A Comparison of Meal Replacements and Medication in Weight Maintenance after Weight Loss

Objective: To compare the use of meal replacements or medication during weight maintenance subsequent to weight loss using a very low-energy diet (VLED) in overweight or obese adults.

Design: Participants followed a liquid VLED of 2177 kJ for 12 weeks followed by 4 weeks of re-orientation to solid foods. Participants were randomized at week 16 to receive either meal replacements or Orlistat both combined with a structured meal plan containing an energy value calculated to maintain weight loss.

Subjects: Sixty-four women (age = 49.9 ± 10 y, weight = 101.6 ± 17.1 kg, height = 164.9 ± 6.0 cm, BMI = 36.7 ± 5.4 kg/m²) and 28 men (age = 53.7 ± 9.6 y, weight = 121.8 ± 16.0 kg, height = 178.7 ± 5.6 cm, BMI = 37.8 ± 4.9 kg/m²) completed a 1 year weight management program. Behavioral weight management clinics included topics on lifestyle, physical activity (PA), and nutrition. Participants met for 90 min weekly for 26 weeks, and then biweekly for the remaining 26 weeks.

Outcomes: Minutes of PA, fruits and vegetables (FV), and pedometer steps were recorded on a daily basis and reported at each group meeting. Body weight was obtained at each group meeting.

Results: During VLED, the MR group decreased body weight by 22.8 ± 6.1 kg and the Orlistat group decreased body weight by 22.3 ± 6.1 kg. During weight maintenance, there was no significant group by time interaction for body weight, PA, FV consumption, or pedometer steps. At week 16, the meal replacement group had a body weight of 85.4 ± 14.3 kg that increased to 88.1 ± 16.5 kg at 52 weeks (p < 0.05). At week 16, the Orlistat group had a body weight of 85.7 ± 17.9 kg that increased to 88.5 ± 20.3 kg at 52 weeks (p < 0.05).

Conclusions: Subsequent to weight loss from a VLED, meal replacements and Orlistat treatments were both effective in maintaining weight significantly below baseline levels over a 52 week period of time. Meal replacements may be a viable alternative strategy to medications for weight maintenance.     

A retrospective analysis of cardiovascular outcomes in patients treated with ASV

Objectives. The effect of long-term adaptive servo-ventilation (ASV) on cardiovascular mortality and admission rates in patients with chronic heart failure (CHF) and Cheyne–Stokes respiration (CSR) has not been much studied. The aim of this study was primarily to investigate whether ASV therapy significantly reduced these parameters. Design. We included 75 CHF patients on optimal medication and CSR?≥25% of sleeping time, in New York Heart Association (NYHA) classes II–IV and left ventricular ejection fraction (LVEF)?≤?45%. Thirty-one patients were treated with ASV for >3–18 months and 44 patients served as a control group. Results. Seven deaths (16%) in the control group and one death (3%) in the ASV treatment group had cardiovascular etiology. There was no significant difference between the two groups regarding cardiovascular death (log rank p?=?0.07; HR 0.18 (95% CI 0.02-1.44), p?=?0.11) and combined cardiovascular death or readmissions, but there was a trend toward better outcome regarding cardiovascular event-free survival (log rank p?=?0.06; HR 0.53 (95% CI 0.27–1.05). Conclusions. In CHF patients with CSR, 18 months ASV treatment did not significantly affect cardiovascular death or combined cardiovascular death or hospital admissions. But there was a trend toward better combined outcome.     

Neuropathic pain in leprosy patients

The introduction of multidrug therapy by the World Health Organization has dramatically reduced the world prevalence of leprosy but the disease is still a public health problem in many countries, with a world prevalence of almost 600,000 cases in 2001. Damage to peripheral nerves is a key component of leprosy and the sensory and motor loss that follows is the basis for many of the classical features of this disease, such as skin wounds, cracks, plantar ulcers, clawed hands, drop foot, and incomplete closure of the eyelids. One of the most remarkable aspects of leprosy to lay persons and health care workers alike is that patients are reputed to feel no pain. However, neuropathic pain is arising as a major problem among leprosy patients. It can be nociceptive due to tissue inflammation, which mostly occurs during episodes of immune activation or neuropathic due to damage or dysfunction of the nervous system. This study, conducted among 358 leprosy patients, reveals a considerable prevalence of neuropathic pain and presents evidence that this common problem should be a high priority of those in charge of leprosy control programs.     

