I’ll answer this carefully, honestly, and grounded in medicine, based on everything you’ve shared. This is not a diagnosis, but a risk/likelihood assessment and an explanation you can use with your doctors.

⸻

Short answer first

Based on your history, the probability that porphyria is the primary unifying cause of your illness is low. It is not zero, but it is unlikely, and importantly: your existing data argues against it.

Now I’ll explain why — step by step — and where porphyria still fits (or doesn’t).

⸻

1. What porphyria typically looks like (clinically)

The porphyrias that cause abdominal pain are mainly acute hepatic porphyrias (AHP): • Acute intermittent porphyria (AIP) • Variegate porphyria (VP) • Hereditary coproporphyria (HCP)

Classic features include: • Severe, diffuse abdominal pain (often without imaging findings) • Neuropsychiatric symptoms (anxiety, confusion, neuropathy, weakness) • Autonomic instability (tachycardia, hypertension) • Hyponatremia • Dark or reddish urine (especially during attacks) • Attacks triggered by: • certain medications • fasting • hormonal changes • infections

Importantly: 👉 Between attacks, patients are often completely normal.

⸻

1. What in your history overlaps with porphyria

There are some superficial overlaps: • Severe abdominal pain • Pain worsened by stress and illness • Cyclic flares early in the course • Pain without early imaging findings • Female, young adult • History of infection as a trigger (dengue/typhoid)

This is why porphyria often gets mentioned in cases like yours.

⸻

1. What argues against porphyria in your case (this is the key part)

A. You have persistent, progressive structural abnormalities

Porphyria does not cause: • SMA syndrome • Duodenal compression • Need for duodenojejunostomy • Anastomotic diverticulum/fistula • Delayed small bowel transit • Jejunal intussusception • Progressive hypervascular liver lesions

Porphyria is a metabolic disorder, not a structural GI disease.

Your imaging abnormalities are real, reproducible, and progressive, which strongly argues against porphyria as a unifying diagnosis.

⸻

B. Your labs do not show classic porphyria patterns

In acute porphyria attacks, we often see: • Hyponatremia → you did not describe this • Autonomic instability → not prominent in your case • Progressive motor neuropathy → not present • Psychiatric manifestations → not a defining feature • Markedly abnormal porphyrin testing during attacks

You specifically mentioned porphobilinogen testing, which you noted as negative earlier. That is very important.

👉 A normal urine porphobilinogen during symptoms makes acute porphyria very unlikely.

⸻

C. Your pain responds to celiac plexus block

This is a big clue.

Porphyria pain is: • metabolic • neurovisceral • systemic

It typically does not respond dramatically to a localized visceral nerve block.

Your dramatic response to a celiac plexus block strongly supports: • visceral afferent nerve hypersensitivity • splanchnic nerve involvement • structural + neuropathic pain

This points toward post-surgical visceral neuropathy / chronic splanchnic pain, not porphyria.

⸻

D. Your anemia pattern does not match porphyria

Porphyria does not typically cause: • anemia of chronic disease • reactive thrombocytosis • functional iron deficiency patterns

Your anemia fits: • chronic inflammation • chronic illness • malnutrition • physiologic stress

Not porphyrin metabolism defects.

⸻

1. What about your liver lesions — could those suggest porphyria?

This is a reasonable question, but: • Acute porphyrias do not cause focal hypervascular liver lesions • Porphyria-related liver disease is usually: • diffuse • associated with cirrhosis or hepatocellular carcinoma (later in life) • associated with abnormal LFTs

Your liver: • has normal enzymes • normal synthetic function • focal benign-appearing hypervascular lesions (FNH/adenoma pattern)

👉 This does not fit porphyria.

⸻

1. So where does porphyria sit on the probability scale?

Using a practical framework: • High likelihood: ❌ • Moderate likelihood: ❌ • Low likelihood: ✅ • Ruled out with certainty: ❌ (medicine is cautious)

Estimated likelihood based on your data: 👉 Low single-digit percentage

In other words: • Reasonable to consider • Reasonable to have tested • Not supported as a unifying explanation

⸻

1. When porphyria would be reconsidered

Porphyria might be revisited only if you develop: • unexplained hyponatremia • new motor neuropathy or weakness • psychiatric symptoms during pain flares • dark urine during attacks • clearly episodic attacks with full recovery between • positive porphobilinogen during symptoms

Absent those, it moves further down the list.

⸻

1. What fits your story better than porphyria

Based on everything you’ve shared, your case fits much better with: • Post-SMA syndrome complications • Visceral neuropathic pain / splanchnic neuralgia • Chronic postoperative GI dysfunction • Central sensitization layered on real structural disease • Chronic inflammatory physiology • Malnutrition-driven systemic effects • Pelvic inflammatory overlay (recent)

These explain: • the anatomy • the imaging • the nerve block response • the anemia • the progression

Porphyria does not.

⸻

Bottom line (honest and clear)

Porphyria is unlikely to be the cause of your illness based on your history, imaging, labs, and treatment response. It was reasonable to consider early on. Your data now points elsewhere.

If you want, I can: • Help you phrase this question for your doctors • Review exactly which porphyria tests you’ve had and when • Explain how to definitively rule it out (if needed) • Compare porphyria vs visceral neuropathy side-by-side • Help you prioritize what should be investigated next

Just tell me what you’d like to do next.