Books: 'Fibrotic and inflammatory conditions'

1

Inflammatory conditions of the colon. New York: Nova Science Publishers, 2009.

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2

Church, Martin, and Clive Robinson, eds. Eicosanoids in Inflammatory Conditions of the Lung, Skin and Joints. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1283-0.

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3

1942-, Bonney R. J., ed. Inflammatory disease therapy: Preclinical and clinical developments. Basel: Birkhäuser Verlag, 1993.

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4

Hashefi, Mandana. PET/CT applications in non-neoplastic conditions. Edited by New York Academy of Sciences. Boston, Mass: Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2011.

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5

Black, Jessica K. Eating your way back to health: A guide to inflammatory cooking - reduce inflammation to help heal cardiovascular disease, arthritis, fibromyalgia, diabetes, allergies, and many more conditions. McMinnville, Ore: A Family Healing Center, 2004.

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6

Yaqoob, Muhammad M., Katherine Bennett-Richards, and Islam Junaid. Retroperitoneal fibrosis. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0357.

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Retroperitoneal fibrosis (RPF) is a rare but multifaceted disease which encompasses a range of conditions characterized by the presence of a fibro-inflammatory tissue, which usually surrounds the abdominal aorta, iliac arteries, and extends into the retroperitoneum to entrap ureters with resultant unilateral or bilateral obstruction, usually at the junction between the middle and lower thirds of the ureter. The condition is progressive: initially, the fibrous tissue is fairly cellular, later becoming relatively acellular. The mechanism by which obstruction occurs is probably due to loss of peristalsis. A histological diagnosis should be obtained if at all possible, and laparotomy is required in order to obtain a sufficiently large sample to differentiate between idiopathic and secondary causes of RPF. Treatment of idiopathic RPF is by corticosteroids in the first instance with ureteric stents or ureterolysis initially and requires regular monitoring.

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7

Recipes for the Specific Carbohydrate Diet: The Grain-Free, Dairy-Free, Sugar-Free Solution to IBD, Celiac Disease, Autism, Cystic Fibrosis, and other ... Conditions (Healthy Living Cookbooks). Fair Winds, 2008.

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8

G, Poór, and Gergely P, eds. Miscellaneous inflammatory musculoskeletal conditions. [Netherland]: Elsevier, 2004.

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9

Gyula, Poór, and Gergely Peter, eds. Miscellaneous inflammatory musculoskeletal conditions. London: Baillière Tindall, 2004.

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10

F, Lioté, and Pascual E, eds. Miscellaneous non-inflammatory musculoskeletal conditions. London: Bailliè Tindall, 2003.

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11

Frédéric, Lioté, and Pascual E, eds. Miscellaneous non-inflammatory musculoskeletal conditions. London: Baillière Tindall, 2003.

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12

undifferentiated, Woolf. Rheumatoid Arthritis And Other Inflammatory Conditions. Martin Dunitz Ltd, 2000.

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13

Gullo, Alberto Lo, and Giuseppe Mandraffino, eds. Chronic Rheumatic Inflammatory Conditions and Cardiovascular Health. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-83250-078-1.

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14

Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Urinary tract obstruction. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0165.

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The urinary tract can become obstructed by various disease processes, including tumours. Obstruction at any level of the urinary tract can impair the free flow of urine and may be partial or complete, and unilateral or bilateral. Bilateral obstruction usually occurs at the level of the bladder or lower. Retroperitoneal fibrosis and extrinsic compression of both ureters by a malignancy are exceptions. Children are affected by congenital vesicoureteric junction obstruction or pelvi-ureteric junction obstruction. Young adults suffer stone disease. The elderly are prone to urothelial cancers, and older men to bladder outflow obstruction. Retroperitoneal fibrosis is an inflammatory condition that typically affects men over 50 years of age. Diagnosis should be confirmed by biopsy to exclude a lymphoma or malignancy.

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15

1942-, Church Martin, and Robinson Clive 1958-, eds. Eicosanoids in inflammatory conditions of the lung, skin, and joints. Lancaster: MTP Press, 1988.

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16

Church, M. K. Eicosanoids in Inflammatory Conditions of the Lung, Skin and Joints. Springer, 2011.

