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Parker, Philip M., i James N. Parker. Liver damage: A medical dictionary, bibliography, and annotated research guide to Internet references. San Diego, CA: ICON Health Publications, 2004.
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Lee, Kirsten. Young alcoholics: The risk of intellectual impairment, cerebral atrophy, cerebral thrombosis and liver damage. København, Århus, Odense: Fadl's Forlag, 1987.
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Mohamed Hatem Fathi El-Saied Wali. Natural history, factors affecting severity and progression rate of hepatitis c virus (HCV) infection in liver transplanted and non-transplanted patients. Birmingham: University of Birmingham, 2002.
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Maxwell, Paul Ross. Human glutathione-S-transferases: Examination of the iso-enzymes alpha and pi as biomarkers of kidney and liver damage. [S.l: The Author], 2003.
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1925-, Dianzani M. U., Gentilini Paolo i Università di Firenze, red. Chronic liver damage: Proceedings of the Annual Meeting of the Italian National Programme on Liver Cirrhosis, San Miniato, Italy, 11-13 January 1990, with the sponsorship of the University of Florence. Amsterdam: Excerpta Medica, 1990.
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McPherson, Andrew. Reversal of Liver Fibrosis: Preventing Further Liver Damage. Independently Published, 2019.
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Chronic Liver Damage (International congress series). Elsevier, 1990.
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FM, Prof Dr Bilqees, Samreen Mirza i Prof Dr Khatoon N. PARAMPHISTOMUM CERVI INFECTION AND LIVER TISSUE DAMAGE IN BUFFALOES: Trematode infection and liver tissue damage in Buffaloes. VDM Verlag Dr. Müller, 2011.
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Levy, Barry S. Liver Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190662677.003.0030.
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This chapter describes occupational and environmental liver disorders. It describes the types of liver function and types of liver damage, and how these functions and this damage can be assessed. Workers in healthcare and solid waste management are at increased risk hepatitis B virus and hepatitis C virus infections. Occupational exposure to swine is associated with hepatitis E virus infection. More than 100 industrial chemicals can be acutely hepatotoxic in experimental animals or humans. Metabolic reactions may affect the hepatotoxicity of chemicals. Occupational exposure to organic solvents can cause toxic hepatitis. Occupational exposure to vinyl chloride monomer has been causally associated with toxicant-associated fatty liver disease as well as a form of non-cirrhotic portal hypertension. Several agents can cause cancer of the liver or bile ducts. Vinyl chloride monomer is causally associated with angiosacoma of the liver. Arsenic causes liver cancer. Dietary exposure to aflatoxins can cause hepatoceulluar carcinoma.
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van Aerts, René M. M., Tom J. G. Gevers i Joost P. H. Drenth. Management of cystic liver disease. Redaktor Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0311_update_001.
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In a subset of autosomal dominant polycystic kidney disease patients, hepatic cysts dominate the clinical picture. These patients may develop polycystic liver disease, and enlargement of the liver leads to compression of adjacent abdominal and thoracic organs. The main risk factors for growth of liver cysts are female sex, exogenous oestrogen use, multiple pregnancies, and severity of renal disease. Treatment is only indicated in those with symptoms, and choice of treatment depends on total liver volume, size, and location of the liver cysts. Current radiological and surgical therapies include aspiration-sclerotherapy, fenestration, segmental hepatic resection, and liver transplantation. They all are palliative in nature and are partially effective and have non-negligible morbidity and mortality. Somatostatin analogues are still in development for polycystic liver disease.
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Publications, ICON Health. Liver Damage - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.
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Keshav, Satish, i Alexandra Kent. Alcoholic liver disease. Redaktorzy Patrick Davey i David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0211.
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Alcoholic liver disease develops in excessive drinkers and can manifest in three forms: alcoholic fatty liver (steatosis; >80%), alcoholic hepatitis (10%–35%), and cirrhosis (10%). The more alcohol consumed, the greater the risk of alcoholic liver disease, although other factors may also be involved. Alcohol can cause significant damage without producing any symptoms, and many patients will only have liver dysfunction detected on routine blood tests. Many patients report non-specific symptoms, such as anorexia, morning nausea, diarrhoea, and vague right upper quadrant abdominal pain. The underlying pathogenesis of alcohol-induced injury is not fully understood but is thought to involve various mechanisms. This chapter discusses alcoholic liver disease, focusing on its etiology, symptoms, demographics, natural history, complications, diagnosis, prognosis, and treatment.
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Brooke, Susan. Battle Against Liver Cirrhosis: The First Book to Provide You with a Detailed Program for Reversing Liver Damage Through Optimal Nutrition. Independently Published, 2019.
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Beattie, R. Mark, Anil Dhawan i John W.L. Puntis. Drug-induced liver injury. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569862.003.0052.
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Epidemiology 374Pathophysiology 374Herbal drugs and alternative medicines 377Risk factors 377Clinical features 378Investigation 379Management 380Drug induced liver injury (DILI) is a variable and complex diagnosis of exclusion, as it can present in different ways. Because of the liver's central role in drug metabolism, most prescribed drugs can cause liver injury. Liver damage can occur through drugs in a predictable, intrinsic dose-related way or in a unpredictable, idiosyncratic dose-unrelated fashion....
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Claire Maureen Barbara.* Holloway. Sinusoidal lining cell damage: the critical injury in cold preservation of liver allografts in the rat. 1991.
