Staging work-up and post-treatment surveillance of patients with melanoma

Strategies based on evidence are required to accurately stage and effectively follow patients with melanoma. The goal of staging is to define the extent of disease at the time of presentation to direct and assign prognosis. Patient surveillance is performed to assess treatment results and detect recurrences amenable to further treatment. Staging and surveillance require careful use of resources to be cost effective. This article addresses preoperative staging and post-treatment surveillance of patients with melanoma and outlines a method of follow-up based on available data.     

Partial venous thrombosis of the pancreatic allografts after simultaneous pancreas-kidney transplantation

Despite new advances in transplantation, complete venous thrombosis (VT) of the pancreas after simultaneous pancreas kidney (SPK) transplantation usually results in graft loss. Data are limited regarding the outcome and treatment of partial VT of the pancreas allograft. From July 1994 to December 1999, 126 patients with IDDM/end-stage renal disease underwent SPK with systemic bladder drainage at the University of Miami. We retrospectively reviewed our experience regarding the outcome and treatment options of partial VT of the pancreas allografts. From July 1994 to April 1997, partial VT was not seen in the first 66 SPK patients induced with anti-CD3 rnAb and oral or intravenous (i.v.) tacrolimus (TAC) in the operating room. From May 1997 to June 1999, 14 (29%) out of 48 patients had VT. These cases were identified following the i.v. use of TAC with anti-IL-2R antibody-induction therapy (7/15) or without (7/33). Partial thrombosis of the splenic vein (PTSV) was documented in 10 patients, 2 had complete thrombosis of the splenic vein (CTSV), 1 had partial thrombosis of the superior mesenteric vein (PTSMV), and 1 patient had PTSV and PTSMV. These were identified incidentally during routine color Doppler ultrasonography (CDU). None of these SPK recipients demonstrates a change in clinical parameters. The first 8 patients were systemically heparinized, followed by oral anticoagulation, except 1 patient with CTSV. He progressed to complete thrombosis of the pancreas allograft and was treated with percutaneous thrombectomy and urokinase infusion, followed by heparinization and oral anticoagulation. One patient required exploration for bleeding. In an attempt to reduce the morbidity of heparinization, we treated the next 6 patients with PTSV with aspirin followed by serial CDU. All 14 patients had preservation of the endocrine and exocrine pancreatic functions. CDU showed resolution with recanalization of the thrombosed vein(s). From July 1999 to December 1999, 12 SPK recipients were administered TAC orally with or without induction therapy with anti-IL-2R antibody. So far, in this group, VT has not been identified. In summary, a total of 14 out of 126 patients (11%) had isolated VT with a mean follow-up of 36.4 months. Based on our experience, we suggest that extensive VT after pancreas transplantation, including splenic and superior mesenteric VT, be treated with heparin and subsequent oral anticoagulation for 3 months. For more limited, partial splenic VT, aspirin may be sufficient. Follow-up CDU is critical for a successful outcome. The i.v. use of TAC appears to be a risk factor for the increased incidence of VT. Currently, using IL-2rmAb as induction, TAC is started orally on postoperative days 3 or 4 and aspirin on postoperative day 2.     

Is it wise to restrict fat in the diets of children?

The proponents of fat-restricted diets for children argue that low-fat diets given in childhood will prevent the development of atherosclerosis in adulthood, low-fat diets given a childhood will condition children to prefer low-fat diets in adulthood, and low-fat diets for children are safe. There is no evidence that low-fat diets in childhood will prevent atherosclerosis in adulthood. In fact, studies of migrating populations indicate that immigrants to the United States from Third World countries who consumed low-fat diets in childhood take on the character of their new environments, including higher serum cholesterol levels and more coronary disease. The prevalence of fatty streaks in childhood bears little relationship to the prevalence of atheromatous plaques in adulthood. In fact, girls have more aortic fatty streaks and higher serum cholesterol values in childhood than boys, but fewer plaques in adulthood and less coronary disease. From the PDAY study, it has also been learned that hypercholesterolemia in childhood enhances fatty streak formation, but not that of plaques. It now seems established from autopsy studies that the progression of atherosclerosis from fatty streaks to plaque is arrested in childhood and does not begin to a significant extent until after puberty in males and after menopause in females. So the oft-repeated statement that atherosclerosis begins in childhood is semantically true but very misleading. The particularly harmful form of atherosclerosis (the plaque) does not become significant until much beyond puberty. The effects of low-fat, low-cholesterol diets on serum lipids and lipoproteins are of a lesser magnitude in children than in adults. The 0.78 mmol/L decrease in LDL cholesterol in the intervention group from controls (change 1.5%) in the DISC study was biologically insignificant and reflects the tighter control of lipoprotein and cholesterol synthesis in children compared with adults. It must be remembered that the human body synthesizes all of the cholesterol it needs from acetyl CoA. In general, the larger the amount of dietary cholesterol absorbed, the smaller the rate of biosynthesis of cholesterol. In some adults and most children this homeostatic control is nearly perfect, but in many adults the correction in biosynthesis of cholesterol with increased dietary input is imperfect and LDL cholesterol values increase. The second argument of the proponents of low-fat diets for children is that they are conditioned to continue low-fat diets in adulthood. From the studies of Birch and Fisher (51) this prediction seems unlikely. These investigators found that restricting access to palatable foods enhanced the interest of 3- to 5-year-old children in those foods and increased their desire to obtain and consume those foods. They concluded that "stringent parental controls can potentiate preference for high-fat energy-dense foods, limit children's acceptance of a variety of foods and disrupt children's regulation of energy intake." Brosin (52) has also observed that food restriction in childhood may lead to gluttony in adulthood. Finally, the claim that low-fat diets are safe in childhood is based on observations over too short a time to establish safety. It is true that growth and development of children studied in the DISC study was not changed from the expected increments, but that is not proof of long-term safety. In addition, the lower content of essential nutrients in low-fat, low-cholesterol diets (calcium, zinc, magnesium, phosphorus, vitamin E, vitamin B-12, thiamin, niacin, and riboflavin) must be considered along-term risk (53,54). Furthermore, the published studies of the safety of low-fat diets have been conducted under intensive surveillance in medical centers, conditions very different from those in the homes of free-living families.     

