PubMed · 7078080
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
L C Anderson, V B Fiedler, B J Cohen, M R Anver, J L Simmons, B R Lucchesi. 1982. Diagnostic exercise.. https://pubmed.ncbi.nlm.nih.gov/7078080/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Neuroblastomas are malignant tumors derived embryonically from the neural crest. Biological diagnosis relies on assay of urinary excretion of homovanillic acid (HVA), vanillylmandelic acid (VMA), and dopamine (DA). Spontaneous regression of these neoplasms has been reported by numerous investigators. The authors report the case of a child with neuroblastoma that illustrates the relationship between catecholamine metabolites and tumor maturation. At 1 month of age, this infant presented an adrenal neuroblastoma with multiple metastases (stage IV); the initial histological diagnosis based on examination of cutaneous metastases was neuroblastoma. At the age of 6 months, after chemotherapy, the primary tumor was resected; hepatic metastases were discovered at laparotomy. The histological diagnosis for all lesions was highly differentiated, mature ganglioneuroma-like tissue. The main biochemical abnormality at the time of diagnosis was an elevation in normetanephrine (NMN). HVA was only slightly increased but rose progressively during chemotherapy; it dropped back to normal levels after the sixth course. This case illustrates the potential benefits of separate assays of urinary methylated catecholamine metabolites for biochemical diagnosis and therapeutic management of neuroblastoma in addition to assays of HVA, VMA, and DA. Case findings suggest existence of a transformation process with maturation of the tumor involving enzymatic regulation and expression of MAO.
PURPOSE: To discern whether the 3,4-dihydroxyphenylglycol produced in adrenal medulla is associated with altered urinary excretion, we compared the tissue and urinary levels of this catecholamine metabolite, epinephrine and norepinephrine in 23 patients with pheochromocytoma and 26 subjects with renal cell carcinoma. MATERIALS AND METHODS: Tissue and urine concentrations of dihydroxyphenylglycol, epinephrine and norepinephrine were determined by catechol-O-methyl-transferase-based radioenzymatic method and high performance liquid chromatography with electrochemical detection. RESULTS: Contents of dihydroxyphenylglycol, epinephrine and norepinephrine in pheochromocytomas were higher than those in normal adrenal medullae. Removal of pheochromocytomas lowered urinary excretion of these catecholamines and dihydroxyphenylglycol. Norepinephrine content correlated closely with dihydroxyphenylglycol content in normal adrenal medullae and pheochromocytomas but not with epinephrine content in either tissue. Contents of norepinephrine and dihydroxyphenylglycol correlated significantly with urinary norepinephrine excretion and dihydroxyphenylglycol excretion in patients with pheochromocytoma but not in subjects with renal cell carcinoma. The norepinephrine-to-dihydroxyphenylglycol ratio in a 24-hour preoperative urine collection from patients with pheochromocytoma was higher than that from subjects with renal cell carcinoma, which was almost similar to that of epinephrine dominant pheochromocytomas. CONCLUSIONS: Our study suggests that dihydroxyphenylglycol in urine in subjects with renal cell carcinoma is predominantly of a neuronal origin and urinary dihydroxyphenylglycol in patients with pheochromocytoma is of tumor origin. A high level of norepinephrine-to-dihydroxyphenylglycol ratio in urine can be used to determine the diagnosis of the norepinephrine dominant type pheochromocytoma. Measurement of at least a few markers is preferable for precise biochemical diagnosis of pheochromocytoma.
The results of our study show that parasympathetic tone was higher in patients with pheochromocytoma than in patients with primary hypertension. An unusual spectral form of vagal activity was seen during excessive beta-adrenergic stimulation, while persistent hypertension with an excessive alpha-adrenergic stimulation was responsible for low cardiac sympathetic tone, probably due to desensitization of beta-adrenergic receptors.