Textbook Oncologic Outcome Summarizes the Perioperative Cancer Journey,but Should it be used to Judge Hospitals?

Annals of Surgical Oncology -     

Subcutaneous growth hormone-releasing hormone therapy in growth hormone-deficient children: first year of therapy.

The purpose of this study was to determine the efficacy and safety of GH-releasing Hormone [GHRH-(1-44)] therapy in GH-deficient children. Twenty previously untreated prepubertal children with GHRH deficiency were treated for 1 yr in a multicenter, open label, company-sponsored study with at least 20 micrograms/kg GHRH-(1-44), sc, half at bedtime and half upon awakening. The main effects were enhancement of linear growth, advancement in bone age, and alteration in general blood chemistries and hormonal values. The mean velocity of the entire group increased from 3.6 +/- 1.1 to 8.1 +/- 1.5 cm/yr (P < 10(-4)) at 1 yr of therapy. After 6 months of therapy, 16 were growing at a mean of 9.4 +/- 2.0 cm/yr and were continued on this dose. In 4 patients who were growing at a rate of 5.5 +/- 1.7 cm/yr, the dose was increased to 40 micrograms/kg daily for the second 6 months. The high dose group increased their mean linear growth velocity for the second 6 months while on the higher dose to 7.6 +/- 0.4 cm/yr (P < 10(-2)). This was equal to the mean velocity for the second 6 months of therapy of the 16 subjects who remained on the 20 micrograms/kg daily therapy (7.6 +/- 1.2 cm/yr). Mean advancement of bone age was 1.3 +/- 0.6 yr during the first year of therapy. No adverse changes in general biochemical, hormonal, or pituitary radiographic analyses were noted. No change in fasting glucose or insulin concentrations, or excessive generation of insulin-like growth factor-I concentrations occurred. We conclude that GHRH in a daily dose of 20-40 micrograms/kg for 1 yr was effective in increasing growth velocity in most GHRH-responsive GH-deficient patients. It was well tolerated without side-effects. Glucose intolerance was not noted.     

New perspectives in cardio-oncology

Journal of Thrombosis and Thrombolysis -     

Mitral valve prolapse

Mitral valve prolapse is a common valvular abnormality that is the most common cause of severe non-ischaemic mitral regurgitation in the USA. The overall prognosis of patients with mitral valve prolapse is excellent, but a small subset will develop serious complications, including infective endocarditis, sudden cardiac death, and severe mitral regurgitation. We present a comprehensive review of mitral valve prolapse, examining normal mitral anatomy, the clinical and echocardiographic features of mitral valve prolapse, and the pathophysiology and genetics of the disorder. We discuss the contemporary management of both asymptomatic and symptomatic prolapse, with particular attention to the timing and technique of surgical repair. We conclude that echocardiography is the method of choice for diagnosing mitral valve prolapse, that clinical and echocardiographic features can predict which patients with prolapse are at highest risk for complications, and that mitral valve repair is the treatment of choice for symptomatic prolapse.     

Functional chest pain of esophageal origin: hyperalgesia or motor dysfunction

OBJECTIVE: Many patients with functional (noncardiac) chest pain exhibit both hypersensitivity and motor dysfunction of the esophageal wall. We aimed to determine whether the sensory or motor dysfunction plays an important role in the pathogenesis of chest pain. METHODS: We performed graded balloon distentions of the esophagus using impedance planimetry in 16 consecutive patients with chest pain and otherwise normal cardiac and esophageal evaluations and in 13 healthy controls. In those patients who experienced chest pain with balloon distention, the test was repeated after atropine was given. Sensory and biomechanical parameters were measured. RESULTS: Balloon distention reproduced typical chest pain in 13/16 patients (81%) and at lower (p < 0.01) sensory thresholds than controls. Pain was reproduced in all 13 patients and at lower (p < 0.05) sensory thresholds after atropine. Also, after atropine, the esophageal cross-sectional area and wall tension increased (p < 0.05), the tension/strain association shifted to the right (p < 0.05), and reactivity decreased (p < 0.002) relative to results before atropine or in healthy controls (i.e., the esophageal wall relaxed and became more deformable). CONCLUSIONS: Even after relaxing the esophageal wall, most patients experienced chest pain and at lower sensory thresholds. Hence, hyperalgesia rather than motor dysfunction appears to be the predominant mechanism for functional chest pain of esophageal origin.     

Does esophageal function vary at the striated and smooth muscle segments in functional chest pain?

OBJECTIVE: Hypersensitivity of the esophageal wall may contribute to the pathogenesis of functional chest pain. Whether the hypersensitivity is more uniformly distributed along the esophageal wall or is segmental is not known. METHODS: Graded balloon distentions were performed randomly at the smooth muscle as well as at the striated muscle portions of the esophagus in 20 patients with functional chest pain and in 15 healthy volunteers, using impedance planimetry. Sensory thresholds and cross-sectional area were examined in relation to the esophageal wall tension, and the results were compared between two levels as well as the two groups of subjects. RESULTS: During balloon distention, 17 (85%) patients reported typical chest pain, 11 (55%) at both levels, four (20%) at the smooth muscle level, and two (10%) at the striated muscle level only. The sensory thresholds for perception, discomfort, or pain were lower in patients than in controls (p < 0.05). The cross-sectional area and the esophageal wall stiffness at the smooth muscle level were lower than those obtained at the striated muscle level both in controls and in patients (p < 0.01). The wall tension at which moderate discomfort and pain were reported was lower in patients than controls (p < 0.05). CONCLUSIONS: Although in most patients the esophagus is uniformly hypersensitive, in some either the smooth muscle or the striated muscle segment can be hypersensitive. If considering balloon distention at only one level, we recommend balloon placement at 10 cm above the lower esophageal sphincter because of a higher yield of hypersensitivity.     

Short-term influences of dichloroacetate on genetically hyperlipemic rats

The effects of short-term (7 days) administration of dichloroacetate (DCA) on carbohydrate and lipid metabolism in the Zucker obese and lean rat were investigated. Metabolic effects of the drug were more pronounced in the obese than in the lean rat. DCA decreased fasting blood glucose concentrations in both lean and obese rats, but more so in the fat animals, probably because of higher initial levels. The hypoglycemic action of DCA is likely attributable to a direct effect on liver and peripheral tissues and not to an indirect action caused by a decrease in the glucagon-to-insulin ratio because the drug induced just the opposite effect. DCA decreased plasma triglycerides (TG) and free fatty acids (FFA) in the hyperlipemic rats but not in lean rats. Intrahepatic triglyceride content diminished after drug treatment in fat rats, suggesting decreased hepatic TG synthesis. Hyperketonemia, induced in both lean and fat rats by DCA treatment, was also greater in the obese animal. This response was probably caused by accelerated hepatic ketone body production due to increased β-oxidation, and not to enhance FFA substrate supply. These data demonstrate that DCA is capable of correcting many of the underlying abnormalities in carbohydrate and fat metabolism in the obese Zucker rat.