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Clinical Trial Details — Status: Not yet recruiting

Administrative data

NCT number NCT04379726
Other study ID # FCMilano
Secondary ID
Status Not yet recruiting
Phase
First received
Last updated
Start date July 1, 2020
Est. completion date September 1, 2023

Study information

Verified date May 2020
Source Fondazione IRCCS Ca' Granda, Ospedale Maggiore Policlinico
Contact Emanuela Orsi, MD
Phone 0255034590
Email emanuela.orsi@policlinico.mi.it
Is FDA regulated No
Health authority
Study type Observational

Clinical Trial Summary

Cystic fibrosis is a genetic disorder caused by mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene, leading to pulmonary infections, sinus disease, pancreatic insufficiency, hepatobiliary disease and male infertility, with respiratory failure being the primary cause of death. Cystic Fibrosis Related Diabetes (CFRD) in one of the most common complication of cystic fibrosis (CF) and it's associated with a worse respiratory and nutritional state, with a negative impact on life expectancy. It differs from type 1 diabetes and type 2 diabetes for particular characteristics making this disease a separated clinical entity.

To date, there is a lack of evidence on many aspects concerning this disease:

- the pathophysiology of the disease: decreased insulin secretion has historically been seen has the major trigger for CFRD, but data about this mechanism are scarce and conflicting. Moreover, the role of insulin-resistance seems to be not consistent, but pulmonary exacerbations are very common and, in this setting, insulin sensitivity can worsen significantly.

- the relationship between its development and particular genetic settings: certain CFTR genotypes are known to be most related to the risk of diabetes, and only few susceptibility genes for type 2 diabetes have been evaluated as potential predisposing factors for CFRD.

- the relationship between the therapeutic optimization and its impact on metabolic status and lung function: CFRD is known to be associated with worse clinical outcomes, reflected in more frequent clinical exacerbations, greater reduction in lung function, poorer nutritional status and decreased survival. It has also been demonstrated that insulin therapy can improve pulmonary function, increase body weight and reduce lung exacerbations. However, no study on the clinical impact of the optimization of insulin therapy on pulmonary outcomes and life expectancy are available in this population.

- finally, no data about potential predisposing pre-transplant risk factors for development of post-transplant DM are available

For this reason, the investigators have structured a study with the aim to:

- characterize the pathophysiological process leading to CFRD, with assessment of the relative contribution of the insulin resistance and the β-cellular secretion impairment

- define the prevalence of CFRD in relation to the mutations of the CFTR gene and to the presence of candidate genes for the development of type 2 diabetes

- perform a proteomic analysis to identify potential proteomic biomarkers among CFRD patients

- evaluate the body composition, muscle performance and respiratory outcomes in patients on insulin therapy, before and after therapeutic optimization, in a follow-up period of 24 months.

- identify eventual predisposing factors for the development of post-transplant diabetes in subjects without pre-transplant CFRD.


Description:

The study aims are:

- Task 1: pathophysiological characterization of CFRD with assessment of the relative contribution of the insulin resistance and the β-cellular secretion impairment through the use of a Minimum Model applied to OGTT for the evaluation of insulin sensitivity and secretion

- Task 2:

2a) determination of the prevalence of CFRD in relation to the mutations of the CFTR gene (presence of mutations with residual function of the CFTR protein) 2b) determination of the prevalence of CFRD in relation to the presence of candidate genes for the devel-opment of type 2 diabetes (NOTCH2, BCL11A, THADA, IGFBP-2, PPARG, ADAMTS9, CDKAL1, VEFGA, JAZF1, CDKN2A / 2B, HHEX, CDC123 / CAMK1D, TCF7L2, KCNJ11, DCD, TSPAN8 / LGR5, FTO, WFS1, SLC30A8 and INS).

2c) determination of variations in the proteomic analysis of CFRD patients compared to CF without DM and a control group of healthy individuals.

- Task 3: evaluation of the effect of the therapeutic optimization of glycometabolic control on body composition and respiratory outcomes in patients on insulin therapy, in a follow-up period of 24 months.