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17

Robinson, C. F., and M. K. Church. Eicosanoids in Inflammatory Conditions of the Lung, Skin and Joints. Springer London, Limited, 2012.

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18

Keshav, Satish, and Alexandra Kent. Inflammatory bowel disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0203.

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Inflammatory bowel disease (IBD) encompasses ulcerative colitis (UC) and Crohn’s disease (CD). Both conditions cause chronic relapsing inflammation in the gastrointestinal (GI) tract, but have different characteristics. UC causes diffuse mucosal inflammation limited to the colon, extending proximally from the anal verge, with the rectum involved in 95% of patients. UC is described in terms of the disease extent: proctitis (confined to the rectum), proctosigmoiditis (disease confined to the recto-sigmoid colon), distal disease (distal to the splenic flexure), and pan-colitis (the entire large intestine). The extent of disease can change, with proximal extension seen in approximately a third of patients with proctitis, although there is great variation between studies. CD causes inflammation that can affect the entire thickness of the wall of the intestine, and is not confined to the mucosa. CD can affect any part of the GI tract. The terminal ileum is affected in approximately 80% of cases, the colon in approximately 60% of cases, and the rectum and perianal region in approximately 40% of cases. CD is classified by location (ileal, colonic, ileocolonic, upper GI tract), by the presence of stricturing or penetrating disease, and by the age of onset (before or after the age of 40). Penetrating disease refers to the development of fistulae, which can lead to complications such as abscesses or perforations. An earlier age at onset is associated with more complicated disease. The diagnosis of UC or CD is established through a combination of clinical, endoscopic, radiological, and histological criteria rather than by any single modality. Occasionally, it is not possible to establish an unequivocal diagnosis of CD or UC in IBD, and a third category, accounting for nearly 10% of cases, is used, termed IBD unclassified.

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19

Bergnaum, Garret. FLUOCINOLONE ACETONIDE: Topical Corticosteroid for the Handling of Inflammatory Skin Conditions. Independently Published, 2019.

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20

Liponis, Mark, and Bettina Martin. An Integrative Approach to the Assessment and Treatment of Inflammatory Conditions. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190241254.003.0017.

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The past two decades have seen great progress in recognizing the importance of inflammation in medicine. Increased focus on inflammation in both prevention and treatment has improved outcomes and quality of life in chronic diseases. Science has improved our understanding of inflammation’s many causes and effects on health, and many advances have been made in the availability of targeted therapeutic options for treating inflammation. This chapter gives an overview of recognizing the many causes of inflammation, its many targeted treatments strategies, and the questions that still surround it. It discusses several integrative approaches to reducing inflammation, including exercise, diet, and different strategies for managing sleep, mood, and stress, such as meditation and massage.

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21

Naturopath, Case Adams. Mucosal Membrane Health: The Key to Preventing Inflammatory Conditions, Infections, Toxicity and Degeneration. Logical Books, 2014.

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22

Kang, Duk-Hee, and Mehmet Kanbay. Urate nephropathy. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0092.

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Gout is a disorder of purine metabolism, characterized by hyperuricaemia and urate crystal deposition within and around the joints. The recognition of increased comorbidity burden in patients with gout rendered it as a systemic disorder rather than simply a musculoskeletal condition. Gout nephropathy (also known as chronic uric acid nephropathy or urate nephropathy) is a form of chronic tubulointerstitial nephritis, induced by deposition of monosodium urate crystals in the distal collecting ducts and the medullary interstitium, associated with a secondary inflammatory reaction. Other renal histologic changes include arteriolosclerosis, glomerulosclerosis, and tubulointerstitial fibrosis. In patients with urate nephropathy, hypertension is common, but usually there is only mild proteinuria and a slight increase in serum creatinine. The reduction of serum uric acid, using xanthine oxidase inhibitors and perhaps low-purine diet, is the mainstay of therapy. There is current research around the question of whether it is beneficial to lower serum uric acid in asymptomatic patients with renal disease or with cardiovascular risk factors.

