Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic autonomic neuropathy (DAN) is a serious and common complication of diabetes. Despite its relationship to an increased risk of cardiovascular mortality and its association with multiple symptoms and impairments, the significance of DAN has not been fully appreciated. The reported prevalence of DAN varies widely depending on the cohort studied and the methods of assessment. In randomly selected cohorts of asymptomatic individuals with diabetes, approximately 20% had abnormal cardiovascular autonomic function. DAN frequently coexists with other peripheral neuropathies and other diabetic complications, but DAN may be isolated, frequently preceding the detection of other complications. Major clinical manifestations of DAN include resting tachycardia, exercise intolerance, orthostatic hypotension, constipation, gastroparesis, erectile dysfunction, sudomotor dysfunction, impaired neurovascular function, "brittle diabetes," and hypoglycemic autonomic failure. DAN may affect many organ systems throughout the body (e.g., gastrointestinal [GI], genitourinary, and cardiovascular). GI disturbances (e.g., esophageal enteropathy, gastroparesis, constipation, diarrhea, and fecal incontinence) are common, and any section of the GI tract may be affected. Gastroparesis should be suspected in individuals with erratic glucose control. Upper-GI symptoms should lead to consideration of all possible causes, including autonomic dysfunction. Whereas a radiographic gastric emptying study can definitively establish the diagnosis of gastroparesis, a reasonable approach is to exclude autonomic dysfunction and other known causes of these upper-GI symptoms. Constipation is the most common lower-GI symptom but can alternate with episodes of diarrhea. Diagnostic approaches should rule out autonomic dysfunction and the well-known causes such as neoplasia. Occasionally, anorectal manometry and other specialized tests typically performed by the gastroenterologist may be helpful. DAN is also associated with genitourinary tract disturbances including bladder and/or sexual dysfunction. Evaluation of bladder dysfunction should be performed for individuals with diabetes who have recurrent urinary tract infections, pyelonephritis, incontinence, or a palpable bladder. Specialized assessment of bladder dysfunction will typically be performed by a urologist. In men, DAN may cause loss of penile erection and/or retrograde ejaculation. A complete workup for erectile dysfunction in men should include history (medical and sexual); psychological evaluation; hormone levels; measurement of nocturnal penile tumescence; tests to assess penile, pelvic, and spinal nerve function; cardiovascular autonomic function tests; and measurement of penile and brachial blood pressure. Neurovascular dysfunction resulting from DAN contributes to a wide spectrum of clinical disorders including erectile dysfunction, loss of skin integrity, and abnormal vascular reflexes. Disruption of microvascular skin blood flow and sudomotor function may be among the earliest manifestations of DAN and lead to dry skin, loss of sweating, and the development of fissures and cracks that allow microorganisms to enter. These changes ultimately contribute to the development of ulcers, gangrene, and limb loss. Various aspects of neurovascular function can be evaluated with specialized tests, but generally these have not been well standardized and have limited clinical utility. Cardiovascular autonomic neuropathy (CAN) is the most studied and clinically important form of DAN. Meta-analyses of published data demonstrate that reduced cardiovascular autonomic function as measured by heart rate variability (HRV) is strongly (i.e., relative risk is doubled) associated with an increased risk of silent myocardial ischemia and mortality. The determination of the presence of CAN is usually based on a battery of autonomic function tests rather than just on one test. Proceedings from a consensus conference in 1992 recommended that three tests (R-R variation, Valsalva maneuver, and postural blood pressure testing)or longitudinal testing of the cardiovascular autonomic system. Other forms of autonomic neuropathy can be evaluated with specialized tests, but these are less standardized and less available than commonly used tests of cardiovascular autonomic function, which quantify loss of HRV. Interpretability of serial HRV testing requires accurate, precise, and reproducible procedures that use established physiological maneuvers. The battery of three recommended tests for assessing CAN is readily performed in the average clinic, hospital, or diagnostic center with the use of available technology. Measurement of HRV at the time of diagnosis of type 2 diabetes and within 5 years after diagnosis of type 1 diabetes (unless an individual has symptoms suggestive of autonomic dysfunction earlier) serves to establish a baseline, with which 1-year interval tests can be compared. Regular HRV testing provides early detection and thereby promotes timely diagnostic and therapeutic interventions. HRV testing may also facilitate differential diagnosis and the attribution of symptoms (e.g., erectile dysfunction, dyspepsia, and dizziness) to autonomic dysfunction. Finally, knowledge of early autonomic dysfunction can encourage patient and physician to improve metabolic control and to use therapies such as ACE inhibitors and beta-blockers, proven to be effective for patients with CAN.
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PMID:Diabetic autonomic neuropathy. 1271 21

