Hepatic enzymes in Hodgkin's and non Hodgkin's lymphoma.

Serum alkaline phosphatase levels in patients with Hodgkin's and non-Hodgkin's lymphoma were studied. The findings were correlated with clinical stage, particularly hepatic involvement, and histologic findings. Serum levels of other hepatic enzymes (SGOT, 5,N and gamma GT) were also measured. The usefulness of these studies for clinical staging was described, as well as speculation on the observed differences in Hodgkin's and non-Hodgkin's patients.

Incidence and sites of bone lesions detected by 99mTc-polyphosphate scans in patients with tumors.

The value of bone scanning with 99mTc-polyphosphate was assessed in 186 patients with various types of tumors. The sensitivity of this technique was greater than that of metastatic roentgenographic series and the reported results of 85-Sr-bone scans, in the detection of osseous involvement by tumors. Three cases with normal bone scans and abnormal roentgenographic studies illustrated the necessity and complementary value of comparing bone scan findings with radiographic studies. Patients with carcinoma of the breast, lung, or prostate displayed characteristic patterns of bone involvement by their tumors. The importance of clinical information, including bone symptoms, antecedent bone disease, and serum calcium and alkaline phosphatase, was stressed in the detection and interpretation of bone scan abnormalities.

Prostaglandins in mice with neuroblastoma.

Male albino mice, with and without transplanted neuroblastoma C1300, had tissues analyzed for prostaglandins by radioimmunoassay. Highest prostaglandin concentrations occurred in tumor tissue, lungs, spleen, and kidneys. Tritiated prostaglandins A1 or E1 and tritiated arachidonic acid were injected intravenously. The concentration (organ/tumor) was higher at 1 hr than at 6 or 24 hr. Prostaglandin E1 and arachidonic acid localized principally in the kidney (likely the excretory organ) whereas prostaglandin A1 showed highest concentration in the liver.

A renal lesion in asphyxiating thoracic dysplasia.

A boy with asphyxiating thoracic dysplasia was studied from age seven months until his death with congestive heart failure at age thirteen months. Aminoaciduria, phosphaturia, increased urate excretion, hyposthenuria, proteinuria, and metabolic acidosis were demonstrated at one year of age. Cardiopulmonary dysfunction and skeletal abnormalities were also studied during life. Cessation of linear growth, overgrowth of membranous bone with retardation of enchondral bone formation, and cartilaginous overgrowth of the chest were prominent findings. At autopsy, an unexpected hepatic fibrosis was discovered, along with renal and skeletal disorganization.