in the blood has nothing to do with this reduction, the liver is believed to be the source of the trypanotidal substances. Several authors tried to use the trypanocidal titer of the serum as a liver fuaction test.

The Treatment of Infantile Scurvy

The Treatment of Infantile Scurvy

A Report of Laboratory Findings in Infantile Scurvy, or Barlow’s Disease

A Report of Laboratory Findings in Infantile Scurvy, or Barlow’s Disease

Ocular Changes in Infantile Scurvy

The general occurrence and characteristics of infantile scurvy are here discussed. A case is reported illustrating the difficulty of its diagnosis and also the very rapid improvement with proper diet.

A Résumé of the Literature of Infantile Scurvy during the Past Two Years

A Résumé of the Literature of Infantile Scurvy during the Past Two Years

INFANTILE SCURVY ASSOCIATED WITH HEREDITARY SYPHILIS

Owing to the prevalence of infantile scurvy and hereditary syphilis, it would seem that the association of these two diseases should not be rare. In view of the scant reference to this possibility in the available literature, it occurred to me that the report of such a case might prove of interest, especially one occurring in a breast fed infant and accompanied by multiple fractures of the long bones of the lower extremities. REPORT OF CASE Case. —Penelope K., a Greek girl, aged 3 months, was admitted to the Pediatric Clinic of the University Hospital, July 1, 1918. Chief complaint, pain on moving the legs. Family History. —Mother has had three miscarriages, one at the third and two at the seventh month, respectively. Birth History. —Papular plantopalmar eruption persisting three weeks and then fading. Feeding History. —Breast fed throughout, with satisfactory gain in weight and unattended by digestive disturbances. Past

Changes in the teeth of the guinea-pig, produced by a scorbutic diet

The pathological anatomy of adult and infantile scurvy has received the attention of many investigators at various times, and is now known in great detail. Not only have the macroscopic but also the microscopic changes been fully studied. Definite characteristic abnormalities in the tissues of the bones, and at the costochondral junctions and the epiphyseal lines in scorbutic subjects, are well recognised. Although the gums are known to be greatly affected in advanced cases of scurvy and the teeth become loose, there has apparently been no chemical or histological work done hitherto on the teeth, since no references to such work can be found in the literature. This is most probably due to the fact that most of the histological work has been carried out in infantile scurvy. During the last few years, research in scurvy has been greatly stimulated by the discovery of the possibility of inducing experimental scurvy in animals. Holst and Frölich (1912) have shown that a pathological condition analogous to scurvy in the human subject can be induced in guinea-pigs by dietetic means. That the condition of the animals thus produced was really scorbutic was further confirmed by the observations of these investigators that it could be prevented by the addition of antiscorbutics to the deficient diet. These observations have since been fully corroborated by many workers. Hart and Lessing (1913) have further demonstrated that monkeys when fed on a diet deficient in antiscorbutic develop scurvy. This has been confirmed by Talbot, Dodd and Peterson (1913), and by Harden and Zilva (1919). The latter investigators have also shown that a monkey suffering from scurvy could be cured by administering an antiscorbutic.

Chemistry of the blood in scurvy

The urea content, CO2 combining power, percentage of sugar, diastatic activity and calcium content of the blood were ascertained in a number of cases of infantile scurvy. Two abnormal variations were found: (a) a moderate acidosis, figures under 40 or 45 obtained according to the Van Slyke method; (b) a deficiency of calcium. Neither appeared to be a basic factor or to run a course parallel to the scorbutic process.The accompanying chart shows the results of calcium tests carried out according to the Halverson and Bergeim deproteinization method with 5 c.c. or more of plasma. The normal content is about 10 mg., so that it will be seen that there was a striking calcium deficiency. None of the cases had convulsions; nor can the results be accounted for by the presence of tetany.

Focal Degeneration of the Lumbar Cord in a Case of Infantile Scurvy

Focal Degeneration of the Lumbar Cord in a Case of Infantile Scurvy

INFANTILE SCURVY

For some years we have been studying various aspects of the symptomatology and dietetics of infantile scurvy. In a recent paper¹it was shown that pasteurized milk brings about this disorder in some cases unless an antiscorbutic food is included in the dietary. The type of scurvy induced under these conditions, as noted elsewhere, is not the textbook variety of this disease, but what has been termed latent or subacute scurvy, characterized by anemia and pallor, failure to gain in weight, rapidity of pulse and respiration, tenderness of the bones, and by a sharp recession of all these signs and symptoms when orange juice or other antiscorbutic foodstuff is given. In asserting that scurvy is brought about by pasteurized milk it should be emphasized that this is not synonymous with saying that this disorder is caused by heating the milk to the temperature of pasteurization. It is for this

SUBACUTE AND LATENT INFANTILE SCURVY

In previous papers on this subject 1 it has been established, I believe, that infantile scurvy may be brought about by a diet of pasteurized milk. An investigation of this question seemed not only indicated but also urgent in view of the increasingly widespread use of pasteurized milk, and of the fact that the National Commission on Milk Standards, a committee of the highest authority, has expressed the opinion that the heating of milk, as carried out in the course of pasteurization, does not destroy its enzymes or other chemical constituents. 2 As stated, my experience did not coincide with this opinion. On the contrary, I found that when the use of orange juice was discontinued in the dietary of a group of infants who were being fed on milk which had been subjected to a temperature of 140 F. for thirty minutes, some of them in the course of

INFANTILE SCURVY

Although we possess in orange juice a specific for infantile scurvy, it is well worth while to look about for other therapeutic agents which are potent in this disturbance. This is desirable from several points of view. In the first place, orange juice cannot be considered an ideal antiscorbutic food, as it is expensive and under certain circumstances difficult to procure, but more especially because it cannot well be embodied in the food. As a result of its having to be prepared and given separately, it is frequently forgotten by the physician or by the nurse, with the result that we encounter cases of latent or subacute scurvy which have come about through this oversight. Furthermore, as long as the true nature of the antiscorbutic vitamin is unknown, we shall gain valuable knowledge of the essential chemical substance which forms the basis of this disorder by ascertaining substances that do