The occurrence of severe acute renal failure in 3 patients who developed diarrhoea while taking angiotensin converting enzyme (ACE) inhibitors led us to undertake a retrospective cohort survey to determine the frequency with which diarrhoea and vomiting are associated with acute renal failure in patients taking this class of drug. Serum creatinine was measured as part of the diagnostic workup of 2398 consecutive admissions to an acute medical receiving unit in a district general hospital. Outcome measures were the presence of diarrhoea and/or vomiting, and whether taking an ACE inhibitor, NSAID or diuretic at the time of admission, also previous, initial and follow up serum creatinine concentrations. Peak serum creatinine in the 3 cases was 1159, 989 and 765 micromol/l. None of the 3 required dialysis and all recovered renal function completely after receiving large volumes of intravenous fluid. In the cohort study, 89 of 2398(3.7%) admissions had serum creatinine >/=200 micromol/l. Nine were regular dialysis patients. Of the remaining patients, 30 (37.5%) were taking an ACE inhibitor. Six of 30 (20%) gave a history of diarrhoea and/or vomiting. Median creatinine concentration in this group was 135 (range 111-209) micromol/l before admission, 292 (216-724) micromol/l when first seen in hospital, and 134 (94-219) micromol/l following the withdrawal of drug therapy and fluid replacement. In conclusion, volume depletion causing acute renal failure in patients taking ACE inhibitors is not uncommon. Such patients and their general practitioners should be aware that reversible renal impairment may occur during intercurrent illnesses, particularly if characterised by diarrhoea and/or vomiting.
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PMID:Diarrhoea, vomiting and ACE inhibitors:--an important cause of acute renal failure. 1276 5

The aim of this work was to determine the concentration of total and ionized magnesium in hair and blood of patients with primary hypertension and the influence of oral magnesium supplementation (Slow-Mag B6) on clinical parameters and blood pressure values. 92 patients were recruited from the Family Care Unit, Pomeranian Academy of Medicine in Szczecin. Each patient was treated during at least 6 months preceding the study with a single antihypertensive agent from one of the following groups: ACE inhibitors, beta-receptor inhibitors, Ca channel blockers, diuretics. The control group included patients with hypertension not treated pharmacologically. Changes in ionized magnesium concentration before and after oral magnesium supplementation were studied in relation to total cholesterol, triglycerides, and other parameters of importance in hypertension. Significantly lower total magnesium concentrations were demonstrated in hair of patients receiving ACE inhibitors and diuretics in comparison to controls. Ionized magnesium concentrations in serum of hypertensive patients were significantly reduced as compared with controls. A highly significant increase in these levels was noted after magnesium supplementation. Blood pressure values after magnesium supplementation were reduced in the study group by an average of 15-20 mmHg for systolic and 5-9 mmHg for diastolic blood pressure. Correlations between ionized magnesium and triglyceride concentrations in patients treated with Ca channel blockers before oral Mg supplementation were found. Patients treated with diuretics demonstrated correlations between total magnesium and total cholesterol concentrations. Following oral magnesium supplementation with Slow-Mag B6 at 320 mg/day, the frequency of complaints reported by patients, including irregular heart beat, pricking heart pain, nervousness, sleep disorders, irritability/tearfulness was reduced. There was no effect on other complaints, such as mental and physical fatigue, constipation/diarrhea, and anxiety.
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PMID:[Level of total and ionized magnesium fraction based on biochemical analysis of blood and hair and effect of supplemented magnesium (Slow Mag B6) on selected parameters in hypertension of patients treated with various groups of drugs]. 1460 71