- Task 4: identification of predisposing factors for the development of post-transplant diabetes in subjects without CFRD.

METHODS:

All CF patients currently followed at the Unit of Pulmonology of our Center (250 subjects) will be considered eligible for the study.

Total duration of the study: 156 weeks (3 years).

The enrolled patients will be divided into two groups:

GROUP 1: subjects with a negative history for CFRD or with a CFRD diagnosis that does not require insulin therapy GROUP 2: subjects suffering from CFRD in insulin therapy

Protocol 1: Group 1; metabolic and anthropometric evaluation and assessment of insulin sensitivity / secretion.

Protocol 2: Group 1 and Group 2; genetic evaluation / proteomic evaluation Protocol 3: Group 2; pre- and post-intervention metabolic, anthropometric and nutritional assessment.

Protocol 4: Group 1 patients without CFRD undergoing lung transplantation (10); genetic, metabolic, an-thropometric and pre-and post-transplant assessment of insulin sensitivity / secretion.

Patients will undergo a:

1. METABOLIC EVALUATION: a venous sampling will be performed for blood glucose, HbA1c, total cholesterol, HDL, triglycerides, blood count, albumin, total proteins, pseudocholinesterase, AST, ALT, GGT, ALP, 25OHvitD

2. GENETIC EVALUATION: the investigators will evaluate the specific genetic mutation of the CFTR gene and the presence of gene variants related to the development of DM2 (NOTCH2, BCL11A, THADA, IGFBP-2, PPARG, ADAMTS9, CDKAL1, VEFGA, JAZF1, CDKN2A / 2B, HHEX, CDC123 / CAMK1D, TCF7L2, KCNJ11, DCD, TSPAN8 / LGR5, FTO, WFS1, SLC30A8 and INS)

3. PROTEOMIC EVALUATION: the investigators will perform a Mass Spectrometry to identify variations in the protein pattern expression in CFRD patients if compared to CF patients without DM and healthy control individuals. The list of analyzed protein is available in supplemental data 2.

4. ANTROPOMETRIC EVALUATION. the anthropometric evaluation will be performed with objective exami-nation (Body Mass Index - BMI, waist circumference - CV and hip circumference - CF) , DEXA total body and bioimpedentiometry

5. DYNAMIC EVALUATION OF INSULIN SENSITIVITY AND β CELL SECRETION. Patients will undergo a 5-hours OGTT with serial blood samples and with the application of a Mathematical Model adapted ad hoc (Appendix 1 for a detailed description of the model), in order to quantify the contribution of insulin resistance and β-cell secretion to the development of CFRD

6. PULMONARY EVALUATION. According to clinical practice, patients will be subjected to respiratory function tests with the calculation of FEV1 (absolute and percentage), exacerbation rate, rate of severe exacerbation (need of hospitalization), patient-reported outcomes (PROs) obtained from the sCF-quality of life questionnaire, which will be provided to patients in paper form.

SAMPLE SIZE AND STATISTICAL ANALYSIS:

Referring to the primary objective of the project, the observational nature of the study and the absence of evidence about the topic make a precise evaluation of the power of the study a difficult issue. However, considering the number of patients available and followed by our Center (n = 136), it has been calculated that the present study will have the power of 80% and an alpha level equal to 5% to show a significant reduction of at least 25% in the 1st phase secretion in the group of diabetics if compared to the non-diabetic group (assuming a mean value in non-diabetics of 1500 (aggiungere udm) and a SD of 500 (udm) (Pass v. 11 NCSS software, LCC, Kaysville, Utah, USA).

