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Books on the topic 'GBM Patients'

Author: Grafiati
Published: 6 September 2023

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1

Group, Diagram, ed. Collins gem patience card games. Glasgow: HarperCollins, 1996.

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2

Herbelin, Yehonathan. Gam ani hayiti sham: I was there. Modiʻin: Kineret, 2019.

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3

Elʻazar, Mosheh ben Shelomoh. Sefer Maʻaneh rakh: Bo yevoʼar ekh yitnaheg ha-adam ... she-lo yikhʻos ṿeshe-lo yaḳpid ṿe-lo yitraʻem ... ṿe-gam ... ʻal ezeh ha-ofanim mutar li-kheʻos ... ṿe-gam yevoʼar ... kol darkhe ha-teshuvah she-mefuzarim ben ha-sefarim ... Bene Beraḳ: Sifre Or ha-ḥayim, 2000.

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4

Health policy in Britain: The politics and organisation of the National Health Service. 2nd ed. Basingstoke: Macmillan, 1985.

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5

Health policy in Britain: The politics and organisation of the National Health Service. 3rd ed. Houndmills, Basingstoke, Hampshire: Macmillan, 1992.

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6

Health policy in Britain: The politics and organisation of the National Health Service. 3rd ed. Basingstoke: Macmillan, 1992.

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7

Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0073_update_001.

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Cyclophosphamide and plasma exchange are the standard of care in rapidly progressive glomerulonephritis or lung haemorrhage caused by antiglomerular basement membrane (anti-GBM) disease, and it is unusual to encounter patients at earlier stages. Steroids are universally used in addition. There is some evidence that plasma exchange may not be a critical part of treatment at an earlier stage. There is no more than anecdotal evidence for other therapies. Slower-onset therapies such as antibodies to B cells are rarely appropriate. If untreated, patients with severe anti-GBM disease will not recover renal function and are at risk of pulmonary haemorrhage. Evidence for the pathogenicity of circulating anti-GBM antibodies provides rationale for removal of circulating antibodies as rapidly as possible, whilst simultaneously inhibiting their synthesis. This was behind the introduction of the combination of plasma exchange with immunosuppressive therapy in mid 1970s, which revolutionized outcomes. Plasmapheresis aims to remove circulating pathogenic antibodies against GBM and possibly other mediators; cyclophosphamide prevents further synthesis of autoantibodies; and steroids act as anti-inflammatory agents to attenuate the glomerular inflammatory response initiated by anti-GBM antibodies. It is clear from experimental models and occasional observations in man that the anti-cell mediated effects of current therapies are important too. Outcomes vary, but in general patient survival is now good, while renal survival remains poor, in many series less than 50% at 1 year. Treatment is toxic and after an early peak in deaths due to pulmonary haemorrhage, secondary infections are the next threat. It may therefore be best not to immunosuppress patients with a very poor renal prognosis who appear to be at low risk of pulmonary haemorrhage. Treatment can usually be curtailed after 3 months without recurrence. ANCA and anti-GBM antibodies occur together in some patients. This is typically an older group which often has features of vasculitis, and the anti-GBM response may often be secondary. Longer treatment as for small vessel vasculitis is usually indicated.
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8

Cui, Zhao, Neil Turner, and Ming-hui Zhao. Alport post-transplant antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0075.

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Alport antiglomerular basement membrane (anti-GBM) disease is a rare example of disease caused by allo-sensitization after renal transplantation, first described in 1992. Because the recipient lacks a specific glomerular basement membrane (GBM) protein, they can become sensitized to the normal molecule present in the GBM of the donor kidney. The disease is restricted to the allograft. Interestingly severe disease arises from this only arises rarely, certainly less than 1 in 20, probably closer to 1 in 50. It characteristically causes late graft loss in a first transplant with accelerated tempo in later allografts, and in its most extreme form recurs within days. However, inexplicably some subsequent transplants do not provoke aggressive recurrence. Treatment of the most aggressive disease is difficult and in most cases has been ultimately unsuccessful. Lower levels of immune response, marked by linear binding of immunoglobulin-G to GBM without glomerular disease, are not uncommon in Alport patients after transplantation and should not lead to altered treatment. Immunoassays for anti-GBM antibodies can be misleading as in most cases the target of antibodies is the α‎‎‎5 chain of type IV collagen, rather than the α‎‎‎3 chain which is the target in spontaneous anti-GBM disease. Overall the outcome of transplantation in Alport syndrome is better than average. This complication is more likely in patients with partial or total gene deletion rather than point mutations, but no other predictive features have been identified.
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9

Cattran, Daniel C., and Heather N. Reich. Membranous glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0064_update_001.

