Saturday, April 25, 2009
Genetically Modified Pig Raises Hope for Organ Transplants
Korean scientists have created a genetically modified pig whose organs can be used for transplanting into human patients. The cloned piglet was born by a surrogate mother on April 3 and remains healthy at a lab at the National Institution of Animal Science in Suwon, Gyeonggi Province.The researchers have predicted the mass production of these hybrid pigs capable of producing humanized organs and organ parts, including pancreatic islets of Langerhans, heart valves and entire hearts. But they have yet to prove the organs can be transplanted into human patients without risk to life. The piglet is part of the ``mini-pig'' species that grow up to just around 80 kilograms. The study was part of a comprehensive project financed by the Ministry of Education, Science and Technology to develop new technologies for drug development and genetically modified organs for use in human transplants. The piglet was born after trial and error tests for the past six years with a budget of $3.38 million.Scientists worldwide have gone all-out to create organ farms in animals, which they believe could help solve one of medicine's fastest growing problems ― the shortage of organs for transplant surgeries. However, creating animal organs that are compatible with the human immune system has proved to be a difficult challenge. Although drugs can stop the body from rejecting a human transplant, the immune system won't accept animal organs for an extended period of time. This is because that the antibodies in human blood are directed to attack alpha 1, 3-galactose, or ``alpha gal,'' which is found in the tissues of all non-primate mammals. The transplanted animal organs often fail to survive for less than a few hours. The Korean researchers were to produce a ``GAL-knockout'' pig, which is genetically removed of alpha gal that triggers the immune rejections. They first removed one of the two genes (a1, 3-Galactosyltransferase) from a somatic cell of a mini-pig and then inserted the cell to an egg removed of its nucleus to create a clone. The produced piglet could eventually be used to breed genetically modified pigs born without alpha gal, which may have a better chance of producing compatible human organs, the scientists said.Lee Kyung-kwang, the leader of the team, died on March 1. Other members include Seoul National University's Jeong Jun-ho, Dankook University's Shim Ho-sup, Konkuk University's Kim Jin-hoi, Animal Science Institute's Park Su-bong and Chonnam National University's Kang Man-jong. A number of breakthroughs have been reported on the research for GAL-knockout pigs. In 2005, a Harvard University team transplanted the heart of a one to a baboon, and the animal lived on for another six months. It could be argued that the track record for xeno-transplantation ― using animal organs to replace human ones ― has been disastrous. In 1984, a newborn baby, called by the media as ``Baby Fae,'' received a baboon heart in California, but managed to live for just 20 days. In 1999, Jeff Getty, an American AIDS patient, received bone marrow from a baboon. Doctors had hopes that the immune cells in the baboon's marrow would replace those Getty had lost to AIDS, as baboon cells are naturally resistant to HIV. However, the cells functioned for only a brief time and Getty died 11 years later from heart failure. In 1999, a 35-year-old American HIV patient received a baboon liver, but died just two months after the transplantation after contracting a virus that is known to only affect the animal
Tuesday, April 21, 2009
Mobile phone may be source of nosocomial infection
Mobile Phones May Be Source of Nosocomial Infections
NEW YORK Mar 05 - The mobile phones of hospital healthcare workers are frequently contaminated with bacteria and fungi, including nosocomial pathogens, a Turkish research team reports in the BMC journal Annals of Clinical Microbiology and Antimicrobials.
Dr. Fatma Ulger and colleagues at Ondokuz Mayis University, Samsun, cultured the dominant hand and the mobile phones of 200 physicians, nurses, and other healthcare staff working in intensive care units and operating rooms.
They found that 95% of telephones were contaminated, often with more than one species. Approximately half of the Staphylococcus aureus isolates were resistant to methicillin, while one third of Gram negative rods were resistant to ceftazidime. Isolated microorganisms from hands and phones were similar.
Of the nosocomial pathogens isolated from phones in intensive care units, the report indicates, 33% were staphylococci, 21% were nonfermentative Gram negative rods, 21% were coliforms, 7% were enterococci, and 12% were yeasts.
Upon questioning the study participants, Dr. Ulger's team found that 90% never cleaned their mobile phones. Thus, they conclude, mobile phones "may facilitate transmission of bacterial isolates from patient to patient in wards or hospitals."
