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      Evaluation of total LDH and its isoenzymes as markers in preeclampsia Translated title: Procena ukupnog LDH i njegovih izoenzima kao markera u preeklampsiji

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          Abstract

          Background

          Preeclampsia, a rapidly progressing pregnancy-specific multi-systemic syndrome is globally the leading cause of maternal and neonatal morbidity and mortality. This study aims to evaluate the serum total Lactate dehydrogenase levels in women with preeclampsia when compared to normotensive pregnant women and assess the electrophoretic pattern of the LDH isoenzymes in normal pregnancy, preeclampsia and eclampsia.

          Methods

          The study, carried out in the Department of Biochemistry of MVJ Medical College, included 30 patients of preeclampsia and 30 normotensive gestational age-matched pregnant women admitted to the Department of OBG. Serum total LDH was analysed by DGKC method. Serum and cord blood samples for isoenzyme distribution analysis were collected from a normal pregnant woman undergoing delivery, a woman with mild eclampsia, two women with eclampsia, and analysed by slab gel electrophoresis followed by activity staining.

          Results

          LDH was significantly elevated in cases as well as between the case (mild and severe) groups, showed a moderate positive statistically significant correlation with systolic, diastolic blood pressure and a sensitivity of 50% and a specificity of 80%. Further, the isoenzyme pattern showed a decreasing distribution of aerobic forms of LDH in preeclampsia-eclampsia.

          Conclusions

          Serum total LDH may serve as a robust and affordable marker of preeclampsia. Serum total LDH, along with its isoenzyme profile, might serve as a predictor and a stronger marker of preeclampsia when compared to serum LDH analysis alone. It may also be used to assess the severity of preeclampsia and hence help in predicting and preventing adverse maternal and foetal outcomes.

          Translated abstract

          Uvod

          Preeklampsija, multisistemski sindrom koji brzo napreduje zbog trudnoće, vodeći je uzrok morbiditeta i mortaliteta majki i novorođenčadi. Ova studija ima za cilj da proceni nivo ukupne laktat dehidrogenaze u serumu kod žena sa preeklampsijom u poređenju sa normotenzivnim trudnicama i proceni elektroforetski obrazac LDH izoenzima u normalnoj trudnoći, preeklampsiji i eklampsiji.

          Metode

          Studija sprovedena na Odeljenju za biohemiju Medicinskog fakulteta MVJ obuhvatila je 30 pacijentkinja sa preeklampsijom i 30 normotenzivnih trudnica u istom stadijumu trudnoće primljenih na odeljenje OBG. Ukupni LDH u serumu je analiziran DGKC metodom. Uzorci seruma i pupčane vrpce za analizu raspodele izoenzima prikupljeni su od pacijentkinje sa normalnom trudnoćom koja je bila na porođaju, žene s blagom eklampsijom, dve žene s eklampsijom, i analizirani su vertikalnom elektroforezom na tankom sloju gela, a detekcija je vršena merenjem odgovarajućih reakcija.

          Rezultati

          LDH je bio značajno povišen u svim grupama, kao i kad se rezultati grupa međusobno porede (blaga i teška preeklampsija), i pokazao je umereno pozitivnu i statistički značajnu povezanost sa sistolnim i dijastolnim krvnim pritiskom, osetljivost od 50% i specifičnost od 80%. Dalje, obrazac izoenzima pokazao je smanjenu distribuciju aerobnih oblika LDH u preeklampsiji-eklampsiji.

          Zaključak

          Ukupni LDH u serumu može poslužiti kao čvrst i pristupačan marker preeklampsije. Ukupni LDH u serumu zajedno sa njegovim izoenzimskim profilom može poslužiti kao prediktor i bolji marker preeklampsije u poređenju sa analizom LDH u serumu. Takođe se može koristiti za procenu ozbiljnosti preeklampsije i tako pomoći u predviđanju i sprečavanju štetnih ishoda po majku i plod.

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          Most cited references23

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          Pre-eclampsia.

          Pre-eclampsia remains a leading cause of maternal and perinatal mortality and morbidity. It is a pregnancy-specific disease characterised by de-novo development of concurrent hypertension and proteinuria, sometimes progressing into a multiorgan cluster of varying clinical features. Poor early placentation is especially associated with early onset disease. Predisposing cardiovascular or metabolic risks for endothelial dysfunction, as part of an exaggerated systemic inflammatory response, might dominate in the origins of late onset pre-eclampsia. Because the multifactorial pathogenesis of different pre-eclampsia phenotypes has not been fully elucidated, prevention and prediction are still not possible, and symptomatic clinical management should be mainly directed to prevent maternal morbidity (eg, eclampsia) and mortality. Expectant management of women with early onset disease to improve perinatal outcome should not preclude timely delivery-the only definitive cure. Pre-eclampsia foretells raised rates of cardiovascular and metabolic disease in later life, which could be reason for subsequent lifestyle education and intervention. Copyright 2010 Elsevier Ltd. All rights reserved.
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            The two stage model of preeclampsia: variations on the theme.