Nutrition for patients with cystic fibrosis.

Cystic fibrosis (CF) is the most frequent, lethal genetic disorder among northern Europeans. The etiology of this autosomal recessive disease is known to be a defect in the cAMP activation of chloride (Cl-) channels in secretory cells in many organs of the body. Although this defect usually leads to severe lung disease, many of these patients also have nutritional deficiencies. Nutrition is one of the key components in the management of CF. Patients are at high risk for malnutrition, which may result in accelerated progression of the disease and increased morbidity. This review will discuss nutrition recommendations for calories, protein, vitamins and minerals, and enteral and parenteral nutrition support practices.     

Hip Adduction and Abduction Strength Profiles Among Bantam,High School,Juniors, and Collegiate American Ice Hockey Players

BackgroundAdductor strains are the most common non-contact musculoskeletal injury sustained in ice hockey. Systematic reviews have determined higher level of play and lower hip adduction to abduction strength ratios to be associated with an increased risk of adductor strain across multiple sports. Limited research exists regarding hip adduction and abduction strength profiles across various levels of ice hockey players.PurposeTo compare isometric hip adduction and abduction strength profiles among bantam, high school, tier one juniors, and NCAA Division I collegiate ice hockey players. A secondary purpose was to identify whether differences in strength profiles between dominant and non-dominant limbs exist.Study DesignCross-sectional cohort study.MethodsA questionnaire of demographic data, hockey, and injury specific information was completed by all subjects. The mean of three reps of maximal hip isometric adduction and abduction strengths were quantified using a handheld dynamometer with external belt-fixation. Ratios of hip adduction-to-abduction strength were calculated and normalized for body weight.ResultsA total of 87 uninjured skaters were included in this study with a mean age of 17 years. Mean hip adductor-to-abductor ratios for Bantam hockey players were 121% followed by collegiate (115%), Juniors (111%), and high school (109%) hockey players. No statistically significant differences were found between peak hip adduction and abduction isometric strength and playing level. In addition, there was no difference between unilateral hip strength ratios and shooting hand or leg dominance. While 34.5% of subjects reported a history of adductor injury, no significant differences existed regarding strength ratios during bilateral comparison or when compared to their team norms. Three subjects were found to have unilateral ratios of less than 80%, while two subjects demonstrated bilateral ratios of less than 80%.ConclusionsSymmetry is illustrated between dominant and non-dominant legs in ice hockey players with and without a history of adductor injury. Results align well with previously established cross-sectional data from Australian football, with ratios of 103% in high school players, 107% in semi-professional players, and 113% in collegiate players.Level of EvidenceLevel 3     

CGS 15435A, a thromboxane synthetase inhibitor with an extended duration of action: a comparison with dazoxiben

CGS 15435A, a novel thromboxane (Tx) synthetase inhibitor (5-chloro-1-methyl-2-(3-pyridyl)-3-indolhexanoic acid HCl), had a selectivity for Tx synthetase 100,000-fold greater than that for cyclooxygenase, PGI2 synthetase and lipoxygenase enzymes. In conscious beagles, 1 h following a single 3 mg/kg p.o. dose, serum TxB2 was inhibited 95% by CGS 15435 and 82% by dazoxiben (DAZ). Unlike the short acting Tx synthetase inhibitor DAZ, CGS 15435A significantly inhibited TxB2 formation 4, 6, 12 and 24 h after dosing. Serum levels of 6-keto PGF1 alpha and PGE2 were significantly increased following the administration of either drug. CGS 15435A and DAZ were further examined in a model with known Tx involvement. Thrombotic sudden death, produced in anesthetized rabbits by injection of 0.75 mg/kg arachidonic acid (AA) i.v. resulted in a 45% fall in the platelet count and 0% survival. Pretreatment with DAZ (8.6 mumol/kg i.v.) at 0.25 or 2 h pre-AA resulted in 3 and 42% thrombocytopenia and 100 and 0% survival respectively. CGS 15435A (8.6 mumol/kg i.v.) prevented the increases in plasma TxB2 levels, thrombocytopenia and sudden death with pretreatment at 0.25 h (0% thrombocytopenia and 100% survival) or 24 h (11% thrombocytopenia and 83% survival) before AA. These data indicate that CGS 15435A is a potent and selective Tx synthetase inhibitor with a long duration of action, and suggest that the compound could be useful in chronic, non-symptomatic indications of Tx involvement.     

The metabolism of 2,3,4-trimethylpentane in male Fischer-344 rats

The urinary metabolites of the potent nephrotoxic hydrocarbon 2,3,4-trimethylpentane (2,3,4-TMP) given Fischer-344 male rats by gavage included 1-hydroxy-2,3,4-trimethylpentane, 2,3,4-trimethyl-1-pentanoic acid and 2,3,4-trimethyl-5-hydroxy-1-pentanoic acid. Analyses were performed by gas-liquid chromatography (GC) and gas-liquid chromatography/mass spectrometry (GC/MS). A comparison of the urinary metabolites of 2,3,4-TMP with those of 2,2,4-trimethylpentane (2,2,4-TMP) showed that more monocarboxylic acid was produced with 2,3,4-TMP.