They recommend routine decontamination of mobile phones with alcohol-containing disinfectants. "In the future," they add, "another way of reducing bacterial contamination on mobile phones might be the use of antimicrobial additive materials."
Ann Clin Microbiol Antimicrob 2009.
NEW YORK Mar 05 - The mobile phones of hospital healthcare workers are frequently contaminated with bacteria and fungi, including nosocomial pathogens, a Turkish research team reports in the BMC journal Annals of Clinical Microbiology and Antimicrobials.
Dr. Fatma Ulger and colleagues at Ondokuz Mayis University, Samsun, cultured the dominant hand and the mobile phones of 200 physicians, nurses, and other healthcare staff working in intensive care units and operating rooms.
They found that 95% of telephones were contaminated, often with more than one species. Approximately half of the Staphylococcus aureus isolates were resistant to methicillin, while one third of Gram negative rods were resistant to ceftazidime. Isolated microorganisms from hands and phones were similar.
Of the nosocomial pathogens isolated from phones in intensive care units, the report indicates, 33% were staphylococci, 21% were nonfermentative Gram negative rods, 21% were coliforms, 7% were enterococci, and 12% were yeasts.
Upon questioning the study participants, Dr. Ulger's team found that 90% never cleaned their mobile phones. Thus, they conclude, mobile phones "may facilitate transmission of bacterial isolates from patient to patient in wards or hospitals."
They recommend routine decontamination of mobile phones with alcohol-containing disinfectants. "In the future," they add, "another way of reducing bacterial contamination on mobile phones might be the use of antimicrobial additive materials."
Ann Clin Microbiol Antimicrob 2009.
Thursday, April 16, 2009
Plastic bottles - Breast cancer
Cancer Update from John Hopkins This information is being circulated at Walter Reed Army Medical Center as well. No plastic containers in microwave. No water bottles in freezer. No plastic wrap in microwave. A dioxin chemical causes cancer, especially breast cancer. Dioxins are highly poisonous to the cells of our bodies. Don't freeze your plastic Bottles with water in them as this releases dioxins from the plastic. Recently, Edward Fujimoto, Wellness Program Manager at Castle Hospital, Was on a TV program to explain this health hazard. He talked about dioxins and how bad they are for us. He said that we should not be heating our food in the Microwave using plastic containers... This especially applies to foods that contain fat.. He said that the combination of fat, high heat, and plastics releases dioxin Into the food and ultimately into the cells of the body... Instead, he recommends using glass, such as Corning Ware, Pyrex or ceramic Containers for heating food... You get the same results, only without the dioxin. So such things as TV dinners, instant ramen and soups, etc., Should be removed from the container and heated in something else. Paper isn't bad but you don't know what is in the paper. It's just safer to use tempered glass, Corning Ware, etc.He reminded us that a while ago some of the fast food restaurants moved away From the foam containers to paper. The dioxin problem is one of the reasons... Also, he pointed out that plastic wrap, such as Saran, is just as dangerous when Placed over foods to be cooked in the microwave. As the food is nuked, the high Heat causes poisonous toxins to actually melt out of the plastic wrap and drip into the food. Cover food with a paper towel instead. This is an article that should be sentTo anyone important inYour life! ALSO ------------------------------------- Bottled water in your car Very dangerous. This is how Sheryl Crow got breast cancer. She was on the Ellen show and said this same exact thing. This has been identified as the most common cause of the high levels in breast cancer, especially in Australia .A friend whose mother was recently diagnosed with breast cancer and the Doctor told her: women should not drink bottled water that has been left in a car.The doctor said that the heat and the plastic of the bottle have certain chemicals that can lead to breast cancer. So please be careful and do not drink bottled water that has been left in a car, and, pass this on to all the women in your life. This information is the kind we need to know and be aware and just might save us! The heat causes toxins from the plastic to leak into the water and they have found these toxins in breast tissue. Use a stainless steel Canteen or a glass bottle when you can!LET EVERYONE WHO HAS A WIFE / GIRL FR IEND / DAUGHTER KNOW PLEASE.
