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1
Adami, J. George. On the relationship between inflammation and sundry forms of fibrosis. [New York?: s.n.], 1985.
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2
Adami, J. George. On the relationship between inflammation and sundry forms of fibrosis. [New York?: s.n.], 1985.
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3
Martins, C. A. RNA turnover and inflammation in adult patients with cystic fibrosis. Roehampton: University of Surrey Roehampton, 2004.
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4
Forte, Elvira, Isotta Chimenti, Gonzalo del Monte-Nieto und Susanne Sattler, Hrsg. Fibrosis and Inflammation in Tissue Pathophysiology. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-497-8.
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5
Sprague, Stuart M., und James M. Pullman. Spectrum of bone pathologies in chronic kidney disease. Herausgegeben von David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0122.
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Histologic bone abnormalities begin very early in the course of chronic kidney disease. The KDIGO guidelines recommend that bone disease in patients with chronic kidney disease should be diagnosed on the basis of bone biopsy examination, with bone histomorphometry. They have also proposed a new classification system (TMV), using three key features of bone histology—turnover, mineralization, and volume—to describe bone disease in these patients. However, bone biopsy is still rarely performed today, as it involves an invasive procedure and highly specialized laboratory techniques. High-turnover bone disease (osteitis fibrosa cystica) is mainly related to secondary hyperparathyroidism and is characterized by increased rates of both bone formation and resorption, with extensive osteoclast and osteoblast activity, and a progressive increase in peritrabecular marrow space fibrosis. On the other hand, low-turnover (adynamic) bone disease involves a decline in osteoblast and osteoclast activities, reduced new bone formation and mineralization, and endosteal fibrosis. The pathophysiological mechanisms of adynamic bone include vitamin D deficiency, hyperphosphataemia, metabolic acidosis, inflammation, low oestrogen and testosterone levels, bone resistance to parathyroid hormone, and high serum fibroblast growth factor 23. Mixed uraemic osteodystrophy describes a combination of osteitis fibrosa and mineralization defect. In the past few decades, an increase in the prevalence of mixed uraemic osteodystrophy and adynamic bone disease has been observed.
6
Delpino, M. Victoria, Guillermo Hernán Giambartolomei, Jorge Quarleri, Sergio C. Oliveira und Gary Splitter, Hrsg. Advances in Liver Inflammation and Fibrosis due to Infectious Diseases. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88966-166-4.
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7
O’Riordan, Stephen MP, und Antoinette Moran. Cystic fibrosis-related diabetes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198702948.003.0008.
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This chapter on CFRD reviews the ever-evolving topic and provides up-to-date information on how to diagnose and manage cystic fibrosis-related diabetes CFRD in the acute and chronic setting. The treatments necessary to treat and prolong life in CF, including their unique dietary requirements, must always be followed as a first priority, with diabetes care adjusted accordingly. Early intervention with insulin has been shown to reverse clinical deterioration, even in those with mild diabetes. Newly emerging treatments for CF which have the potential to restore defective chloride channels may have implications for the development and treatment of CFRD. Whilst CFRD shares features of both type 1 and type 2 diabetes, there are important differences which necessitate a unique approach to diagnosis and management. Factors specific to CF that variably affect glucose metabolism include chronic respiratory infection and inflammation, increased energy expenditure, malnutrition, glucagon deficiency, and gastrointestinal abnormalities.
8
Braga, Tarcio Teodoro, Ivan C. Moura, Ana Paula Lepique und Niels Olsen Saraiva Camara, Hrsg. Macrophages Role in Integrating Tissue Signals and Biological Processes in Chronic Inflammation and Fibrosis. Frontiers Media SA, 2017. http://dx.doi.org/10.3389/978-2-88945-332-0.
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9
Schiller, Adalbert, Adrian Covic und Liviu Segall. Chronic tubulointerstitial nephritis. Herausgegeben von Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0086_update_001.
