Search PubMed⌕ Search

Biomedical subjects

B H Landing

Publications and source records attributed to B H Landing.

At least 91 records · Page 5Linked to original sources
PubMed1981

Lymphomatoid granulomatosis-like lesions in a child with leukemia in remission.

This case report describes an eight year old leukemic child who was in remission for four and one-half years and showed hypogammaglobulinemia and deficient leukocyte chemotaxis and migration. She developed pulmonary lesions with laryngeal and tracheobronchial disease and died from pulmonary hemorrhage. The lesions found at autopsy were lymphomatoid granulomatosis-like, but were atypical in their anatomic distribution, behavior, and histologic features.

Child, Preschool↗
PubMed1980

Medulloblastoma presenting as neck tumors in 2 infants.

Extension of neuroepithelial neoplasms outside the neuraxis, though uncommon, is well known and usually follows surgical intervention. More unusual is the brain tumor that appears beyond the bounds of the central nervous system prior to operative manipulation. Two infants presented with soft tissue masses in the neck that proved to be medulloblastomas. Autopsy examination in both infants showed primary medulloblastoma of the cerebellar vermis with extensive spread through the subarachnoid spaces. The neck masses may have been direct extensions from the central nervous system tumors, though this was not proved in either case.

Cerebellar Neoplasms↗
PubMed1980

Hepatitis B infection in pediatric dialysis and transplant patients: significance of e antigen.

We examined the clinical significance of hepatitis Be antigenemia in 36 HBsAg positive pediatric dialysis and renal transplant patients. One hundred twenty-seven sera were tested for HBeAg and anti-HBe. Seventy-three sera (57%) from 29 patients (81%) contained HBeAg. The presence of HBeAg was associated with an increased titer of HBsAg (P < 0.005) and with the presence of the HBsAg carrier state (P < 0.001). HBeAg was found in 40% of specimens taken from dialysis patients, and in 70% of specimens from transplant patients (P < 0.001). No serum contained anti-HBe, although 28 of 29 sera (97%) tested had antibody to HBcAg. No association was found between the presence of HBeAg and serum aminoleucine transferase levels or the histologic evidence of chronic active hepatitis. Fifteen HBeAg negative sera from patients persistently positive for HBsAg were tested for HBV-specific DNA polymerase activity; 7 (47%) had significant activity. Since both HBeAg and DNA p are indicators of infectivity, many HBeAg negative sera from immunosuppressed HBsAg carriers may be infectious.

Adolescent↗
PubMed1980

Nesidioblastosis and other islet cell abnormalities in hyperinsulinemic hypoglycemia of childhood.

The histologic findings are described in 16 subtotal pancreatectomies performed in patients with hyperinsulinemic hypoglycemia over a 17 year period. All patients had nesidioblastosis, defined as the presence of small packets of two to 25 islet cells scattered throughout acinar tissue and separate from islets of Langerhans. The proliferating islet cells were a mixture of beta, alpha, and delta cells. Two histologic subgroups were apparent: Group I patients had diffuse hyperplasia of the islets of Langerhans as well as nesidioblastosis, and group II patients had more subtle nesidioblastosis alone. The patients in groups I and II were remarkably age segregated. All but one of the group I patients were eight months old or younger. Group II patients ranged in age from three to 15 years. The incidence of nesidioblastosis in the patients undergoing pancreatectomy was higher than the incidence in a group of age matched autopsy controls.

Adolescent↗
PubMed1980

Morphometric analysis of liver lesions in cystic diseases of childhood.

Morphometric analysis of the liver lesions in patients with various forms of cystic disease of the liver in childhood demonstrates that the entities called the congenital, perinatal, and infantile forms of polycystic disease produce the same liver lesion. The data suggest that these entities are actually the same disorder, for which the name infantile polycystic disease (of the liver and kidneys) is recommended. In all patients with this autosomal recessive disorder there is involvement of both the liver and the kidneys, and patients present with hepatonephromegaly at birth or in early infancy. Similarly, the entity called the juvenile form of polycystic disease produces the same liver lesion as does the disease to which the term congenital hepatic fibrosis has been applied to describe patients presenting in later childhood with portal hypertension. The latter name is recommended to distinguish this condition from infantile polycystic disease. Nephromegaly is not a feature of this also autosomal recessive disease, but renal insufficiency, progressing slowly through later childhood and adolescence, is. The hepatic lesions of infantile polycystic disease and congenital hepatic fibrosis differ from those of other disorders causing cystic lesions of the liver and kidneys, either regularly (Meckel's syndrome, Jeune's syndrome) or variably (vaginal atresia syndrome, tuberous sclerosis, medullary cystic disease).