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Cobb, Shannon Idell. Effect of supplemental zinc as zinc oxide and zinc methionine on liver vitamin A, interleukin-2 activity, and severity of staphylococcus mastitis in mice. 1985.
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Vinod, Nikhra. COVID-19 and Long Covid: Organs Damage and Dysfunctions, and Implications for Clinical Course. Heighten Science Publications Inc., 2021. http://dx.doi.org/10.29328/ebook1005.
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Like any other infectious disease, the prognosis of COVID-19 is influenced by infecting agent, the SARS-CoV-2 virus load and the extent of organs affliction and damage. COVID-19 having a propensity for multiorgan involvement carries an adverse prognosis during the clinical course as well as later during the post-recovery period persisting as Long Covid. The direct cytopathic effects of SARS-CoV-2 virus and the erratic and hyper-inflammatory response lead to tissue injury in various organs coupled with physiological dysfunctions and complications. In fact, the multi-system manifestations of COVID-19 are caused by a combination of specific host defence responses with associated inflammatory activity and vascular involvement with coagulopathy and a distinct propensity to develop thromboembolic complications. Simultaneously, comorbidities such as diabetes, hypertension and cardiovascular diseases influence the disease severity and mortality.
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The alpha lipoic acid breakthrough: The superb antioxidant that may slow aging, repair liver damage, and reduce the risk of cancer, heart disease, and diabetes. Rocklin, Calif: Prima Health, 1998.
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Glasper, Edward Alan, Gillian McEwing i Jim Richardson, red. Nursing care of the sick child. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780198569572.003.0006.
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Management of procedural pain 104Pain assessment tools 106Pre-operative care 108Procedure-related pain is a major source of distress to the child and family. Poorly managed pain will result in the child continuing to display high levels of distress in future procedures. To a child there is no such thing as a minor procedure. Often the extent of tissue damage correlates poorly with the severity of pain that the child experiences....
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Nauta, Joske, Willem van Mechelen i Evert ALM Verhagen. Epidemiology and prevention of sports injuries. Redaktorzy Neil Armstrong i Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0040.
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Although sports injuries in children are common, prevention of these injuries is paramount. In order to set out effective prevention programmes, epidemiological studies need to be conducted on incidence, severity, and aetiology of sports injuries. Furthermore, the effectiveness of a preventive measure must be assessed, and the eventual implementation of a programme closely evaluated. When conducting epidemiological studies in sports injuries the injury definition used can have a large impact on the outcome, especially as the aetiology of sports injuries is highly multi-causal and recursive. In addition to distinguishing between ‘sports injury’, ‘sports injury incidence’ and ‘sports participation’, the severity of the injury must be defined by taking six indices into consideration: nature of sports injuries, duration and nature of treatment, sports time loss, working/school time loss, permanent damage, and costs of sports injuries.
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Hooper, Amanda J., i John R. Burnett. Abetalipoproteinemia and Hypobetalipoproteinemia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0037.
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Abetalipoproteinemia and hypobetalipoproteinemia are characterized by marked hypocholesterolemia and are classified depending on the lipid biochemical phenotype, gene involved, and mode of inheritance of the condition together with the severity of the mutation or mutations present. These disorders may or may not be associated with clinical manifestations such as fat malabsorption, growth failure, fat-soluble vitamin deficiency, fatty liver disease, and neuro-ophthalmological dysfunction. Early diagnosis and treatment with dietary modification and replacement of fat-soluble vitamins can prevent the clinical complications.
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Trzcinka, Agnieszka. Aspiration Pneumonitis. Redaktorzy Matthew D. McEvoy i Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0016.
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Aspiration pneumonitis during the perioperative period is a serious complication and involves passage of sterile gastric contents into the airway resulting in alveolar damage. The mechanism of aspiration pneumonitis is characterized by a significant inflammatory reaction. The risk of aspiration is highest during anesthesia induction, but it is also present during emergence and extubation. The risk factors include delayed gastric emptying (gastritis, pain, pregnancy, obesity, elevated intracranial pressure), emergency surgery, upper abdominal surgery, and difficulty securing the airway. Anesthesiologists should focus on prevention of pulmonary aspiration with consideration of the patient’s NPO status and risk factors when planning anesthesia induction and emergence. If aspiration of gastric contents occurs, the patient may exhibit a variety of symptoms, with severity based on the volume and pH of the aspirate. Subsequently, patients with observed or suspected aspiration need supportive treatment that varies depending on the severity of symptoms.
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Martin, David, i Junzheng Wu. Cystic Fibrosis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199764495.003.0021.
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Cystic fibrosis (CF) is an inherited chronic disease that affects about 30,000 children and adults in the United States and 70,000 worldwide. CF is the most common fatal inherited disorder affecting Caucasians in the United States. While its presentation can vary in severity, the most common clinical manifestations are progressive lung damage and chronic digestive problems due to exocrine gland dysfunction and the production of thick viscous mucus. Careful perioperative management is important to avoid respiratory complications.
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Donaghy, Michael. Focal peripheral neuropathy. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0487.