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23

Elewaut, Dirk, Heleen Cypers, Matthew L. Stoll, and Charles O. Elson. Extra-articular manifestations: inflammatory bowel disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0017.

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A significant overlap exists between spondyloarthritis (SpA) and inflammatory bowel disease (IBD), particularly in the IL-23/IL-17 pathway. Shared immunologic mechanisms include aberrant innate immune responses, an excess of Th1/Th17-mediated immunity, and inadequate immune regulation. Many genetic factors associated with IBD are involved in host–pathogen interactions and intestinal barrier function, and the intestinal microbiota do appear to play an important role in disease development. Hence the current hypothesis for IBD pathogenesis is that it stems from a dysregulated immune response to intestinal microbiota in a genetically susceptible host. In SpA, evidence for a role of intestinal microbiota is less abundant, but given the overlap with IBD, it is plausible that gut microbiota are important players in SpA pathogenesis as well. However, there are significant genetic differences between these two conditions, as well as differing responses to biologic therapy.

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24

Research & Forecasts, Inc., ed. Arthritis and other chronic pain conditions: Problems associated with drug therapy. New York, N.Y. (110 E. 59th St., New York 10022): Research & Forecasts, 1985.

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25

Morgan, D. W., R. J. Booney, and Niall S. Doherty. Inflammatory Disease Therapy: Preclinical and Clinical Developments (Agents and Actions Supplements). Birkhauser, 1993.

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26

Monahan, Annabelle. M0TRlN: Anti-Inflammatory Drug Used to Reduce Fever and Treat Pain or Inflammation Caused by Many Conditions. Independently Published, 2019.

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27

Klocko, Rosanna. CLθBETASθl PRθPIONATE: An Exceptionally Powerful Topical Corticosteroid Treatment for Inflammatory Skin Conditions. Independently Published, 2019.

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28

Miller, Aaron E., and Teresa M. DeAngelis. Progressive Multifocal Leukoencephalopathy Syndrome and Immune Reconstitution Inflammatory Syndrome. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199732920.003.0007.

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Progressive multifocal leukoencephalopathy (PML), an opportunistic viral infection of the central nervous system caused by the JC virus, typically manifests in severely immunocompromised conditions, ranging from HIV/AIDS to lymphoproliferative malignancies to the consequence of immunosuppressant medications such as natalizumab, a monoclonal antibody approved for the treatment of relapsing forms of MS. In this chapter, we discuss the typical symptomatology and radiographic findings of PML and how to distinguish it from those of MS. In addition, we review the management of PML in natalizumab-treated MS patients as well as the features of immune reconstitution inflammatory syndrome (IRIS), the potentially life-threatening consequence of natalizumab withdrawal in patients with PML.

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29

Yilmaz, Ali, and Anca Florian. Myocarditis: imaging techniques. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0367.

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The clinical presentation of myocarditis is multifaceted and electrocardiogram (ECG) changes as well as biomarkers tend to be non-specific. Therefore, the diagnosis of myocarditis can be challenging and should be based on an integrated approach including patient history, physical examination, non-invasive tests such as ECG and serum biomarkers, and non-invasive cardiac imaging. As myocarditis may lead to global ventricular dysfunction, regional wall motion abnormalities, and/or diastolic dysfunction, echocardiography should be routinely performed. However, hallmarks of acute myocarditis comprise structural changes such as cardiomyocyte swelling, an increase in extracellular space and water content, accumulation of inflammatory cells, potential necrosis or apoptosis of cardiomyocytes, and myocardial remodelling with fibrotic tissue replacement that can be depicted by cardiovascular magnetic resonance. Nuclear techniques are still not routinely recommended for the work-up of myocarditis—with the possible exception of suspected sarcoidosis—due to limited data, limited diagnostic specificity, limited availability, and risk from radiation exposure. This chapter focuses on those non-invasive cardiac imaging techniques that are used in daily clinical practice for work-up of suspected myocarditis. However, as research continues and novel imaging techniques become available, it is hoped that even more accurate and timely diagnosis of myocarditis will be possible in the near future.

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30

Tsai, Ching-Wei, Sanjeev Noel, and Hamid Rabb. Pathophysiology of Acute Kidney Injury, Repair, and Regeneration. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0030.

