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Journal articles on the topic 'Cystic fibrosis'

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Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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1

Marin, Angelica-Cristina, Dana-Teodora Anton-Păduraru, Nicoleta-Bianca Cloşcă, Doina Mihăilă, and Marin Burlea. "Cystic fibrosis and Helicobacter pylori infection." Romanian Journal of Infectious Diseases 19, no. 2 (June 30, 2016): 54–59. http://dx.doi.org/10.37897/rjid.2016.2.2.

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Helicobacter pylori infection is the most frequent bacterian infection and the main cause of duodenal ulcerations. The prevalence in patients with cysic fibrosis is controversial. The paper present generale data about Helicobacter pylori and the particularities of this infection in cystic fibrosis (cystic fibrosis paradox). The authors concluded that although the prevalence of Helicobacter pylori and its role in gastroduodenal disease in cystic fibrosis are controversial, however, its role should not be underestimated.

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2

Jones, Andrew. "Cystic Fibrosis and Non-Cystic Fibrosis Bronchiectasis." Seminars in Respiratory and Critical Care Medicine 36, no. 02 (March 31, 2015): 167–68. http://dx.doi.org/10.1055/s-0035-1547317.

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3

&NA;. "Cystic fibrosis and fibrosing colonopathy." Advances in Anatomic Pathology 3, no. 2 (March 1996): 112. http://dx.doi.org/10.1097/00125480-199603000-00015.

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4

Smyth, R. L. "Fibrosing colonopathy in cystic fibrosis." Archives of Disease in Childhood 74, no. 5 (May 1, 1996): 464–68. http://dx.doi.org/10.1136/adc.74.5.464.

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5

LYON, IAN C. T., and DIANNE R. WEBSTER. "Newborn Screening for Cystic Fibrosis." Pediatrics 87, no. 6 (June 1, 1991): 954–55. http://dx.doi.org/10.1542/peds.87.6.954.

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To the Editor.— The report on newborn screening for cystic fibrosis1 illustrates the need for continued evaluation of such programs. The authors state that the identification of cases of cystic fibrosis (CF) by an elevated level of immunoreactive trypsinogen (IRT) in second (follow-up) samples from infants with positive initial screening tests could result in false negatives in 27% of cases of cystic fibrosis without meconium ileus (MI). We have screened 401 122 infants using the method originally reported.2

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6

Grody, Wayne W. "Cystic Fibrosis." Archives of Pathology & Laboratory Medicine 123, no. 11 (November 1, 1999): 1041–46. http://dx.doi.org/10.5858/1999-123-1041-cf.

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Abstract Objective.—To review the current status of scientific knowledge and opinion regarding molecular genetic testing of mutations in the CFTR gene for purposes of diagnosis and population carrier screening of cystic fibrosis (CF). Data Sources.—Published research findings on the nature of the CFTR gene, pilot population screening studies in the United States and Europe, and ongoing deliberations of professional and governmental agencies considering implementation of widespread testing. Study Selection.—Findings relevant to the molecular heterogeneity of CFTR mutations and its implications for population carrier screening were considered. Data Extraction.—Information was extracted from studies published by us and others, as made available to recent consensus panels and professional committees. Data Synthesis.—These data were reevaluated in light of recent movements in professional and public policy regarding acceptability and desirability of widespread CF mutation testing. Effects to date of such testing on patient outcomes is reported. Conclusions.—The ability to test for CFTR mutations at the molecular level has already improved the diagnosis of symptomatic patients and expanded the reproductive options of family members of CF patients. The same technology also holds promise of identifying asymptomatic carriers and at-risk couples without family history in the general population so that they too might be offered prenatal diagnosis or other options. However, a number of key questions remain to be worked out before a widespread national screening program can be put into practice. These include the target population to be offered testing (the entire population vs high-risk ethnic groups), the size and nature of the mutation test panel (universal vs ethnic specific), the inclusion or exclusion of CFTR variants that do not cause classical CF, the optimal testing technology, appropriate standards for laboratory quality assurance, and the development of sufficient educational materials and genetic counseling resources for test delivery, reporting, and interpretation. The answers to these questions will be relevant not only to CF testing but also to many other large-scale molecular genetic screening programs being considered in the future.

