Posts by Kate Collins67

vividotter7 said:The second I felt this, pure panic set in—I dropped my cigarettes immediately. At first, I tried to convince myself I was just imagining things, but then how else do you explain these random chest pains? Could my body be having some kind of violent reaction to nicotine, or is it something else entirely?

You’ve only been smoking for five months and you’re already acting like you’re terminal... He claims he smokes, yet he’s being "super careful" about his health... what does that even mean? What kind of logic is that?

If you realize right now that you don't have cancer, you'll just go right back to lighting up—and then you'll just toss the pack again the next time your chest starts hurting...

And then people like this turn around and complain when we try to implement actual health education programs in our public schools.

@Lisa Myers.

Look, if you have Hypertension, you take antihypertensives. It’s that simple.

And if your blood pressure spikes every single time you get worked up—well, maybe just stop getting worked up? Seriously.

So, here is the real question: who was the first doctor to prescribe this regimen to you, and what exactly were they basing it on?

If you're actually feeling stuck in this dilemma—and I'm not talking about readings hitting over 200 mmHg here—just taper off the antihypertensives over the course of a week. Then, go see a private specialist for a 24-hour blood pressure monitor test. Once you have those numbers, it'll be crystal clear whether you actually need the medication or not.

Mixing Amlodipine with Ramace... did Sanofi sponsor some medical conference or something? Because let's be honest, that isn't changing a thing for your actual situation.

So, the plan is to use either Zoloft or propylthiouracil to get that hyperthyroidism under control first. Once the hormone levels stabilize, we’re looking at thyroid surgery. After that's done, if everything goes smoothly—meaning, if they don't end up dealing with cholecystitis or pancreatitis in the meantime—we move forward with gallbladder surgery to get things regulated. Of course, if one of those issues pops up beforehand, we'll likely have to stick to conservative therapy to calm the inflammation before even thinking about the gallbladder. Unless, of course, the surgeon happens to be available right when an acute case of cholecystitis hits, in which case they might just go ahead and remove the gallbladder immediately.

Look, they could just perform a lobectomy—say, take out one lobe—and leave the other one intact. You might end up with hypothyroidism, sure, but there's a decent chance the remaining part of the thyroid will be enough to handle things.

The surgery itself is basically routine, though let's be real—there’s always that underlying risk of everything going sideways with any surgical procedure. But if that part goes smoothly? Then the rest of the recovery is relatively harmless.

If that toxic adenoma reading is actually accurate—and I mean really, truly accurate—then we're looking at hyperthyroidism, which pretty much means surgery is the move.

Nancy Morris5 said:🤣 but I'm worried.
I get that I'm not technically anemic yet, but I honestly can't tell if these levels have dropped too much over the last 7 months.

Look, you know exactly when it becomes necessary to run tests—it's when you're actually willing to pay out of your own pocket just to get some clarity. This whole system isn't going to fix itself as long as this "just because we can" mentality keeps running things. It’s like people think services are just free handouts. Would you even bother paying for extra labs just to see if there's a tiny difference between two perfectly fine results, or would you grab a few more just to be absolutely certain?$33 If you were in my shoes, would you spend your own money investigating minor fluctuations, or would you just move on?

There are hundreds of thousands of people just like you—maybe even more—and that's exactly how all that money just vanishes. And let me be clear: the issue isn't that you're asking for answers. The real problem is that the system actually gives in and lets you drain your bank account for it.

But anyway, back to the medical side of things. If your new ferritin level ends up sitting around 5, then you are well on your way to developing actual anemia within a few months. It always follows a pattern with the type of anemia you're dealing with (iron deficiency): first the ferritin drops, then the serum iron, and finally the hemoglobin. That sequence is set in stone.

@Nancy Morris5/">@@Nancy Morris5

Are you actually losing it just a little bit?

I mean, this kind of obsessive, active hunting for symptoms when nothing is even wrong...

Let’s play out a scenario here: suppose what you’re feeling in your joints actually is polyarthritis—and I mean real deal stuff, not just some vague systemic pain caused by a fever. If your antibodies are coming back positive, and if we just ignore that absolute nonsense about needing two minor criteria plus one major one to clinch a diagnosis (I mean, let’s be honest, practically everyone with any kind of infection meets those "minor" criteria anyway), then you’d basically just be one single criterion away from this being classified as rheumatic fever.

We’re talking about something like this: carditis—which would show up on an EKG or an echocardiogram, and honestly, you should probably expect elevated cardiac enzymes if there's myocarditis involved—maybe some minor chorea (those involuntary, purposeless movements, though that's less likely, still possible), erythema marginatum (that very specific rash with the pale patches and reddish borders), or even subcutaneous nodules.

But look, the absolute priority here is determining whether your heart is being affected. If it is, you need corticosteroid therapy to get those inflammatory markers and symptoms under control—assuming, of course, you aren't currently fighting off a recurring infection, in which case you'd need antibiotics like penicillin first. If the diagnosis ends up being confirmed, you're looking at long-term prophylaxis with monthly penicillin doses.

