A 63-year-old man was referred to Modarres Hospital, Tehran.

He had gradual onset of obscure generalized abdominal pain six hours before admission.

His pain was located in the epigastric and periumbilical region.

There was no radiation of pain to anywhere else.

There was moderate abdominal distension.

There was periumbilical abdominal tenderness.

Initial blood tests showed white cell count (WBC) of 21.7 × 109/L.

Initial blood tests showed neutrophils 84.2%.

Initial blood tests showed hemoglobin (Hb) 15.2 g/dL.

About five hours after resuscitation and appropriate fluid therapy, he has not felt better.

Abdominopelvic CT-scan showed evidence of hematoma near the head of pancreas.

Abdominopelvic CT-scan showed perihepatic and perisplenic fluid.

He was transferred to operating room emergently.

Massive intraperitoneal hematoma was evacuated.

Right medial visceral rotation, the Cattell-Braasch maneuver, was performed.

Active bleeding in the base of IPDA was detected.

IPDA was suture ligated at the base with 4/0 nonabsorbable stitch.

The post-operative period was uneventful.

Oral fluids were started the day after the surgery.

The patient was discharged from the hospital two days after the surgery.

One week after discharge, he had a normal follow-up.

There were no concerning problems one week after discharge.

The patient had idiopathic spontaneous intraperitoneal hemorrhage.

The hemorrhage was caused by spontaneous rupture of non-aneurysmal inferior pancreaticoduodenal artery.


Your body needs to keep your blood clean and your organs working well. If your kidneys aren’t doing their job, it’s like having a leaky faucet — waste builds up, and you might feel tired or sick. You should talk to a doctor if you notice these signs so they can check your kidneys and help you feel better.

Kidney function is essential for filtering waste and excess fluids from the blood. When kidney function declines, toxins accumulate, leading to symptoms like fatigue, swelling, and high blood pressure. Early detection through regular screening is key to managing the condition and preventing complications. Lifestyle changes and medical monitoring can help maintain kidney health.

The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and reduce cardiovascular risk.

The patient had multiple yellowish elevated masses in different locations of the body.

The masses were located on the dorsum of the hands, elbows, buttocks, and feet.

The patient had bilateral arcus cornealis.

The size of the masses varied from 1 × 1 × 1 cm to 8 × 8 × 5 cm.

The masses increased progressively in size.

The patient reported discomfort and difficulty dressing and sitting due to large masses in the buttocks.

The patient reported difficulty wearing sandals due to the masses in the feet.

The patient felt inferior when in contact with others.

The patient decided to divorce because of psychological influences related to abnormalities in the body.

The chest X-ray, abdominal ultrasound, electrocardiogram, and echocardiogram of the patient were normal.

The patient's family medical history was not taken because the patient did not wish to disclose it.

The patient's LDL-C level was 10.04 mmol/L.

The reference value for LDL-C is <2.6 mmol/L.

The patient was diagnosed with Familial hypercholesterolemia (FH) based on the Simon Broome Criteria.

The patient agreed to be admitted to the hospital for surgery to remove the masses.

Lipid-lowering therapy was administered with Atorvastatin 40 mg/day.

After 4 days of hospitalization, the patient underwent surgery to remove the masses.

The resected masses had a surface of normal skin.

The core of the masses looked yellowish-colored, uniform, relatively solid, without necrosis.

The masses were localized in the subcutaneous layer without invading the muscle or joint capsule.

The skin incision was oval around the circumference of the masses with the longitudinal axis parallel to the Langer's line.

After removing the masses, all defects were sutured directly.

The remaining 2 masses on the finger were not removed because the patient still had to use the fingers to take care of himself.

The remaining 2 masses would be removed during the next surgery.

Histopathology showed a typical xanthoma with infiltration of foam cells.

All sutures were removed 14 days after surgery.

The patient was discharged and continued treatment with atorvastatin 40 mg/day.

Gene sequencing test showed homozygous LDL-C receptor gene mutation on chromosome 19.

The patient's family members did not undergo gene sequencing to find mutations causing FH.

At 1.5 months postoperatively, the LDL-C level of the patient was reduced to 8.8 mmol/L.

At 1.5 months postoperatively, the wounds healed well.

At 1.5 months postoperatively, no re-appearance of masses was observed.

The patient had multiple large tuberous xanthomas related to FH.

There were 15 masses in different body parts.