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7

Wendekier, Camille, and Katheryn Wendekier-Raybuck. "Cystic fibrosis." Nursing 51, no. 6 (June 2021): 32–38. http://dx.doi.org/10.1097/01.nurse.0000751344.57701.75.

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8

Davis, P. B. "Cystic Fibrosis." Pediatrics in Review 22, no. 8 (August 1, 2001): 257–64. http://dx.doi.org/10.1542/pir.22-8-257.

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9

Montgomery, G. S., and M. Howenstine. "Cystic Fibrosis." Pediatrics in Review 30, no. 8 (July 31, 2009): 302–10. http://dx.doi.org/10.1542/pir.30-8-302.

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10

Paranjape, S. M., and P. J. Mogayzel. "Cystic Fibrosis." Pediatrics in Review 35, no. 5 (May 1, 2014): 194–205. http://dx.doi.org/10.1542/pir.35-5-194.

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11

Radlovic, Nedeljko. "Cystic fibrosis." Srpski arhiv za celokupno lekarstvo 140, no. 3-4 (2012): 244–49. http://dx.doi.org/10.2298/sarh1204244r.

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Cystic fibrosis (CF) is a multisystemic autosomal recessive disease caused by a defect in the expression of CFTR protein, i.e. chloride channel present in the apical membrane of respiratory, digestive, reproductive and sweat glands epithelium. It primarily occurs in the Caucasians, while being considerably or exceptionally rare in persons of other races. Absence, deficit or structural and functional abnormalities of CFTR protein lead to mucosal hyperconcentration in the respiratory, digestive and reproductive systems and malabsorption of chloride and sodium in the sweat glands. Thus, the clinical features of patients? with CF are predominated by respiratory, digestive and reproductive disorders, as well as the tendency to dehydration in the condition of increased sweating. Beside genotype variations, the degree of disease manifestation is also essentially influenced by various exogenous factors, such as the frequency and severity of respiratory infections, the level of aero-pollution, quality of immunoprophylaxis, patients? nutritional condition and other. Chloride concentration of over 60 mmol/L in sweat, a high level of immunoreactive chymotrypsinogen in blood and the verification of homozygous mutation of CFTR gene are the basic methods in the diagnostics of the disease. CF belongs to the group of severe and complex chronic diseases, and therefore requires multidisciplinary therapeutic approach. Owing to the improvement of healthcare provision, most patients with CF now survive into adulthood. In addition, their quality of life is also considerably improved.

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12

Dickinson, Kimberly M., and Joseph M. Collaco. "Cystic Fibrosis." Pediatrics in Review 42, no. 2 (February 2021): 55–67. http://dx.doi.org/10.1542/pir.2019-0212.

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13

Colin, A. A., and M. E. B. Wohl. "Cystic Fibrosis." Pediatrics in Review 15, no. 5 (May 1, 1994): 192–200. http://dx.doi.org/10.1542/pir.15-5-192.

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14

Mellis, Craig M. "Cystic fibrosis." Medical Journal of Australia 143, no. 6 (September 1985): 227–28. http://dx.doi.org/10.5694/j.1326-5377.1985.tb122950.x.

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15

Leitch, AE, and HC Rodgers. "Cystic fibrosis." Journal of the Royal College of Physicians of Edinburgh 43, no. 2 (June 4, 2013): 144–50. http://dx.doi.org/10.4997/jrcpe.2013.212.

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16

Orenstein, David M., and A'Delbert Bowen. "CYSTIC FIBROSIS." Radiologic Clinics of North America 31, no. 3 (May 1993): 617–30. http://dx.doi.org/10.1016/s0033-8389(22)02609-4.

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17

Yashin, S. S., Y. R. Yunusova, N. V. Isakova, and Y. V. Serdobolskaya. "CYSTIC FIBROSIS." Современные проблемы науки и образования (Modern Problems of Science and Education), no. 5 2022 (2022): 5. http://dx.doi.org/10.17513/spno.32008.

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18

Shteinberg, Michal, Iram J. Haq, Deepika Polineni, and Jane C. Davies. "Cystic fibrosis." Lancet 397, no. 10290 (June 2021): 2195–211. http://dx.doi.org/10.1016/s0140-6736(20)32542-3.

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19

Paranjape, Shruti M., and Peter J. Mogayzel. "Cystic Fibrosis." Pediatrics In Review 35, no. 5 (May 1, 2014): 194–205. http://dx.doi.org/10.1542/pir.35.5.194.