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Acute kidney injury (AKI), regardless of its aetiology, can elicit persistent or permanent kidney tissue changes that are associated with progression to end-stage renal disease and a greater risk of chronic kidney disease (CKD). In other cases, AKI may result in complete repair and restoration of normal kidney function. The pathophysiological mechanisms of renal injury and repair include vascular, tubular, and inflammatory factors. The initial injury phase is characterized by rarefaction of peritubular vessels and engagement of the immune response via Toll-like receptor binding, activation of macrophages, dendritic cells, natural killer cells, and T and B lymphocytes. During the recovery phase, cell adhesion molecules as well as cytokines and chemokines may be instrumental by directing the migration, differentiation, and proliferation of renal epithelial cells; recent data also suggest a critical role of M2 macrophage and regulatory T cell in the recovery period. Other processes contributing to renal regeneration include renal stem cells and the expression of growth hormones and trophic factors. Subtle deviations in the normal repair process can lead to maladaptive fibrotic kidney disease. Further elucidation of these mechanisms will help discover new therapeutic interventions aimed at limiting the extent of AKI and halting its progression to CKD or ESRD.

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31

Houghton, Kristin. Childhood regional conditions. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0158.

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Musculoskeletal (MSK) complaints are common in childhood. The majority of causes are benign and self-limiting, but MSK symptoms may be the presenting feature of serious life-threatening illness or chronic disease. Pain is often attributed to minor trauma, and atraumatic causes including infectious, inflammatory, and oncologic conditions, amplified musculoskeletal pain syndromes, and normal skeletal growth variants need to be considered. The age of the child helps identify the possible developmental conditions unique to the growing paediatric skeleton. Evaluation and management requires a thorough history and physical examination, and understanding of normal development. This chapter reviews common MSK regional conditions in childhood.

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32

Houghton, Kristin. Childhood regional conditions. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199642489.003.0158_update_001.

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Musculoskeletal (MSK) complaints are common in childhood. The majority of causes are benign and self-limiting, but MSK symptoms may be the presenting feature of serious life-threatening illness or chronic disease. Pain is often attributed to minor trauma, and atraumatic causes including infectious, inflammatory, and oncologic conditions, amplified musculoskeletal pain syndromes, and normal skeletal growth variants need to be considered. The age of the child helps identify the possible developmental conditions unique to the growing paediatric skeleton. Evaluation and management requires a thorough history and physical examination, and understanding of normal development. This chapter reviews common MSK regional conditions in childhood.

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33

Wright, Deborah E. Beat Autoimmune Diseases with Ketogenic Diet: How to Control Autoimmune Conditions Naturally, Preventing Inflammation by Consuming Anti-Inflammatory Diet. Independently Published, 2019.

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34

Hughes, Jeremy. Proteinuria as a direct cause of progression. Edited by 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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35

Nienow, Johann. PR0PIONATE GEL: An Outstandingly and Potent Remedy for Inflammatory Skin Conditions Such As Severe Dermatitis and Skin Inflammation in Human. Independently Published, 2019.

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36

Dow, Julia Martin, and Jessica Amy Samuel. Anti-Inflammatory Diet Cookbook: The Beginner's Diet Plan to Heal and Build the Immune System and Restore Overall Health Conditions. Sam Amoo, 2020.

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37

Dow, Julia Martin, and Jessica Amy Samuel. Anti-Inflammatory Diet Cookbook: The Beginner's Diet Plan to Heal and Build the Immune System and Restore Overall Health Conditions. Independently Published, 2020.

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38

Thaisetthawatkul, Pariwat, and Eric Logigian. Guillain-Barré Syndrome and Chronic Inflammatory Demyelinating Polyradiculoneuropathy in Pregnancy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190667351.003.0026.