The masses were located on the dorsum of the hands, elbows, buttocks, feet, and Achille's tendon.

The largest masses in the buttocks measured 8 × 8 × 5 cm.

Surgical removal of 13 masses was carried out in combination with medical treatment.

The skin incision was oval around the circumference of masses with the longitudinal axis parallel to the Langer's line.

Skin defects were closed directly or dissected on both sides of the incision to reduce tension.

After 1.5 months, there was no recurrence of xanthomas.

The patient had bilateral arcus cornealis.

The masses increased progressively in size.

The patient's LDL-C level was 10.04 mmol/L.

The reference value for LDL-C is <2.6 mmol/L.

The resected masses had a surface of normal skin.

All sutures were removed 14 days after surgery.

**System Role:**

You are an expert medical editor and Health Literacy specialist. Your task is to transform complex medical text into three distinct versions based on the reader's health literacy level. You must maintain the source language of the input while adjusting the linguistic complexity. Use the provided Gold Summary as the factual anchor to ensure the simplified versions remain accurate and focused on the most important information.

**User Prompt:**

Please process the following medical Source Text and its corresponding Gold Summary to generate three versions tailored to different health literacy levels.
### Instructions for Each Level:

1. Level: Low Health Literacy (High Readability)

Target: Individuals needing the simplest terms for immediate action.

Linguistic Goal: Use "living room" language. Replace all medical jargon with functional descriptions (e.g., "renal" becomes "kidney").

Information Density: Focus strictly on the "need-to-know" info found in the Gold Summary.

Strategy: High paraphrasing using analogies. One idea per sentence.

Faithfulness: Must align perfectly with the Gold Summary.

2. Level: Intermediate Health Literacy (Medium Readability)

Target: The general public (news-reading level).

Linguistic Goal: Standard vocabulary. Common medical terms are okay, but technical "doctor-speak" must be simplified.

Information Density: Balanced. Use the Gold Summary as the lead, supplemented by necessary context from the Source Text.

Strategy: Moderate paraphrasing. Remove minor technical details to avoid information overload.

Faithfulness: Maintains the main narrative of the Gold Summary.

3. Level: Proficient Health Literacy (Low Readability)

Target: Researchers, clinicians, or highly informed patients.

Linguistic Goal: Technical and academic language. Prioritize clinical nuance and medical accuracy.

Information Density: High. Use the Full Source Text to include data, physiological mechanisms, and statistics.

Strategy: Minimal paraphrasing. Retain all original technical terminology.

Faithfulness: Adhere to the Source Text; you may add related subclaims that provide deeper scientific context.

I will provide the following information:

- Input Language: <<<SOURCE_LANGUAGE>>>
- Gold Summary (the anchor reference summary): <<<GOLD_SUMMARY>>>
- Source Text (detailed content): <<<FULL_TEXT>>>

**Output Format (JSON only):**
    {
    "low_health_literacy": "...",
    "intermediate_health_literacy": "...",
    "proficient_health_literacy": "..."
    }


The patient is a 57-year-old Ashkenazi Jew woman.

She had no family or personal history of malignancy.

She was admitted to the department of general surgery for treatment of her transverse colon tumor.

Four months prior, she had begun experiencing periumbilical abdominal pain.

Upon physical examination, no masses were palpated.

There were no other pathologic findings.

The colonoscopy revealed a large mass that involved nearly the whole circumference of the colon.

The mass seemed to be adjacent to the cecum.

The biopsies failed to demonstrate any colonic pathology.

She underwent computed tomography (CT) of the chest and abdomen.

The CT demonstrated a huge mass that occupied the whole colonic lumen.

The mass caused a colocolic intussusception.

Considerable mesenteric lymphadenopathy was seen.

The nodes were up to 28 × 21 mm in diameter.

The lymphadenopathy was deemed to be evidence of positive tumoral lymph node involvement.

No inguinal, pelvic, retroperitoneal, or other lymphadenopathy was seen.

A laparoscopic right extended hemicolectomy was performed.

During surgery, considerable mesocolic lymphadenopathy was seen.

The mesocolic lymphadenopathy was widely resected accordingly.

Pathology of the surgical specimen showed findings consistent with small B cell lymphoproliferative disorders with plasmacytoid differentiation.

Primary lymphoma of the colon was considered in the differential diagnosis.

The disease was thought to be part of systemic dissemination of lymphoma.