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It has been clear for several decades from comparison with the rodent model disease Heymann nephritis that membranous glomerulonephritis (MGN) is an immune condition in which antibodies, usually autoantibodies, bind to targets on the surface of podocytes. However, the antigen in Heymann nephritis, megalin, is not present on human podocytes. The first potential antigen was identified by studying rare examples of maternal alloimmunization, leading to congenital membranous nephropathy in the infant caused by antibodies to neutral endopeptidase. More recently, the target of autoantibody formation in most patients with primary MGN has been identified to be the phospholipase A2 receptor, PLA2R. Genome-wide association studies identify predisposing genetic loci at HLADQ and at the locus encoding the autoantigen itself. So antibodies to at least two different molecular targets can cause MGN, and it seems likely that there may be other targets in secondary types of MGN, and possibly haptenized or otherwise modified molecules are implicated in drug- and toxin-induced MGN. Once antibodies are fixed, animal models and human observations suggest that complement is involved in mediating tissue damage. However, immunoglobulin G4, not thought to fix complement, is the predominant isotype in human MGN, and the mechanisms are not fully unravelled. Podocyte injury is known to cause proteinuria. In MGN, antibody fixation or cell damage may stimulate production of extracellular matrix to account for the increased GBM thickness with ‘podocyte type’ basement membrane collagen isoforms, and ultimately cell death and glomerulosclerosis.
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10

Group, Diagram, and Group Diagram. Patience Card Games (Collins Gem). HarperCollins Publishers, 1996.

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11

Group, Diagram, and Group Diagram. Patience Card Games (Collins Gem). HarperCollins Publishers, 1996.

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12

Hellerstein, David J., and Ron B. Aviram. Supportive Psychotherapy and Case Management. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199997510.003.0018.

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Psychotherapy of borderline personality disorder (BPD) has often focused on specialized and putatively more effective treatments such as dialectical behavioral therapy. In recent years, accumulating evidence suggests that many BPD patients benefit equally well from well-structured but less specialized care designed to meet their needs. Supportive psychotherapy (SPT) and various forms of clinical management, such as structured clinical management (SCM) and general psychiatric management (GPM), have been successfully adapted for treatment of BPD. This chapter describes the theoretical backgrounds for these approaches, main treatment techniques, and how they can be implemented to provide good outcomes for individuals diagnosed with BPD.
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13

Sanghani, Rupa Mehta, and Kim Allan Williams. Radionuclide Angiography. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199392094.003.0005.

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This chapter discusses the technique and use of radionuclide angiography with planar and tomographic imaging. Planar techniques have given way to tomographic imaging in recent years. An overview of RNA is given, including technical issues such as radiopharmaceutical administration, and performance aspects including image acquisition and data interpretation. First-pass RNA (FPRNA), gated planar equilibrium RNA (ERNA) and gated tomographic equilibrium blood pool imaging (GBP-SPECT) are discussed in detail. The use of RNA in select patient populations, including coronary artery disease, valvular disease and for monitoring chemotherapy is discussed. In addition, the use of RNA for the assessment of dyssynchrony is discussed.
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14

Filippi, Massimo, and Maria A. Rocca. Multiple Sclerosis: White Matter versus Gray Matter Involvement (The Cause of Disability in MS). Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0083.

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The classic view of multiple sclerosis (MS) as a chronic, inflammatory-demyelinating condition affecting solely the white matter (WM) of the central nervous system (CNS) has been challenged by the demonstration, from pathologic and magnetic resonance imaging (MRI) studies, of an extensive and diffuse involvement of the gray matter (GM). This observation has driven the application of modern MR technology and methods of analysis to quantify the extent and distribution of damage to the different compartments of the CNS, with the ultimate goal of improving our understanding of the factors associated with the accumulation of clinical disability and cognitive impairment in these patients.
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15

Venet, Fabienne, and Alain Lepape. Immunoparesis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0313.

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In parallel with an exaggerated pro-inflammatory response, critically-ill patients develop an immunosuppressive phase, termed immunoparesis/immunoparalysis or immune reprogramming. Innate and adaptive immune responses are affected. In particular, impaired neutrophil recruitment to injury sites and abnormal accumulation in remote sites; monocyte deactivation with preferential anti-inflammatory cytokine production and altered antigen presentation capacity; and a dramatic lymphopenia associated with major induction of apoptosis, functional, and phenotypic alterations have been described. The intensity and duration of this injury-induced immune dysfunction have been associated with an increased risk of death and secondary nosocomial infections. Innovative therapeutic strategies aiming at restoring immunological functions are currently being tested. GM-CSF appears to be an interesting candidate while IFN-γ‎ and IL-7 represent novel future therapeutic approaches. There is thus an urgent need for further clinical trials of such immunoadjuvant therapies that should include large cohorts of critically-ill patients stratified by relevant markers of immune dysfunction.
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16

Cassiman, David, Pascal Laforêt, and Fanny Mochel. Glycogen Storage Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0001.

