Transurethral microwave thermotherapy of nonbacterial prostatitis and prostatodynia: initial experience.

OBJECTIVES: To report our early experience using transurethral microwave thermotherapy (TUMT) to treat patients with nonbacterial prostatitis (NBP) and prostatodynia. METHODS: Nineteen patients with NBP (symptoms, negative cultures, no response to antibiotics, leukocytosis in expressed prostatitic fluid) and 5 patients with prostatodynia (symptoms, negative cultures, no response to antibiotics, no leukocytosis in expressed prostatitic fluid) were treated with TUMT at interstitial temperatures of 45 degrees to 60 degrees C for 1 hour. Response was assessed by a consistent symptom severity index and global assessment of symptoms. RESULTS: A marked and significant early (3 months) favorable response was noted in nearly one half of the NBP group but little benefit was found in the prostatodynia group. The treatment was associated with few adverse experiences. CONCLUSIONS: TUMT appears to be a potentially effective therapy for NBP, but its real efficacy as well as the durability of the response needs to be confirmed with a randomized double-blind sham-controlled trial.

An immunohistochemical, ultrastructural, and physiologic study of pancreatic islets from copper-deficient, penicillamine-treated rats.

Murine copper deficiency induced by diet and supplemented with a copper chelator is known to produce a progressive atrophy of pancreatic acinar tissue largely replaced by noninflammatory lipomatosis, while the ductal and endocrine systems appear to remain unaffected. The islets were studied morphologically and physiologically in animals rendered copper deficient by diet and supplemented with D-penicillamine. Using immunohistochemistry, the distribution of islet cell types from copper-deficient animals exhibited a normal cellular complement for A-, B-, D-, and PP-cells. Ultrastructural analysis showed the islet tissue remains normal in appearance during the course of the metal-deficient state. Physiologic data based on the response of islets to a low- and high-glucose load in perfused, isolated pancreata as well as intravenous glucose tolerance tests indicated that insulin-secreting B-cells were functionally normal. Because of the accessibility of islets enhanced by atrophy of acini, this model may be adopted for the isolation of viable islets and for in situ physiologic studies of islet hormone secretion.

Peptidergic regulation in neuroendocrine and autonomic systems.

Neuropeptides are found in dense networks of neuronal perikarya, fibers and terminals within numerous brain regions. Among the more striking of these collections are sites within the central nervous system that are presumed to regulate either endocrine or autonomic function. A recent example of a neuropeptide which is likely to play a significant role in endocrine regulation is cortocotropin releasing factor (CRF). Immunohistochemical studies revealed that CRF immunoreactivity was found in many brain regions, including the paraventriculo-infundibular pathway. CRF released from nerve terminals belonging to this pathway presumably regulates ACTH release. Treatment of rats with reserpine depletes CRF as well as vasopressin from the external layer of the median eminence, suggesting tonic, monoaminergic inhibition of CRF and vasopressin containing neurons. CRF antisera were found which stain urotensin I immunoreactivity within the caudal neurosecretory system of fish. Numerous putative neurotransmitters impinge upon preganglionic sympathetic neurons within the intermediolateral cell column of the spinal cord. Preganglionic sympathetic neurons which innervate the adrenal medulla appear to have a specific input from somatostatin immunoreactive fibers. In addition, binding sites for serotonin and alpha-2 adrenergic ligands are more highly concentrated over sympathoadrenal neurons. Finally, the pancreatic islet contains peptide producing endocrine cells which possess several neuron-like properties. Some of these properties are reviewed, especially the finding that the insulin producing cells contain glutamate decarboxylase immunoreactivity, the biosynthetic enzyme for GABA. Further studies revealed that GABA agonists inhibit somatostatin release from islet cells.