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Chronic tubulointerstitial nephropathies (CTINs) are a group of renal diseases, characterized by variable interstitial inflammation and fibrosis and tubular atrophy, and a slow course towards end-stage renal disease (ESRD). The causes of CTIN are numerous, including nephrotoxic drugs and chemicals, infections, autoimmune diseases, obstructive uropathies, and metabolic disorders. Taken together, CTIN are responsible for less than 10% of all ESRD cases requiring renal replacement therapy. The clinical manifestations of CTIN typically comprise low-grade proteinuria, leucocyturia, and variably reduced glomerular filtration rate (GFR), whereas the blood pressure is usually normal or moderately increased. Tubular abnormalities are common, including type 2 (proximal) renal tubular acidosis, Fanconi syndrome, nephrogenic diabetes insipidus, and type 1 (distal) renal tubular acidosis, with hypokalaemia and nephrolithiasis. Radiology exams reveal shrunken kidneys, sometimes with irregular outlines. A renal biopsy is often required for the diagnosis of CTIN and its aetiology. The treatment of CTIN mainly involves discontinuation of exposure to nephrotoxins and specific therapy of renal infections, urinary tract obstruction, or underlying systemic diseases. Agents like ACE inhibitors and pirfenidone, which might reduce interstitial inflammation and fibrosis, are still under clinical evaluation.
10
Davey, Patrick, Sherif Gonem und David Sprigings. Interstitial lung disease. Herausgegeben von Patrick Davey und David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0139.
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The interstitial lung diseases, also known as the diffuse or diffuse parenchymal lung diseases, are a broad group of pulmonary disorders which mainly affect the lung parenchyma as opposed to the airways. By convention, infectious and malignant conditions are excluded from this definition. Thus, the interstitial lung diseases comprise a group of conditions characterized by variable degrees of inflammation and fibrosis, centred on the lung interstitium and alveolar airspaces.
11
Segall, Liviu, und Adrian Covic. Immune-mediated tubulointerstitial nephritis. Herausgegeben von Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0093_update_001.
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Immune-mediated tubulointerstitial nephritides (TINs) are generally encountered in the context of systemic or extrarenal autoimmune diseases, such as sarcoidosis, Sjögren syndrome, systemic lupus erythematosus, inflammatory bowel disease, TIN and uveitis (TINU) syndrome, and immunoglobulin G4-related disease. The pathogenesis of these TINs is complex and more or less unclear; it usually involves leucocyte activation, autoantibodies, immune complex deposition, complement activation, and release of inflammatory cytokines and growth factors. Tubulointerstitial inflammation most commonly has a chronic pattern, although acute forms of TIN may also occur. Furthermore, inflammation may be granulomatous (as in sarcoidosis or Crohn’s disease) or non-granulomatous. Immunofluorescence staining can sometimes reveal immune complex deposits and even antitubular basement membrane autoantibodies. Systemic immunosuppressive therapies are almost always required to prevent progression to irreversible interstitial fibrosis, tubular atrophy, and end-stage renal disease.
12
Kriemler, Susi, Thomas Radtke und Helge Hebestreit. Exercise, physical activity, and cystic fibrosis. Herausgegeben von Neil Armstrong und Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0027.
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Cystic fibrosis (CF) is a genetic disease resulting in an impaired mucociliary clearance, chronic bacterial airway infection, and inflammation. The progressive destruction of the lungs is the main cause of morbidity and premature death. Diverse other organ systems such as heart, muscles, bones, gastro-intestinal tract, and sweat glands are often also affected and interfere with exercise capacity. Hence, exercise capacity is reduced as the disease progresses mainly due to reduced functioning of the muscles, heart, and/or lungs. Although there is still growing evidence of positive effects of exercise training in CF on exercise capacity, decline of pulmonary function, and health-related quality of life, the observed effects are encouraging and exercise should be implemented in all patient care. More research is needed to understand pathophysiological mechanisms of exercise limitations and to find optimal exercise modalities to slow down disease progression, predict long-term adherence, and improve health-related quality of life.
13
Ware, Lorraine B. Pathophysiology of acute respiratory distress syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0108.