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20

Colin, Andrew A., and Mary Ellen B. Wohl. "Cystic Fibrosis." Pediatrics In Review 15, no. 5 (May 1, 1994): 192–200. http://dx.doi.org/10.1542/pir.15.5.192.

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Cystic fibrosis (CF) is an autosomal recessive inherited disorder caused by mutations of both alleles of the CF gene. These mutations result in abnormalities in the production or function of the gene product, a protein known as the cystic fibrosis membrane conductance regulator (CFTR). The CF gene is large (250 000 base pairs) and located on chromosome 7. A deletion of three base pairs that results in the absence of phenylalanine at codon 508 is the most common defect (designated F 508) and accounts for about 70% of the mutant genes in North American populations. Other genotypes observed with some frequency (but <3%) are G542X, G551D, W1282X, W1303K, and R553X. The twelve most common CF gene mutations account for approximately 85% of cases in North America. Mutations other than F508 number more than 200 and account for the remaining cases. Most of these 200-odd mutations are "private," observed only in the affected kindred. Because the CF locus has so many DNA sequence changes associated with disease, precise genetic testing cannot replace clinical criteria for diagnosis, and the sweat test remains an important diagnostic test. The CF gene is expressed in epithelial cells of the pancreas, sweat and salivary glands, intestine, and reproductive and respiratory tracts, particularly in the submucosal glands.

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21

Montgomery, Gregory S., and Michelle Howenstine. "Cystic Fibrosis." Pediatrics In Review 30, no. 8 (August 1, 2009): 302–10. http://dx.doi.org/10.1542/pir.30.8.302.

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22

Davis, Pamela B. "Cystic Fibrosis." Pediatrics In Review 22, no. 8 (August 1, 2001): 257–64. http://dx.doi.org/10.1542/pir.22.8.257.

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23

Wendekier, Camille, and Katheryn Wendekier-Raybuck. "Cystic fibrosis." Nurse Practitioner 46, no. 9 (September 2021): 48–55. http://dx.doi.org/10.1097/01.npr.0000769756.82495.f3.

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24

Krauth, Christian, Noushin Jalilvand, Tobias Welte, and Reinhard Busse. "Cystic Fibrosis." PharmacoEconomics 21, no. 14 (2003): 1001–24. http://dx.doi.org/10.2165/00019053-200321140-00002.

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25

Cleghorn, Geoffrey, and Ross Shepherd. "Cystic fibrosis." Medical Journal of Australia 144, no. 2 (January 1986): 109–10. http://dx.doi.org/10.5694/j.1326-5377.1986.tb113679.x.

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26

Reis, Francisco J. C., and Neiva Damaceno. "Cystic fibrosis." Jornal de Pediatria 74, no. 7 (November 15, 1998): 76–94. http://dx.doi.org/10.2223/jped.489.

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27

Rowe, Steven M., Stacey Miller, and Eric J. Sorscher. "Cystic Fibrosis." New England Journal of Medicine 352, no. 19 (May 12, 2005): 1992–2001. http://dx.doi.org/10.1056/nejmra043184.

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28

Geddes, Duncan. "Cystic fibrosis." Clinical Medicine 7, no. 5 (October 1, 2007): 445–46. http://dx.doi.org/10.7861/clinmedicine.7-5-445.

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29

Freeman, M. V. "Cystic fibrosis." Journal of Ultrasound in Medicine 8, no. 5 (May 1989): 285–86. http://dx.doi.org/10.7863/jum.1989.8.5.285.

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30

Figarella, Catherine. "Cystic Fibrosis." Journal of Pediatric Gastroenterology and Nutrition 13, no. 4 (November 1991): 437. http://dx.doi.org/10.1097/00005176-199111000-00026.

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31

Williams, Rachel, and Helen Barker. "Cystic Fibrosis." InnovAiT: Education and inspiration for general practice 3, no. 12 (November 19, 2010): 743–52. http://dx.doi.org/10.1093/innovait/inq072.

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32

Elborn, J. Stuart, and Margaret McCloskey. "Cystic fibrosis." Current Opinion in Infectious Diseases 10, no. 2 (April 1997): 128–32. http://dx.doi.org/10.1097/00001432-199704000-00011.

