scholarly journals Grossly elevated serum angiotensin-converting enzyme activities are still suppressible with ACE inhibitor therapy

2002 ◽  
Vol 3 (2) ◽  
pp. 138-138
Author(s):  
Miles D Witham ◽  
Stuart D Hutcheon ◽  
Callum G Fraser ◽  
Marion ET McMurdo ◽  
Allan D Struthers
2003 ◽  
Vol 23 (2) ◽  
pp. 111-115 ◽  
Author(s):  
Mira Varagunam ◽  
Daniel J. McCloskey ◽  
Paul J. Sinnott ◽  
Martin J. Raftery ◽  
Muhammed M. Yaqoob

Objectives To study the effect of angiotensin-converting enzyme (ACE) polymorphisms II, ID, and DD on erythropoietin (EPO) requirement in patients on continuous ambulatory peritoneal dialysis (CAPD) therapy. Design Retrospective observational study. Setting CAPD Unit, Royal London/St. Bartholomews Hospital, London, UK. Patients 46 patients on the transplant waiting list (age 20 – 70 years), on CAPD therapy for an average of 28 months, seen consecutively over a period of 3 months in the outpatients department. Main Outcome Measures Primary end point: EPO dose requirement in different ACE genotypes. Secondary end points: C-reactive protein, ferritin, parathyroid hormone, Kt/V, duration of dialysis, folate, cause of renal failure, and whether or not patients were on ACE inhibitor therapy. Results There was a statistically significant difference ( p < 0.05) in EPO requirement in the II/ID group compared to the DD group. The mean ± standard error of EPO for the II/ID group was 144 ± 15 U/kg/week, and for the DD group, 87 ± 9 U/kg/ week. The difference in EPO requirement could not be explained by age, C-reactive protein, ferritin, parathyroid hormone, Kt/V, duration of dialysis, folate, cause of renal failure, or whether or not patients were on ACE inhibitor therapy. Conclusion In CAPD patients, ACE genotype has predictive value when determining the EPO dosage, as the II/ID genotype may be associated with a suboptimal response.


Endocrinology ◽  
2011 ◽  
Vol 152 (3) ◽  
pp. 1195-1195
Author(s):  
Wendy A. Davis ◽  
Simon G. A. Brown ◽  
Ian G. Jacobs ◽  
Max Bulsara ◽  
John Beilby ◽  
...  

Abstract Aims/Hypotheses: The aims of this study were to determine whether the angiotensin-converting enzyme (ACE) gene I/D polymorphisms independently predict severe hypoglycemia in community-dwelling type 2 patients. Methods: Six hundred two patients who were ACE genotyped at baseline and assessed in 1998 were followed up to the end of June 2006. Severe hypoglycemia was defined as that requiring documented health service use as the primary diagnosis. Cox proportional hazards modeling was used to determine the predictors of first episode and zero-inflated negative binomial regression modeling identified predictors of frequency. Results: Forty-nine patients (8.1%) experienced 63 episodes of severe hypoglycemia. After adjusting for previously identified significant independent predictors of time to first episode, both ACE DD genotype and ACE inhibitor therapy, but not their interaction, added to the model [hazard ratio (95% confidence interval): 2.34 (1.29–4.26), P = 0.006, and 1.77 (0.99–3.13), P = 0.052, respectively]. Similarly, after adjusting for previously identified risk factors for multiple episodes of severe hypoglycemia, ACE DD genotype was independently associated with increased risk [incidence relative risk (95% confidence interval): 1.80 (1.00–3.24), P = 0.050]. Conclusions/Interpretation: ACE DD genotype is associated with an increased the risk of the first episode of severe hypoglycemia and its subsequent frequency approximately 2-fold in well-characterized patients with type 2 diabetes. Consistent with previous case-control studies, ACE inhibitor therapy was a weak predictor of severe hypoglycemia. ACE I/D genotyping might provide useful adjunctive prognostic information when intensive glycemic control measures are contemplated.


