scholarly journals Case-control study of acute renal failure in patients with cystic fibrosis in the UK

Thorax ◽  
2008 ◽  
Vol 63 (6) ◽  
pp. 532-535 ◽  
Author(s):  
A Smyth ◽  
S Lewis ◽  
C Bertenshaw ◽  
I Choonara ◽  
J McGaw ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Risk Factor ◽  
Case Control Study ◽  
Case Control ◽  
Increased Risk ◽  
Long Term Treatment ◽  
The Uk ◽  
Control Study

Background:There has been a recent increase in the number of reported cases of acute renal failure (ARF) in cystic fibrosis (CF). A case-control study was conducted to determine the factors which are associated with an increased risk of ARF.Methods:24 cases of confirmed ARF were identified in patients with CF from 20 UK CF centres presenting between 1997 and 2004. Using the UK CF database, sex- and age-matched controls were identified. Risk factors were analysed by conditional logistic regression and Mantel-Haenszel analysis.Results:21 of the 24 patients with ARF had received an aminoglycoside at the time of their episode of ARF or in the preceding week compared with only 3 of 42 controls during the same time period (OR 81.8, 95% CI 4.7 to 1427, p<0.001). In the year before the episode of ARF, significantly more cases than controls had received gentamicin (19/24 cases vs 1/42 controls, p<0.001). The numbers receiving tobramycin were similar (9/24 cases vs 16/42 controls, p = 0.9). A known risk factor for renal impairment (prior renal disease, acute dehydration or long-term treatment with a nephrotoxic drug) was present in 18/24 cases and 7/42 controls (OR 24.0, 95% CI 3.1 to 186.6, p = 0.002).Conclusions:In patients with CF the use of an intravenous aminoglycoside is a risk factor for ARF; gentamicin is more nephrotoxic than tobramycin. Most patients who develop ARF have a risk factor which necessitates withholding aminoglycosides or more closely monitoring their use.

Incidence and risk factors of cancer in individuals with cystic fibrosis in the UK; a case-control study

2021 ◽  
Author(s):  
Olga Archangelidi ◽  
Paul Cullinan ◽  
Nicholas J. Simmonds ◽  
Emmanouil Mentzakis ◽  
Daniel Peckham ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cystic Fibrosis ◽  
Case Control Study ◽  
Case Control ◽  
The Uk ◽  
Control Study

scholarly journals Dietary intake of folate, vitamin B6, vitamin B12 and riboflavin and risk of Parkinson's disease: a case–control study in Japan

2010 ◽  
Vol 104 (5) ◽  
pp. 757-764 ◽  
Author(s):  
Kentaro Murakami ◽  
Yoshihiro Miyake ◽  
Satoshi Sasaki ◽  
Keiko Tanaka ◽  
Wakaba Fukushima ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dietary Intake ◽  
Case Control Study ◽  
Case Control ◽  
B Vitamins ◽  
Vitamin B ◽  
Increased Risk ◽  
The Uk ◽  
Control Study

Increased homocysteine levels might accelerate dopaminergic cell death in Parkinson's disease (PD) through neurotoxic effects; thus, increasing intake of B vitamins involved in the regulation of homocysteine metabolism might decrease the risk of PD through decreasing plasma homocysteine. However, epidemiological evidence for the association of dietary B vitamins with PD is sparse, particularly in non-Western populations. We conducted a hospital-based case–control study in Japan to examine associations between dietary intake of folate, vitamin B6, vitamin B12 and riboflavin and the risk of PD. Patients with PD diagnosed using the UK PD Society Brain Bank criteria (n 249) and controls without neurodegenerative diseases (n 368) were recruited. Dietary intake during the preceding month was assessed at the time of study recruitment using a validated, self-administered, semi-quantitative, comprehensive diet history questionnaire. After adjustment for potential dietary and non-dietary confounding factors, intake of folate, vitamin B12 and riboflavin was not associated with the risk of PD (P for trend = 0·87, 0·70 and 0·11, respectively). However, low intake of vitamin B6 was associated with an increased risk of PD, independent of potential dietary and non-dietary confounders. Multivariate OR (95 % CI) for PD in the first, second, third and fourth quartiles of vitamin B6 were 1 (reference), 0·56 (0·33, 0·94), 0·69 (0·38, 1·25) and 0·48 (0·23, 0·99), respectively (P for trend = 0·10). In conclusion, in the present case–control study in Japan, low intake of vitamin B6, but not of folate, vitamin B12 or riboflavin, was independently associated with an increased risk of PD.

