De Quervain’s (Subacute) Thyroiditis

Photograph from my Kirsty Glitterhead photoshoot.

Just like Katy Perry, you’re hot then you’re cold.

The story

In June 2021, I noticed I was starting to sweat a lot. I mean, I knew I wasn’t the fittest after COVID lockdowns, but I shouldn’t be sweating this much walking from the car to my paediatric placement. Just while standing in handover for 20 minutes, I could feel beads of sweat rolling down my back. Lovely. 

A week into the third-year placement, I felt otherwise great as I had found a speciality I enjoyed. I’d developed a bit of a sore throat that weirdly didn’t get worse on swallowing, but I put that down to catching something from the kids. Taking some ibuprofen reliably settled the pain for 8 hours.

Sleeping soon became an issue as I continued to drench in sweat under even the lightest of duvets at night. I resorted to sleeping on towels and taking showers at 3 am after waking up soaked. That’s if I could fall asleep, as my thumping heart prevented me from lying on my left side. Along with palpitations, my heart rate had begun to rocket from its usual resting rate (50-55 bpm) up to 75-80 bpm. It jumped over 100bpm as soon as I began moving. Wearing shorts became a necessity.

After a couple of weeks, I began to put the puzzle pieces together. I called the GP and explained, “I think I have De Quervain’s Thyrotoxicosis,” a niche thyroid pathology typically seen in middle-aged women. He quizzically called me in to take some blood and look at my neck for any lumps (none) or throat inflammation (none) and soon agreed that I indeed showed the signs. 

The GP prescribed me Propranolol 40mg TDS to calm the vasomotor symptoms and reduce the chance of my heart skipping into an irregular rhythm (atrial fibrillation). 

The thyroid function tests (TFTs) came back the next day as Free T4: 80 [normal range 9 - 23] and TSH: unrecordable[normal range 0.4 - 4]. I was severely hyperthyroid. I was referred to endocrine and prescribed Carbimazole 20mg OD to calm my thyroid and temporarily stop further thyroxine production. Since it’s a specialised medication, the doctor carefully explained the potential side effects, including pancytopenia (a dangerous drop in all blood cell types, including the immune system). He advised that any signs of infection, such as a sore throat, require immediate assessment in A&E as they could quickly worsen. My platelets were slightly raised (472), likely as an acute phase reactant related to my neck pain.

The propranolol immediately started to calm me down, and the carbimazole ensured I stayed that way. This graph shows how dramatic the fall in my heart rate back to baseline was over the next few weeks. I wish I had started wearing my Fitbit when the symptoms began.

Thankfully my sweating and palpitations began to subside too. I estimate I lost about 5kg over 3 weeks. Thankfully I had avoided some other typical hyperthyroid symptoms, such as loose stools and agitation. 

My results a week later were Free T4: 36 [9 - 23], TSH: unrecordable [0.4 - 4], platelets: high, other cells: normal.

A month later, we rechecked my bloods and found the TFTs had reversed, as expected with subacute thyroiditis. Free T4: unrecordable [9 - 23], TSH: 50 [0.4 - 4], platelets & other cells: normal.

I was now severely hypothyroid. We stopped my medications and hoped my thyroid would kick back in again to replace my absence of thyroxine. My weight rose back to normal. Eventually my sweating, racing heat and palpitations thankfully subsided, though it took 3 months until I could wear trousers again.

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My struggles with hypothyroidism surprisingly only got worse over time as my thyroid levels returned to normal-ish values. I gradually became much more lethargic, replacing weight lifting with napping which persists to this day. My mental health deteriorated. My weight didn’t rocket, but I’m certainly not as fit as I once was. When once I couldn’t tolerate the slightest heat, now I can’t get enough blankets at the slightest chill.

I was considered subacutely hypothyroid as my TSH ranged between 5 - 9 [normal range 0.4 - 4] over the coming months. Frustratingly this meant I wasn’t considered eligible for levothyroxine to correct. Whether my new career working as a foundation doctor only made the symptoms worse, or I struggled because of the symptoms, I’m not sure. But it wasn’t enjoyable.

Thankfully(?) I developed TPO-antibodies in December 2023, meaning I was clinically hypothyroid and required thyroxine replacement. I’m not sure why they weren’t present before. I’ve so far been titrated up to 75 micrograms levothyroxine daily, but I still struggle with the lethargy and energy. Whether this is the natural development of familial hypothyroidism or was triggered by the illness, I’ll never know.

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So it turns out that while you may not feel a virus take hold, other body parts may do, leaving you with surprising results. I hope this story helps someone better understand the process of subacute thyroiditis from the patient’s perspective - whether you’re contending with the thyroid rollercoaster yourself, or a medical student studying the thyroid. 

The science in a nutshell

Thyroiditis Basics

Your thyroid, a butterfly-shaped gland in your neck, produces hormones - primarily thyroxine (T4) and triiodothyronine (T3) - that regulate metabolism, body temperature, and energy levels. I think of it like the speedometer for your body. When it’s inflamed due to subacute thyroiditis, it freaks out and dumps its stored thyroid hormone all at once, sending the body into temporary hyperthyroidism.

Hyperthyroidism Phase: A Thyroid Flood

The initial inflammation, often triggered by a viral infection (which I probably caught in paediatrics), causes damage to thyroid follicular cells, which release massive amounts of pre-made thyroid hormones into the bloodstream. This sudden spike in T4 and T3 pushes the body's metabolism into overdrive. Your body essentially hits "fast forward": faster heart rate, sweating, and sometimes weight loss as every system burns through resources more quickly. The high hormone levels then suppress TSH (thyroid-stimulating hormone), the hormone that typically tells the thyroid when to work harder, so TSH becomes undetectable.

Hypothyroid Phase: The Crash

After exhausting its hormone reserves, the thyroid needs time to recover and rebuild. However, because TSH is still low, the thyroid doesn’t immediately kick back in, and hormone production is minimal. This leads to hypothyroidism - a sluggish thyroid state. Symptoms flip, and the body now has slowed metabolism, which can bring fatigue, weight gain, sensitivity to cold, and low mood.

Back to Normal (Hopefully)

As inflammation gradually settles, TSH levels can return to normal and stimulate the thyroid to resume balanced hormone production. Some people experience full recovery, while others might develop chronic hypothyroidism, particularly if thyroid peroxidase antibodies (TPO antibodies) are detected later, suggesting autoimmune thyroiditis as a possible next chapter.

In all, subacute thyroiditis sends the body on a thyroid rollercoaster, from hyperthyroid highs to hypothyroid lows—each with its unique set of challenges.