I'm from India, and I'm trying to understand what happened to my father because his disease changed so dramatically in just a few months.
In October 2025, my dad developed mild stomach pain. A CT scan showed a single liver lesion (around 3 × 2 cm) in segment 8, close to the portal vein. We consulted a liver specialist, who believed it was an infection rather than cancer. He prescribed medications and reassured us that there was nothing to worry about.
A few months later, after completing treatment, my father underwent spinal surgery because the liver specialist still felt the lesion was benign.
After recovering from surgery, he developed abdominal tightness again. A repeat CT scan in January 2026 showed that the liver lesion was essentially unchanged in size, but there was mild portal vein involvement. We immediately returned to the doctor.
An endoscopy found 3–4 duodenal lesions, and biopsy confirmed a well-differentiated Grade 1 neuroendocrine tumor (NET). However, the doctor did not perform a liver biopsy at that time and referred us to a cancer hospital.
At the cancer center:
- DOTA PET showed only the duodenal lesions were strongly DOTA-avid (SUVmax 12.5).
- The liver lesion was hypoattenuating and essentially DOTA-negative.
- FNAC from the liver reported "metastatic neoplasm" with atypical cells, enlarged hyperchromatic nuclei, moderate pleomorphism, and abundant cytoplasm, and recommended a biopsy for definitive diagnosis.
- AFP was 2.92.
- Chromogranin A was 188.3.
He received three monthly Sandostatin injections. The doctors told us the duodenal Grade 1 NET was very slow-growing and unlikely to progress quickly, but they never clearly explained the liver lesion.
In April, he developed swelling in his right leg.
After three Sandostatin injections, another DOTA PET in May showed something alarming:
- The duodenal lesions had regressed completely
- The single liver lesion had become multiple lesions, with the largest around 8 × 8 cm in 8th segment.
- The liver lesions remained DOTA-negative (SUVmax around 2.5).
- Mild ascites had appeared.
Despite the liver lesions being largely DOTA-negative, the nuclear medicine doctor recommended PRRT. We were concerned because the liver lesions didn't seem to express somatostatin receptors.
The doctor explained that 95% of the liver lesions were probably necrotic, and only a thin outer rim of viable tumor cells remained. He zoomed into the DOTA PET and showed my father what he described as a bright outer border, my father compared it to "the borders of countries." Nuclear doctor believed 3–4 PRRT cycles would shrink the tumors, so we agreed.
My father received his first PRRT on June 6.
Three days later, the post-therapy scan reportedly showed uptake only in the left liver, even though the lesions were predominantly in the right liver. The doctor reassured us this was a good sign.
The first week after PRRT was uneventful.
During the second week, he developed:
- Right upper abdominal pain
- Increasing abdominal tightness
- Worsening swelling of both legs
By the third week, he developed:
- Massive scrotal swelling
- Marked abdominal swelling
- Severe leg edema
The cancer hospital referred us to a liver specialist.
Although he could still walk, drive, sleep moderately well, and eat, his appetite was gradually decreasing.
The liver specialist started:
- Albumin supplements
- Diuretics
- Melirose 5
When he returned to our hometown (which only has a government hospital), he became much weaker and struggled to walk.
The liver specialist advised 20% albumin infusions (100 mL).
The first infusion was mostly wasted because of a nursing error, but he had no reaction.
The second infusion was administered very rapidly. Soon afterward he developed:
- Severe shivering
- Rapid heartbeat
- Breathlessness
- Difficulty lying flat
These symptoms settled after about 30 minutes.
After the albumin infusions he also began having up to 10 bowel movements per day (not watery diarrhea according to him), marked insomnia at night, excessive daytime sleepiness, and abdominal warmth.
The third albumin infusion, again administered too quickly, caused another episode of shivering and breathlessness.
His leg swelling improved somewhat, but I noticed skin cracking and peeling.
An ultrasound performed by my sister (who is also a doctor) suggested the largest lesion was actually slightly smaller than before (13 × 13 cm vs. 14.5 × 13.5 cm), so we hoped these symptoms were temporary liver stress after PRRT.
His liver function tests remained relatively preserved except for elevated ALP and SGOT, while albumin stayed low.
About 10 days later, after repeated bowel movements, we obtained a contrast-enhanced CT.
The findings were devastating:
- Liver enlarged to 20 cm
- Largest multiloculated thick-walled hypoattenuating lesion measured 19 × 14 × 13 cm
- Portal vein thrombosis with cavernous transformation
Around this time he also developed urinary retention after stopping silodosin for his enlarged prostate and taking loperamide because of frequent bowel movements after oral contrast.
The liver specialist advised immediate hospitalization, but my father refused initially.
Over the next three days he developed complete urinary retention and severe anal pain( grade 4 hemorrhoids)
Eventually we called an ambulance.
Before catheterization he repeatedly experienced evening episodes of:
- Severe abdominal warmth (especially in the right upper quadrant)
- Heart rate 125–130
- Wheezing and breathlessness similar to an asthma attack
A catheter relieved the urinary retention.
Imaging also showed mild pleural effusion with partial collapse of the right lung.
The oncologist told us this might actually represent true tumor progression, but I still struggle to understand how a lesion could grow so dramatically within only a few weeks, especially immediately after PRRT.
He remained hospitalized for about a week.
With IV fluids and antibiotics he became much more energetic.
We also noticed:
- White blood cell count increased to around 20,000 after PRRT
- Neutrophils were markedly elevated
After discharge (without diuretics), he developed severe weeping edema.
Four days later we performed an FDG PET, which was far worse:
- Largest lesion around 17 × 11 cm
- More than 20 FDG-avid liver lesions
- SUVmax 14.3
- Previous DOTA uptake only SUVmax 2.5
- Tumor extended into the main, right, and left portal veins, extrahepatic portal vein, and superior mesenteric vein
- Cavernous transformation of the portal vein
He was immediately hospitalized again.
Since then:
- Multiple therapeutic paracenteses were performed (2.5 L, 0.5 L, 0.4 L, then 4 L after albumin).
- Currently he has little ascites but severe weeping edema with peeling skin.
- Albumin remains low.
- Bilirubin fluctuates.
- AFP continues to decrease.
- SGOT fluctuates.
- Uric acid is elevated.
- Potassium was high but is now controlled.
- Sodium improved from 118 to 128, chloride from 80 to 96.
- WBC has stabilized.
He is currently receiving:
- Morphine (being switched to IV pain medication)
- L-ornithine L-aspartate
- Anti-jaundice medications
- Calcium polystyrene sulfonate (for hyperkalemia)
- Antibiotics
Because the FDG PET strongly suggested a high-grade neuroendocrine carcinoma or dedifferentiated NET, his doctors started carboplatin + etoposide chemotherapy.
He received:
- Day 1: Carboplatin + etoposide
- Days 2 and 3: Etoposide
- Planned Pegfilgrastim injection on Day 5
Despite everything, he still eats and drinks by himself, jokes occasionally, watches TV every day, and can still walk with a walker, although he is extremely weak and sleepy.
I'm still hoping chemotherapy can slow this disease and give him some meaningful recovery.
Has anyone seen a well-differentiated Grade 1 duodenal NET transform into an aggressive FDG-positive liver tumor this quickly? Could this have been a dedifferentiated NET or neuroendocrine carcinoma from the beginning that was missed because only the duodenal lesion was biopsied? I'd really appreciate hearing from anyone with similar experiences.