Frank Rodriguez5 said:Look, I’m trying to figure this out—my AST/ASO levels are sitting at 1160.
It hasn't budged in three months. Who knows how long it’s been this high? It could be months, could even be years... I’ve been dealing with strep throat infections for about four years now.

The real issue is that lately—over the last two months—I’ve been feeling pain around my heart area. Then for the past three weeks, my knees have been aching, my joints are acting up occasionally, and I’m running low-grade fevers hitting around 99.5°F. To me, it all feels like something is going on—something rheumatic.

My last bout of strep was back in September. All my swabs come back clean—I can't find any strep anywhere—but yet that AST/ASO level just won't drop. I'm honestly terrified it's going to mess with my heart, my knees, or my kidneys. What am I supposed to do here? Should I be looking into getting injections, or is there some other way to bring those titers down?

If we were living fifty years ago, I’d tell you it sounds like a classic case of rheumatic fever.
But nowadays, things aren't quite that straightforward.
Without an EKG, it’s hard to say anything for sure, but if you're feeling that pain behind your sternum alongside everything else you mentioned, there could definitely be some changes occurring. If they suspect what you're worried about, doctors really need to either rule it out or confirm it—it's a bad spot to be in when things are left up in the air.

I have to admit, I’m struggling to wrap my head around why—given that we’re talking about an inherited genetic mutation here—the symptoms don't start showing up until so much later in life.

I can maybe wrap my mind around it for women, considering the monthly blood loss compensation, but even then, if there’s no cycle for the first twelve years, how does the ferritin not build up enough to cause damage by then? And for men, seeing them show up in their 40s with low ferritin levels just doesn't add up. If they couldn't get those levels up by age 40 and they aren't losing blood from anywhere else, isn't it safe to assume they won't be able to raise it in the next forty years either? Unless, of course, this specific mutation has some sort of upper limit on iron absorption and the guy is just living off a diet of iron supplements.

How is this even scientifically explained?

Even if you end up getting a diagnosis for hemochromatosis, you aren't going to qualify for any kind of treatment with ferritin levels that low—I mean, what's the point? The whole goal of therapy is to bring those ferritin numbers down, right? Maybe things will shift once you hit menopause and your ferritin starts climbing because you aren't losing blood anymore.

Look, it’s not like hemochromatosis is my area of expertise, so please, don't go treating my take as the final word on the matter.

His ferritin levels are way too low for hemochromatosis, right?

There’s this weird finding in the results that doesn't fit the standard textbook patterns—you could easily write it off as some insignificant outlier or just a medical curiosity.

Unless, of course, she's been dealing with heavy periods her entire life.

What is his problem?

Where on earth did he catch malaria?

swiftbear86 said:What’s actually the point of getting a metabolic syndrome diagnosis if we just end up treating every individual issue based on the standard medical guidelines anyway?
Is there some specific set of protocols just for metabolic syndrome, or how does it differ from the usual way things are handled?
I totally get that having a bunch of different risk factors stacked up increases the chances of cardiovascular issues.
Also, does anyone know what the ICD code for metabolic syndrome is?

Where is modern medicine even heading? Metabolic... my foot.

They claim people are getting overweight more often, yet the prerequisite for labeling it "metabolic syndrome" is central obesity... seriously?

Unfortunately, we’re living in a world overflowing with PhDs, associate professors, and various academic elites who seem obsessed with churning out scientific papers on absolutely anything just to cling to their tenured positions. (Honestly, when you dig through the literature, half of them read like, "if a breeze blows on a Saturday, two seniors over 65 will die per 4 million people"—it's all just variations of that nonsense)....

And the absolute worst part? They cite studies that eventually get debunked, but because those flawed results and assumptions spawned hundreds of follow-up papers, they continue to be accepted as gospel. It’s a self-perpetuating cycle of garbage conclusions.

Personally, I don't recognize metabolic syndrome as a valid diagnosis—unless, of course, some Big Pharma company pays me to start acknowledging it.😉

Let’s be real here—he could have said whatever he wanted. When you're dealing with something where proving the actual cause of a spike is practically impossible, what does it really matter? The bottom line is that the numbers normalized and you didn't end up developing any clinical symptoms. That’s the win. Just don't go getting them tested for no reason moving forward, alright?😉

Maria Fisher46 said:I agree that deciding where to even begin—what to do versus what to leave alone—is pretty debatable. But honestly? If nothing else, I’d at least double-check those lab results one more time.

Stop the hormones and monitor the D-dimer levels, though I have no clue how long after stopping therapy we should be checking them.

If someone had actually bothered to teach me how to perform a Doppler, and then a patient walked in with random D-dimer readings like that—especially at only 35 years old—I’d check her veins. Honestly, I’d probably do it just to satisfy my own curiosity rather than because I actually expect to find anything, but you can never be too sure (that’s the one thing I know for certain).

Ugh, you really spooked them there.

@Charles Murphy6: Look, in the medical field, you can't just claim anything with absolute certainty.

@Charles Murphy6 & el Gato:
So, I went ahead and read the article, and here’s my take on the whole thing:
1. We are looking at a Case Report here. Period.