CHEST Journal ◽  
1984 ◽  
Vol 85 (3) ◽  
pp. 307-310 ◽  
Author(s):  
Scott F. Davies ◽  
Michael S. Rohrbach ◽  
Vicki Thelen ◽  
Joel Kuritsky ◽  
Robert Gruninger ◽  
...  

2013 ◽  
Vol 98 (10) ◽  
pp. 4023-4029 ◽  
Author(s):  
Peter J. Donovan ◽  
Lana Sundac ◽  
Carel J. Pretorius ◽  
Michael C. d'Emden ◽  
Donald S. A. McLeod

Abstract Context: Hypercalcemia mediated by 1,25-dihydroxy vitamin D (calcitriol) is uncommon, with evidence on etiology limited to small case series or case reports. Objective: The objective of the study was to systematically identify a large series of cases of calcitriol-mediated hypercalcemia and document the presentation, demographics, and clinical course across etiologies. Design, Setting, and Patients: The study was a hospital-based, retrospective case series, identifying subjects from 1999 through 2009 across the public hospital system in Queensland, Australia. All patients aged over 18 years were identified that had persistent hypercalcemia associated with elevated or inappropriately normal calcitriol concentration or elevated serum angiotensin-converting enzyme. Results: A total of 101 cases were identified. Sarcoidosis was the most common etiology (49%), followed by hematological malignancy (17%) and infections (8%). Etiologies not previously described include squamous cell carcinoma of the tongue, ovarian cystadenocarcinoma, and chronic lymphocytic leukemia. Median serum angiotensin-converting enzyme was higher in sarcoid patients compared with all other causes [218 U/L (176–277) vs 155 U/L (110–208), P &lt; .001], but a level above the normal range did not discriminate well between cases of sarcoidosis and other causes (specificity at cutoff of 130 U/L was only 31%). However, a value greater than 250 U/L was highly specific (89%) for sarcoidosis but lacked sensitivity (31%). A calcitriol level greater than 300 pmol/L was not seen in sarcoidosis but was seen with other etiologies. Cases with neoplastic etiologies were older (61.4 ± 11.4 y) than all other subjects (51.7 ± 15.0 y, P = .006). Conclusions: Hypercalcemia mediated by calcitriol remains a rare presentation. In almost half the cases, sarcoidosis was the underlying cause, whereas a third of patients had cancer or systemic infections.


2011 ◽  
Vol 96 (4) ◽  
pp. E696-E700 ◽  
Author(s):  
Wendy A. Davis ◽  
Simon G. A. Brown ◽  
Ian G. Jacobs ◽  
Max Bulsara ◽  
John Beilby ◽  
...  

Abstract Aims/hypotheses: The aim of this study was to determine whether the angiotensin-converting enzyme (ACE) gene I/D polymorphisms independently predict severe hypoglycemia in community-dwelling type 2 patients. Methods: Six hundred and two patients who were ACE genotyped at baseline and assessed in 1998 were followed up to the end of June 2006. Severe hypoglycemia was defined as that requiring documented health service use as the primary diagnosis. Cox proportional hazards modeling was used to determine the predictors of first episode and zero-inflated negative binomial regression modeling identified predictors of frequency. Results: Forty-nine patients (8.1%) experienced 63 episodes of severe hypoglycemia. After adjusting for previously identified significant independent predictors of time to first episode, both ACE DD genotype and ACE inhibitor therapy, but not their interaction, added to the model [hazard ratio (95% confidence interval): 2.34 (1.29–4.26), P = 0.006, and 1.77 (0.99–3.13), P = 0.052, respectively]. Similarly, after adjusting for previously identified risk factors for multiple episodes of severe hypoglycemia, ACE DD genotype was independently associated with increased risk [incidence relative risk (95% confidence interval): 1.80 (1.00–3.24), P = 0.050]. Conclusions/interpretation: ACE DD genotype was associated with an approximately 2-fold increased risk of the first episode of severe hypoglycemia and its subsequent frequency in well-characterized patients with type 2 diabetes. Consistent with previous case-control studies, ACE inhibitor therapy was a weak predictor of severe hypoglycemia. ACE I/D genotyping might provide useful adjunctive prognostic information when intensive glycemic control measures are contemplated.


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