Wolf W. Zuelzer

MYELOKATHEXIS--A NEW FORM OF CHRONIC GRANULOCYTOPENIA. REPORT OF A CASE.

THE quantitative analysis of granulopoiesis requires knowledge not only of the complex relations between cytologic compartments within the bone marrow but also of the distribution and fate of cells...

Renal Vascular Disease

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Persistent jaundice in infancy

I have collected the opinions of a number of pediatricians and pediatric pathologists regarding the causes of persistent jaundice during infancy. Most would discard the term “inspissated bile syndrome”, but there is less unanimity regarding the meaning of “neonatal hepatitis”, the significance of giant cells in the liver, and the value of needle biopsies. The many causes of infantile jaundice are mentioned, and hepatic physiology during the neonatal period is discussed. Finally, a program is outlined for the study of the infant with persistent jaundice. The value of the determination of the excretion of radioactive rose bengal in differentiating complete biliary atresia from other causes of jaundice is emphasized.

The Emily Cooley Lecture. Etiology and Pathogenesis of Acquired Hemolytic Anemia

The demonstration of recurrent lymphadenitis attributable to CMV during periods of hemolysis in a patient with chronic acquired hemolytic anemia of autoimmune type, led to the investigation of the possible etiologic relationship between this virus and acquired hemolytic anemia. In children a frequent association was demonstrated. Previously unrecognized clinical manifestations attributable to CMV were frequently observed. In this age group lymphadenopathy was a prominent finding in the majority of the cases and appeared to correspond to periods of rapid virus multiplication. It was noted that the predominant cellular lesion was not the well known pathognomonic large inclusion‐bearing cell which is a comparatively rare end state in the cellular response to the virus but less fully developed cellular lesions representing early and intermediate states. Recognition of these lesions permitted a rough appraisal of the extent of viral activity and showed that the latter generally correlated well with the hemolytic process.

Idiopathic thrombopenic purpura in childhood.

THE syndrome of idiopathic or primary thrombopenic purpura has been discussed by a number of authors,1 2 3 4 but these studies usually have included all age groups or have used large subdivisions of age ranges. The condition as it is seen in childhood has not been dealt with specifically or in detail for some time. McLean5 in 1932 reported a short follow-up study of 21 cases, and Diamond6 briefly summarized the results of therapy in 28 cases in 1938. Since then, except for studies on congenital purpura,7 no comprehensive publications have appeared on thrombopenic purpura in childhood. This paper reports on 47 .xa0.xa0.

Adrenocortical insufficiency in infants with the adrenogenital syndrome; a clinical and pathologic study of four cases.

Summary This paper deals with clinical, chemical, and pathologic observations on fourinfants who presented the picture of adrenal cortical insufficiency in association with bilateral adrenal hypoplasia as shown at autopsy. The condition was found in 0.52 per cent of autopsies done on infants under1 year of age, indicating a higher incidence than is suggested by the literature. The familial pattern which was apparent in two of our patients remains unexplained and requires endocrinologic studies of the mothers of such infants. In our own group and in all eases thus far reported the patients were either female pseudohermaphrodites with a characteristic deformity of the genitalia or else true males. In the latter, external manifestations of virilism are not apparent in early infancy. The presenting clinical features were gastrointestinal symptoms, especiallydiarrhea, vomiting, and dehydration. Serial chemical studies performed in two cases showed a lowering of the“total base,” bicarbonate and chloride values in the plasma. The blood sugar levels were found normal in three patients. Anatomic and histologic examination of the adrenals showed diffuse hyperplasia of the cortex with apparent replacement of the zona glomerulosa by eosinophilic cells which often contained fuchsinophil granules. A correlation of these findings with the clinical manifestations is suggested. The physiologic disturbance appears to be one of overproduction with respect to N hormone and underproduction of substances regulating salt and water metabolism. The apparently intact carbohydrate metabolism differentiates these patients from those with true Addisons disease as regards the manifestations of adrenal insufficiency. Further studies of the carbohydrate metabolism in such patients are needed. It is suggested that the administration of DOCA and salt may be a complete substitution therapy in patients exhibiting this syndrome.

Hemophilia A in chromosomal female subjects

Two unrelated female subjects with a hemorrhagic diathesis associated with pure AHGdeficiency are presented. The father of one girl has classical hemophilia; the mother of the other is a “carrier”. Pedigree analyses indicate no reason for believing that either of these girls has a genetic constitution other than heterozygous for the hemophilia gene von Willebrands disease was excluded by appropriate laboratory studies. Possible genetic mechanisms which might have resulted in severe AHG deficiency in these patients are discussed.

Parapertussis pneumonia: Report of two fatal cases

Summary 1. Two cases of fatal pertussis-like infections in infants are reported with autopsy studies. 2. The etiologic agent was demonstrated to be B. parapertussis , instead of H. pertussis , upon bacteriologic, rather than pathologic, evidence. 3. The diagnosis of pertussis at autopsy should not be made without bacteriologicconfirmation. 4. Parapertussis may be a more serious disease than formerly thought.

Hemolytic anemias; mechanisms and diagnostic aspects.

Summary To sum up, hemolytic anemias are either due to inherited intracorpuscular defects or to extrinsic factors acting on the red corpuscles. Table I gives a graphic summary of the basic features of the main hemolytic syndromes. The common intrinsic defects are characterized by more or less diagnostic shape anomalies. Chemical identification of abnormal hemoglobins or stroma components should soon become a practical diagnostic tool. In doubtful cases erythrocyte survival studies may decide the issue. Among the extracorpuscular hemolytic anemias those due to immune mechanisms can nearly always be separated from all others by the Coombs test. In the majority of the remainder either a direct hemolytic agent, infectious, chemical, or physical, can be elicited, or a primary disease, neoplastic or metabolic, should be looked for. The correct therapy usually flows from the diagnosis.

Rh hemolytic disease in ABO-incompatible offspring: Observations on the protective effect of heterospecific pregnancy

Abstract Heterospecific pregnancy is generally believed to protect the mother against Rh sensitization and not to protect the child against Rh hemolytic disease. This study shows that: (1) Rh hemolytic disease was less severe in 126 infants ABO incompatible with their mothers than in 366 compatible infants. The 126 included 53 with combined Rh and ABO hemolytic disease and 73 with only Rh hemolytic disease. Since the height of the maternal Rh titer was not solely responsible for the mildness, it is suggested that possibly Rh antibody is retained in the placenta and related to the binding of anti-A or -B. (2) The sensitization caused by heterospecific pregnancy in 22 per cent of the mothers analyzed showed low titer Rh antibody, which indicates only partial protection by heterospecific pregnancy.