2. Any patient showing up with "rectal bleeding" is immediately suspected of having colorectal cancer until proven otherwise—that's just how it works. Now, they have a patient with rectal bleeding and elevated D-dimer levels (though, frankly, I don't see what the actual indication was for testing those D-dimers in the first place). So, if we assume the patient has cancer and then find elevated D-dimers? Well, that’s exactly what you’d expect to see.

I'm not sure if I'm making myself clear enough: if someone has cancer, you should expect their D-dimer levels to be high; however, just because someone has high D-dimer levels doesn't mean they suddenly have a tumor.
It's like the analogy with smokers and lung cancer—if someone has lung cancer, there’s a huge probability they’re a smoker, but if you only look at smokers (using that as your sole criterion), the actual statistical chance of any single one of them having lung cancer is still quite low.

3. If they had chosen a subject who wasn't already symptomatic—and I honestly get the impression they're downplaying the significance of the rectal bleeding just to make the article seem more "impactful"—it would have been a much more meaningful observation. As it stands, it feels like they missed the cancer entirely, and then we just got lucky that we didn't know why the D-dimers were up, allowing us to locate what should have been discovered regardless of the D-dimer levels.

4. A much better observation in this paper would have been stating that you shouldn't just write off rectal bleeding as hemorrhoids until a full colonoscopy has been performed.

5. Sure, it’s possible their observation is spot on, but you damn well cannot draw sweeping conclusions from a single case study.

6. Personally, I have no idea why someone would have elevated D-dimers. If anyone can actually give me an official answer and prove it, then please, by all means, teach me something.

7. As far as I'm concerned, you don't need to address me using formal language on this forum (and yeah, that goes for el Gato).🙂

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3273370/

So, let's talk about D-dimers

I have to admit, I’m still a bit fuzzy on this whole extravascular coagulation thing—I’ve seen people claim that’s how it works, but... when we're talking about the uterine lining shedding, isn't the basic assumption that we're looking at capillary bleeding? And if that's the case, shouldn't that bleeding be stopped by aggregation and coagulation? If those fibrin strands eventually form a structural barrier, wouldn't that naturally lead to D-dimer release into the bloodstream later on?

I get that coagulation happens outside the vessels if we're talking about blood reaching the decidua, but how else does the bleeding stop if not through coagulation? If I'm not mistaken, when a hematoma is being resorbed, you see a spike in D-dimers, right?

The real headache with D-dimers—at least in the context of pulmonary embolisms—is that from a diagnostic standpoint, there's practically no difference between a value of 0.51 and a 5.

In any case, it begs the question: what are we supposed to do with patients who show elevated D-dimer levels that are just incidental findings without any actual clinical symptoms?

Do we run routine Doppler ultrasounds on the upper and lower extremities? Or go straight to a CT angiography of the pulmonary arteries?

Personally, I wouldn't even bother testing them if I didn't have a specific reason to do so. Since I don't just order these tests routinely without cause, I honestly don't have much experience dealing with an elevated result that lacks a clear clinical picture.

Since birth control can trigger DVT, there's a theoretical scenario where clots are indeed forming, but some innate fibrinolytic activity prevents them from actually staying put or getting lodged. In that case, their breakdown would drive up D-dimer levels without ever showing up as a physical clinical manifestation.

But then the question remains: in a situation like that, should you even be hunting for a clot? And if so, where exactly are you looking?

If a gynecologist ordered D-dimer tests specifically to prove a procoagulant state, you could argue they've effectively proven it and that hormone therapy needs to be discontinued immediately—but hey, I'm not a gynecologist, and I have no idea how their clinical decision-making process works.

Betty Sanchez58 said:So, does that mean Rocaltrol isn't actually good for calcium? I am seriously confused here. Completely lost.
I'm sitting here reading the medication insert right now and—surprise, surprise—that's exactly what it says. So what am I even supposed to take? This is ridiculous...
If my endocrinologist doesn't know, who on earth am I supposed to ask?

Look, let's break this down. Rocaltrol (which is just the active form of Vitamin D that your body can't produce on its own anymore after those parathyroid glands were removed—and by the way, since you had two put back, you really ought to be checking your PTH levels to see how they're actually functioning) is what allows your gut to absorb calcium. But get this: you could swallow a mountain of Rocaltrol, but if you aren't actually consuming enough calcium through food or supplements, there’s nothing there to absorb! It's basic biology.

The logic your endocrinologist is likely using is pretty straightforward: her calcium levels are dropping, the parathyroids are gone, so the culprit is clearly a lack of active Vitamin D (Rocaltrol), not a lack of calcium intake. They prescribe the Rocaltrol, the calcium still drops, and then you're left with a few possibilities—maybe the dose of Rocaltrol is too low, or maybe she's just not eating nearly enough calcium, or some other variable that probably isn't the main issue here.

Honestly, things would be a hell of a lot easier to navigate if they actually sat down and looked at the full picture—PTH, Ca++, Vitamin D 1-25 OH, and Vitamin D 25 OH. Sure, a doctor can sometimes make an educated guess without running every single test, but that's exactly how people run into dead ends—by making assumptions instead of looking at the hard data.