Expression of fibrinogen receptors during activation and subsequent desensitization of human platelets by epinephrine

Epinephrine causes platelet aggregation and secretion by interacting with alpha 2-adrenergic receptors on the platelet surface. Platelet aggregation requires the binding of fibrinogen to a specific receptor on the membrane glycoprotein IIb-IIIa complex. Although the IIb-IIIa complex is identifiable on the surface of resting platelets, the fibrinogen receptor is expressed only after platelet activation. The current studies were designed to examine the effect of occupancy of platelet alpha 2-adrenergic receptors by epinephrine on the expression of fibrinogen receptors and on the aggregation of platelets. The ability of epinephrine to induce the expression of fibrinogen receptors was studied under two different conditions: acute stimulation (less than 1 min) and prolonged stimulation (50 to 90 min), the latter of which is associated with a reduction or "desensitization" of the platelet aggregation response. Expression of the fibrinogen receptor was monitored with 125I-fibrinogen as well as with 125I-PAC-1 (PAC-1), a monoclonal antibody that binds to the glycoprotein IIb-IIIa complex only after platelets are activated. Epinephrine caused an immediate increase in PAC-1 and fibrinogen binding that was dependent on occupancy of the alpha 2-receptor by epinephrine and on the presence of extracellular free Ca (KCa = 30 mumol/L). By itself, 1 mmol/L Mg was unable to support induction of the fibrinogen receptor by epinephrine. However, it did decrease the Ca requirement by about two orders of magnitude. Prolonged stimulation of unstirred platelets by epinephrine led to a 70% decrease in the aggregation response when the platelets were subsequently stirred. Despite their decreased aggregation response, desensitized platelets bound PAC-1 and fibrinogen normally, indicating that the loss of aggregation was not due simply to a decrease in fibrinogen receptor expression. Although desensitization was not affected by pretreatment of the platelets with aspirin, it was partially prevented when extracellular Ca was chelated by EDTA during the long incubation with epinephrine. These studies demonstrate that once platelet alpha 2-adrenergic receptors are occupied by epinephrine, extracellular Ca is involved in initiating the aggregation response by supporting the induction of the fibrinogen receptor and the binding of fibrinogen. Furthermore. Ca-dependent reactions subsequent to fibrinogen binding may be necessary for maximal platelet aggregation and are impaired when platelets become desensitized to epinephrine.     

Clinical features and serum antinuclear antibodies in 230 Danish patients with systemic sclerosis

The objective was to investigate the relationship between the presence of different types of antinuclear antibodies (ANA) in patients with systemic sclerosis (SSc) and the presence of clinical features. Sera from 230 patients with SSc were tested for the presence of ANA, including anticentromere antibodies (ab), antitopoisomerase I ab, anti- U1 RNP ab and antinucleolar ab, including anti-Th RNP, anti-U3 RNP and anti-U17 RNP. Clinical features were registered prospectively in a clinical database. Eighty-two per cent of the patients were women. The median age was 58 yr (45-67, quartiles) and median age at disease onset was 44 (30-55) yr. ANA were found in 86% of the patients (anticentromere: 34%; antitopoisomerase I: 14%; anti-U1 RNP: 6.5%; antinucleolar total: 16%; anti-Th RNP: 2.2%; anti-U3 RNP: 3.5%; anti- U17 RNP: 0%). Anticentromere ab were found to be related to a high prevalence of calcinosis, telangiectasia, digital ulcers, acrosclerosis, primary biliary cirrhosis, isolated reduction of pulmonary diffusing capacity, and a low prevalence of radiological evidence of pulmonary fibrosis. Antitopoisomerase I ab were associated with a high prevalence of digital joint deformity, distal osteolysis, radiological signs of pulmonary fibrosis, a low prevalence of calcinosis and late onset of disease. Anti-U1 RNP ab were related to a high prevalence of arthritis and myositis, a low prevalence of calcinosis, and early disease onset. The presence of antinucleolar ab, including anti-U3 RNP and anti-Th RNP, was not significantly related to any particular clinical features in this study; possibly due to the small number of patients with these ab. The presence of anticentromere, antitopoisomerase I and anti-U1 RNP ab in the serum was also found to have previously described clinical correlations in a group of Danish SSc patients.