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Books on the topic 'Dependency syndrome'

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Published: 4 June 2021
Last updated: 18 February 2022

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1

Namka, Lynne. The doormat syndrome. Deerfield Beach, Fla: Health Communications, 1989.

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2

Kobierzycki, Tadeusz. Beyond love and freedom: The psychological dependency syndrome. Warsaw: Muzaios, 2009.

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3

Reese, Robert. Roots and remedies of the dependency syndrome in world missions. Pasadena, Calif: William Carey Library, 2010.

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4

Roots and remedies of the dependency syndrome in world missions. Pasadena, Calif: William Carey Library, 2009.

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5

Reese, Robert. Roots and remedies of the dependency syndrome in world missions. Pasadena, Calif: William Carey Library, 2009.

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6

Petrakis, Peter L. Acquired immune deficiency syndrome and chemical dependency: Report of symposium. Rockville, Md: U.S. Dept. of Health and Human Services, Public Health Service, Alcohol, Drug Abuse, and Mental Health Administration, National Institute on Alcohol Abuse and Alcoholism, 1987.

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7

Reese, Robert. Roots and remedies of the dependency syndrome in world missions. Pasadena, Calif: William Carey Library, 2009.

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8

Mwanza, Frederick K. Chasing the winds and dependency syndrome: Topical issues on Zambia's political economy. Lusaka: MFK Management Consultancy Services, 1993.

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9

Smart, Hans. Le syndrome colonial: L'art de se tirer dans le pied! St.-Zénon, Québec: L. Courteau, 2004.

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10

Barnes, C. G. Cabbage syndrome: The social construction of dependence. London: Falmer Press, 1990.

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11

Kobierzycki, Tadeusz. Poza miłością i wolnością: Syndrom uzależnienia psychologicznego. 2nd ed. Warszawa: Muzaios, 2000.

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12

1927-, Schäfer Harald, and Titlbach Milan 1928-, eds. Histophysiology of the obesity-diabetes syndrome in sand rats. Berlin: Springer-Verlag, 1994.

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13

Thompson, Miles. Mutation screening of dopamine and serotonin candidate genes in Tourette's syndrome and alcohol-dependent patients. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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14

Type 2 diabetes, pre-diabetes, and the metabolic syndrome. 2nd ed. New York: Humana Press, 2011.

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15

Das, Undurti N. Metabolic syndrome pathophysiology: The role of essential fatty acids. Ames, Iowa: Wiley-Blackwell, 2010.

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16

Gaetano, Crepaldi, Tiengo Antonio, and Manzato E, eds. Diabetes, obesity, and hyperlipidemias, V: The plurimetabolic syndrome : proceedings of the European Symposium on Metabolism, Padova, 24-26 May 1993. Amsterdam: Excerpta Medica, 1993.

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17

Codario, Ronald A. Type 2 diabetes, pre-diabetes, and the metabolic syndrome: The primary care guide to diagnosis and management. Totowa, N.J: Humana Press, 2005.

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18

Heroin, AIDS, and society. London: Hodder and Stoughton, 1987.

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19

Petrakis, Peter L. Acquired Immune Deficiency Syndrome and Chemical Dependency. Diane Pub Co, 1988.

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20

L, Petrakis Peter, American Medical Society on Alcoholism and Other Drug Dependencies., National Council on Alcoholism, and AIDS and Chemical Dependency Forum (1986 : San Francisco, Calif.), eds. Acquired Immune Deficiency Syndrome and chemical dependency: Report of symposium. Rockville, Md: U.S. Dept. of Health and Human Services, Public Health Service, Alcohol, Drug Abuse, and Mental Health Administration, National Institute on Alcohol Abuse and Alcoholism, 1987.

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21

Opdebeeck, Sybille. Afhankelijkheid en het beeindigen van partnergeweld. Garant, 1993.

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22

Newell-Price, John, Alia Munir, and Miguel Debono. Cushing syndrome. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0189.

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Endogenous Cushing’s syndrome results from chronic, excessive, and inappropriately high cortisol exposure. It comprises a large group of signs and symptoms. Pseudo-Cushing’s syndrome is a state of hypercortisolaemia that may have some of the clinical features of Cushing’s syndrome, but the clinical and biochemical features resolve when the underlying condition is treated: causes include alcohol dependence and depression.
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23

Prout, Jeremy, Tanya Jones, and Daniel Martin. General therapeutics. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199609956.003.0007.