Wednesday, April 8, 2009
Pregnancy Outcomes After Kidney Donation
The outcome of pregnancy in kidney donors has generally
been viewed to be favorable. We determined fetal
and maternal outcomes in a large cohort of kidney
donors. A total of 2102 women have donated a
kidney at our institution; 1589 donors responded to
our pregnancy surveys; 1085 reported 3213 pregnancies
and 504 reported none. Fetal and maternal outcomes
in postdonation pregnancies were comparable
to published rates in the general population. Postdonation
(vs. predonation) pregnancies were associated
with a lower likelihood of full-term deliveries (73.7%
vs. 84.6%, p = 0.0004) and a higher likelihood of fetal
loss (19.2% vs. 11.3%, p < 0.0001). Postdonation
pregnancies were also associated with a higher risk
of gestational diabetes (2.7% vs. 0.7%, p = 0.0001),
gestational hypertension (5.7% vs. 0.6%, p < 0.0001),
proteinuria (4.3% vs. 1.1%, p < 0.0001) and preeclampsia
(5.5% vs. 0.8%, p < 0.0001). Women who had both
pre- and post-donation pregnancies were also more
likely to have these adverse maternal outcomes in their
postdonation pregnancies. In this large survey of previous
living donors in a single center, fetal and maternal
outcomes and pregnancy outcomes after kidney
donation were similar to those reported in the general
population, but inferior to predonation pregnancy
outcomes.
been viewed to be favorable. We determined fetal
and maternal outcomes in a large cohort of kidney
donors. A total of 2102 women have donated a
kidney at our institution; 1589 donors responded to
our pregnancy surveys; 1085 reported 3213 pregnancies
and 504 reported none. Fetal and maternal outcomes
in postdonation pregnancies were comparable
to published rates in the general population. Postdonation
(vs. predonation) pregnancies were associated
with a lower likelihood of full-term deliveries (73.7%
vs. 84.6%, p = 0.0004) and a higher likelihood of fetal
loss (19.2% vs. 11.3%, p < 0.0001). Postdonation
pregnancies were also associated with a higher risk
of gestational diabetes (2.7% vs. 0.7%, p = 0.0001),
gestational hypertension (5.7% vs. 0.6%, p < 0.0001),
proteinuria (4.3% vs. 1.1%, p < 0.0001) and preeclampsia
(5.5% vs. 0.8%, p < 0.0001). Women who had both
pre- and post-donation pregnancies were also more
likely to have these adverse maternal outcomes in their
postdonation pregnancies. In this large survey of previous
living donors in a single center, fetal and maternal
outcomes and pregnancy outcomes after kidney
donation were similar to those reported in the general
population, but inferior to predonation pregnancy
outcomes.
Monday, April 6, 2009
How Effective Are ACE Inhibitors for Hypertension? A Best Evidence Review
Introduction
Angiotensin-converting enzyme (ACE) inhibitors are some of the most commonly prescribed medications for hypertension. Indeed, they were cited in a recent survey of primary care supervisors in Australia[1] as the treatment most often recommended by guidelines and favored over other antihypertensive drugs as first-line agents. This enthusiasm for ACE inhibitors is somewhat inconsistent with current recommendations,[2] which prefer thiazide diuretics as first-line medication for uncomplicated cases of hypertension. ACE inhibitors are seen as more appropriate for first-line use when other high-risk conditions are present, such as diabetes. Still, given clinicians' favorable experience with ACE inhibitors and the increasing prevalence of type 2 diabetes in the population, it is clear that ACE inhibitors will maintain an important role in the treatment of hypertension.
With the popularity of ACE inhibitors in mind, investigators conducted a systematic review of published studies to determine how effective the drugs actually are in reducing blood pressure. They also examined dose effectiveness, adverse effects, and the role of co-occurring conditions.
The Study Findings
Researchers looked for double-blind studies comparing ACE inhibitors and placebo. All included studies were at least 3 weeks in duration and measured blood pressure as an endpoint at 3-12 weeks. Studies that featured a response-dependent titration of medications were included in the review. Only research that focused on patients with a blood pressure above 140/90 mm Hg was reviewed.
The review included 92 trials with a total of 12,954 participants (mean age, 54 years). Mean baseline blood pressure was 157/101 mm Hg and mean pulse pressure was 56 mm Hg. The majority (75%) of included studies was industry-sponsored, and 82% of the trials examined fixed-dose ACE inhibitors. The duration of trials was generally short, which limited data with regard to adverse events and study withdrawals.