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The acute respiratory distress syndrome (ARDS) is a syndrome of acute respiratory failure characterized by the acute onset of non-cardiogenic pulmonary oedema due to increased lung endothelial and alveolar epithelial permeability. Common predisposing clinical conditions include sepsis, pneumonia, severe traumatic injury, and aspiration of gastric contents. Environmental factors, such as alcohol abuse and cigarette smoke exposure may increase the risk of developing ARDS in those at risk. Pathologically, ARDS is characterized by diffuse alveolar damage with neutrophilic alveolitis, haemorrhage, hyaline membrane formation, and pulmonary oedema. A variety of cellular and molecular mechanisms contribute to the pathophysiology of ARDS, including exuberant inflammation, neutrophil recruitment and activation, oxidant injury, endothelial activation and injury, lung epithelial injury and/or necrosis, and activation of coagulation in the airspace. Mechanical ventilation can exacerbate lung inflammation and injury, particularly if delivered with high tidal volumes and/or pressures. Resolution of ARDS is complex and requires coordinated activation of multiple resolution pathways that include alveolar epithelial repair, clearance of pulmonary oedema through active ion transport, apoptosis, and clearance of intra-alveolar neutrophils, resolution of inflammation and fibrinolysis of fibrin-rich hyaline membranes. In some patients, activation of profibrotic pathways leads to significant lung fibrosis with resultant prolonged respiratory failure and failure of resolution.
14
Kriemler, Susi. Exercise, physical activity, and cystic fibrosis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199232482.003.0033.
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Cystic fibrosis (CF) is the most common genetic autosomal recessive disease of the Caucasian race, generally leading to death in early adulthood.1 The frequency of the gene carrier (heterozygote) is 1:20–25 in Caucasian populations, 1:2000 in African-Americans, and practically non-existent in Asian populations. The disease occurs in about 1 in every 2500 life births of the white population. Mean survival has risen from 8.4 years in 1969 to 32 years in 2000 due to improvements in treatment. The genetic defect causes a pathological electrolyte transport through the cell membranes by a defective chloride channel membrane transport protein [cystic fibrosis transmembrane conductance regulator (CFTR)]. With respect to the function, this affects mainly the exocrine glands of secretory cells, sinuses, lungs, pancreas, liver, and the reproductive tract of the human body leading to a highly viscous, water-depleted secretion. The secretion cannot leave the glands and in consequence causes local inflammation and destruction of various organs. The main symptoms include chronic inflammatory pulmonary disease with a progressive loss of lung function, exocrine and sometimes endocrine pancreas insufficiency, and an excessive salt loss through the sweat glands.1 A summary of the signs and symptoms of CF will be given with a special emphasis on the effect of exercise performance and capacity.
15
Guzik, Tomasz J., und Rhian M. Touyz. Vascular pathophysiology of hypertension. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0019.
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Hypertension is a multifactorial disease, in which vascular dysfunction plays a prominent role. It occurs in over 30% of adults worldwide and an additional 30% are at high risk of developing the disease. Vascular pathology is both a cause of the disease and a key manifestation of hypertension-associated target-organ damage. It leads to clinical symptoms and is a key risk factor for cardiovascular disease. All layers of the vascular wall and the endothelium are involved in the pathogenesis of hypertension. Pathogenetic mechanisms, whereby vascular damage contributes to hypertension, are linked to increased peripheral vascular resistance. At the vascular level, processes leading to change sin peripheral resistance include hyper-contractility of vascular smooth muscle cells, endothelial dysfunction, and structural remodelling, due to aberrant vascular signalling, oxidative and inflammatory responses. Increased vascular stiffness due to vascular remodelling, adventitial fibrosis, and inflammation are key processes involved in sustained and established hypertension. These mechanisms are linked to vascular smooth muscle and fibroblast proliferation, migration, extracellular matrix remodelling, calcification, and inflammation. Apart from the key role in the pathogenesis of hypertension, hypertensive vasculopathy also predisposes to atherosclerosis, another risk factor for cardiovascular disease. This is linked to increased transmural pressure, blood flow, and shear stress alterations in hypertension, as well as endothelial dysfunction and vascular stiffness. Therefore, understanding the mechanisms and identifying potential novel treatments targeting hypertensive vasculopathy are of primary importance in vascular medicine.