A series of descriptive analyzes will be performed: the continuous variables will be presented as averages and standard deviations or median with interquartile ranges, depending on the distribution. Frequency distributions will be presented as numbers and percentages. Data will also be presented graphically with histograms and "Box-and-Whisker" plots in order to evaluate potential anomalous values, allowing a further data-check phase in order to have reliable data for subsequent analyzes. Differences between the groups will be analyzed using parametric tests (t-test or ANOVA) without repeated tests or repeated tests, depending on the task of the project. If the normality of the distributions were violated (normal test based on the Shapiro-Wilk statistics), non-parametric technical correspondents will be used. Categorical data will be compared using contingency tables through the Chi-square test or Fisher's exact test, where appropriate. All tests will be two-tailed and p-values less than 5% will be considered statistically significant.

A series of descriptive analyzes will be performed: the continuous variables will be presented as averages and standard or median deviations with interquartile ranges, depending on the distribution. Frequency distributions will be presented as numbers and percentages. The data will also be presented graphically through histograms and "Box-and-Whisker" plots in order to evaluate potential anomalous values that will allow a further data-check phase in order to have valid data for subsequent analyzes. The differences between the groups will be analyzed using parametric techniques (t-test or ANOVA) without repeated tests or with repeated tests, depending on the task of the project. If the normality of the distributions was violated (normality test based on the Shapiro-Wilk statistics), corresponding non-parametric techniques will be used. Categorical data will be compared using contingency tables through the Chi-square test or Fisher's exact test, where appropriate. All tests will be two-tailed and a p-values less than 5% will be considered statistically significant.


Recruitment information / eligibility

Status Not yet recruiting
Enrollment 150
Est. completion date September 1, 2023
Est. primary completion date July 1, 2023
Accepts healthy volunteers No
Gender All
Age group 18 Years to 45 Years
Eligibility Inclusion Criteria:

- written informed

- diagnosis of cystic fibrosis

Exclusion Criteria:

- celiac disease

- pregnancy

- diagnosis of T1DM

Study Design


Intervention

Behavioral:
therapeutic optimization
patients with diagnosis of CFRD will undergo the gold standard treatment for the disease (insulin therapy)

Locations

Country Name City State
n/a

Sponsors (1)

Lead Sponsor Collaborator
Fondazione IRCCS Ca' Granda, Ospedale Maggiore Policlinico

References & Publications (40)

Adler AI, Shine BS, Chamnan P, Haworth CS, Bilton D. Genetic determinants and epidemiology of cystic fibrosis-related diabetes: results from a British cohort of children and adults. Diabetes Care. 2008 Sep;31(9):1789-94. doi: 10.2337/dc08-0466. Epub 2008 — View Citation

Ali BR. Is cystic fibrosis-related diabetes an apoptotic consequence of ER stress in pancreatic cells? Med Hypotheses. 2009 Jan;72(1):55-7. doi: 10.1016/j.mehy.2008.07.058. Epub 2008 Oct 11. — View Citation

Association AD. 1. Improving Care and Promoting Health in Populations: Standards of Medical Care in Diabetes-2020. Diabetes Care. 2020 Jan;43(Suppl 1):S7-S13. doi: 10.2337/dc20-S001. Review. — View Citation

Austin A, Kalhan SC, Orenstein D, Nixon P, Arslanian S. Roles of insulin resistance and beta-cell dysfunction in the pathogenesis of glucose intolerance in cystic fibrosis. J Clin Endocrinol Metab. 1994 Jul;79(1):80-5. — View Citation

Blackman SM, Commander CW, Watson C, Arcara KM, Strug LJ, Stonebraker JR, Wright FA, Rommens JM, Sun L, Pace RG, Norris SA, Durie PR, Drumm ML, Knowles MR, Cutting GR. Genetic modifiers of cystic fibrosis-related diabetes. Diabetes. 2013 Oct;62(10):3627-3 — View Citation

Blackman SM, Tangpricha V. Endocrine Disorders in Cystic Fibrosis. Pediatr Clin North Am. 2016 Aug;63(4):699-708. doi: 10.1016/j.pcl.2016.04.009. Review. — View Citation

Bonadonna RC, Heise T, Arbet-Engels C, Kapitza C, Avogaro A, Grimsby J, Zhi J, Grippo JF, Balena R. Piragliatin (RO4389620), a novel glucokinase activator, lowers plasma glucose both in the postabsorptive state and after a glucose challenge in patients wi — View Citation