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Glucose is the body’s major energy source, and carbohydrate serves as fuel—particularly during high-intensity exercise that requires rapid energy release. A deficiency of any of the enzymes involved in the catabolism of glycogen to glucose may cause symptoms, with hypoglycemia and exercise intolerance as the most common presentations. Glycogen storage disorders (GSD) affect muscle, liver, and brain. The most common GSDs affecting muscle are GSD II (Pompe disease) and GSD V (McArdle disease). GSDs affecting mainly the liver are GSD I, III, IV, VI, IX, XI. Most liver-GSDs present during infancy, with symptoms of hypoglycemia, impressive hepatomegaly, and retarded growth. Adult presentations have been reported for GSD Ia, III, IV, and IX.Adult polyglucosan body disease (APBD) is the main GSD affecting primarily the brain and mainly characterized by spastic paraplegia, axonal neuropathy and leukodystrophy. APBD is a subtype of GSD IV and is due to a deficiency of glycogen branching enzyme (GBE). Besides GSD IV, other GSDs have been reported to have CNS effects in some patients—notably GSD II and GSD III.
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17

Ver, Maria R., and Tammy S. Fouse. Vertical Banded Gastroplasty. Edited by Tomasz Rogula, Philip Schauer, and Tammy Fouse. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190608347.003.0036.

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Vertical banded gastroplasty (VBG) is the construction of a small vertical pouch using a linear stapler, with addition of a Marlex band placed through a window formed by a circular stapler. Compared to gastric bypass, VBG maintains a more normal anatomy of the upper gastrointestinal tract. However, due to poor long-term outcomes and a high percentage of patients requiring revisional surgery, most bariatric surgeons have abandoned VBG as a primary bariatric procedure. Early complications include acute gastric distention and gastric leaks. Late complications include mesh migration or erosion, stomal stenosis, staple-line disruption, and gastrogastric fistulas. The most common revision is to Roux-en-Y gastric bypass (RYGB). There are reports of other revisions, such as the vertical banded gastroplasty−gastric bypass (VBG-GB), re-VBG, RYGB-on-VBG, VBG to duodenal switch, VBG to biliopancreatic diversion, VBG to sleeve gastrectomy, VBG to adjustable gastric band, and VBG reversal, as well as endoscopic alternatives.
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18

Karmali, Mohamed A., and Jan M. Sargeant. Verocytotoxin-producing Escherichia coli (VTEC) infections. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0008.

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Verocytotoxin (VT)-producing Escherichia coli (VTEC), also known as Shiga toxin producing E. coli (STEC), are zoonotic agents, which cause a potentially fatal illness whose clinical spectrum includes diarrhoea, haemorrhagic colitis, and the haemolytic uraemic syndrome (HUS). VTEC are of serious public health concern because of their association with large outbreaks and with HUS, which is the leading cause of acute renal failure in children. Although over 200 different OH serotypes of VTEC have been associated with human illness, the vast majority of reported outbreaks and sporadic cases of VTEC-infection in humans have been associated with serotype O157:H7.VTs constitute a family of related protein subunit exotoxins, the major ones implicated in human disease being VT1, VT2, and VT2c. Following their translocation into the circulation, VTs bind to endothelial cells of the renal glomeruli, and of other organs and tissues via a specific receptor globotriosylceramide (Gb 3), are internalized by a process of receptor-mediated endocytosis, and cause subcellular damage that results in the characteristic microangiopathic disease observed in HUS.The incubation period of VTEC-associated illness is about 3–5 days. After ingestion VTEC (especially of serotype O157:H7) multiply in the bowel and colonize the mucosa of probably the large bowel with a characteristic attaching and effacing (AE) cytopathology. Colonization is followed by the translocation of VTs into the circulation and the subsequent manifestation of disease.The majority of patients with uncomplicated VTEC infection recover fully with general supportive measures. Historically, the case-fatality rate was high for HUS. However, improvement in the treatment of renal failure and the attendant biochemical disturbances has substantially improved the outlook, although long-term sequelae may develop.Ruminants, especially cattle, are the main reservoirs of VTEC. Infection is acquired through the ingestion of contaminated food, especially under-cooked hamburger, through direct contact with animals, via contaminated water or environments, or via personto-person transmission.The occurrence of large outbreaks of food-borne VTEC-associated illness has promoted close scrutiny of this zoonoses at all levels in the chain of transmission, including the farm, abattoir, food processing, packaging and distribution plants, the wholesaler, the retailer and the consumer. While eradication of VTEC O157 at the farm may not be an option, interventions to increase animal resistance or to decrease animal exposure are being developed and validated. Hazard Analysis and Critical Control Programmes are being implemented in the processing sector and appear to be associated with temporal decreases in VTEC serotype O157 illness in humans. Education programmes targeting food handling procedures and hygiene practices are being advocated at the retail and consumer level. Continued efforts at all stages from the farm to the consumer will be necessary to reduce the risk of VTEC-associated illness in humans.
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19

Ham, Christopher. Health Policy in Britain: The Politics and Organisation of the National Health Service; Fifth Edition (Public Policy and Politics). 5th ed. Palgrave Macmillan, 2004.

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20

Ham, Christopher. Health Policy in Britain: The Politics and Organization of the National Health Service (Studies in Social Policy). 2nd ed. Baywood Pub Co, 1986.

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21

Ham, Christopher. Health Policy in Britain: The Politics and Organisation of the National Health Service; Fifth Edition (Public Policy and Politics). 5th ed. Palgrave Macmillan, 2004.

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22

Ham, Christopher. Health Policy in Britain: The Politics and Organization of the National Health Service. Taylor & Francis Group, 2019.

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