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Some causes of focal peripheral nerve damage are self-evident, such as involvement at sites of trauma, tissue necrosis, infiltration by tumour, or damage by radiotherapy. Focal compressive and entrapment neuropathies are particularly valuable to identify in civilian practice, since recovery may follow relief of the compression. Leprosy is a common global cause of focal neuropathy, which involves prominent loss of pain sensation with secondary acromutilation, and requires early antibiotic treatment. Mononeuritis multiplex due to vasculitis requires prompt diagnosis and immunosuppressive treatment to limit the severity and extent of peripheral nerve damage. Various other medical conditions, both inherited and acquired, can present with focal neuropathy rather than polyneuropathy, the most common of which are diabetes mellitus and hereditary liability to pressure palsies. A purely motor focal presentation should raise the question of multifocal motor neuropathy with conduction block, which usually responds well to high-dose intravenous immunoglobulin infusions.
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Lories, Rik. Mechanisms of bone destruction and proliferation in psoriatic arthritis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0008.
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Psoriatic arthritis is a chronic inflammatory joint disease that can affect both the peripheral and axial skeleton. The clinical presentation of psoriatic arthritis is very heterogeneous and different subforms have been described. Structural damage to the joint is a feared complication of psoriatic arthritis. The severity of joint inflammation and subsequent damage can range from mild to extreme. Over the last decade, insights into the molecular and cellular mechanisms that underlie the skeletal changes in psoriatic arthritis have gradually increased although translational validation of concepts using patient-derived materials still lags behind. Current treatment strategies directed against key mediators of inflammation appear to have good effects on joint destruction, but their short and long-term impact on new bone formation and ankylosis is still unclear. The identification of the role that key growth factors play in the latter process identifies new opportunities for therapeutic interventions.
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D’Haese, Patrick C., Benjamin A. Vervaet i Anja Verhulst. Heavy metal-induced tubulointerstitial nephritis. Redaktor Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0088.
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Environmental and occupational exposure to heavy metals should be considered an important health hazard, even more so since evidence has been provided in recent literature for toxic effects occurring even at low levels. The kidney is highly vulnerable to metal toxicity and the extent of renal damage depends on the nature, dose, route, and duration of exposure. Both acute and chronic intoxication have been demonstrated to cause kidney injury, with various levels of severity, ranging from tubular dysfunctions to severe chronic kidney disease. The epidemiology of heavy metals poisoning, their renal handling, pathophysiological mechanisms of renal toxicity, diagnosis, and monitoring, as well as therapeutic aspects are dealt with. The metals discussed include lead, cadmium, mercury, uranium, arsenic, and chromium.
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Robert, Philippe, Elsa Leone, Hélène Amieva i David Renaud. Managing behavioural and psychological symptoms in Alzheimer’s disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198779803.003.0009.
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This chapter focuses on the behavioural and psychological symptoms of Alzheimer's disease and the different approaches clinicians can take in their treatment of the condition. The behavioural and psychological symptoms are defined as primary manifestations of cerebral dysfunction, and appear specifically as a result of damage to a system or circuit such as the limbic system or the cortico-subcortical circuits. During the progression of Alzheimer’s disease, the presence of at least one BPSD is common and can vary, depending especially on the severity of the dementia-related syndrome at the time of diagnosis. Management of BPSD should preferentially be based on non-pharmacologic approaches first. Pharmacologic treatments should constitute second line treatment and are to be prescribed only after assessment of the individual risk:benefit ratio.
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Devlin, Hugh, i Rebecca Craven. Diabetes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198759782.003.0007.
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Diabetes in relation to dentistry is the topic of this chapter. The incidence of diabetes is increasingly rapidly, hand-in-hand with the increase in obesity. Obesity predisposes patients to an increased insulin resistance, i.e. reduces their ability to increase the glucose transport into adipocytes, muscle, and liver cells. The pancreas responds by producing more insulin but when it can no longer produce enough to overcome the insulin resistance, the blood glucose rises. Diabetes is characterized by raised blood glucose. We describe the devastating long-term effects of diabetes, in particular the microvascular and macrovascular medical complications. The dental complications include an increased severity of periodontal disease, oral candidiasis, and dry mouth but in those who are poorly controlled the impaired defence mechanisms can lead to severe head and neck infections and osteomyelitis. A final summary lists the important clinical recommendations for treatment of diabetic patients.
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Orellana, Renán A., i Jorge A. Coss-Bu. Nutrition and Gastrointestinal Emergencies. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199918027.003.0014.
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Appropriate nutrition must be tailored to the specific needs of individual patients. Needs depend on the child’s baseline nutritional status, the severity of disease, and specific organ dysfunction. Enteral nutrition is preferable whenever possible. Parenteral nutrition may be necessary when efforts to supply adequate nutrition enterally are contraindicated or unsuccessful. Patients with symptoms of acute abdomen require prompt recognition of surgical and nonsurgical disorders. Upper gastrointestinal hemorrhage may require transfusion of blood products, vasoactive drug infusion to minimize ongoing losses, and endoscopy following stabilization. Pancreatitis typically requires an orogastric/nasogastric tube for decompression, aggressive pain management, and radiological evaluations. Abdominal compartment syndrome needs to be recognized promptly to avoid further injury. Acute liver failure commonly leads to multiorgan system dysfunction and death. Specific therapy is available only in a minority of cases, and outcome depends on excellent supportive care, prompt evaluation by a pediatric gastroenterologist, and referral to a transplant center.
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Thomas, David F. M. Vesicoureteric reflux. Redaktor David F. M. Thomas. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0115.