Cobelli C, Toffolo GM, Dalla Man C, Campioni M, Denti P, Caumo A, Butler P, Rizza R. Assessment of beta-cell function in humans, simultaneously with insulin sensitivity and hepatic extraction, from intravenous and oral glucose tests. Am J Physiol Endocrin — View Citation

Dobson L, Hattersley AT, Tiley S, Elworthy S, Oades PJ, Sheldon CD. Clinical improvement in cystic fibrosis with early insulin treatment. Arch Dis Child. 2002 Nov;87(5):430-1. — View Citation

Edlund A, Esguerra JL, Wendt A, Flodström-Tullberg M, Eliasson L. CFTR and Anoctamin 1 (ANO1) contribute to cAMP amplified exocytosis and insulin secretion in human and murine pancreatic beta-cells. BMC Med. 2014 May 28;12:87. doi: 10.1186/1741-7015-12-87 — View Citation

Edlund A, Pedersen MG, Lindqvist A, Wierup N, Flodström-Tullberg M, Eliasson L. CFTR is involved in the regulation of glucagon secretion in human and rodent alpha cells. Sci Rep. 2017 Mar 7;7(1):90. doi: 10.1038/s41598-017-00098-8. — View Citation

Farrell PM, White TB, Ren CL, Hempstead SE, Accurso F, Derichs N, Howenstine M, McColley SA, Rock M, Rosenfeld M, Sermet-Gaudelus I, Southern KW, Marshall BC, Sosnay PR. Diagnosis of Cystic Fibrosis: Consensus Guidelines from the Cystic Fibrosis Foundatio — View Citation

Grancini V, Trombetta M, Lunati ME, Zimbalatti D, Boselli ML, Gatti S, Donato MF, Resi V, D'Ambrosio R, Aghemo A, Pugliese G, Bonadonna RC, Orsi E. Contribution of ß-cell dysfunction and insulin resistance to cirrhosis-associated diabetes: Role of severit — View Citation

Guo JH, Chen H, Ruan YC, Zhang XL, Zhang XH, Fok KL, Tsang LL, Yu MK, Huang WQ, Sun X, Chung YW, Jiang X, Sohma Y, Chan HC. Glucose-induced electrical activities and insulin secretion in pancreatic islet ß-cells are modulated by CFTR. Nat Commun. 2014 Jul — View Citation

Haardt M, Benharouga M, Lechardeur D, Kartner N, Lukacs GL. C-terminal truncations destabilize the cystic fibrosis transmembrane conductance regulator without impairing its biogenesis. A novel class of mutation. J Biol Chem. 1999 Jul 30;274(31):21873-7. — View Citation

Hudson VM. Rethinking cystic fibrosis pathology: the critical role of abnormal reduced glutathione (GSH) transport caused by CFTR mutation. Free Radic Biol Med. 2001 Jun 15;30(12):1440-61. Review. — View Citation

Kelly A, Moran A. Update on cystic fibrosis-related diabetes. J Cyst Fibros. 2013 Jul;12(4):318-31. doi: 10.1016/j.jcf.2013.02.008. Epub 2013 Apr 3. Review. Erratum in: J Cyst Fibros. 2014 Jan;13(1):119. — View Citation

Koivula FNM, McClenaghan NH, Harper AGS, Kelly C. Islet-intrinsic effects of CFTR mutation. Diabetologia. 2016 Jul;59(7):1350-1355. doi: 10.1007/s00125-016-3936-1. Epub 2016 Mar 31. Review. Erratum in: Diabetologia. 2017 Dec;60(12):2544. — View Citation

Lanng S, Thorsteinsson B, Røder ME, Nerup J, Koch C. Insulin sensitivity and insulin clearance in cystic fibrosis patients with normal and diabetic glucose tolerance. Clin Endocrinol (Oxf). 1994 Aug;41(2):217-23. — View Citation

