Albumin Substitution in Decompensated Liver Cirrhosis: Don't Forget Zinc.

Decompensated liver cirrhosis has a dismal prognosis, with patients surviving on average for 2-4 years after the first diagnosis of ascites. Albumin is an important tool in the therapy of cirrhotic ascites. By virtue of its oncotic properties, it reduces the risk of cardiovascular dysfunction after paracentesis. Treatment with albumin also counteracts the development of hepatorenal syndrome and spontaneous bacterial peritonitis. More recently, the positive impact of long-term albumin supplementation in liver disease, based on its pleiotropic non-oncotic activities, has been recognized. These include transport of endo- and exogenous substances, anti-inflammatory, antioxidant and immunomodulatory activities, and stabilizing effects on the endothelium. Besides the growing recognition that effective albumin therapy requires adjustment of the plasma level to normal physiological values, the search for substances with adjuvant activities is becoming increasingly important. More than 75% of patients with decompensated liver cirrhosis do not only present with hypoalbuminemia but also with zinc deficiency. There is a close relationship between albumin and the essential trace element zinc. First and foremost, albumin is the main carrier of zinc in plasma, and is hence critical for systemic distribution of zinc. In this review, we discuss important functions of albumin in the context of metabolic, immunological, oxidative, transport, and distribution processes, alongside crucial functions and effects of zinc and their mutual dependencies. In particular, we focus on the major role of chronic inflammatory processes in pathogenesis and progression of liver cirrhosis and how albumin therapy and zinc supplementation may affect these processes.

Zinc Deficiency-An Independent Risk Factor in the Pathogenesis of Haemorrhagic Stroke?

Zinc is an essential trace element for human health and plays a fundamental role in metabolic, immunological and many other biological processes. The effects of zinc are based on the intra- and extracellular regulatory function of the zinc ion (Zn2+) and its interactions with proteins. The regulation of cellular zinc homeostasis takes place via a complex network of metal transporters and buffering systems that react to changes in the availability of zinc in nutrition, chronic diseases, infections and many other processes. Zinc deficiency is associated with impairment of numerous metabolic processes, reduced resistance to infections due to impaired immune functions, changes in skin and its appendages and disorders of wound healing and haemostasis. While ischemic heart attacks (myocardial infarction) occur more frequently with meat-based normal diets, haemorrhagic strokes are more frequently observed with vegetarian/vegan diets. The causes are discussed as deficiencies of various micronutrients, such as vitamin B12, vitamin D, various amino acids and also zinc. In the present review, after a description of the functions of zinc and its resorption, a discussion of daily food intake will follow, with a special focus on the importance of food composition and preparation for the zinc balance. The close interrelationships between proteins, especially albumin and zinc will be discussed. Finally, the possible causes and consequences of a zinc deficiency on the blood vessels and blood coagulation are considered.

SHOULDER EXTERNAL ROTATOR STRENGTH IN RESPONSE TO VARIOUS SITTING POSTURES: A CONTROLLED LABORATORY STUDY.

BACKGROUND: The forward head rounded shoulder (FHRS) sitting posture has been associated with decreased shoulder complex muscle strength and function. Upon clinical observation, the adverse effects of the FHRS sitting posture on shoulder complex isometric muscle strength is also present when testing controls for scapular position. HYPOTHESIS/PURPOSE: The purpose of the study was to assess the effect of various sitting postures on shoulder external rotator muscle isometric strength when the strength testing controls for scapular position. STUDY DESIGN: A cohort study, with subjects serving as their own controls. METHODS: One hundred subjects ages 20-26 participated in the study. Each subject was placed in a neutral cervical sitting (NCS) posture which was maintained for five minutes after which the strength of the dominant shoulder external rotators was immediately tested with the glenohumeral joint in the neutral position using a Micro-FET3 Hand Held Muscle Testing Dynamometer (HHMTD). Each subject was returned to the NCS posture for subsequent external rotator strength testing after five minutes in a FHRS sitting posture, five additional minutes in the NCS posture and five minutes in a retracted cervical sitting (RCS) posture resulting in each subjects' external rotator strength being tested on four occasions. Subjects were randomized for order between the FHRS and RCS postures. RESULTS: Mean strength values for each condition were normalized to the mean strength value for the 1st NCS condition for each subject. A statistically significant decline in shoulder external rotator strength following the FHRS sitting posture occurred compared to the appropriate postural conditions (p<.05). A frequency analysis revealed that 36% of the subjects demonstrated greater than 10% decline in external rotator strength following five minutes in the FHRS sitting posture. The average percentage of strength decline in those with greater than a 10% reduction in external rotator strength was 19%. Sixty-four percent of the subjects experienced less than a 10% decline in shoulder external rotator strength in response to the FHRS sitting posture. CONCLUSION: Shoulder external rotator strength declined 8% following five minutes in the FHRS sitting posture. A sub-population of 36% demonstrated an average decline of 19% in shoulder external rotator strength following five minutes in the FHRS sitting posture. The strength decline appears to resolve over the short-term by returning to the NCS posture. LEVEL OF EVIDENCE: Level III.