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Drugs used during the perioperative period may have implications for both the patient and the environment. Drugs may cause toxicity such as propofol infusion syndrome or dependency problems in the long-term. Perioperative anaphylaxis, the triggers, recognition and management is detailed. Management of patients with acute poisoning is included with general assessment and supportive management as well as specific antidotes. The clinical consequences of paracetamol poisoning are discussed in detail.
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24

Medforth, Janet, Linda Ball, Angela Walker, Sue Battersby, and Sarah Stables. Maternal emergencies during pregnancy, labour, and postnatally. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198754787.003.0022.

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Maternal emergencies during pregnancy, labour, birth, and the postnatal period are covered. Blood tests during pregnancy and detecting deviations from the norm are included. Maternal emergencies and their management considered include: major obstetric haemorrhage, uterine rupture, eclampsia, emboli (pulmonary embolus and amniotic fluid embolus), HELLP syndrome, disseminated intravascular coagulation, uterine inversion, shock, and maternal resuscitation. Guidelines for admission to a high-dependency unit and current maternal morbidity and mortality data are included.
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25

Swift, Robert M. Pharmacotherapy of Substance Use, Craving, and Acute Abstinence Syndromes. Edited by Kenneth J. Sher. Oxford University Press, 2015. http://dx.doi.org/10.1093/oxfordhb/9780199381708.013.12.

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Advances in the understanding of the neurobiological basis of addiction have led to a better understanding of the causes of drug and alcohol dependence, as well as to new alternatives in the treatment of these disorders. By addressing some of the underlying neurobiological changes that cause and maintain drug and alcohol dependence, pharmacotherapies can provide an important adjunctive treatment for alcohol- and drug-dependent and behaviorally addicted patients. During detoxification, pharmacotherapies can reduce the severity of withdrawal. After detoxification, pharmacotherapies can be useful as an adjunct to psychosocial treatments to help maintain abstinence or reduced addictive behaviors by reducing craving, reducing the rewarding effects of drugs, and improving the allostasis that accompanies abstinence. This chapter describes the neurobiology of drugs and alcohol, how chronic use leads to brain adaptations that result in addiction, and the actions of medications used to treat addictive disorders.
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26

Barañano, Kristin W. Angelman Syndrome. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0055.

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Angelman syndrome (AS) is a severe neurodevelopmental disorder caused by maternal deficiency of the epigenetically imprinted gene UBE3A. It is characterized by severe developmental delay, an ataxic gait disorder, an apparent happy demeanor with frequent smiling or laughing, and severe expressive language impairments. Understanding the neurobiology of AS has focused on understanding how UBE3A is regulated by neuronal activity, as well as the targets of its ubiquitin E3 ligase activity. This has led to a model of the role of UBE3A in the regulation of experience-dependent sculpting of synaptic circuits. At this time, treatment is largely supportive, but efforts directed toward reversing the epigenetic silencing machinery may lead to improved synaptic function in AS patients.
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27

Henri, Begleiter, and Kissin Benjamin 1917-, eds. The pharmacology of alcohol and alcohol dependence. New York: Oxford University Press, 1996.

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28

Perspectives of the hyperinsulinemia/insulin resistance syndrome in NIDDM: From pathophysiology to clinical implications. München: MMV Medizin Verlag, 1990.

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29

Crepaldi, Gaetano, and Antonio Tiengo. Diabetes, Obesity and Hyperlipidemias: 5: Plurimetabolic Syndrome (Physical Sciences Data). Excerpta Medica, 1993.

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30

Markolf, Hanefeld, and Leonhardt Wolfgang, eds. The metabolic syndrome: An integrated concept for the diagnosis and therapy of a cluster of diseases of civilisation. Jena: G. Fischer, 1997.

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31

Preventing Type 2 Diabetes: Beyond Diet and Exercise. BelVista Publishers, LLC, 2008.

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32

Codario, Ronald A. Type 2 Diabetes, Pre-Diabetes, and the Metabolic Syndrome (Current Clinical Practice). Humana Press, 2005.