16
Schaible, Hans-Georg, und Rainer H. Straub. Pain neurophysiology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0059.
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Physiological pain is evoked by intense (noxious) stimuli acting on healthy tissue functioning as a warning signal to avoid damage of the tissue. In contrast, pathophysiological pain is present in the course of disease, and it is often elicited by low-intensity stimulation or occurs even as resting pain. Causes of pathophysiological pain are either inflammation or injury causing pathophysiological nociceptive pain or damage to nerve cells evoking neuropathic pain. The major peripheral neuronal mechanism of pathophysiological nociceptive pain is the sensitization of peripheral nociceptors for mechanical, thermal and chemical stimuli; the major peripheral mechanism of neuropathic pain is the generation of ectopic discharges in injured nerve fibres. These phenomena are created by changes of ion channels in the neurons, e.g. by the influence of inflammatory mediators or growth factors. Both peripheral sensitization and ectopic discharges can evoke the development of hyperexcitability of central nociceptive pathways, called central sensitization, which amplifies the nociceptive processing. Central sensitization is caused by changes of the synaptic processing, in which glial cell activation also plays an important role. Endogenous inhibitory neuronal systems may reduce pain but some types of pain are characterized by the loss of inhibitory neural function. In addition to their role in pain generation, nociceptive afferents and the spinal cord can further enhance the inflammatory process by the release of neuropeptides into the innervated tissue and by activation of sympathetic efferent fibres. However, in inflamed tissue the innervation is remodelled by repellent factors, in particular with a loss of sympathetic nerve fibres.
17
Lupton, Joshua. Hospital Acquired Pneumonia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0023.
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Pneumonia consists of inflammation of the pulmonary parenchyma, typically resulting from a microbial infection. Hospital-acquired pneumonia (HAP) occurs in (typically elderly) patients in long-term care facilities, with regular IV therapy, with immunosuppression, or with a history of recent treatment at a hospital. It is associated with high mortality. The majority HAP patients present with some constellation of cough, fever, sputum production, and pleuritic chest pain. Patients with chronic obstructive pulmonary disease (COPD) and cystic fibrosis are at increased risk for pneumonia. The Infectious Disease Society of America requires infiltrates on chest x-ray or other imaging for the diagnosis of pneumonia. For hospitalized patients, empiric antimicrobial therapy for HAP should be given as soon as pneumonia is highly suspected. There is currently a vaccine available against Streptococcus pneumonia that all patients should be offered before discharge from the hospital. The elderly are already more susceptible to HAP due to decreased mobility and increased comorbidities.
18
Tjärnlund, Anna, und Ingrid E. Lundberg. Diagnostic and classification criteria. Herausgegeben von Hector Chinoy und Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0002.
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Diagnosis of idiopathic inflammatory myopathies (IIM) is based on clinical features such as subacute progress of symmetrical weakness of proximal muscle and muscle fatigue, in combination with laboratory confirmation of myopathy, including elevated muscle enzyme levels in serum and histological demonstration of skeletal muscle inflammation, as well as fibre regeneration and degeneration in muscle biopsies. Several classification criteria for IIM have historically been proposed. New classification criteria for IIM have been developed, and are based on real patient data from adult and juvenile IIM cases worldwide. These criteria provide a probability of having IIM with defined cut-off values for categorizing ‘possible’, ‘probable’, and ‘definite’ IIM. Autoantibodies in IIM are becoming increasingly important for diagnosis and classification, and newly identified autoantibodies specific for inclusion body myositis may provide a future diagnostic tool.
19
McDougall, Jason J., und 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.
20
APGAR, Virginia. Cleanse to Heal: Detox Your Body from Gastric Problems, Coronary, Diabetes, Obesity, Inflammation, Irritable Bowel Syndrome, Fibrosis, and Liver, Increase Metabolism and Potassium, Low Cholesterol. Independently Published, 2022.
