Diet therapy of chronic renal failure

PROTEINLowproteindiethadbeensuggestedformorethan50yearsforCRFpatientsalthoughcontroversyaboutitseffect.Lowproteindietwillresultinmalnutritionwhichcanincreasemortalityandinci-dence.Therefore,someresearcherssuggestedthatoptimumnutritionstatusshouldbemaintainedduringnutritiontreatment.Recently,ametaanalysisindicatedthatdietproteincaneffectivelydelaysub-stitutiontherapy,relieveGFRmoderately,anddelayuremia犤1犦.Founque犤2犦analyzed7controlled,randomizedtrialsof40studiessince1975andinvestigate…     

Is chronic tension-type headache a vascular headache? The relation between chronic tension-type headache and cranial hemodynamics

Twenty-seven patients with chronic tension-type headache were studied as to end-tidal PCO2, heart rate, mean blood pressure, diameter and blood flow of the common carotid arteries, cranial vascular resistance, and headache intensity at supine rest, after administration of nitroglycerin, and at head down tilt. The results were compared to the results of nitroglycerin and head down tilt provocations in age- and sex-matched controls. During supine rest, no change in chronic tension-type headache occurred. Nitroglycerin and tilting induced significant increase of the headache intensity compared to baseline in patients with chronic tension-type headache (P=0.01 and P<0.05, respectively) in contradistinction to controls who did not develop significant headache. Common carotid artery blood flow changes were similar during nitroglycerin provocations in the two groups, but greater (P<0.05) during head down tilt in patients than in controls. Lumbar cerebrospinal fluid pressure was found to be greater than 20 but less than 26 cm H2O in 45% of the 22 patients studied with chronic tension-type headache. The results indicate that the pain in chronic tension-type headache is related to cranial hemodynamics, presumably to distention of intracranial veins.     

Does chronic pain predict future psychological distress?

Cross-sectional studies have consistently shown a relationship between chronic widespread pain, the clinical hallmark of fibromyalgia, and psychological distress. These studies cannot distinguish the direction of any causal relationship. Recent population based studies have reported that such pain is predictive of future distress. However, chronic pain is often associated with physical and psychological co-morbid features which may confound this relationship. The aim of this study was to examine the hypothesis that chronic widespread pain increases the risk of future distress after adjusting for the effects of possible confounding factors. A population based survey of 1953 individuals identified subjects' psychological status and whether they satisfied criteria for chronic widespread pain. At baseline co-morbid features of chronic widespread pain, including reporting other somatic symptoms, abnormal illness behaviour, health anxiety, fatigue and low levels of self-care, were measured. All subjects were followed up after 12 months to determine levels of psychological distress. Subjects with chronic widespread pain at baseline were much more likely to be distressed at follow up (OR=4.0, 95% CI (2.5,6.3)). As levels of distress at follow up may simply reflect those at baseline the association was adjusted for baseline levels of distress. Chronic widespread pain was, however, still associated with future distress although the relationship was slightly attenuated (odds ratio, OR=3.0, 95% CI (1.8,5.1)). To examine our main hypothesis a final analysis was undertaken adjusting this association for those co-morbid features assessed at baseline. Following these adjustments chronic widespread pain was no longer significantly associated with future distress (OR=1.5, 95% CI (0.8,2.9)). Chronic widespread pain was associated with increased levels of psychological distress at follow up. However, a more rigorous analysis indicated that the association between baseline pain status with future distress was explained by concomitant features of chronic pain rather than pain per se. These findings indicate that it is those persons with chronic widespread pain in the presence of other physical and psychosocial factors who will become distressed.     

Why does chronic inflammatory joint disease persist?

Inflammation is a beneficial host response to tissue damage. Most episodes of inflammation resolve spontaneously and do not persist. However, in rheumatoid arthritis (RA), as in a number of other chronic inflammatory diseases, the inflammatory response persists and a stable inflammatory infiltrate accumulates in the joint. What drives this persistence and the relative contribution of infiltrating leucocytes and stromal cells such as fibroblasts to the stability of the inflammatory process are the subject of this article. Fibroblasts play an important role in defining the disordered synovial microenvironment in RA. Through their production of a variety of cytokines and constitutive chemokines they directly alter the behaviour of infiltrating leucocytes, leading to their inappropriate survival and retention. These findings suggest that stromal cells such as fibroblasts play an important role in the switch from acute resolving to chronic persistent arthritis by allowing lymphocytes to accumulate in the wrong place at the wrong time.     

Effect observation of microwave therapy of chronic pharyngodynia

Background：Microwaveisakindofmagneticwavewithhighfrequency．Itproducespyreticeffectwhenitactsonbiologicaltis－sue，whichwillbepropitioustotheabsorptionofinflammationandedemaofpharyngealtissue，enhancethetissuebloodcirculationaswellasthemetabolismandimmunefunction．Objective：ToinvestigatethetreatmenteffectofmicrowavecombinedwithChinesetraditionalmedicineinchronicpharyngody－nia．Unit：AffiliatedHospitalofLuzhouMedicalCollege．Subject：１８０casesofchronicpharyngodyniapatientsweredividedin…     

Is there hope for chronic pain and headache?

Currently the clinical needs for pain and headache management are not met. Despite the numerous and exciting recent advances in understanding the molecular and cellular mechanisms that originate pain, we cannot yet fully explain the mechanism underlying the biology of chronic pain. Pain is a natural mechanism preserving our species survival; however, when the protective quality is lost, physiologic changes to the peripheral and central nervous systems result in the formation of chronic pain states. Once we understand how this chronic pain state is created, either through genetic, environmental, therapeutic, or other triggers we may be able to enhance our species existence, limiting maladaptive pain and suffering. The future therapeutic targets will need to address the genetics, neurophysiologic changes of the neurons and brain as well as help control immune systems including the glia. The key to successful headache and pain therapy is research aimed at prevention and minimizing the plastic changes triggering chronic pain.