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The term vesicoureteric reflux (VUR) describes the retrograde flow of urine from the bladder into the upper urinary tract. VUR is not a disease entity in its own right. Nevertheless, it has the potential to cause significant morbidity by preventing effective emptying of the urinary tract and by facilitating the transport of bacteria into the upper tract and renal parenchyma. Mechanisms of renal damage associated with VUR include pyelonephritic scarring and congenital dysplasia or hypoplasia. The long-term complications of pyelonephritic scarring may include hypertension, renal failure, and an increased risk of complications during pregnancy. VUR of mild or moderate severity is best managed conservatively and surgical intervention is generally reserved for failed medical management and high grade or complex VUR. Although the introduction of endoscopic correction has revolutionized surgical management, there remains a role for open surgery for the correction of higher grades of reflux.
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Kortgen, Andreas, i Michael Bauer. Hepatic function in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0175.
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The liver with its parenchymal and non-parenchymal cells plays a key role in the organism with manifold functions of metabolism, synthesis, detoxification, excretion, and host response. This requires a portfolio of different tests to obtain an overview of hepatic function. In the critically ill hepatic dysfunction is common and potentially leading to extrahepatic organ dysfunctions culminating in multi-organ failure. Conventional laboratory measures are used to evaluate hepatocellular damage, cholestasis, or synthesis. They provide valuable (differential) diagnostic data and can yield prognostic information in chronic liver diseases, especially when used in scoring systems such as the ‘model for end-stage liver disease’. However, they have short-comings in the critically ill in assessing rapid changes in hepatic function and liver blood flow. In contrast, dynamic quantitative liver function tests measure current liver function with respect to the ability to eliminate and/or metabolize a specific substance. In addition, they are dependent on sinusoidal blood flow. Liver function tests have prognostic significance in the critically ill and may be used to guide therapy.
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Hooper, Timothy, i David Lockey. Assessment and management of ballistic trauma. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0340.
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The severity of ballistic trauma is dependent upon multiple factors including bullet type, velocity, tissue type penetrated, and energy transfer. Patient management needs a considered approach with careful assessment, appropriate imaging and directed treatment of the wounds found. Triage, treatment and transport form the framework of effective prehospital care. In the emergency department a rapid primary survey is essential to reveal any injuries that need immediate intervention. The decision to operate and nature of surgery is determined by the patient’s suspected injuries, physiological condition and expertise available with some patients benefiting from damage control resuscitation and surgery. Indications for intensive care admission include the need for ongoing organ support, cardiovascular instability, and injuries that require close observation. Attention should be paid to cardiovascular status, coagulation, nutrition, thromboprophylaxis, infective issues, and management of specific injuries. Patients may require protracted hospital stays and extensive reconstructive surgery. The psychological and social impact of these injuries should not be underestimated.
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Speed, Cathy. Pharmacological pain management in sports injuries. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199533909.003.0015.
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The perception of pain is a biological mechanism which warns that damage has occurred and protects against further damage, allowing healing to occur. Acute pain often acts as an indicator of injury severity and progression or healing. The same may apply in some with chronic injuries, but in others pain may not correlate with tissue damage and/or may not be a sign that the tissue needs to be protected from mechanical stress. The management of most sports injuries involves early mobilization where possible, and pain management in the treatment of these injuries is important to allow rehabilitation to proceed and to ease distress. Modalities play an important role in this respect, and are discussed elsewhere (Chapter 2.4). Injection therapies are also discussed elsewhere (Chapter 2.6). Thorough counselling of the athlete is a priority to ensure that he/she understands what the pain represents, as this will be likely to affect compliance. For example, a degree of pain during eccentric exercise protocols in the rehabilitation of chronic tendinopathies would be anticipated, and would not contraindicate continuation of a set programme. In contrast, when an athlete is returning to sporting activities after injury, pain that is experienced during the activity would not be acceptable, and the athlete is also advised during this period that conclusions as to the tissue’s reaction to activity should not be drawn until the day after the training session. Athletes should also be taught appropriate self-help strategies to manage their pain and when this involves medication, how and when to take it. Principles for the use of medications in pain management are given in ...
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Burton, Derek, i Margaret Burton. Metabolism, homeostasis and growth. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198785552.003.0007.
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Metabolism consists of the sum of anabolism (construction) and catabolism (destruction) with the release of energy, and achieving a fairly constant internal environment (homeostasis). The aquatic external environment favours differences from mammalian pathways of excretion and requires osmoregulatory adjustments for fresh water and seawater though some taxa, notably marine elasmobranchs, avoid osmoregulatory problems by retaining osmotically active substances such as urea, and molecules protecting tissues from urea damage. Ion regulation may occur through chloride cells of the gills. Most fish are not temperature regulators but a few are regional heterotherms, conserving heat internally. The liver has many roles in metabolism, including in some fish the synthesis of antifreeze seasonally. Maturing females synthesize yolk proteins in the liver. Energy storage may include the liver and, surprisingly, white muscle. Fish growth can be indeterminate and highly variable, with very short (annual) life cycles or extremely long cycles with late and/or intermittent reproduction.
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Lavand’homme, Patricia, i Fabienne Roelants. Persistent pain after caesarean delivery and vaginal birth. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0025.