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33

Das, Undurti N. Metabolic Syndrome Pathophysiology: The Role of Essential Fatty Acids. Wiley & Sons, Incorporated, John, 2009.

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34

Swift, Carrie S. Overcoming type 2 diabetes. 2015.

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35

Gaitanis, John, Phillip L. Pearl, and Howard Goodkin. The EEG in Degenerative Disorders of the Central Nervous System. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0013.

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Nervous system alterations can occur at any stage of prenatal or postnatal development. Any of these derangements, whether environmental or genetic, will affect electrical transmission, causing electroencephalogram (EEG) alteration and possibly epilepsy. Genetic insults may be multisystemic (for example, neurocutaneous syndromes) or affect only the brain. Gene mutations account for inborn errors of metabolism, channelopathies, brain malformations, and impaired synaptogenesis. Inborn errors of metabolism cause seizures and EEG abnormalities through a variety of mechanisms, including disrupted energy metabolism (mitochondrial disorders, glucose transporter defect), neuronal toxicity (amino and organic acidopathies), impaired neuronal function (lysosomal and peroxisomal disorders), alteration of neurotransmitter systems (nonketotic hyperglycinemia), and vitamin and co-factor dependency (pyridoxine-dependent seizures). Environmental causes of perinatal brain injury often result in motor or intellectual impairment (cerebral palsy). Multiple proposed etiologies exist for autism, many focusing on synaptic development. This chapter reviews the EEG findings associated with this myriad of pathologies occurring in childhood.
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36

Lheureux, Philippe, and Marc Van Nuffelen. Management of benzodiazepine poisoning. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0320.

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The wide use of benzodiazepines is associated with some inconveniences and are most frequently implicated in acute self-poisoning and accidental poisoning in children. Some of them are recognized as submission drugs, used to commit date rape or robbery. Prolonged use of a benzodiazepine leads to dependence, with a risk of developing a life-threatening withdrawal syndrome. Overdose has usually a good prognosis—most patients recover well with careful observation and prevention of complications, although care should be taken with elderly people, and patients with chronic obstructive pulmonary disease or liver dysfunction. Fast-acting agents and co-ingestion of other central nervous system depressants may be present greater risk. Early administration of activated charcoal in patients able to protect their airway is only needed if there are co-ingestants. Flumazenil may help confirm the diagnosis, improve alertness, and prevent the need for respiratory support in some patients, especially after accidental poisoning in children. Contraindications include patients on long-term treatment and/or dependent on benzodiazepines, or those who have simultaneously ingested proconvulsant or prodysrhythmic substances or at risk of increased intracranial pressure.
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37

Ireland. National Advisory Committee on Drugs. and National Medicines Information Centre (Ireland), eds. Report to the National Advisory Committee on Drugs on 'Use of buprenorphine as an intervention in the treatment of opiate dependence syndrome'. 2002.

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38

United States. Congress. Office of Technology Assessment., ed. The Effectiveness of drug abuse treatment: Implications for controlling AIDS/HIV infection. Washington, D.C: Congress of the U.S., Office of Technology Assessment, 1990.

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39

Babor, Thomas F., Jonathan Caulkins, Benedikt Fischer, David Foxcroft, Keith Humphreys, María Elena Medina-Mora, Isidore Obot, et al. Matters of substance. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198818014.003.0002.

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Psychoactive substances vary tremendously in their pharmacological properties, cultural symbolism, and reinforcing effects. Comparative risk assessments indicate that legal substances like tobacco and alcohol are at least as dangerous to health and social welfare as many illicit substances. Any consideration of the public health impact of psychoactive substances needs to take into account three important mechanisms of harm: the physical toxicity of the substance, the intoxicating effects it produces, and its potential for creating a syndrome of drug dependence. Policies on substance use should reflect the social and pharmacological complexities of psychoactive substances as well as the relative differences among them.
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40

(Editor), Syed F. Ali, Toshitaka Nabeshima (Editor), and Tomoji Yanagita (Editor), eds. Current Status of Dependence/Abuse Studies: Cellular and Molecular Mechanisms of Drugs of Abuse and Neurotoxicity (Annals of the New York Academy of Sciences). New York Academy of Sciences, 2004.