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21
MEYER, Joyal. Cleanse to Heal: Guide to Cleanse and Detox from Gastric Problems, Diabetes, Fibrosis, Liver, Obesity, Inflammation, Coronary, Irritable Bowel Syndrome, Low Cholesterol, Increase Potassium and Metabolism. Independently Published, 2021.
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22
Radović, Milan, und Adalbert Schiller. Balkan endemic nephropathy. Herausgegeben von Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0090_update_001.
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Balkan endemic nephropathy (BEN) is a chronic, slowly progressive tubulointerstitial nephritis, with familial clustering, occurring in several endemic rural regions in countries of the Balkan Peninsula. BEN is characterized by anaemia, tubular proteinuria, renal shrinkage, and slowly declining glomerular filtration rate (GFR). Up to one-third of patients may also develop upper urothelial tumours. The aetiology of BEN is unclear; chronic exposure to aristolochic acid and a polygenic predisposition are the most likely contributing factors. The major pathological characteristics of BEN are symmetrically shrunken, smooth-shaped kidneys, with interstitial fibrosis, mild interstitial inflammation, and tubular atrophy. Diagnosis is usually based upon positive family history of BEN, past or current residence in endemic regions, tubular proteinuria, tubular dysfunctions (such as urine acidification defects, salt wasting, and impaired excretion of ammonia, uric acid, and phosphate), scant urinary sediment, bilateral and symmetrically reduced kidney size, accompanied by severe anaemia, disproportionate to the degree of GFR reduction. There is no specific therapy for BEN; patients should therefore be treated as all patients with chronic kidney disease, in general. The use of distant water supplies or moving to another residence area should be advised to affected families. Careful evaluation for urothelial cancers is mandatory in patients with haematuria.
23
Turner, Neil. Crescentic (rapidly progressive) glomerulonephritis. Herausgegeben von Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0070.
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Crescent formation refers to the appearance of proliferating cells in Bowman’s space in response to severe glomerular inflammation. Any aggressive ‘nephritic’ diseases that cause basement membrane breaks may provoke this. Specific serum proteins appear to be responsible for provoking crescent formation as it is largely abolished by defibrination in animal models. The cells in the crescent are initially mostly hypertrophying and proliferating parietal epithelial cells that normally line Bowman’s capsule. Foci of proliferation of these cells (extracapillary proliferation) are the first steps of crescent formation. Monocytes are frequently seen in established crescents. At this stage recovery of glomerular structure and function is possible in many circumstances. However, if Bowman’s capsule is ruptured, fibroblast ingress followed by fibrosis and glomerulosclerosis are likely. Crescentic nephritis is a histological description, but it fits closely with the clinical picture of rapidly progressive glomerulonephritis (RPGN), in which renal function is lost over days to weeks. The diseases most likely to cause this clinical picture are small vessel vasculitis, anti-GBM disease, lupus nephritis, and post-infectious glomerulonephritis. Any ‘nephritic’ disease may provoke crescent formation, but it is frequently encountered in immunoglobulin A nephropathy/Henoch–Schönlein purpura, and in post-infective glomerulonephritis. Recognizing the clinical picture is important as aggressive immunosuppression can be effective in saving glomerular function in some of the conditions causing it.
24
Gilchrist, Francis J., und Alex Horsley. Management of respiratory exacerbations. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198702948.003.0005.
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Cystic fibrosis lung disease is characterized by chronic infection, inflammation and a progressive loss of lung function. Patients are also affected by recurrent episodes of increased respiratory symptoms, called exacerbations which have a detrimental effect on quality of life, the rate of lung function decline, and mortality. Early diagnosis and treatment is vital. Diagnosis relies on a combination of symptoms, examination findings, the results of laboratory tests, and lung function. Antibiotics are the mainstay of treatment but airway clearance, nutrition, and glucose homeostasis must also be optimized. Mild exacerbations are usually treated with oral antibiotics and more severe exacerbations with intravenous antibiotics. The choice of antibiotic is guided by the patient’s chronic pulmonary infections, the in-vitro antibiotic sensitivities, known antibiotic allergies, and the previous response to treatment. In patients with chronic Pseudomonas aeruginosa infection, antibiotic monotherapy is thought to increase the risk of resistance and treatment with 2 antibiotics is therefore suggested (usually a β-lactam and an aminoglycoside). Although there is a lack of evidence on the duration of treatment, most patients receive around 14 days. This can be altered according to the time taken for symptoms and lung function to return to pre-exacerbation levels. If patients are carefully selected and receive appropriate monitoring, home intravenous antibiotics can be as effective as in-patient treatment. They are also associated with decreased disruption to patients / family life, decreased risk of cross infection and decreased costs.
