The aim of this study was to investigate the effect of a cyclooxygenase (COX)-2 inhibitor on the recovery of muscle function, inflammation, regeneration after, and adaptation to, unaccustomed eccentric exercise. Thirty-three young males and females participated in a double-blind, placebo-controlled experiment. Seventy unilateral, voluntary, maximal eccentric actions with the elbow flexors were performed twice (bouts 1 and 2) with the same arm, separated by 3 weeks. The test group participants were administered 400 mg/day of celecoxib for 9 days after bout 1. After both bouts 1 and 2, concentric and isometric force-generating capacity was immediately reduced (approximately 40-50%), followed by the later appearance of muscle soreness and increased serum creatine kinase levels. Radiolabelled autologous leukocytes (detected by scintigraphy) and monocytes/macrophages (histology) accumulated in the exercised muscles, simultaneously with increased satellite cell activity. These responses were reduced and recovery was faster after bout 2 than 1, demonstrating a repeated-bout effect. No differences between the celecoxib and placebo groups were detected, except for muscle soreness, which was attenuated by celecoxib. In summary, celecoxib, a COX-2 inhibitor, did not detectably affect recovery of muscle function or markers of inflammation and regeneration after unaccustomed eccentric exercise, nor did the drug influence the repeated-bout effect. However, it alleviated muscle soreness.

Pituitary adenomas result in clinical sequelae and accelerated mortality due to central mass effects or pituitary hormone hypersecretion and/or insufficiency. The low annual incidence and prolonged natural history of these rare tumors has hindered efforts to evaluate long-term clinical outcomes. Care of these patients is often provided by larger tertiary specialist referral centers. A novel evidence-based computerized pituitary tumor registry was developed to systematically evaluate epidemiological, biochemical, and clinical outcome data. Retrospective registration of 371 patients [99 clinically nonfunctioning tumors (CNFTs), 176 acromegalics, and 96 prolactinomas] with radiological, biochemical, and clinical evidence of pituitary tumors was performed. Analysis of this primarily specialist-referred population revealed a female predominance among CNFT (60%) and prolactinoma (69%) patients. Males had a significantly greater frequency of macroadenomas than females for CNFTs (92% vs. (68%) and for prolactinomas (74% vs. 40%). Males with prolactinomas also had higher mean pretreatment serum PRL levels (1206 vs. 219 ng/mL). Concurrent hyperprolactinemia was present in CNFT (47%) and acromegaly (33%) patients. Radiographic cure, defined as absence of visualized tumor, was achieved in 21% of CNFTs, 34% of acromegalies, and 21% of prolactinomas. Biochemical remission, defined by normalization of hormonal tumor markers, was observed in 35% of acromegaly and 39% of prolactinoma patients in the registry, thus reflecting the tertiary referral patterns. Nine premature deaths (patients aged < or =65 yr) occurred in the acromegaly subpopulation, whereas no premature deaths were encountered in nonacromegalic patients. In conclusion, this unique and comprehensive pituitary tumor registry enables identification of diagnostic and prognostic markers and evaluation of long-term clinical outcomes. Prospectively, this registry will improve therapeutic guidelines and cost-effective pituitary tumor management.

Ectopic GHRH-secreting tumors, such as carcinoid, rarely cause acromegaly. As protracted exposure to high levels of GH is associated with considerable morbidity and mortality, these patients require early and effective medical therapy to control hormonal hypersecretion. We employed a prolonged release somatostatin analog, lanreotide, to treat a patient with disseminated GHRH-producing carcinoid. Before treatment, the patient had a biochemical profile characteristic of active acromegaly. Plasma GHRH levels were markedly elevated (200-fold), and urinary 5-hydroxyindolacetic acid (5-HIAA) levels were increased (4-fold). Magnetic resonance imaging revealed a large asymmetrical pituitary mass consistent with somatotroph hyperplasia. Somatostatin receptor scintigraphy revealed multiple bony and soft tissue lesions as well as striking pituitary uptake. Lanreotide (30 mg) was administered weekly by im injection for 12 weeks. Rapid and sustained symptomatic clinical improvement with diminished soft tissue swelling and hyperhidrosis was observed. GHRH levels decreased by 70%; glucose-suppressed GH and insulin-like growth factor I levels were reduced by 90% and 75%, respectively, to near normal values; urinary 5-HIAA levels normalized; and the pituitary mass remained unchanged. Unfortunately, the patient died due to complications of osteogenic sarcoma. In conclusion, prolonged release lanreotide induced clinical and biochemical remission in this patient with diffusely metastatic GHRH-producing carcinoid. This long-acting drug thus offers an effective, well tolerated, and convenient medical therapy for control of hormonal hypersecretion induced by excess GHRH.

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