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Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) are both immune-mediated diseases of the peripheral nervous system that typically present with symmetric, progressive muscle weakness, areflexia, and sensory symptoms or signs. GBS evolves rapidly with a nadir at 2–4 weeks usually with an antecedent viral illness, while CIDP progresses more slowly over months to years. GBS is sometimes complicated by life-threatening respiratory failure or dysautonomia. Onset of GBS and relapse of CIDP can occur during pregnancy or postpartum. But with appropriate supportive care and immunotherapy, maternal and fetal outcome in both conditions is typically excellent. The exception is fetal outcome in GBS triggered by maternal CMV or Zika infection transmitted to the fetus. Full-term vaginal delivery and regional anesthesia are preferred in maternal GBS and CIDP, but if C-section and general anesthesia are indicated, non-depolarizing agents such as succinylcholine should be avoided.

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39

Mills, Gary H. Pulmonary disease and anaesthesia. Edited by Philip M. Hopkins. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0082.

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Respiratory adverse events are the commonest complications after anaesthesia and have profound implications for the recovery of the patient and their subsequent health. Outcome prediction related to respiratory disease and complications is vital when determining the risk:benefit balance of surgery and providing informed consent. Surgery produces an inflammatory response and pain, which affects the respiratory system. Anaesthesia produces atelectasis, decreases the drive to breathe, and causes muscle weakness. As the respiratory system ages, closing capacity increases and airway closure becomes an increasing issue, resulting in atelectasis. Increasing comorbidity and polypharmacy reduces the patient’s ability to eliminate drugs. The proportion of major operations on older frailer patients is rising and postoperative recovery becomes more complicated and the demand for critical care rises. At the same time, the population is becoming more obese, producing rapid decreases in end-expiratory lung volume on induction, together with a high incidence of sleep-disordered breathing. Despite this, many high-risk patients are not accurately identified preoperatively, and of those that are admitted to critical care, some are discharged and then readmitted to the intensive care unit with complications. Respiratory diseases may lead to increases in pulmonary vascular resistance and increased load on the right heart. Some lung diseases are primarily fibrotic or obstructive. Some are inflammatory, autoimmune, or vasculitic. Other diseases relate to the drive to breathe, the nerve supply to, or the respiratory muscles themselves. The range of types of respiratory disease is wide and the physiological consequences of respiratory support are complex. Research continues into the best modes of respiratory support in theatre and in the postoperative period and how best to protect the normal lung. It is therefore essential to understand the effects of surgery and anaesthesia and how this impacts existing respiratory disease, and the way this affects the balance between load on the respiratory system and its capacity to cope.

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40

Farquhar-Smith, Paul. The key role of nerve growth factor in inflammatory pain processing. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0021.

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This paper was one of several that cemented the key role of nerve growth factor (NGF) in sensory neurons in inflammatory pain processing. It used a novel way of biologically ‘removing’ NGF using a sequestration molecule that could then investigate the effect of the absence of NGF in pain paradigms. These data contributed to the robust evidence base indicating the importance of NGF and, although there had been issues in developing usable anti-NGF moieties in human pain conditions, this study could be considered part of the journey that has led to the introduction of antagonists to NGF actions for the treatment of pain in bone.

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41

J, Judd Sandra, ed. Respiratory disorders sourcebook: Basic consumer health information about infectious, inflammatory, and chronic conditions affecting the lungs and respiratory system, including pneumonia, bronchitis, influenza, tuberculosis, sarcoidosis, asthma, cystic fibrosis, chronic obstructive pulmonary disease, lung abscesses, pulmonary embolism, occupational lung diseases, and other bacterial, viral, and fungal infections; along with facts about the structure and function of the lungs and airways, methods of diagnosing respiratory disorders, and treatment and rehabilitation options, a glossary of related terms, and a directory of resources for additional help and information. 2nd ed. Detroit: Omnigraphics, 2008.

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42

Hagendorff, Andreas. Systemic diseases and other conditions: introduction. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0054.

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Cardiac structures and their function as well as the vascular system can be affected by general systemic influences. Exceptional physiological conditions like competitive sports or pregnancy cause typical, but normally reversible alterations in the heart. Certain systemic diseases will cause cardiovascular alteration and damage, which can be life-threatening or can introduce the development of myocardial failure due to humoral, immunological, or inflammatory affections on the myocardium or the valves. In the following chapters in this section, the echocardiographic findings which can be documented due to the physiological compensatory effects in athlete’s heart as well as in pregnancy are described. Then, the typical echocardiographic characteristics in patients with systemic diseases are described with respect to the main cardiac target which is affected. The targets of the systemic diseases are the coronary arteries, the heart valves, the myocardium, the pericardium, as well as the right ventricle.