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Persistent pain after childbirth has recently received a lot of attention as potentially many women could be affected. Several pain syndromes including pelvic girdle pain, low back pain, and headaches occur during the pregnancy and can persist after delivery. The prevalence of chronic pain directly related to the delivery, at 6 months and later after childbirth, is however very low (< 2%) compared to chronic pain which occurs after other types of tissue trauma as in common surgical procedures. Acute pain is a major risk factor in the development of persistent pain after surgery and trauma. After childbirth, the severity of acute pain, independent of the mode of delivery (i.e. the degree of tissue damage) only predicts an increased risk of persistent pain (a 2.5-fold increase) at 2 months but not later. An individual’s pain response seems to be the most relevant factor in the development of persistent pain. In retrospective studies, patient-specific risk factors, such as a pre-existing chronic pain condition or pain elsewhere, were predictive factors. In prospective studies, the low incidence of persistent pain at 6 and 12 months make the analysis of risk factors unreliable.
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Nolan, Jerry P., i Michael J. A. Parr. Management after resuscitation from cardiac arrest. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0066.
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Systemic ischaemia during cardiac arrest and the reperfusion response after return of spontaneous circulation (ROSC) cause the post-cardiac arrest syndrome (PCAS). The severity and duration of this syndrome is determined by the cause and duration of cardiac arrest, quality of resuscitation, and interventions after ROSC. Four key clinical components are recognized—post-cardiac arrest brain injury, myocardial dysfunction, other organ ischaemia/reperfusion (e.g. liver, kidney), and potential persistence of the precipitating pathology causing the cardiac arrest. The interventions applied after ROSC impact significantly on the quality of survival. All components of the PCAS need to be addressed if outcome is to be optimized; treatment should start immediately after ROSC. An ‘ABCDE’ (Airway, Breathing, Circulation, Disability, Exposure) systems approach is used to identify and treat physiological abnormalities and organ injury. All survivors of out-of-hospital cardiac arrest should be considered for urgent coronary angiography unless the cause of cardiac arrest is clearly non-cardiac or continued treatment is considered futile. Targeted temperature management (mild hypothermia and avoidance of hyperthermia) should be considered for those patients who remain comatose after ROSC. If targeted temperature management has been used, early prognostication on outcome is unreliable and should be delayed until 3 days after return to normothermia; it should not rely on just one modality.
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Scott, David L. Outcomes. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0029.
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Outcomes evaluate the impact of disease. In rheumatology they span measures of disease activity, end-organ damage, and quality of life. Some outcomes are categorical, such as the presence or absence of remission. Other outcomes involve extended numeric scales such as joint counts, radiographic scores, and quality of life measures. Outcomes can be measured in the short term—weeks and months—or over years and decades. Short-term outcomes, though readily related to treatment, may have less relevance for patients. Clinical trials focus on short-term outcomes whereas observational studies explore longer-term outcomes. The matrix of rheumatic disease outcomes is exemplified by rheumatoid arthritis. Its outcomes span disease activity assessments like joint counts, damage assessed by erosive scores, quality of life evaluated by disease-specific measures like the Health Assessment Questionnaire (HAQ) or generic measures like the Short Form 36 (SF-36), overall assessments like remission, and end result such as joint replacement or death. Outcome measures are used to capture the impact of treating rheumatic diseases, and are influenced by both disease severity and the effectiveness of treatment. However, they are also influenced by a range of confounding factors. Demographic factors like age, gender, and ethnicity can all have crucial impacts. Deprivation is important, as poverty invariably worsens outcomes. Finally, comorbidities affect outcomes and patients with multiple comorbid conditions usually have worse quality of life with poorer outcomes for all diseases. These multiple confounding factors mean comparing outcomes across units without adjustment will invariably show major differences.
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Scott, David L. Outcomes. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0029_update_001.
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Outcomes evaluate the impact of disease. In rheumatology they span measures of disease activity, end-organ damage, and quality of life. Some outcomes are categorical, such as the presence or absence of remission. Other outcomes involve extended numeric scales such as joint counts, radiographic scores, and quality of life measures. Outcomes can be measured in the short term—weeks and months—or over years and decades. Short-term outcomes, though readily related to treatment, may have less relevance for patients. Clinical trials focus on short-term outcomes whereas observational studies explore longer-term outcomes. The matrix of rheumatic disease outcomes is exemplified by rheumatoid arthritis. Its outcomes span disease activity assessments like joint counts, damage assessed by erosive scores, quality of life evaluated by disease-specific measures like the Health Assessment Questionnaire (HAQ) or generic measures like the Short Form 36 (SF-36), overall assessments like remission, and end result such as joint replacement or death. Outcome measures are used to capture the impact of treating rheumatic diseases, and are influenced by both disease severity and the effectiveness of treatment. However, they are also influenced by a range of confounding factors. Demographic factors like age, gender, and ethnicity can all have crucial impacts. Deprivation is important, as poverty invariably worsens outcomes. Finally, comorbidities affect outcomes and patients with multiple comorbid conditions usually have worse quality of life with poorer outcomes for all diseases. These multiple confounding factors mean comparing outcomes across units without adjustment will invariably show major differences.
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Perez-Ruiz, Fernando, Irati Urionagüena i Sandra P. Chinchilla. Long-term management of gout. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0046.