The main potential source of bias in the research was a lack of information with regard to how the studies were blinded. In addition, the reviewers suggested that the researchers could have preferentially selected patients more likely to respond to ACE inhibitors. This selection bias could make ACE inhibitors appear more effective than they truly are.
The studies covered 14 ACE inhibitors. The degree of homogeneity with regard to their efficacy in reducing blood pressure was remarkable. No one medication appeared superior to others.
Overall, ACE inhibitors had a modest collective effect in reducing blood pressure. The mean reduction in systolic blood pressure ranged between 6 mm Hg and 9 mm Hg, and the mean reduction in diastolic blood pressure was 4-5 mm Hg. Less data were available with regard to the blood pressure effects of ACE inhibitors at 1-12 hours after dosing, but the average decrease in blood pressure with ACE inhibitors around their peak concentration was greater than their average efficacy (11.4/6.4 mm Hg).
Dose Effectiveness
The study provided some important information about the relationship between the dose of ACE inhibitors and their effect on blood pressure. Doses lower than the manufacturers' maximum recommended dosage had the same blood pressure-lowering effect as the maximum dose. For example, doses of one eighth to one quarter of the maximum achieved the blood pressure-lowering effect of the maximum dose in 60% to 70% of cases. Half of the maximum dose achieved it 90% of the time. There was no blood pressure-lowering effect at or below one sixteenth of the maximum suggested dose. These data suggest that use of the maximum dosage of ACE inhibitors to achieve greater blood pressure control is usually unnecessary.
The research also identified dosing information for individual ACE inhibitors and suggested that the manufacturers' recommended starting doses of benazepril, moexipril, and ramipril are higher than the minimum dose needed to reduce blood pressure. Conversely, captopril did not appear effective in reducing blood pressure at the manufacturers' recommended starting dose. Most of the maximum blood pressure-lowering effect of lisinopril was achieved at only one eighth of the recommended maximum dose.
ACE inhibitor dosing was also one of the biggest deficits in the current review. It was clear to the review authors that not all data in regard to the efficacy of different doses of ACE inhibitors were published. Instead, the data were supplied to regulators privately to determine the appropriate dosing range of ACE inhibitors.
Only half of trials provided data in regard to the rate of withdrawal due to adverse events. Collectively, there was no difference between ACE inhibitors and placebo in this critical outcome. ACE inhibitors did not significantly affect patients' heart rate.
The Role of ARB Inhibitors
The main finding of the current review is that ACE inhibitors as a class of medications have a fairly weak effect in reducing blood pressure in hypertension. Physicians might therefore consider an alternative inhibitor of the renin-angiotensin system, an angiotensin receptor blocker (ARB). These newer medications have been heavily promoted for the treatment of hypertension, and they are not associated with cough, which is one of the most prevalent side effects of ACE inhibitors.
However, a systematic review of the efficacy of ARBs for hypertension,[3] published concurrently with the review of ACE inhibitors, suggested that these medications have very similar efficacy. The reviewers studied 46 randomized controlled trials examining 9 ARBs, and found that the overall efficacy in reducing systolic and diastolic blood pressure was -8 mm Hg and -5 mm Hg, which was similar to an ACE inhibitor. The peak effect of ARBs was also similar, with an average blood pressure reduction of approximately 12/7 mm Hg. Much like ACE inhibitors, ARBs were effective at one eighth to one half of the manufacturers' recommended doses.
Addressing Other Health Issues
Physicians might choose ACE inhibitors to treat hypertension for other possible health benefits associated with these medications, especially the potential to prevent type 2 diabetes. ACE inhibitors can have a positive effect on glucose metabolism through multiple mechanisms, and previous research suggested that they could prevent incident diabetes compared with other antihypertensive medications. Specifically, the Captopril Prevention Project[4] demonstrated a 14% relative reduction in this outcome among participants receiving captopril vs a diuretic or beta-blocker. This benefit, associated with captopril, was evident regardless of the baseline risk for diabetes, although the incidence of diabetes was not a primary outcome of the study.