The patient was referred to the hematology clinic for further investigation.

The bone marrow biopsy result was normal.

Positron emission tomography-CT showed no other focus of lymphoma.

A test for Epstein-Barr virus infection was negative.

These results support the diagnosis of a primary colonic NHL small B-cell LPD with plasmacytoid differentiation.

The disease is an exceedingly rare disease.

There are only two such reports in the current literature.

We describe a case of an Ashkenazi Jew patient.

The patient presented in the typical way that carcinoma of the colon might present.

The patient turned out to have a very rare type of tumor.


She presented to the emergency department in significant respiratory distress.

She had a known past medical history of tobacco dependence.

She had a known past medical history of chronic obstructive pulmonary disease.

She had a known past medical history of hypertension.

On arrival, the patient was noted to be apneic.

She was actively being ventilated with a bag-valve-mask ventilation.

She rapidly progressed from an irregularly irregular cardiac rhythm to sinus bradycardia.

She then progressed into a pulseless electrical activity (PEA) arrest within minutes of arrival.

She underwent approximately 30 minutes of cardiopulmonary resuscitation.

Endotracheal intubation was performed via video laryngoscopy.

After intubation, she was noted to have significant resistance to bagging.

After return of spontaneous circulation, she was noted to have high peak pressures on the ventilator.

On examination, she was noted to have distant, rhonchorous, and wheezy breath sounds bilaterally.

She was treated for her bronchospasm with nebulized albuterol-ipratropium solution.

She was treated with continuous nebulized albuterol.

She was treated with methylprednisolone.

She was treated with subcutaneous terbutaline.

She was treated with titratable epinephrine.

She was noted to have continuously high peak pressures.

An intravenous push of vecuronium was given.

There was no improvement in ventilation after vecuronium.

There were continuously high peak airway pressures noted on the ventilator.

She had an electrocardiogram concerning for new-onset atrial fibrillation with rapid ventricular response.

She had an electrocardiogram showing left axis deviation.

She had an electrocardiogram showing a new right bundle branch block.

She had an electrocardiogram showing a left anterior fascicular block.

The electrocardiogram showed signs of right heart strain.

Given her difficulty with ventilation and hypotension, she was taken for a computed tomography (CT) with pulmonary embolism protocol.

The CT revealed no evidence of pulmonary embolism.

The CT showed evidence of alveolar rupture with pneumomediastinum consistent with the Macklin effect.

The CT showed a small left-sided pneumothorax.

The CT showed associated medial left hemi diaphragmatic rupture.

The CT showed pneumoretroperitoneum tracking along the left upper abdomen.

The CT showed pneumoretroperitoneum tracking along the left perinephric space.

The CT showed left-sided nondisplaced rib fractures of the fifth and sixth ribs.

A CT of the abdomen and pelvis showed a small amount of free air consistent with pneumoretroperitoneum.

The CT of the abdomen and pelvis showed free air adjacent to the gastric cardia.

The CT of the abdomen and pelvis showed free air adjacent to the left kidney.

The CT of the abdomen and pelvis showed free air adjacent to the left adrenal gland.

There was no definitively identified intra-abdominal traumatic injury.

Further history from the family revealed she had been complaining of difficulty breathing earlier in the day.

She subsequently suffered a witnessed fall down a flight of stairs.

The fall was associated with head trauma.

The fall was associated with apparent loss of consciousness.

The patient’s physical examination revealed no external signs of trauma on initial arrival.

The patient was admitted to the medical intensive care unit.

The admission was in the setting of cardiac arrest with prolonged down time.

The patient’s pneumomediastinum improved with lung-protective ventilation strategies.

The patient’s pneumoretroperitoneum improved with lung-protective ventilation strategies.

The patient was treated with paralytics.

The patient’s treatment for her COPD exacerbation included continuous albuterol nebulization of 40 milligrams (mg) over four hours.

The patient’s treatment included intermittent scheduled three-milliliter ipratroprium-albuterol nebulizers every six hours.

The patient’s treatment included 0.25 mg of budesonide twice daily.

The patient’s treatment included 0.5 mg of ipratroprium four times daily.

The patient’s treatment included isolated two mg of magnesium sulfate administration daily if worsening wheeze on examination.

The patient’s treatment included 80 mg of methylprednisolone daily.

The patient received a one-time dose of 0.25 mg of subcutaneous terbutaline.