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33

Brennan, Amanda L., and Duncan M. Geddes. "Cystic fibrosis." Current Opinion in Infectious Diseases 15, no. 2 (April 2002): 175–82. http://dx.doi.org/10.1097/00001432-200204000-00013.

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34

LITTLEWOOD, J. M. "Cystic fibrosis." Archives of Disease in Childhood 77, no. 5 (November 1, 1997): 463. http://dx.doi.org/10.1136/adc.77.5.463j.

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35

Brennan, Amanda L., and Duncan M. Geddes. "Cystic fibrosis." Current Opinion in Internal Medicine 1, no. 4 (August 2002): 363–70. http://dx.doi.org/10.1097/00132980-200201040-00007.

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36

Wicks, Emma. "Cystic fibrosis." BMJ 334, no. 7606 (June 14, 2007): 1270–71. http://dx.doi.org/10.1136/bmj.39188.741944.47.

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37

Davies, Jane C., Eric W. F. W. Alton, and Andrew Bush. "Cystic fibrosis." BMJ 335, no. 7632 (December 13, 2007): 1255–59. http://dx.doi.org/10.1136/bmj.39391.713229.ad.

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38

Standen, Jen. "Cystic fibrosis." InnovAiT: Education and inspiration for general practice 13, no. 1 (November 27, 2019): 39–46. http://dx.doi.org/10.1177/1755738019883322.

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In the UK over 10 000 people live with cystic fibrosis (CF), with 1-in-25 people being carriers of the disease. Multidisciplinary care is provided by tertiary care CF centres, with or without local secondary service shared care agreements. There are still, however, several reasons why CF sufferers or their families present to their GPs. This article aims to provide a brief overview of CF and its management. It also gives the information needed to guide patients about genetic testing and neonatal screening for the disease.

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39

Harris, A. "Cystic Fibrosis." Journal of Medical Genetics 27, no. 2 (February 1, 1990): 144. http://dx.doi.org/10.1136/jmg.27.2.144.

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40

Shale, D. J. "Cystic Fibrosis." Journal of Medical Genetics 29, no. 3 (March 1, 1992): 216. http://dx.doi.org/10.1136/jmg.29.3.216-b.

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41

Welsh, Michael J., and Alan E. Smith. "Cystic Fibrosis." Scientific American 273, no. 6 (December 1995): 52–59. http://dx.doi.org/10.1038/scientificamerican1295-52.

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42

Taussig, Lynn, and Louis Landau. "Cystic Fibrosis." Seminars in Respiratory and Critical Care Medicine 1, no. 02 (March 20, 2008): 167–82. http://dx.doi.org/10.1055/s-2007-1018904.

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43

Drotar, Dennis. "Cystic Fibrosis." Journal of Pediatric Psychology 20, no. 4 (1995): 413–16. http://dx.doi.org/10.1093/jpepsy/20.4.413.

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44

Mearns, M. B. "Cystic fibrosis." Archives of Disease in Childhood 60, no. 3 (March 1, 1985): 272–77. http://dx.doi.org/10.1136/adc.60.3.272.

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45

David, T. J. "Cystic fibrosis." Archives of Disease in Childhood 65, no. 1 (January 1, 1990): 152–57. http://dx.doi.org/10.1136/adc.65.1.152.

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46

FARRALL, MARTIN, and PETER J. SCAMBLER. "Cystic fibrosis." Nature 338, no. 6210 (March 1989): 24. http://dx.doi.org/10.1038/338024c0.

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47

&NA;. "Cystic fibrosis." Inpharma Weekly &NA;, no. 803 (September 1991): 6. http://dx.doi.org/10.2165/00128413-199108030-00013.

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48

Peckham, Daniel G., and Steve Conway. "Cystic fibrosis." Medicine 32, no. 1 (January 2004): 124–28. http://dx.doi.org/10.1383/medc.32.1.124.28472.

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49

Lewis, Myra J., Eugene H. Lewis, Jean A. Amos, and Gregory J. Tsongalis. "Cystic Fibrosis." Pathology Patterns Reviews 120, suppl_1 (December 1, 2003): S3—S13. http://dx.doi.org/10.1309/duuvfr11w595v7fe.

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50

Nelson, R. "Cystic Fibrosis." BMJ 310, no. 6984 (April 8, 1995): 949. http://dx.doi.org/10.1136/bmj.310.6984.949.

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