The Diabetes Reduction Assessment with Ramipril and Rosiglitazone Medication (DREAM) trial[5] directly examined the effect of ramipril vs placebo on the incidence of diabetes. This study examined patients with impaired fasting glucose levels or reduced insulin sensitivity but no history of cardiovascular disease. After a median of 3 years of treatment, ramipril was not associated with a significantly lower incidence of diabetes compared with placebo. Median fasting plasma glucose levels were also similar at the end of the trial. However, ramipril was associated with a higher rate of return to normoglycemia. An editorial[6] accompanying this article concluded that ACE inhibitors could not be recommended to reduce the risk for incident diabetes, although they might still confer some benefit on glucose metabolism.
Physicians might also consider using ACE inhibitors for hypertension in order to prevent incident heart failure. However, although ACE inhibitors are associated with numerous positive outcomes, including reduced mortality, among patients with known heart failure,[7] little evidence exists that they provide special protection against new heart failure. In a study of quinapril and placebo initiated shortly after myocardial infarction, there was no difference between treatment groups in a composite outcome of cardiovascular death and significant cardiovascular events.[8] Specifically, no difference was found in the risk for heart failure among those patients at high cardiovascular risk. Similarly, in the Antihypertensive and Lipid-Lowering Treatment to Prevent Hearth Attack Trial (ALLHAT), the incidence of heart failure was similar among patients receiving lisinopril and chlorthalidone.[9]
Commentary
Although ACE inhibitors may not provide special protection against diabetes or heart failure among patients with hypertension, physicians should still consider these medications when managing hypertension. In fact, the nature of hypertension management dictates that they have to because most patients require more than 1 medication initially. In a recent study of men receiving care at a Veteran Affairs hospital, 60.4% of subjects with hypertension and significant cardiovascular risk were receiving multiple antihypertensive medications.[10] Nevertheless, only 28% of these same patients had reached their goal blood pressure levels, indicating that they needed titration of their medications, if not the addition of other antihypertensive drugs.
If most patients require multiple medications, physicians would be wise to spend more time focusing on which combinations of medications work best, as opposed to fretting about the choice of initial treatment. The current review of ACE inhibitors (and ARBs) is also a reminder that physicians should consider adding another medication prior to prescribing the full dose of these drugs. With these principles in mind, both physician and patient will get the maximum benefit from the chosen antihypertensive regimen.
Clinical Pearls
In the current review, ACE inhibitors were associated with an average reduction in systolic blood pressure between 6 mm Hg and 9 mm Hg and in diastolic blood pressure of 4-5 mm Hg;
ACE inhibitors achieved most of their power in reducing blood pressure at half of the maximum recommended dose, or less;
ARBs provide similar reductions in blood pressure compared with ACE inhibitors; and
There is no strong evidence that ACE inhibitors can prevent incident diabetes mellitus or heart failure.
Angiotensin-converting enzyme (ACE) inhibitors are some of the most commonly prescribed medications for hypertension. Indeed, they were cited in a recent survey of primary care supervisors in Australia[1] as the treatment most often recommended by guidelines and favored over other antihypertensive drugs as first-line agents. This enthusiasm for ACE inhibitors is somewhat inconsistent with current recommendations,[2] which prefer thiazide diuretics as first-line medication for uncomplicated cases of hypertension. ACE inhibitors are seen as more appropriate for first-line use when other high-risk conditions are present, such as diabetes. Still, given clinicians' favorable experience with ACE inhibitors and the increasing prevalence of type 2 diabetes in the population, it is clear that ACE inhibitors will maintain an important role in the treatment of hypertension.
With the popularity of ACE inhibitors in mind, investigators conducted a systematic review of published studies to determine how effective the drugs actually are in reducing blood pressure. They also examined dose effectiveness, adverse effects, and the role of co-occurring conditions.
The Study Findings
Researchers looked for double-blind studies comparing ACE inhibitors and placebo. All included studies were at least 3 weeks in duration and measured blood pressure as an endpoint at 3-12 weeks. Studies that featured a response-dependent titration of medications were included in the review. Only research that focused on patients with a blood pressure above 140/90 mm Hg was reviewed.
The review included 92 trials with a total of 12,954 participants (mean age, 54 years). Mean baseline blood pressure was 157/101 mm Hg and mean pulse pressure was 56 mm Hg. The majority (75%) of included studies was industry-sponsored, and 82% of the trials examined fixed-dose ACE inhibitors. The duration of trials was generally short, which limited data with regard to adverse events and study withdrawals.
