Captopril Patient Views

It was prescribed for me, but dropped my blood pressure too much so it was stopped.

Over-exertion while taking an ACE inhibitor came close to killing me twice, as it led to dangerously-low blood sodium (hyponatraemia), putting me in hospital the second time. Just a little lower and I could have died. I realised then that the saying "Hard work never killed anyone" was untrue.

I am also interested in where you read about this ACE inhibitor approach to treating ME/CFS, my friend. And I'd be interested to know: was there any particular reason why you chose lisinopril, since there are many ACE inhibitors and ARBs to choose from. Though I did some Googling, and found the following from Dr David Moskowitz: > ACE appears to be at the source of virtually all common diseases except prostate cancer. In particular, all autoimmune diseases, such as Lupus, Rheumatoid Arthritis, Multiple Sclerosis, and even allergies to penicillin and sulfa drugs, start with overactivity of ACE. The logical treatment to try, then, especially for diseases with no good treatment yet, is an ACE inhibitor or an angiotensin II blocker (ACE makes angiotensin II). > Since activated macrophages express ACE on their surface membrane, ACE has something to do with their activated state. The product of ACE, angiotensin II, is probably an activating hormone, or "cytokine," for macrophages. Blocking the macrophage with an ACE inhibitor or angiotensin II receptor blocker ("arb") is a very gentle, benign way of trying to tone down the inflammation. We have seen it work for several diseases already characterized by overly exuberant inflammation or even outright autoimmune disease. > Source: Treating Chronic Fatigue Syndrome and Fibromyalgia: Interview with David Moskowitz, M.D. > > Click to expand... Note: both angiotensin converting enzyme inhibitors (ACE inhibitors) and angiotensin II receptor blockers (ARBs) perform equivalent functions: these drugs respectively block the production or the action of the hormone angiotensin II. Note: the Marshall Protocol, which some people use to treat ME/CFS, involves taking the drug Benicar (olmesartan), which is an ARB drug.

Thank you. But please note what I said in my post:

Not a single one of the numerous doctors I saw during that time realised that the drug I had been prescribed shortly before I first became ill with it was the cause of my illness.

Not one doctor. Many, including a hospital consultant (senior doctor). I have looked online several times since then to see if there are yet any warnings about hyponatraemia with ACE inhibitors. I can still hardly find any mention anywhere. This appears to be the latest info given to doctors in the UK. There is still no clear, specific warning about hyponatraemia being caused by the drug, just a few references to salt and hyponatraemia in other contexts and with regard to concomitant diuretic use (and AFAIK these are still prescribed to patients also taking ACE inhibitors, despite it being dangerous to take ACE inhibitors when one is dehydrated - see this thread). I was put on fluid restriction in hospital when I had hyponatraemia! I know that this is recommended in the case of overhydration, but I was dehydrated, which docs failed to recognise or acknowledge.

I turned to an online pharmacy when a doctor stopped another medication - desmopressin - because she and other doctors seemed to have convinced themselves that it was desmopressin that had caused my first episode of hyponatraemia, notwithstanding the fact that my previous doctor had dismissed the episode as a panic attack and left me with no treatment for it. When I was finally well enough to get to my GP, it was found that I was (still) moderately hyponatraemic, which I think was the first time this was recorded. Docs at that practice, and maybe docs generally, seem obsessed with desmopressin posing a threat of hyponatraemia through excessive fluid retention/overhydration through drinking too much fluid. My meticulously-compiled charts (produced at docs' request and then ignored) showed my fluid intake to be normal and my output to be excessive - I was polyuric. But the doc just stopped the desmopressin with no warning, discussion or explanation. Reminder - ACE inhibitors are particularly dangerous when one is dehydrated, so this in fact put me at greater risk, although I didn't know it at the time. I had been taking desmo with no problems for 7 years when I had my first hyponatraemic episode, but docs decided desmo was to blame rather than the ACE inhibitor I had only started shortly before - going onto the top dose just 10 days before the episode. Desmopressin had transformed my life for the better. At last I could go shopping without multiple trips to disgusting public toilets. I could use buses again. I could sleep without having to get up multiple times to urinate. And I wasn't constantly thirsty. So after a lot of research, and with trepidation, I tried what appeared to be a reputable online pharmacy - and have never looked back. I do not look for medical knowledge at a pharmacy of any kind. I use scientific papers and authoritative sites, including government sites.

Are you in the USA? When I have repeatedly pointed out my high albumin levels to doctors as evidence for dehydration, they have said that that's not why they test albumin (I KNOW - but it can be used as evidence for this!), and that they use other measures for hydration status. When I have asked what measures they use, they have come up with stupid responses, such as levels of other things that need to be interpreted IN LIGHT of hydration status. But my explanations have fallen on deaf ears, and I have been the one to suffer misdiagnosis and related problems. I have recently discovered the probable cause of my hyponatraemia that I have suffered on and off for 7 years - my ACE inhibitor, which can cause hyponatraemia through natriuresis - sodium loss in urine, typically occurring in a hypovolaemic context. But all this time the doctors insisted that the cause was overhydration/hypervolaemia due to excessive fluid intake and overuse of desmopressin. I knew that they were wrong, but they wouldn't listen. But I didn't know it was the ACE inhibitor. I have suffered a hell of a lot over those 7 years as a result. Severe and frightening illness, loss of income, abuse from doctors and more. Yesterday a doctor agreed with my self-diagnosis.

Well, one of those assumptions came close to costing the patient their life in 2007, when their GP/PCP decided over the phone, despite their weak but desperate protestations - that they were having a panic attack (of which they have no history) when it eventually turned out that they were suffering severe hyponatraemia (low blood sodium) almost-certainly caused by the ACE inhibitor they had been prescribed shortly before. I later found that a friend's relative had died shortly after being told by the same doctor that her symptoms were all in her mind. Makes me wonder how many people die due to such idiotic and disrespectful decisions. I fear that it may be a lot.

What if your body is making angiotensin ii because you are ill and do need to lay down? This sound like it could be a 'beating the tired horse' type of treatment. I think it should be approached with caution.

Hi Richard, can you explain in more detail how an ACE inhibitor can reduce sickness behavior? Where did you learn about this approach? I tried searching online but couldn't find much info.