Recently, plasma exchange (PE) has been added to the treatment regimen for patients with steroid-, cyclophosphamide-, and cyclosporine-resistant nephrotic syndrome. This is a case report of a female patient with severe acute renal failure (ARF) during the relapse of steroid-resistant nephrotic syndrome (SRNS) who recovered completely after PE and became steroid-sensitive in further follow-up of 48 months. An 8-year-old girl was referred to Nephrology Department of the University Children's Hospital due to relapse of SRNS complicated with ARF. Her nephrotic syndrome (mesangioproliferative glomerulonephritis) was diagnosed at the age of 17 months. During the following 6 years, she was given several therapeutic regimens including pulse prednisolone, cyclophosphamide, Cyclosporine (CyA), but she continued to have frequent relapses and during the last six months she was steroid- and cyclosporine-resistant. Three days before admission, she was febrile, had cellulites of the lower abdominal wall, diarrhea, vomiting, hypovolemic shock with generalized edema, severe hypoproteinemia and hypoalbuminemia. In a local hospital, she was treated with fresh frozen plasma, albumin, methylprednisolone, furosemide and antibiotics, but she became anuric and was referred to our hospital. There were no signs of hemolysis. Anuria lasted for 12 days. She was discharged after 42 days in remission with normal GFR. Principal treatment included: 13 sequential hemodialysis sessions (30% of body weight was removed as excess volume), 6 PE, corticosteroids, CyA, ACE inhibitor, antibiotics, antimycotics, and cimetidine. Six PE sessions were performed every other day. In further 48-month follow-up, while under the treatment of CyA the patient had a few steroid-sensitive relapses, the first being 6 months after PE. The second kidney biopsy showed focal segmental glomerulosclerosis with no signs of apparent CyA nephrotoxicity. "Malignant" course of disease in our patient was a good reason to introduce PE into the treatment. Since PE was the only additional mode of treatment, it is believed that its effect was crucial for milder activity of the disease.
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PMID:[The benefit of plasmapheresis in a patient with steroid-resistant nephrotic syndrome and anuria--long-term follow-up]. 1561 78

A 67 year old woman developed acute renal failure with serum potassium 9.4 mmol/l requiring emergency dialysis after seven days of diarrhoea while taking an ACE inhibitor for vascular disease. Review of the literature, the British National Formulary, and the patient information leaflets for each of the 11 ACE inhibitors currently marketed in the UK suggests that this potentially life threatening complication of ACE inhibition is not yet widely recognised.
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PMID:Life threatening hyperkalaemia with diarrhoea during ACE inhibition. 1566 77

HFR is an integrated hemodiafiltration system that utilizes a double chamber filter to separate convection from diffusion. The ultrafiltrate is regenerated by passage through a sorbent cartridge made up of resin and activated carbon. A small percentage of patients using this technique had gastrointestinal symptoms that included nausea/vomiting, diarrhea and/or stomach cramps approximately 1-2 hours after the start of HFR. We undertook a series of investigations to try and elucidate the cause of these reactions. Since the majority of the patients were taking ACE inhibitors, attention was focused on contact phase activation. Healthy and uremic plasma were incubated with different components of the HFR circuit. The activated carbon caused a moderate activation of factor XII and production of kallikrein, while there was no activation for the lines, double filter or resin. Patients taking ACE inhibitors may be at risk for treatments involved with contact phase activation as ACE inhibitors also block the degradation of bradykinin. A new sorbent cartridge has now been developed that contains only resin.
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PMID:[Contact phase activation can occur with certain types of activated carbon]. 1574 7

HEMOLYTIC UREMIC SYNDROME POST-PARTUM: We describe a case of a 37-year-old woman admitted for severe renal failure to our hospital immediately after the delivery by caesarean section of twins. She had anuria, anemia, and moderate thrombocytopenia. A diagnosis of hemolytic-uremic syndrome was made. Plasma exchange was started, substitution was performed with fresh frozen plasma and eight consecutive plasmapheresis sessions were given. She received hydrocortisone and ACE inhibitors. After about fifteen days from the beginning of the illness, signs of active haemolysis disappeared and renal function was partially recovered. A genetic study demonstrated the absence of HF1 and MCP mutations but a polymorphic variant of the HF1 gene (C-257T promoter region). This polymorphism is strongly associated with non-diarrhoea-HUS (D-HUS). Post-partum HUS is quite a rare syndrome and has a poor outcome; however prompt diagnosis and efficacious therapy could save lives without clinical consequences. The excellent outcome of this patient seems to corroborate this concept.
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PMID:A post-partum hemolytic-uremic-like-syndrome in a patient with pre-eclampsia: description of a clinical case. 1642 9