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Long-term management of gout comprises several aspects. Although in the short term, prophylaxis and treatment of acute episodes of inflammation are of great importance, the milestone for the long-term management of gout is targeted, sustained, and long-term control of hyperuricaemia. Treating to target subsaturating serum urate (SUA) levels, which may be initially dependent on the severity of the disease in the individual patient, is associated with a progressive reduction to no episodes of acute inflammation, regression and disappearance of subcutaneous and articular monosodium urate deposits and associated chronic inflammation, and improvement in patient-reported, health-related quality of life. Early and effective urate-lowering treatment to target levels will also prevent the development of structural damage. Urate-lowering treatment includes any measure intending to reduce SUA levels to target: lifestyle changes, modifications of concomitant medications favouring hyperuricaemia, and urate-lowering medications (ULMs). Availability of ULMs is variable worldwide, and prescription should be judicious, according to approved labels, and always considering associated health conditions and concomitant medications. Effectiveness and safety should be periodically monitored. Long-term treatment of gout still remains suboptimal in the twenty-first century. As practising clinicians, we cannot afford to neglect a ‘curable disease’.
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Bernal, William, i Alberto Quaglia. Normal physiology of the hepatic system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0173.
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Hepatic blood inflow is from two sources—high-pressure, well-oxygenated blood from the hepatic artery and low-pressure, partly deoxygenated blood from the portal vein. Hepatic inflow is maintained by variation in flows in these two systems. Although less than a third of total blood flow is delivered via the hepatic artery, it is responsible for the majority of hepatic oxygen supply. The liver can be subdivided into eight functionally independent segments, each with its own vascular inflow, outflow, and biliary drainage. The tri-dimensional hepatic microstructure is complex with geographic heterogeneity of hepatocellular function, and resistance to toxic, ischaemic, and metabolic damage. The liver is central to a wide variety of synthetic, metabolic, and detoxification functions. The overall balance of activity may be altered rapidly in response to systemic inflammatory stimuli.
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Raggi, Paolo, i Luis D’Marco. Imaging for detection of vascular disease in chronic kidney disease patients. Redaktor David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0116.
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The well-known severity of cardiovascular disease in patients suffering from chronic kidney disease (CKD) requires an accurate risk stratification of these patients in several clinical situations. Imaging has been used successfully for such purpose in the general population and it has demonstrated excellent potential among CKD patients as well. Two main forms of arterial pathology develop in patients with CKD: atherosclerosis, with accumulation of inflammatory cells, lipids, fibrous tissue and calcium in the subintimal space, and arteriosclerosis. The latter is characterized by accumulation of deposits of hydroxyapatite and amorphous calcium crystals in the muscular media of the vessel wall, and is believed to be more closely associated with alterations of mineral metabolism than with traditional atherosclerosis risk factors. The result is the development of what appears to be premature arterial ageing, with loss of elastic properties, increased stiffness, and increased overall fragility of the arterial system. Despite intensifying research and increasing awareness of these issues, the underlying pathophysiology of the aggressive vasculopathy of CKD remains largely unknown. As a consequence, there are currently very limited pathways to prevent progression of vascular damage in CKD. The indications, strengths and weaknesses of several imaging modalities employed to evaluate vascular disease in CKD are described, focusing on coronary arterial circulation and the peripheral arteries, with the exclusion of the intracranial arteries.
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McDougall, Jason J., i Joel A. Vilensky. The innervation of the joint and its role in osteoarthritis pain. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0007.
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Diarthrodial joints possess an extensive network of sensory and sympathetic nerve fibres whose physiological functions are varied and complex. Nerves are primarily located in the synovium but also innervate the subchondral bone, the outer third of menisci, and the superficial surface of tendons and ligaments. Large-diameter, myelinated neurons are involved in joint position sense while small-diameter neurons with thin or no myelin typically sense pain. The small-diameter nerves in conjunction with sympathetic fibres control synovial blood flow and maintain joint homeostasis. In patients with osteoarthritis (OA), the sensory nerves become sensitized and increase their firing rate in response to normal movement. This peripheral sensitization is mediated by numerous algogenic agents released into the OA knee including neuropeptides, eicosanoids, and proteinases. A portion of joint afferents fire in the absence of mechanical stimuli and encode pain at rest. Interestingly, the firing rate of joint afferents does not correlate with OA severity, indicating that pain is a poor predictor of joint pathology. Evidence is accumulating to suggest that a subpopulation of OA patients who are unresponsive to classical non-steroidal anti-inflammatory drugs may be suffering from neuropathic pain in which there is damage to the joint nerves themselves. Better understanding of the biology of joint nerves could help in the development of patient-targeted therapies to alleviate OA pain and inflammation.
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Gapstur, Susan M., i Philip John Brooks. Alcohol and Cancer Risk. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0012.
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In 2010, alcoholic beverage consumption caused an estimated 3.3 million deaths worldwide, and contributed to injuries, violence, liver cirrhosis, social disruption and at least seven different types of cancer. The International Agency for Research on Cancer (IARC) classifies exposure to both ethanol in alcoholic beverages and acetaldehyde, the primary metabolite of ethanol, as carcinogenic to humans (Group 1) based on “sufficient” evidence that alcoholic beverage consumption is causally related to cancers of the oral cavity, pharynx, larynx, esophagus, liver, colorectum and female breast. The biologic mechanisms by which alcohol and its primary metabolite acetaldehyde affect cancer risk appear to vary across anatomic sites. Broadly, these mechanisms involve DNA and protein damage from acetaldehyde and oxidative stress, nutritional malabsorption and metabolic effects, and for breast cancer, increased estrogen levels. The World Health Organization has increased global surveillance of alcohol consumption and encourages national efforts to apply evidence-based policies to reduce consumption.