The main potential source of bias in the research was a lack of information with regard to how the studies were blinded. In addition, the reviewers suggested that the researchers could have preferentially selected patients more likely to respond to ACE inhibitors. This selection bias could make ACE inhibitors appear more effective than they truly are.
The studies covered 14 ACE inhibitors. The degree of homogeneity with regard to their efficacy in reducing blood pressure was remarkable. No one medication appeared superior to others.
Overall, ACE inhibitors had a modest collective effect in reducing blood pressure. The mean reduction in systolic blood pressure ranged between 6 mm Hg and 9 mm Hg, and the mean reduction in diastolic blood pressure was 4-5 mm Hg. Less data were available with regard to the blood pressure effects of ACE inhibitors at 1-12 hours after dosing, but the average decrease in blood pressure with ACE inhibitors around their peak concentration was greater than their average efficacy (11.4/6.4 mm Hg).
Dose Effectiveness
The study provided some important information about the relationship between the dose of ACE inhibitors and their effect on blood pressure. Doses lower than the manufacturers' maximum recommended dosage had the same blood pressure-lowering effect as the maximum dose. For example, doses of one eighth to one quarter of the maximum achieved the blood pressure-lowering effect of the maximum dose in 60% to 70% of cases. Half of the maximum dose achieved it 90% of the time. There was no blood pressure-lowering effect at or below one sixteenth of the maximum suggested dose. These data suggest that use of the maximum dosage of ACE inhibitors to achieve greater blood pressure control is usually unnecessary.
The research also identified dosing information for individual ACE inhibitors and suggested that the manufacturers' recommended starting doses of benazepril, moexipril, and ramipril are higher than the minimum dose needed to reduce blood pressure. Conversely, captopril did not appear effective in reducing blood pressure at the manufacturers' recommended starting dose. Most of the maximum blood pressure-lowering effect of lisinopril was achieved at only one eighth of the recommended maximum dose.
ACE inhibitor dosing was also one of the biggest deficits in the current review. It was clear to the review authors that not all data in regard to the efficacy of different doses of ACE inhibitors were published. Instead, the data were supplied to regulators privately to determine the appropriate dosing range of ACE inhibitors.
Only half of trials provided data in regard to the rate of withdrawal due to adverse events. Collectively, there was no difference between ACE inhibitors and placebo in this critical outcome. ACE inhibitors did not significantly affect patients' heart rate.
The Role of ARB Inhibitors
The main finding of the current review is that ACE inhibitors as a class of medications have a fairly weak effect in reducing blood pressure in hypertension. Physicians might therefore consider an alternative inhibitor of the renin-angiotensin system, an angiotensin receptor blocker (ARB). These newer medications have been heavily promoted for the treatment of hypertension, and they are not associated with cough, which is one of the most prevalent side effects of ACE inhibitors.
However, a systematic review of the efficacy of ARBs for hypertension,[3] published concurrently with the review of ACE inhibitors, suggested that these medications have very similar efficacy. The reviewers studied 46 randomized controlled trials examining 9 ARBs, and found that the overall efficacy in reducing systolic and diastolic blood pressure was -8 mm Hg and -5 mm Hg, which was similar to an ACE inhibitor. The peak effect of ARBs was also similar, with an average blood pressure reduction of approximately 12/7 mm Hg. Much like ACE inhibitors, ARBs were effective at one eighth to one half of the manufacturers' recommended doses.
Addressing Other Health Issues
Physicians might choose ACE inhibitors to treat hypertension for other possible health benefits associated with these medications, especially the potential to prevent type 2 diabetes. ACE inhibitors can have a positive effect on glucose metabolism through multiple mechanisms, and previous research suggested that they could prevent incident diabetes compared with other antihypertensive medications. Specifically, the Captopril Prevention Project[4] demonstrated a 14% relative reduction in this outcome among participants receiving captopril vs a diuretic or beta-blocker. This benefit, associated with captopril, was evident regardless of the baseline risk for diabetes, although the incidence of diabetes was not a primary outcome of the study.
