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Books on the topic 'Porphyrin metabolism'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Moore, Michael R., Kenneth E. L. McColl, Claude Rimington, and Abraham Goldberg. Disorders of Porphyrin Metabolism. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-1277-2.

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2

International Congress on Porphyrins and Porphyrias (2nd 1985 Paris, France). Porphyrins and porphyrias =: Porphyrines et porphyries : proceedings of the Second International Congress on Porphyrins and Porphyrias held in Paris (France), 19-22 June, 1985. J. Libbey, 1986.

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3

International, Congress on Porphyrins and Porphyrias (2nd 1985 Paris France). Porphyrins and porphyrias: Proceedings of the Second International Congress on Porphyrins and Porphyrias held in Paris (France) 19-22 June, 1985 = Porphyrines et porphyries. Editions INSERM, 1986.

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4

The chemistry and biochemistry of N-substituted porphyrins. VCH Publishers, 1987.

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5

Parker, James N., and Philip M. Parker. Porphyria: A bibliography and dictionary for physicians, patients, and genome researchers [to Internet references]. ICON Health Publications, 2007.

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6

R, Moore Michael, and Wintrobe Maxwell Myer 1901-, eds. Disorders of porphyrin metabolism. Plenum Medical Book Co., 1987.

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7

A, Goldberg, K. E. L. McColl, and M. R. Moore. Disorders of Porphyrin Metabolism. Springer, 2012.

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8

Wolstenholme, G. E. W., and Elaine C. P. Millar. Porphyrin Biosynthesis and Metabolism. Wiley & Sons, Incorporated, John, 2009.

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9

Goldberg, Sir Abraham. Disorders of Porphyrin Metabolism. Springer, 2012.

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10

Webb, S. M., and R. A. Hoffman. Harderian Glands: Porphyrin Metabolism, Behavioral, and Endocrine Effects. Springer, 1992.

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11

1952-, Webb S. M., ed. Harderian glands: Porphyrin metabolism, behavioral, and endocrine effects. Springer-Verlag, 1992.

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12

Sybert, Virginia P. Metabolic Disease. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780195397666.003.0011.

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Porphyrias – Congenital Erythropoietic Porphyria – Erythropoietic Protoporphyria – Hereditary Coproporphyria – Porphyria Cutanea Tarda – Variegate Porphyria – Mucopolysaccharidoses – Hunter Syndrome – Other Metabolic Disorders – Acrodermatitis Enteropathica – Alkaptonuria – Biotinidase Deficiency – Familial Cutaneous Amyloidosis – Prolidase Deficiency

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13

Sybert, Virginia P. Metabolic Disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190276478.003.0011.

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Chapter 11 covers Porphyrias (Congenital Erythropoietic Porphyria, Erythropoietic Protoporphyria, Hereditary Coproporphyria, Porphyria Cutanea Tarda, and Variegate Porphyria), Mucopolysaccharidoses (Hunter Syndrome), and Other Metabolic Disorders (Acrodermatitis Enteropathica, Alkaptonuria, Biotinidase Deficiency, Familial Cutaneous Amyloidosis, and Prolidase Deficiency). Each condition is discussed in detail, including dermatologic features, associated anomalies, histopathology, basic defect, treatment, mode of inheritance, prenatal diagnosis, and differential diagnosis.

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14

K, Silbergeld Ellen, Fowler Bruce A, and New York Academy of Sciences., eds. Mechanisms of chemical-induced porphyrinopathies. New York Academy of Sciences, 1987.

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15

Deegan, Patrick. Porphyria. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0179.

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This chapter discusses six diseases caused by inborn errors of metabolism affecting the biosynthesis of haem. Haem is a tetracyclic metal-binding compound involved in oxygen transport (in haemoglobin and myoglobin) and redox reactions (e.g. in the cytochrome P450 system). Each of these conditions is caused by a single gene defect in one of the enzymes involved in the biosynthesis of haem. Inheritance is usually autosomal dominant with incomplete penetrance. The enzyme defect results in disease, not as a result of deficiency of the reaction product, but as a result of accumulation of precursors

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16

Nageshwaran, Sathiji, Heather C. Wilson, Anthony Dickenson, and David Ledingham. Metabolic disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199664368.003.0016.

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This chapter discusses the clinical features and management of inborn errors of metabolism (lysosomal storage disorders, peroxisomal disorders, Wilson’s disease, porphyria, and phenylketonuria), vitamin and nutrient deficiency syndromes, and neurological toxicity syndromes.

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17

Dierdorf, Stephen F. Introduction to Metabolic and Endocrine Diseases. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0024.

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Patients may have metabolic and endocrine dysfunction that is primary and results in surgical pathology, or the surgical condition can produce metabolic changes that influence the administration of anesthesia. These disorders can vary with incidence of occurrence from commonly encountered situations such as hyperkalemia, to more rare disorders such as the porphyrias. Knowledge of the metabolic/endocrine derangements can lead to treatment that can be life-saving during the perioperative period. While it is important to periodically review the new developments in metabolism and endocrinology dis

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18

Kuimov, Krivosheev, and Krivosheev. Medical disease at of an manifest and latent violations of a porphyrinic metabolism. Infra-M Academic Publishing House, 2013. http://dx.doi.org/10.12737/1135.

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19

Aldridge, W. Norman, and Francesco De Matteis. Heme and Hemoproteins. Springer-Verlag Berlin Heidelberg New York, 2011.

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20

Jolly, Elaine, Andrew Fry, and Afzal Chaudhry, eds. Endocrine. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199230457.003.0007.

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Chapter 7 covers the basic science and clinical topics relating to the endocrine system which trainees are required to learn as part of their basic training and demonstrate in the MRCP. It covers endocrine physiology, acid-base balance, thyrotoxicosis, hypothyroidism, goitre and thyroid nodule, Cushing syndrome, acromegaly, hyperprolactinaemia, hypopituitarism, diabetes insipidus, adrenal incidentaloma, primary hyperaldosteronism, adrenal insufficiency, phaeochromocytoma and paraganglioma , male hypogonadism and Gynaecomastia, menstrual disorders and anovulation, hirsutism and the polycystic o

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21

Cassiman, David, and Wouter Meersseman. Tyrosinemia Type I. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0013.

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Tyrosinemia type 1 (HT-1) is a rare metabolic disorder affecting degradation pathways of the amino acid tyrosine. HT-1 presents with liver, kidney and/or bone disease and can cause acute porphyria attacks. Biochemical diagnosis is made by measuring raised plasma tyrosine and detection of succinylacetone in urine. Long-term management with diet and nitisinone leads to excellent short term results, but since long term effects are largely unknown, life-long treatment and follow-up for liver malignancy, bone disease and kidney disease seem necessary. HT-1 is treatable by liver transplantation.

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22

Wiffen, Philip, Marc Mitchell, Melanie Snelling, and Nicola Stoner. Patient management issues. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198735823.003.0010.

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This chapter outlines information relevant to pharmacists and other healthcare professionals on patient management issues related to special populations. It covers management of patients with liver impairment, including drug use, drug dosing, and hepatorenal syndrome. Drug use and dosing in renal impairment is discussed and the various methods of assessing or calculating glomerular filtration rate are reviewed. The use of drugs in pregnancy and breastfeeding is discussed with guidance given on assessing the risks versus benefits of drug use in these situations. Drugs and dietary considerations

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