Travellers' diarrhoea is defined as diarrhoea that develops while a person is abroad in or shortly after return from a developing country. Different pathogens cause diarrhoea in travellers. Campylobacter jejuni is one of the most prominent agents for this illness. Diarrhoea is defined as an abnormally increased frequency or decreased consistency of stools for less than one week. Antibiotics are effective in preventing travellers' diarrhoea, but routine prophylaxis with antibiotics, should be discouraged. Vaccination is promising but no vaccine against C. jejuni is available at the moment. This article presents the ACE BioSciences strategy for the discovery of protein based vaccine candidates using a cell surface proteomics approach of C. jejuni. New targets for C. jejuni protein vaccines were identified. As proof of concept, we could demonstrate decreased colonization of C. jejuni in mice after vaccination with some of these candidates. It is likely that the proteomics based ACE-Biosciences approach will result in reliable travellers' diarrhoea protein-vaccines in the future.
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PMID:Campylobacter jejuni proteomics for new travellers' diarrhoea vaccines. 1729 16

Over a period of six months, 55 patients out of 11,216 (0.49%) admitted to the hospital developed acute renal failure (ARF). The diagnosis of ARF was based on the usual criteria, a sudden rise in blood urea nitrogen and creatinine with or without oliguria. Patients age ranged between 15 and 81 years with a mean of 51.9 years. Renal ischemia (69%) and nephrotoxic drugs (16.3%) were the two main etiologic factors. Among the causes of ischemia, septic shock was the commonest (29%), followed by severe hypotension due to several causes such as hemorrhage, burns, severe diarrhea and cardiogenic shock (25.4%), and ACE inhibitors (10.9%). ARF was associated with an average of 15.8 days stay in hospital versus 5.1 days for the overall hospital admissions. Immediate management of hypotension by intravenous fluid replacement, vasopressor agents and the necessary surgical intervention was appropriately considered. Intravenous frusemide was used for oliguric patients. Intermittent hemodialysis was used in 18 patients and continuous venovenous hemofiltration in six patients. Twelve patients with ARF due to ischemia died, while there were no deaths in the nephrotoxic group (p < 0.05). The overall mortality was (21.8%), which had no correlation with patient age. All non-oliguric patients survived with the mortality being exclusively in the oliguric group.
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PMID:Acute renal failure: six months pilot study in qatar. 1840 4

Intensive efforts have been spent to discover therapeutic, non-peptide and orally effective hypertensive drugs. One drug that emerged from this effort is aliskiren, a direct human renin inhibitor that blocks the conversion of angiotensinogen to angiotensin I (Ang I). In contrast to other antihypertensive agents, aliskiren decreases plasma renin activity (PRA). In healthy human subjects, doses of between 40 and 640 mg of aliskiren exert a dose-dependent reduction in PRA and Ang I and Ang II levels. The bioavailability of aliskiren is low (2%), peak plasma concentrations are reached within one to three hours and the binding with plasma proteins achieves approximately 47-51%. Aliskiren is slightly metabolized (20%) by CYP3A4. The most common adverse events include diarrhea, headache, back pain and gastrointestinal disorders. Aliskiren is well tolerated, and may be used alone or in combination with other antihypertensive agents. Aliskiren belongs to a new class of agents that effectively and specifically inhibit the RAS. This drug functions through a novel mechanism of action and has the potential to become a true alternative to angiotensin converting enzyme inhibitors and angiotensin receptor blockers in the therapy of hypertension and other cardiovascular and renal disorders.
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PMID:Pharmacokinetics and pharmacodynamics of aliskiren, an oral direct renin inhibitor. 1906 8


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