The Diabetes Reduction Assessment with Ramipril and Rosiglitazone Medication (DREAM) trial[5] directly examined the effect of ramipril vs placebo on the incidence of diabetes. This study examined patients with impaired fasting glucose levels or reduced insulin sensitivity but no history of cardiovascular disease. After a median of 3 years of treatment, ramipril was not associated with a significantly lower incidence of diabetes compared with placebo. Median fasting plasma glucose levels were also similar at the end of the trial. However, ramipril was associated with a higher rate of return to normoglycemia. An editorial[6] accompanying this article concluded that ACE inhibitors could not be recommended to reduce the risk for incident diabetes, although they might still confer some benefit on glucose metabolism.
Physicians might also consider using ACE inhibitors for hypertension in order to prevent incident heart failure. However, although ACE inhibitors are associated with numerous positive outcomes, including reduced mortality, among patients with known heart failure,[7] little evidence exists that they provide special protection against new heart failure. In a study of quinapril and placebo initiated shortly after myocardial infarction, there was no difference between treatment groups in a composite outcome of cardiovascular death and significant cardiovascular events.[8] Specifically, no difference was found in the risk for heart failure among those patients at high cardiovascular risk. Similarly, in the Antihypertensive and Lipid-Lowering Treatment to Prevent Hearth Attack Trial (ALLHAT), the incidence of heart failure was similar among patients receiving lisinopril and chlorthalidone.[9]
Commentary
Although ACE inhibitors may not provide special protection against diabetes or heart failure among patients with hypertension, physicians should still consider these medications when managing hypertension. In fact, the nature of hypertension management dictates that they have to because most patients require more than 1 medication initially. In a recent study of men receiving care at a Veteran Affairs hospital, 60.4% of subjects with hypertension and significant cardiovascular risk were receiving multiple antihypertensive medications.[10] Nevertheless, only 28% of these same patients had reached their goal blood pressure levels, indicating that they needed titration of their medications, if not the addition of other antihypertensive drugs.
If most patients require multiple medications, physicians would be wise to spend more time focusing on which combinations of medications work best, as opposed to fretting about the choice of initial treatment. The current review of ACE inhibitors (and ARBs) is also a reminder that physicians should consider adding another medication prior to prescribing the full dose of these drugs. With these principles in mind, both physician and patient will get the maximum benefit from the chosen antihypertensive regimen.
Clinical Pearls
In the current review, ACE inhibitors were associated with an average reduction in systolic blood pressure between 6 mm Hg and 9 mm Hg and in diastolic blood pressure of 4-5 mm Hg;
ACE inhibitors achieved most of their power in reducing blood pressure at half of the maximum recommended dose, or less;
ARBs provide similar reductions in blood pressure compared with ACE inhibitors; and
There is no strong evidence that ACE inhibitors can prevent incident diabetes mellitus or heart failure.
seminal vesicle cyst
Seminal vesicle cyst is a rare urological problem.[1],[2],[3] First case reported by Zinner in 1941. Seminal vesicle cysts may be congenital or acquired [1]. Present since birth, congenital cysts develop and become symptomatic in young adulthood. Accumulation of secretions in the gland owing to insufficient drainage, which is associated with atresia of the ejaculatory ducts, causes subsequent distension of the seminal vesicles, leading to formation of a cyst [6]. The cysts are usually unilateral with no predilection for side [3]. Acquired cysts are often bilateral and are seen in an older age group after a history of chronic prostatitis or prostate surgery. The seminal vesicles are paired secretory glands just posterior to the bladder. Congenital anomalies of the seminal vesicles including ectopia, hypoplasia, cyst formation and agenesis and other internal genital abnormalities are frequently associated. Most seminal vesical cysts remain asymptomatic until puberty, but with the widespread use of ultrasonography during pregnancy and infancy there are likely to be more asymptomatic cases [1, 2]. The potential complications are infection, compression of the surrounding structures [3–6], infertility and malignant degeneration. Most patients with this anomaly are asymptomatic or present during early adulthood with non-specific symptoms. Usually the cysts are 5.0 cm or less in diameter and are either a symptomatic or present during early adulthood with symptoms such as urgency, burning, hematuria and hypogastric pain mainly after coitus. Less frequently cysts larger than 8-10 cm occur and such giant cysts can result in colon or bladder obstruction with palpation of mass per rectum. Here we report a young male presenting with bilateral hydronephrosis hydroureter with acute renal failure because of giant seminal vesicle cyst causing urinary retention
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