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43

Hajhosseiny, Reza, Kaivan Khavandi, and David J. Goldsmith. Sudden cardiac death in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0108.

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Epidemiological data demonstrate the unique vulnerability of chronic kidney disease (CKD) subjects to cardiovascular disease, the most catastrophic being sudden cardiac death (SCD). In patients with declining kidney function there is a continuum of cardiovascular risk. In those individuals who survive to reach end-stage renal disease (ESRD), the risk of suffering a cardiac event is extremely high. Some of this risk is explained by the common risk factors and traditional cardiovascular events, namely atherosclerotic plaque fissure and rupture, but there is now evidence of a distinct ‘later CKD’ mechanism, notably arrhythmias. This appears particularly true in later stages of CKD and corresponds with the multifaceted range of myocardial and vascular insults operating. The physiological milieu of disordered vessel autoregulation, sequestered vasoprotective agents, loss of conduit and small artery elasticity/compliance, a stiffened and fibrotic myocardium, with calcified and diseased coronary arteries, all within an inflammatory environment, all contribute to arrhythmia generation. The final insult is changes in volume and electrolyte status. Risk stratification tools would be helpful in guiding clinicians to recognize those subjects likely to benefit from specific interventional strategies. These might include the novel, or emerging serum, haemodynamic, or electrocardiographic biomarkers in CKD. Current tools—such as those used for stratifying risk for SCD and determining the need for ICD implantation—are not valid in ESRD patients. Beta blockers appear likely to be generally advisable, blood pressure permitting, for patients with significant cardiomyopathy. Evidence for implantable cardiac defibrillators (ICD) is lacking. There is good reason to think that young dialysis patients at high risk of sudden death may benefit, but the risk/benefit ratio for older patients is less likely to be advantageous. These hypotheses need further investigation.

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44

Ruiz-Villalba, Adrián, Nikolaos Frangogiannis, and José Maria Pérez-Pomares. Origin and diversity of cardiac fibroblasts: developmental substrates of adult cardiac fibrosis. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0012.

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Cardiac connective tissues are primarily formed by cardiac fibroblasts (CF) of diverse embryonic origins. Whereas CF specific roles in cardiac morphogenesis remain under-researched, their involvement in adult cardiac fibrosis is clinically relevant. Cardiac fibrosis is a common element of several chronic cardiac conditions characterized by the loss of ventricular wall mechanical function, ultimately driving to heart failure. In the ischaemic heart early reparative fibrosis evidences the very restricted regenerative potential of the myocardium. In non-ischaemic diseases fibrosis is activated by unknown signals. We summarize current knowledge on the origin of CFs and their developmental roles, and discuss the differential disease-dependent response of different CF subpopulations to various pathological stimuli. We also describe the characteristic cell-cell and cell-matrix interactions that determine the fibrotic remodelling of the myocardium. We analyse experimental models for the study of cardiac fibrosis, and suggest future directions in the search for new markers and therapeutic targets.

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45

1943-, Riddell Robert H., Crohn's & Colitis Foundation of America., National Institutes of Health (U.S.), and Rebecca Meyerhoff Philanthropic Fund, eds. Dysplasia and cancer in colitis. New York: Elsevier, 1991.

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46

Laing, Susan. Love Your Liver Feel Alive: Liver and Gallbladder Detox with Plant-Based, Anti-inflammatory, Mucus-free Raw Food Recipes. Plus Tips, Diagrams, Photos for Candida; a Fatty Liver and Most Health Conditions. Independently Published, 2019.

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47

Denton, Christopher P., and Pia Moinzadeh. Systemic sclerosis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0121.