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41

Drug addiction treatment research: German and American perspectives. Malabar, Fla: Krieger Pub. Co., 1992.

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42

Medjeral-Thomas, Nicholas, Anna Richards, and Matthew C. Pickering. Molecular basis of complement-mediated renal disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0333.

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Abnormal regulation of complement is intimately associated with C3 glomerulopathy and atypical haemolytic uraemic syndrome. Atypical haemolytic uraemic syndrome is characterized by renal thrombotic microangiopathy due to an inability to regulate complement activation along the renal endothelium. The development of thrombosis is critically dependent on the ability to activate C5. Eculizumab, a monoclonal anti-C5 antibody, is an effective therapy for this condition. C3 glomerulopathy refers to glomerular lesions characterized by accumulation of C3 in the absence of immunoglobulin. The prototypic example is dense deposit disease. This condition is associated with impaired regulation of the alternative pathway in plasma. In other subtypes of C3 glomerulopathy, familial studies have identified mutations within the complement factor H-related protein family. Polymorphic variation within this protein family also influences susceptibility to IgA nephropathy. The mechanism underlying these associations remains unknown and is the subject of ongoing research efforts.
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43

Freda, Benjamin J., and Gregory L. Braden. Other toxic acute tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0085.

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Chronic kidney disease (CKD) is often the result of incomplete recovery of renal function from a variety of causes of acute tubulointerstitial injury. Exposure to ethylene glycol, chlorinated hydrocarbons, paraquat, or toxic mushrooms often causes severe acute kidney injury (AKI), leading to chronic tubulointerstitial nephritis (TIN) and CKD, including end-stage renal disease. Ethylene glycol intoxication often leads to chronic TIN and CKD from direct renal tubular toxicity and from interstitial calcium oxalate deposition. Chlorinated hydrocarbon exposure can cause dialysis-dependent AKI, but only rarely causes CKD from interstitial calcium deposition. Paraquat intoxication causes dose-dependent AKI and often Fanconi syndrome in up to 50% of patients, but only 15% of these patients survive, so CKD is rarely seen as a complication. The toxic mushrooms Cortinarius and Amanita phalloides often cause delayed AKI leading to CKD, chronic dialysis, or renal transplantation.
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44

Pillai, Jagan A., and Jeffrey L. Cummings. Conclusions on Neurodegenerative Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0019.

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Neurodegenerative diseases strip an individual of his or her cognitive powers, functional capacity, and autonomy while increasing dependence on others. They are an existential threat to an aging society in its ability to provide a meaningful and high quality of life to all its citizens. The classical view of neurodegenerative disorders (NDDs) emphasized the distinctness of each NDD ,with a definable clinical syndrome of neurological deficits, behavioral changes, and progressive functional decline, underpinned by inexorable neuronal loss that is pathological for the age of the subject. Neurodegenerative Disorders: Unifying Principles has covered each of these themes from multiple expert domains to basic science to clinical therapeutics. This detailed overview emphasizes the work recently accomplished to uncover shared themes across NDDs and further posits questions for the future.
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45

Wurmser, Rachel, and Kirsten Wilkins. Buprenorphine versus Methadone During Pregnancy. Edited by Ish P. Bhalla, Rajesh R. Tampi, Vinod H. Srihari, and Michael E. Hochman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190625085.003.0036.

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This chapter provides a summary of a landmark study in women’s mental health. The study addresses the question of whether buprenorphine is an alternative treatment option to methadone for pregnant women with opioid use disorders. The chapter describes the basics of the study, including funding, location, population studied, study design, interventions, results, and limitations. In short, the study demonstrated that neonates born to mothers with opioid dependence taking buprenorphine during pregnancy required less morphine for the treatment of Neonatal Abstinence Syndrome (NAS), shorter periods of treatment for NAS, and shorter hospital stays compared with neonates born to mothers treated with methadone. The chapter briefly reviews other relevant literature and discusses implications. It concludes with a case to help the reader apply the study to clinical practice.
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46

Rees, Gayla, Benjamin Shapiro, and Matthew Torrington. Integrative Approach to Sedative-Hypnotic Use Disorder. Edited by Shahla J. Modir and George E. Muñoz. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190275334.003.0005.