25
Hughes, Jeremy. Proteinuria as a direct cause of progression. Herausgegeben von 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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Izzedine, Hassan, und Victor Gueutin. Drug-induced acute tubulointerstitial nephritis. Herausgegeben von Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0084.
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Drug-induced acute tubulointerstitial nephritis (ATIN) is the most common aetiology of ATIN and a potentially correctable cause of acute kidney injury (AKI). An interval of 7–10 days typically exists between drug exposure and development of AKI, but this interval can be considerably shorter following re-challenge or markedly longer with certain drugs. It occurs in an idiosyncratic and non-dose-dependent manner. Antibiotics, NSAIDs, and proton pump inhibitors are the most frequently involved agents, but the list of drugs that can induce ATIN is continuously increasing. The mechanism of renal injury is postulated to involve cell-mediated immunity, supported by the observation that T cells are the predominant cell type comprising the interstitial infiltrate. A humoral response underlies rare cases of ATIN, in which a portion of a drug molecule (i.e. methicillin) may act as a hapten, bind to the tubular basement membrane (TBM), and elicit anti-TBM antibodies. The classic symptoms of fever, rash, and arthralgia may be absent in up to two-thirds of patients. Diagnostic studies, such as urine eosinophils and renal gallium-67 scanning provide only suggestive evidence. Renal biopsy remains the gold standard for diagnosis, but it may not be required in mild cases or when clinical improvement is rapid after removal of an offending medication. Pathologic findings include interstitial inflammation, oedema, and tubulitis. The time until removal of such agents and the severity of renal biopsy findings provide the best prognostic value for the return to baseline renal function. Poor prognostic indicators are the long duration of AKI (> 3 weeks), a patient’s advanced age, and the high degree of interstitial fibrosis. Early recognition and appropriate therapy are essential to the management of drug-induced ATIN, because patients can ultimately develop chronic kidney disease. The mainstay of therapy is timely discontinuation of the causative agent, whereas controversy persists about the role of steroids.
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MacLean, Allan B. Vulval pain. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198749547.003.0009.
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Vulval pain or pain involving the vulval tissue is discussed in Chapter 9. It becomes chronic when lasting for at least three months. Vulvodynia is a subset of chronic vulval pain, once known causes (infective, inflammatory, neoplastic, neurological, traumatic, iatrogenic and hormone deficiencies) are excluded. It reportedly affects one in six women at some stage of their lives. Uncertain terminology has hampered understanding. Even the latest classification from the International Society for the Study of Vulvovaginal Disease has deficiencies but it allows the discarding of previously used unhelpful terms. Differentiating features between provoked (entry dyspareunia), and unprovoked, localised and generalised, overlap, both in diagnosis and management. Older theories on causation included infection, irritation and inflammation but laboratory-based research has not supported these. Hormonal and neural mechanisms seem more likely to cause the pain, while the interplay of biological, psychological, and social factors has recently gained credence. Publications on successful management demonstrate a powerful placebo effect. The role of specially designated vulval pain clinics, multidisciplinary approaches, and team working is emphasised. General measures in vulval care, such as wearing clothes made of natural fibre, using emollients or carrying out pelvic floor exercises besides reducing stress, can minimise the pain. Topical anaesthetic creams or systemic treatments with antidepressants or anti-epileptics have advocates. Treatment is most effective when careful selection, adequate counselling, and ongoing psychosomatic evaluation address all the interactive factors that initiate, and maintain vulval pain besides modulating patient response. Case scenarios illustrate the complexities of diagnosis and management.