Calcium Use Increases Risk of Calciphylaxis: A Case-Control Study

1999 ◽  
Vol 19 (3) ◽  
pp. 248-252 ◽  
Author(s):  
James M. Zacharias ◽  
Bunny Fontaine ◽  
Adrian Fine
Keyword(s):  
Risk Factor ◽  
Peritoneal Dialysis ◽  
Calcium Carbonate ◽  
Case Control Study ◽  
Conditional Logistic Regression ◽  
Laboratory Data ◽  
Case Control ◽  
Calcium Deposition ◽  
Increased Risk ◽  
Control Study

Objective To investigate the risk factors for the development of calciphylaxis in renal failure, a poorly understood and often fatal condition characterized by calcium deposition in tissues. Design Retrospective case-control study. Setting University hospital peritoneal dialysis center. Patients Eight continuous ambulatory peritoneal dialysis (CAPD) patients with calciphylaxis were identified in a 3-year period. We matched up to five controls for dialysis modality and length of time on dialysis with each case. Statistics Multivariate conditional logistic regression analysis for matched case-controls. Main Outcome Measures Laboratory data and demographics were collected as well as cumulative calcium and vitamin D ingestion over the year prior to disease onset. Results All the patients were female, versus only 38% (14/37) of controls ( p < 0.0001). While not statistically significant, a majority of the patients were diabetic [62.5% (5/8) vs 32% (12/37)]. Peak and average levels of serum calcium, phosphate, calcium x phosphate product, parathyroid hormone (PTH), albumin, iron, total iron-binding capacity (TIBC), and ferritin were not significantly different in cases compared with controls. The use of calcitriol alone or with calcium carbonate was not found to be a significant risk factor for the development of calciphylaxis. In a multivariate analysis, iron intake seemed to be protective, contrary to previous reports, while the use of calcium carbonate was associated with a strong trend to increased risk of calciphylaxis development (odds ratio = 1.029/g and 1.011/g calcium ingested per month, at 1 and 2 – 3 months prior to calciphylaxis development; p = 0.0556 and 0.0565, respectively). Conclusion These data, although limited by the small numbers of index cases, suggest that calcium ingestion is a risk factor for calciphylaxis. The increased use of calcium salts as a phosphate binder in recent years might explain the apparent increased incidence of calciphylaxis in our and other centers. The preponderance of female diabetics among cases reported elsewhere was confirmed in our study.

Helicobacter Pylori Infection and the Risk of Myocardial Infarction: Role of Fibrinogen and Its Genetic Control

1999 ◽  
Vol 82 (07) ◽  
pp. 14-18 ◽  
Author(s):  
Francesco Zito ◽  
Augusto Di Castelnuovo ◽  
Andria D’Orazio ◽  
Riccardo Negrini ◽  
Domenico De Lucia ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Helicobacter Pylori ◽  
Risk Factor ◽  
Genetic Control ◽  
Case Control Study ◽  
Case Control ◽  
Increased Risk ◽  
Confounding Variables ◽  
Control Study

SummaryThe contribution of Helicobacter pylori (HP) infection to the risk of myocardial infarction was evaluated. The role of fibrinogen and its genetic control as a possibile mechanism by which HP may influence myocardial infarction risk was explored in this context. A case-control study was performed in 101 patients with myocardial infarction and in 101 controls.HP infection was associated with an increased risk of myocardial infarction independently for confounding variables (OR 4.1, CI95: 1.8-9.4). HP infection was significantly associated with higher levels of fibrinogen, both in cases and in controls. Furthermore, there was an additive effect of HP infection and B2 allele of BclI fibrinogen poly-morphism in increasing fibrinogen levels. HP infection showed a stronger effect on the risk of myocardial infarction in B2 allele carriers (OR 7.6, CI95: 1.8-31.6) as compared to subjects carrying the B1B1 genotype (OR 3.3, CI95: 1.2-9.2).We showed that a previous HP infection is a risk factor for myocardial infarction. An increase in fibrinogen levels is a possible mechanism by which HP may act. Concomitant conditions, like a genetic predisposition in increasing fibrinogen levels, seem to further increase the effect of HP on myocardial infarction risk.

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