Adolescent↗
PubMed1979

Histochemical methods for dissociated muscle fibers.

Skeletal or cardiac muscle fibers can be separated by brief (3--5 second) dissociation of formalin-fixed pieces with a Willems Polytron (Brinkmann Instrument Co.). Such separated fibers are useful for demonstration of abnormal accumulations of lipids, carbohydrates, proteins and minerals in metabolic diseases. Staining techniques for demonstration of various stored materials include: 1) toluidine blue at pH 2.8 for acid mucopolysaccharide in skeletal muscle fibers in Pompe's glycogenesis 2, 2) one-step trichrome stain for nemaline myopathy and for abnormal mitochondria in X-linked infantile cardiomyopathy, 3) periodic acid-methenamine silver stain for glycolipid-containing lysosomes in I-cell disease (mucolipidosis 2), 4) Sudan black B stain for lipid in skeletal muscle fibers in Reye's syndrome, infantile lactic acidosis, Leigh's infantile subacute necrotizing encephalopathy and Jansky-Bielschowsky late infantile ceroid lipofuscinosis, 5) iron stain for iron in cardiac and skeletal muscle fibers in thalassemia with advanced hemosiderosis, and 6) autofluorescence for "ceroid" in skeletal muscle fibers in Jansky-Bielschowsky disease.

Carbohydrates↗
PubMed1978

Scintigraphic abnormalities in glycogen storage disease.

Fifteen patients with glycogen-storage disease type 1 (von Gierke's disease) were evaluated by serial scintigraphy, with a clearly recognizable pattern of an enlarged liver with diminished radionuclide accumulation, splenomegaly with considerably increased uptake and renomegaly. In seven of these patients with GSD-1 scintigraphy demonstrated focal defects of varying size. Small or stable defects suggest benign hepatic adenomata, whereas malignant change occurred in growing large lesions. The potential malignant end-point of hepatic-cell carcinoma in GSD-1 warrants careful serial liver scintigraphy with scintiangiography on a routine basis.

Adenoma↗
PubMed1977

Pathologic and immune factors in thyroid disease.

Thyroid glands from 33 children with hyperthyroidism and nine with juvenile lymphocytic thyroiditis were examined histologically and for IgG, IgA, IgM, and C3 by immunofluorescent staining. There was no significant difference between glands with JLT and those with hyperthyroidism in the degree of lymphoid infiltration or lymphoid follicle formation. In thyroiditis there was no correlation between the degree of histologic abnormalities and the presence of immunofluorescent staining for IgG, IgM, or IgA. In hyperthyroidism there was a correlation between the degree of histologic abnormalities and the presence of IgG. In both groups of patients LI and LFF were distinctly more severe in glands positive for C3. Postsurgical hypothyroidism correlated with LI but not with LFF, IgG, or C3.

Adolescent↗
PubMed1977

HBs antigenemia in renal allograft recipients.

Serial HBs Ag determinations were performed on 98 renal allograft recipients with functioning grafts for 6 to 108 months, 85 of whom were followed from the initiation of dialysis. Twenty-six (27%) recipients had HBs antigenemia following transplantation. Thirteen (50%) of the 26 recipients were HBs Ag positive during the period of dialysis and 13 developed HBs antigenemia 1 to 44 months following transplantation. Seventeen (65%) of the 26 HBs Ag positive patients had hepatic dysfunction which was detected by biochemical surveillance and not associated with clinical symptomatology. There was no evidence of progressive hepatic insufficiency. HBs Ag persisted in 24 (92%) recipients for 6 to 49 months. Clearing of antigenemia occurred in only two patients, both of whom ultimately rejected their grafts. The presence of HBs Ag had no adverse effect on graft function. Temporary reduction in azathioprine dosage with hepatic dysfunction was not associated with rejection episodes. The major hazard posed by the HBs Ag positive recipient is the potential reservoir for spread to the general population because of the persistence of antigenemia.

Alanine Transaminase↗