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The term 'scleroderma' describes a group of conditions in which the development of thickened, fibrotic skin is a cardinal feature. This includes localized forms of scleroderma (e.g. morphoea) and also systemic forms of the disease that are more correctly termed systemic sclerosis. Systemic sclerosis (SSc) is a multiorgan, autoimmune disease that has a high clinical burden and mortality, due to affecting the skin as well as internal organs. As with other related diseases there is a female predominance and marked clinical diversity. The pathogenesis of SSc is not fully elucidated; it includes endothelial cell injury fibroblast activation and autoimmunity that lead to skin and internal organ manifestations. The majority of cases exhibit characteristic serum autoantibodies. Some of these antibodies are scleroderma-specific reactivities including anti-centromere (ACA), anti-topoisomerase-1 (ATA or Scl 70) or anti-RNA polymerase III antibodies. These anti-nuclear antibody (ANA) patterns are generally mutually exclusive and serve as useful clinical markers of disease subgroups. Additional subsetting of scleroderma cases, based on the extent of skin sclerosis, permits classification into limited and diffuse subsets. Because of the heterogeneity of the disease patients may suffer from different organ manifestations, such as lung fibrosis, hypertensive renal crisis, severe cardiac disease, gastrointestinal involvement, and pulmonary arterial hypertension. Although outcomes have improved recently, systemic sclerosis still has the highest case-specific mortality of any of the autoimmune rheumatic diseases and requires careful and systematic investigation, management and follow-up. Treatment includes symptomatic strategies with attention to each involved organ system; it is still an area where therapeutic progress and better understanding of pathogenesis is increasingly anticipated.

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48

Miller, Michelle A. Sleep, inflammation, and disease. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198778240.003.0012.

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Sleep is a fundamental requirement for living individuals. Sleep disturbances and sleep disorders have extensive effects on the immune system, affecting one’s susceptibility to, and ability to fight off, infections—both bacterial and viral—and the subsequent development of different diseases. This is mediated by the increase in pro-inflammatory cytokines associated with sleep loss and disruption. A number of common conditions, such as obesity, cardiovascular disease, metabolic syndrome, obstructive sleep apnoea syndrome, rheumatoid arthritis, and systemic lupus erythematosus, all share pro-inflammatory mechanisms and the presence of sleep disturbances. Early identification of sleep disorders, and the associated adverse inflammatory and metabolic risk factors, in affected individuals would have a clear clinical benefit.

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Turner, Neil. Mechanisms of glomerular injury. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0045.

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Proteinuric diseases, historically termed ‘nephrosis’, are characterized by subtle abnormalities in podocytes or by abnormal glomerular matrix, including the scarring laid down by inflammatory diseases. Angiotensin blockers, corticosteroids, calcineurin inhibitors, and a wide range of other drugs known or believed to be effective in different renal diseases, appear to have direct effects on podocytes that reduce proteinuria that may be important to their effectiveness. Several of these have previously been assumed to work via haemodynamic, immune or other modes. Haematuric diseases are characterized by inflammatory disruption of the glomerular basement membrane (GBM) (‘nephritis’), or less commonly by fragile GBM without inflammation. The majority of haematuric conditions are slowly or rapidly destructive diseases associated with infiltration of inflammatory cells, and proliferation of endogenous cells of the glomerulus, probably in attempts at repair. With time, many haematuric diseases are associated with the development of proteinuria, possibly as a consequence of scarring and its effects on podocyte function.

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Rosh, Joel R., Leo A. Heitlinger, and Walter D. Rosenfeld, eds. AM:STARs: Clinical GI Challenges in the Adolescent, Vol. 27, No. 1. American Academy of Pediatrics, 2016. http://dx.doi.org/10.1542/9781581109382.

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It is now recognized that the prevalence of atopic disorders including (EoE) and immune based conditions such as celiac disease and inflammatory bowel disease are on the rise. This changing epidemiology coupled with advancements in the diagnosis of these conditions have led to greater numbers of adolescents needing treatment. Topics include: Swallowing disorders and eosinophilic esophagitis Celiac and gluten-related disorders Functional GI disorders Advances in inflammatory bowel disease Advances in hepatology Obesity Fad diets, FODMAPS Vitamin D and bone health Gut microbiome and probiotics GI issues in adolescents with eating disorders Health maintenance in adolescents with chronic GI disorders Transition of care

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Books on the topic 'Fibrotic and inflammatory conditions'

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