            The Two Stage Model of preeclampsia proposes that a poorly perfused placenta (Stage 1) produces factor(s) leading to the clinical manifestations of preeclampsia (Stage 2). Stage 1 is not sufficient to cause the maternal syndrome but interacts with maternal constitutional factors (genetic, behavioral or environmental) to result in Stage 2. Recent information indicates the necessity for modifications of this model. It is apparent that changes relevant to preeclampsia and other implantation disorders can be detected in the first trimester, long before the failed vascular remodeling necessary to reduce placental perfusion is completed. In addition, although the factor(s) released from the placenta has usually been considered a toxin, we suggest that what is released may also be an appropriate signal from the fetal/placental unit to overcome reduced nutrient availability that cannot be tolerated by some women who develop preeclampsia. Further, it is evident that linkage is not likely to be one factor but several, different for different women. Also although the initial model limited the role of maternal constitutional factors to the genesis of Stage 2, this does not appear to be the case. It is evident that the factors increasing risk for preeclampsia are also associated with abnormal implantation. These several modifications have important implications. An earlier origin for Stage 1, which appears to be recognizable by altered concentrations of placental products, could allow earlier intervention. The possibility of a fetal placental factor increasing nutrient availability could provide novel therapeutic options. Different linkages and preeclampsia subtypes could direct specific preventive treatments for different women while the role of maternal constitutional factors to affect placentation provides targets for prepregnancy therapy. The modified Two Stage Model provides a useful guide towards investigating pathophysiology and guiding therapy.
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              Diagnosis and Treatment of Hyponatremia: Compilation of the Guidelines.

              Hyponatremia is a common water balance disorder that often poses a diagnostic or therapeutic challenge. Therefore, guidelines were developed by professional organizations, one from within the United States (2013) and one from within Europe (2014). This review discusses the diagnosis and treatment of hyponatremia, comparing the two guidelines and highlighting recent developments. Diagnostically, the initial step is to differentiate hypotonic from nonhypotonic hyponatremia. Hypotonic hyponatremia is further differentiated on the basis of urine osmolality, urine sodium level, and volume status. Recently identified parameters, including fractional uric acid excretion and plasma copeptin concentration, may further improve the diagnostic approach. The treatment for hyponatremia is chosen on the basis of duration and symptoms. For acute or severely symptomatic hyponatremia, both guidelines adopted the approach of giving a bolus of hypertonic saline. Although fluid restriction remains the first-line treatment for most forms of chronic hyponatremia, therapy to increase renal free water excretion is often necessary. Vasopressin receptor antagonists, urea, and loop diuretics serve this purpose, but received different recommendations in the two guidelines. Such discrepancies may relate to different interpretations of the limited evidence or differences in guideline methodology. Nevertheless, the development of guidelines has been important in advancing this evolving field.
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                Author and article information

                Contributors
                Journal
                J Med Biochem
                J Med Biochem
                JOMB
                Journal of Medical Biochemistry
                Society of Medical Biochemists of Serbia, Belgrade
                1452-8258
                1452-8266
                02 September 2020
                02 September 2020
                02 September 2020
                : 39
                : 3
                : 392-398 (pp. 392-398)
                Affiliations
                [1 ] orgnameMVJ Medical College and Research Hospital, Department of Biochemistry, Hoskote, Bangalore, Karnataka, India
                [2 ] orgnameManipal Academy of Higher Education (MAHE), Kasturba Medical College, Department of Biochemistry, Manipal, Karnataka, India
                Author notes

                Correspondence to: Dr Swetha Chandru, MD, Assistant Professor, Department of Biochemistry, MVJ Medical College and Research Hospital, Bangalore, Karnataka (562114), India drswethac@ 123456gmail.com

                Article
                jomb-39-3-2003392S
                10.2478/jomb-2019-0045
                7682784
                33269027
                aba8667a-9a0c-442d-88f8-ef68744d8079
                2020 Fazal Rimsha Saleem, Swetha Chandru, Monalisa Biswas, published by CEON/CEES

                This work is licensed under the Creative Commons Attribution 4.0 License.

                History
                : 09 September 2019
                : 28 June 2019
                Funding
                Funded by: We express our sincere gratitude to the ICMR STS team for encouraging us by approving the study for ICMR STS 2018 (Reference ID: 2018-02850);
                Categories
                Original Paper

                preeclampsia,eclampsia,lactate dehydrogenase,preeklampsija,eklampsija,laktat dehidrogenaza

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