Lewis C, Blackman SM, Nelson A, Oberdorfer E, Wells D, Dunitz J, Thomas W, Moran A. Diabetes-related mortality in adults with cystic fibrosis. Role of genotype and sex. Am J Respir Crit Care Med. 2015 Jan 15;191(2):194-200. doi: 10.1164/rccm.201403-0576OC — View Citation

MacKenzie T, Gifford AH, Sabadosa KA, Quinton HB, Knapp EA, Goss CH, Marshall BC. Longevity of patients with cystic fibrosis in 2000 to 2010 and beyond: survival analysis of the Cystic Fibrosis Foundation patient registry. Ann Intern Med. 2014 Aug 19;161( — View Citation

Mari A, Camastra S, Toschi E, Giancaterini A, Gastaldelli A, Mingrone G, Ferrannini E. A model for glucose control of insulin secretion during 24 h of free living. Diabetes. 2001 Feb;50 Suppl 1:S164-8. — View Citation

Mari A, Pacini G, Murphy E, Ludvik B, Nolan JJ. A model-based method for assessing insulin sensitivity from the oral glucose tolerance test. Diabetes Care. 2001 Mar;24(3):539-48. Erratum in: Diabetes Care. 2014 Jul;37(7):2063. — View Citation

Marshall BC, Butler SM, Stoddard M, Moran AM, Liou TG, Morgan WJ. Epidemiology of cystic fibrosis-related diabetes. J Pediatr. 2005 May;146(5):681-7. — View Citation

Milla CE, Warwick WJ, Moran A. Trends in pulmonary function in patients with cystic fibrosis correlate with the degree of glucose intolerance at baseline. Am J Respir Crit Care Med. 2000 Sep;162(3 Pt 1):891-5. — View Citation

Moran A, Brunzell C, Cohen RC, Katz M, Marshall BC, Onady G, Robinson KA, Sabadosa KA, Stecenko A, Slovis B; CFRD Guidelines Committee. Clinical care guidelines for cystic fibrosis-related diabetes: a position statement of the American Diabetes Associatio — View Citation

Moran A, Diem P, Klein DJ, Levitt MD, Robertson RP. Pancreatic endocrine function in cystic fibrosis. J Pediatr. 1991 May;118(5):715-23. — View Citation

Moran A, Doherty L, Wang X, Thomas W. Abnormal glucose metabolism in cystic fibrosis. J Pediatr. 1998 Jul;133(1):10-17. Review. — View Citation

Moran A, Dunitz J, Nathan B, Saeed A, Holme B, Thomas W. Cystic fibrosis-related diabetes: current trends in prevalence, incidence, and mortality. Diabetes Care. 2009 Sep;32(9):1626-31. doi: 10.2337/dc09-0586. Epub 2009 Jun 19. — View Citation

Moran A, Pekow P, Grover P, Zorn M, Slovis B, Pilewski J, Tullis E, Liou TG, Allen H; Cystic Fibrosis Related Diabetes Therapy Study Group. Insulin therapy to improve BMI in cystic fibrosis-related diabetes without fasting hyperglycemia: results of the cy — View Citation

Moran A, Pyzdrowski KL, Weinreb J, Kahn BB, Smith SA, Adams KS, Seaquist ER. Insulin sensitivity in cystic fibrosis. Diabetes. 1994 Aug;43(8):1020-6. — View Citation

Mozzillo E, Franzese A, Valerio G, Sepe A, De Simone I, Mazzarella G, Ferri P, Raia V. One-year glargine treatment can improve the course of lung disease in children and adolescents with cystic fibrosis and early glucose derangements. Pediatr Diabetes. 20 — View Citation

Ntimbane T, Comte B, Mailhot G, Berthiaume Y, Poitout V, Prentki M, Rabasa-Lhoret R, Levy E. Cystic fibrosis-related diabetes: from CFTR dysfunction to oxidative stress. Clin Biochem Rev. 2009 Nov;30(4):153-77. — View Citation