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Keshav, Satish, i Palak Trivedi. Viral hepatitis. Redaktorzy Patrick Davey i David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0212.
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Hepatitis means ‘inflammation of the liver’ and is manifest with symptoms that include malaise, anorexia, fever, flu-like symptoms, and pain in the right upper quadrant of the abdomen, with the pain being caused by swelling of the liver and its capsule. Elevations in circulating hepatic enzymes, particularly aspartate transaminase and alanine transaminase, are common, with jaundice occurring some time after the onset of other symptoms and signs. There are five viruses that primarily cause viral hepatitis: hepatitis A, B, C, D, and E viruses, abbreviated HAV, HBV, HCV, HDV, and HEV, respectively. These viruses are all hepatotrophic, in that the liver is the primary site of infection. HAV, HBV, and HEV are usually acute, self-limiting infections that may, nonetheless, cause morbidity and, in the case of HEV, fatality. However, HBV and, more so, HCV can cause chronic carriage of the virus over many years, as well as the development of chronic hepatitis. HDV is only pathogenic in conjunction with HBV. After recovery from acute infection with HAV, individuals have long-lasting immunity against further infection. The same holds true for the majority of individuals with acute HBV infection. There seems to be little natural immunity to HCV infection, and a significant proportion of cases result in chronic hepatitis. Immunity to HEV is not long-lasting, and repeated infections are possible. Many other viruses can cause hepatitis, of which cytomegalovirus, herpes simplex virus, Epstein–Barr virus, and flaviviruses such as dengue and yellow fever are the most important. The liver, however, is not their primary site of replication or cellular damage.
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Fox, Susan H. Seizures and Shakes. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0017.
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Wilson’s disease is an autosomal recessive, treatable heredodegenerative disorder characterized by excessive deposition of copper in the liver, brain, and other tissues including the kidneys, pancreas, and joints. Early recognition of the disorder, which can present with a variety of movement disorders and neuropsychiatric phenomena, is critical to avoid irreversible end organ damage through the initiation of copper chelating agents. Diagnosis relies first on demonstrating evidence of brain iron deposition on magnetic resonance imaging of brain and elevated urinary copper excretion in the appropriate clinical context. Genetic testing for mutations in the ATP7B gene will identify a mutation in up to 90% of cases.
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Johnson, Steven B. Pathophysiology and management of abdominal injury. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0334.
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Abdominal injuries are common following blunt and penetrating trauma. They can result in a spectrum of severity from benign to potentially life-threatening conditions. Soon after injury, haemorrhage is the predominant concern, and leading cause of morbidity and mortality. Active haemorrhage resulting in shock requires emergent operative intervention and aggressive haemostatic resuscitation. However haemodynamically-stable patients benefit from non-operative management of solid organ injuries with or without angiographic embolization. Sepsis usually occurs as a result of intra-abdominal infections from missed bowel perforations or anastomotic leaks. Sterile systemic hyperinflammatory conditions can result from major hepatic necrosis or pancreatic injuries, and closely mimic infectious conditions. Damage control surgery is a valuable adjunct to the operative management of major abdominal trauma. This concept recognizes that the time and procedures required to perform definitive operative repair may be detrimental when physiological derangements are excessive. By limiting operations to controlling haemorrhage and enteric contamination, further deterioration, and the ‘vicious bloody cycle of trauma’ can be avoided. The operative and critical care management of patients with abdominal trauma should be closely integrated to correct physiological derangements with rapid stabilization and reversal of hypoperfusion. Abdominal compartment syndrome, characterized by intra-abdominal hypertension and resultant remote organ dysfunction, is a risk in patients undergoing high-volume fluid resuscitation. Emergent decompressive laparotomy is indicated in patients with abdominal compartment syndrome and results in rapid reversal of physiological compromise. Paramount to optimal management of abdominal injuries is the close integration of operative and critical care approaches.
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Eckert, J., P. Deplazes i P. Kern. Alveolar echinococcosis (Echinococcus multilocularis). Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0061.
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In this chapter three forms of echinococcosis in humans are described that are caused by a larval stage (metacestode) of Echinococcus multilocularis Leuckart, 1863, Echinococcus oligarthrus (Diesing, 1863) or Echinococcus vogeli Rausch and Bernstein, 1972. E. multilocularis is the causative agent of alveolar echinococcosis (AE). In the human host the metacestode of E. multilocularis behaves like a malignant tumour, characterized by infiltrative proliferation and the potential to induce serious disease. The liver is nearly exclusively the primary site of metacestode development, but metastases may by formed in adjacent and distant organs. Typically AE exhibits a chronic progressive clinical course, which finally leads to death in up to 90% of untreated patients within 10 years after diagnosis. An undefined proportion of cases are abortive with inactivation of the parasite. Evidence has accumulated in recent years that anti-parasitic therapy with benzimidazoles (albendazole or mebendazole) over many years or lifelong, if necessary combined with interventional procedures, can inhibit disease progression and improve or stabilse the patient’s clinical condition. Radical surgery in an early stage of the infection combined with anti-parasitic therapy for two years may lead to cure. The introduction of benzimidazole therapy of AE (1977), combined with improved diagnostic and surgical procedures, has resulted in significantly increased life-expectancies of adequately treated AE patients. In highly endemic areas ultrasound population screening (partially combinated with antibody detection) has been successfully used for early detection of AE cases. Countrywide annual AE incidence rates are mostly low at approximately < 0.1 to 2.0 per 100,000 inhabitants, but they can be much higher locally. Furthermore, there are indications of emerging case numbers in some areas of Europe and Asia. In spite of relatively low case numbers, AE is a significant disease due to its severity and high costs of treatment (median costs of approximately 145,800 per case).