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Sedatives, hypnotics, and anxiolytics are CNS depressants with GABAergic activity that are potentially habit-forming due to their activity in brain reward pathways. They are central in the drug overdose epidemic with benzodiazepines (BZD) being involved in approximately 31% of all fatal overdoses. There are 4 withdrawal syndromes: High dose minor and major withdrawal, low dose withdrawal, and protracted withdrawal. Benzodiazepines are chemically related positive allosteric modulators of the GABA at the GABA-A receptor. In differential expression 5 different receptor subunits play a role in acute and prolonged withdrawal syndromes. Benzodiazepines have supplanted barbiturates for treatment of anxiety and insomnia due to their wider therapeutic index. Barbiturates can be helpful managing opiate and benazodiazapeine withdrawal. Traditional Chinese Medicine can improve hypnotics-dependent insomnia. Mindfulness-based relapse prevention and yoga may offer benefits but are poorly studied.
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47

Walsh, Richard A. Parkinson’s Disease with an Unusual Tremor. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0009.

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Multiple system atrophy represents a form of atypical parkinsonism that is challenging to manage and results in rapidly progressive disability and dependence in the absence of effective disease-modifying or symptomatic therapies. Two syndromes are recognized, both associated with autonomic dysfunction—MSA-C and MSA-P, with a predominance of parkinsonian and cerebellar features, respectively. Magnetic resonance imaging can assist with an early diagnosis, demonstrating certain features that can be considered diagnostic in the right clinical context. The typical changes described may not be apparent on an initial scan, so it is worth repeating imaging 1 or 2 years later if the clinical features and course are typical of multiple system atrophy.
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48

McAuley, Danny F., and Thelma Rose Craig. Measurement of extravascular lung water in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0140.

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The accumulation of fluid in the interstitium and alveolar space is known as extravascular lung water (EVLW). EVLW is associated with increased morbidity and mortality in critically ill patients and is elevated in patients with cardiogenic pulmonary oedema, acute lung injury (ALI), and the acute respiratory distress syndrome (ARDS). Pulmonary oedema is a consequence of increased pulmonary capillary hydrostatic pressure and/or an increased capillary permeability. The quantity of pulmonary oedema fluid is dependent on the balance of fluid formation and clearance, and this contributes to the overall dynamic net lung fluid balance. Measurement of EVLW is therefore an indirect surrogate measurement of the alveolar epithelial and endothelial damage in ALI/ARDS. The single indicator transpulmonary thermodilution technique is an available bedside technique to measure EVLW.
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49

Widera, Eric, and Rachelle Bernacki. Dementia. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0154.

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Dementia is caused by a variety of disorders that result in a progressive loss of both cognitive and functional abilities. Despite the heterogeneity of disorders, there is a common set of problems that patients and families face living with this syndrome. Symptoms such as pain, eating difficulties, depression, and agitation are all common. As the disease progresses to the advanced stages, the different disorders share a common functional trajectory that includes persistently severe disability with complete dependence on others for basic activities of daily living. Care for individuals with dementia should involve a number of important palliative interventions. Advance care planning should occur early on in the disease process as it is anticipated that an individual will lose capacity to make medical and financial decisions at some point in their illness; specialized programmes for end-of-life care, such as hospice, should be considered for all patients with advanced dementia.
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50

Meyrier, Alain, and Patrick Niaudet. Primary focal segmental glomerulosclerosis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0058_update_001.

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The proportion of cases of primary focal segmental glomerulosclerosis responsive to treatment with corticosteroids is variable and depends on histological type, patient age and duration, and dose of steroid treatment, but overall complete remission rate is estimated at 20–25% in white and Asian patients, and lower in black patients. Partial response dependent on a high dose of steroids is common. Despite anxieties about nephrotoxicity, there may be justification for adding calcineurin inhibitors to control nephrotic syndrome if it is severe. Data for additional agents is not very encouraging. Plasma exchange appears to remove a circulating factor that causes proteinuria in focal segmental glomerulosclerosis, as illustrated by responses to this treatment when proteinuria recurs acutely after kidney transplantation. This is rarely pursued clinically except after transplantation, in advance of severe glomerular injury.
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