Ode KL, Moran A. New insights into cystic fibrosis-related diabetes in children. Lancet Diabetes Endocrinol. 2013 Sep;1(1):52-8. doi: 10.1016/S2213-8587(13)70015-9. Epub 2013 May 23. Review. — View Citation

Rowe SM, Miller S, Sorscher EJ. Cystic fibrosis. N Engl J Med. 2005 May 12;352(19):1992-2001. — View Citation

Schaedel C, de Monestrol I, Hjelte L, Johannesson M, Kornfält R, Lindblad A, Strandvik B, Wahlgren L, Holmberg L. Predictors of deterioration of lung function in cystic fibrosis. Pediatr Pulmonol. 2002 Jun;33(6):483-91. — View Citation

Sheikh S, Gudipaty L, De Leon DD, Hadjiliadis D, Kubrak C, Rosenfeld NK, Nyirjesy SC, Peleckis AJ, Malik S, Stefanovski D, Cuchel M, Rubenstein RC, Kelly A, Rickels MR. Reduced ß-Cell Secretory Capacity in Pancreatic-Insufficient, but Not Pancreatic-Suffi — View Citation

Smyth AR, Bell SC, Bojcin S, Bryon M, Duff A, Flume P, Kashirskaya N, Munck A, Ratjen F, Schwarzenberg SJ, Sermet-Gaudelus I, Southern KW, Taccetti G, Ullrich G, Wolfe S; European Cystic Fibrosis Society. European Cystic Fibrosis Society Standards of Care — View Citation

Sun X, Yi Y, Xie W, Liang B, Winter MC, He N, Liu X, Luo M, Yang Y, Ode KL, Uc A, Norris AW, Engelhardt JF. CFTR Influences Beta Cell Function and Insulin Secretion Through Non-Cell Autonomous Exocrine-Derived Factors. Endocrinology. 2017 Oct 1;158(10):33 — View Citation

Yoon JC. Evolving Mechanistic Views and Emerging Therapeutic Strategies for Cystic Fibrosis-Related Diabetes. J Endocr Soc. 2017 Oct 30;1(11):1386-1400. doi: 10.1210/js.2017-00362. eCollection 2017 Nov 1. Review. — View Citation

* Note: There are 40 references in allClick here to view all references

Outcome

Type Measure Description Time frame Safety issue
Primary TASK 1: derivative control (DC) index of first phase insulin secretion, calculated using the Minimum Model applied to the OGTT in patients with CF and various degrees of glucose homeostasis 2 YEARS
Primary TASK 1: proportional control (PC) index of second phase insulin secretion, calculated using the Minimum Model applied to the OGTT in patients with CF and various degrees of glucose homeostasis 2 YEARS
Primary TASK 1: OGIS-2H index of insulin sensitivity, calculated with the appropriate formula applied to the OGTT in patients with CF and various degrees of glucose homeostasis 2 YEARS
Primary TASK 2: prevalence of CFRD in relation to the classes of mutations in the CFTR gene 2 YEARS
Primary TASK 3: variation of FEV1 difference between pre- and post-institution of an optimal glycemic control 2 YEARS
Primary TASK 4: incidence of post-transplant diabetes in subjects without CFRD 2 YEARS
Secondary TASK 2: prevalence of candidate genes for DM2 in the population with CF 2 YEARS
Secondary TASK2: variations in the protein pattern expression in CFRD population highlighted with a proteomic analysis 2 YEARS
Secondary TASK 3: variations of other respiratory and muscle-performance parameters n° episodes of exacerbation/year, n° of severe exacerbation (need of hospitalization)/year, and patient-reported outcomes (PROs) obtained from a specific validated questionnaire (CF-quality of life questionnaire, 9 quality of life domains: Physical Functioning, Vitality, Emotional state, Social limitations, Role Limitations/School Performance, Embarrassment, Body Image, Eating Disturbances, Treatment Constraints. 3 symptom scales: Respiratory, Digestive, Weight. 1 health perception scale: Health Status (present/evolution).Scores range from 0 to 100, with higher scores indicating better health) 2 YEARS
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