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Hughes, Jeremy. Proteinuria as a direct cause of progression. Redaktor David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0137.
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Proximal tubular cells reabsorb any filtered proteins during health via cell surface receptors such as megalin and cubulin so that very low levels of protein are present in the excreted urine. Significant proteinuria is a common finding in patients with many renal diseases. Proteinuria is a marker of glomerular damage and podocyte loss and injury in particular. The degree of proteinuria at presentation or during the course of the disease correlates with long-term outcome in many renal diseases. Proteinuria per se may be nephrotoxic and thus directly relevant to the progression of renal disease rather than simply acting as a marker of the severity of glomerular injury and podocytes loss. Seminal studies used the atypical renal anatomy of the axolotl to instill proteins directly into the tubular lumen without requiring passage through the glomerulus. This indicated that tubular protein could be cytotoxic and induce interstitial inflammation and fibrosis in the peritubular region. Cell culture studies demonstrate that exposure to proteins results in proximal tubular cell activation and the production of pro-inflammatory and pro-fibrotic mediators. Proximal tubular cell death occurred in some studies reinforcing the potential of protein to exert cytotoxic effects via oxidative stress or endoplasmic reticulum stress. Analysis of renal biopsy material from both experimental studies using models of proteinuric disease or patients with various proteinuric diseases provided evidence of activation of transcription factors and production of chemokines and pro-inflammatory mediators by proximal tubular cells. These data strongly suggest that although proteinuria is the result of glomerular disease it also represents an important cause of progression in patients with chronic kidney disease associated with proteinuria.
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Lopez, Berenice, i Patrick J. Twomey. Biochemical investigation of rheumatic diseases. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0062.
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It is important for rheumatologists to have an understanding of biochemical tests including an awareness of their limitations. The biological variability of an analyte both within and between individuals, the limitations of the measurement technology, the sensitivity of laboratory internal quality control and external quality assurance procedures, as well as interlaboratory variations in practices including sample collection procedures, may all impact on the interpretation of a result. Biochemical tests are often requested to monitor organ-specific dysfunction arising as an adverse consequence of pharmacotherapy or as a component of a systemic rheumatic disease, although dysfunction may also reflect infection or coincidental pathology. Patients with rheumatic diseases are at high risk of renal and hepatic disease. Serum creatinine and its derivative estimated glomerular filtration rate (eGFR) are the most readily available surrogate markers of GFR and are used to assess renal impairment and monitor its course. However, the use of creatinine alone lacks sensitivity and a substantial loss of function must occur before creatinine levels are increased. Additional biochemical screening for kidney damage can be performed by assessment of glomerular integrity, including proteinuria or albuminuria and haematuria. A wide spectrum of rheumatic diseases can affect the liver with various degrees of involvement and hepatic pathology. These often present with cholestatic or hepatitic biochemical profiles. The medical management of rheumatic diseases also involves medications that are hepatotoxic, and routine monitoring of liver function is recommended. This approach is not problem-free and may be improved by quantitative determinations of non-invasive markers of liver fibrosis in the future. Together with imaging techniques, biochemical tests play an important role in the assessment and differential diagnosis of metabolic bone disease.
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Bhopal, Raj S. Epidemic of Cardiovascular Disease and Diabetes. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198833246.001.0001.
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Coronary heart disease (CHD) and stroke, collectively cardiovascular disease (CVD), are caused by narrowing and blockage of the arteries supplying the heart and brain, respectively. In type 2 diabetes (DM2) insulin is insufficient to maintain normal blood glucose. South Asians have high susceptibility to these diseases. Drawing upon the scientific literature and discussions with 22 internationally recognized scholars, this book focuses on causal explanations and their implications for prevention and research. Genetically based hypotheses are considered together with the developmental origins of health and disease (DOHAD) family of hypotheses. The book then considers how CHD, stroke, and DM2 are closely linked to rising affluence and the accompanying changes in life-expectancy and lifestyles. The established causal factors are shown to be insufficient, though necessary, parts of a convincing explanation for the excess of DM2 and CVD in South Asians. In identifying new explanations, this book emphasizes glycation of tissues, possibly leading to arterial stiffness and microcirculatory damage. In addition to endothelial pathways to atherosclerosis an external (adventitial) one is proposed, i.e. microcirculatory damage to the network of arterioles that nourish the coronary arteries. In addition to the ectopic fat in their liver and pancreas as the cause of beta cell dysfunction leading to DM2, additional ideas are proposed, i.e. microcirculatory damage. The high risk of CVD and DM2 in urbanizing South Asians is not inevitable, innate or genetic, or acquired in early life and programmed in a fixed way. Rather, exposure to risk factors in childhood, adolescence, and most particularly in adulthood is the key. The challenge to produce focused, low cost, effective actions, underpinned by clear, simple, and accurate explanations of the causes of the phenomenon is addressed.