Rinsho byori. The Japanese journal of clinical pathology
-
Cachexia is among the most debilitating and life-threatening aspects of cancer. Associated with anorexia, fat and muscle tissue wasting, psychological distress, and a lower quality of life, cachexia arises from a complex interaction between the cancer and the host. This process results from a failure of the adaptive feeding response seen in simple starvation and includes cytokine production, release of lipid-mobilizing and proteolysis-inducing factors, and alterations in intermediary metabolism. ⋯ These include antiserotonergic drugs, gastroprokinetic agents, branched-chain amino acids, eicosapentanoic acid, cannabinoids, melatonin, and thalidomide, all of which act on the feeding-regulatory circuitry to increase appetite and inhibit tumor-derived catabolic factors to antagonize tissue wasting and/or host cytokine release. The outcomes of drug studies in cancer cachexia should focus on the symptomatic and quality-of-life advantages rather than simply on nutritional end points, since the survival of cachexia cancer patients may be limited to weeks or months due to the incurable nature of the underlying malignancy. As weight loss shortens the survival time of cancer patients and decreases their performance status, effective therapy would extend patient survival and improve quality of life.
-
This is the essence of my last lecture to the medical students of Hiroshima University. My 38-year career as a medical school teacher can be sectioned three parts. My main four studies are shown at the third part. 1) We advocated respiratory physiologic-chemistry based on the relationships between pulmonary function and the constitutive chemical components of lungs. 2) We proved the mechanisms of hypertension at the molecular level by renin-angiotensin-adrenaline theory. 3) We showed the difference of mitochondria DNA in Diabetes Mellitus patients between Japanese and Chinese. 4) We suggested the necessity of standardization and holding common national reference values of main clinical laboratory tests by reporting our data. I am delighted that the very good studies of my colleagues achieved 500 IFs and express my gratitude for my colleagues' cooperation.
-
In 2004, the Japanese Committee of Clinical Laboratory Standards (JCCLS) published a standard phlebotomy guideline, which not only ensures the safety of the patients and phlebotomists but is adopted to the healthcare setting in Japan. This phlebotomy standard is also essential for the standardization of clinical laboratory tests. ⋯ The content of the guideline includes necessary facilities and equipment, a step by step safe but practical venipuncture procedure, an explanation of the individual steps, and other supplementary information such as alternative methods. The first edition, published as tentative guideline, is planned to be revised after a set period of time based on the comments and suggestions from a wide range of people concerned, so that it can be published as an approved guideline.
-
EDTA-dependent pseudothrombocytopenia (EDTA-PTCP) is a phenomenon caused by EDTA-dependent anti-platelet antibody. This antibody induces platelet agglutination in vitro, resulting in a decrease in platelet counts. It is necessary for clinicians to consider the possible presence of PTCP in cases of patients having low platelet counts without any hemorrhagic tendency. In this article, we describe some aspects of EDTA-PTCP including, (1) characteristics of platelet agglutination, (2)possible mechanisms for antibody production, (3) several methods to determine the true platelet number, and also (4) a few similar phenomena induced by antibodies independent of EDTA.
-
Heparin-induced thrombocytopenia(HIT) due to immunological mechanisms is known as an important adverse reaction to heparin treatment, and heparin treatment should be applied while keeping in mind the risk of onset of HIT 5-14 days after the initiation of heparin. The presence of HIT had not been fully recognized in clinical practice in Japan despite the management of HIT being well confirmed in Western countries. Recognition of HIT has increased since argatroban, a direct thrombin inhibitor, obtained the approval of the FDA for prevention and treatment of HIT. ⋯ Treatment of HIT should be started at the time of recognition of thrombocytopenia while antibody testing for HIT is performed. As an alternative anticoagulant to heparin, argatroban should immediately be applied to avoid complication of thrombosis. Thrombocytopenia and hypercoagulability quickly recover to the preheparin level by the appropriate use of argatroban.