The patient received a one-time dose of one microgram (μg) of epinephrine.

Sedation was maintained with ketamine at 1.5 mg per kilogram (kg) per hour.

Sedation was maintained with propofol at 20 μg/kg per minute.

The patient was treated with epinephrine as the first-line vasopressor choice.

The patient’s cardiac arrest resulted in severe hypoxic brain injury.

The patient had subsequent diffuse cerebral edema.

The patient had effacement of the basal cisterns.

The patient had tonsillar herniation seen on CT of her head.

The patient became increasingly hypertensive.

The patient was weaned off vasopressors.

The patient was started on titratable nicardipine at a maximum of 12.5 mg per hour.

The patient was given a hypertonic saline bolus.

The patient lost all evidence of brainstem reflexes five days after suffering cardiac arrest.

The patient continued to trigger some spontaneous breaths on the ventilator.

Multiple family meetings were held regarding patient prognosis.

The patient suffered a cardiac arrest after a fall.

The cardiac arrest occurred during a chronic obstructive pulmonary disease exacerbation.

She had a known past medical history of tobacco dependence.

She had a known past medical history of hypertension.

On arrival, the patient was noted to be apneic.

She was actively being ventilated with a bag-valve-mask ventilation.

She underwent approximately 30 minutes of cardiopulmonary resuscitation.

Endotracheal intubation was performed via video laryngoscopy.

After intubation, she was noted to have significant resistance to bagging.

She was treated with continuous nebulized albuterol.

She was treated with methylprednisolone.

She was treated with subcutaneous terbutaline.

She was treated with titratable epinephrine.

She was noted to have continuously high peak pressures.

An intravenous push of vecuronium was given.

There was no improvement in ventilation after vecuronium.

She had an electrocardiogram showing left axis deviation.

She had an electrocardiogram showing a new right bundle branch block.

She had an electrocardiogram showing a left anterior fascicular block.

The electrocardiogram showed signs of right heart strain.

The CT revealed no evidence of pulmonary embolism.

The CT showed a small left-sided pneumothorax.

The CT showed associated medial left hemi diaphragmatic rupture.

The CT showed pneumoretroperitoneum tracking along the left upper abdomen.

There was no definitively identified intra-abdominal traumatic injury.

She subsequently suffered a witnessed fall down a flight of stairs.

The fall was associated with head trauma.

The fall was associated with apparent loss of consciousness.

The patient was admitted to the medical intensive care unit.

The patient was treated with paralytics.

The patient’s treatment included 0.25 mg of budesonide twice daily.

The patient’s treatment included 0.5 mg of ipratroprium four times daily.

The patient’s treatment included 80 mg of methylprednisolone daily.

The patient received a one-time dose of one microgram (μg) of epinephrine.

Sedation was maintained with propofol at 20 μg/kg per minute.

The patient’s cardiac arrest resulted in severe hypoxic brain injury.

The patient had subsequent diffuse cerebral edema.

The patient had effacement of the basal cisterns.

The patient had tonsillar herniation seen on CT of her head.

The patient became increasingly hypertensive.

The patient was weaned off vasopressors.

The patient was given a hypertonic saline bolus.

Multiple family meetings were held regarding patient prognosis.


The patient was admitted with an uncontrolled itching sensation.

Six months prior, the patient had experienced intractable itching.

The patient had obstructive-pattern jaundice.

Endoscopic retrograde cholangiopancreatography (ERCP) and endoscopic retrograde biliary drainage were performed.

ERCP and endoscopic retrograde biliary drainage ruled out malignancy.

The patient's medical history included hypertension.

The patient's medical history included diabetes mellitus.

The patient's hypertension and diabetes mellitus were well controlled by medication.

The patient was an ex-smoker of ten years.

There was no family history of oncologic diseases.

There was no family history of rheumatic diseases.

The physical examination revealed icteric sclerae.

The physical examination revealed multiple itching scratches on the skin.

The patient’s platelet count was 348000/L.

The patient’s aspartate aminotransferase was 71 U/L.

The patient’s alanine aminotransferase level was 44 U/L.

The patient’s gamma-glutamyl transferase level was 233 U/L.

The patient’s alkaline phosphatase level was 315 U/L.

The patient’s total bilirubin level was 8.6 mg/dL.

The patient’s creatinine level was 1.37 mg/dL.

The patient’s erythrocyte sedimentation rate was 120 mm/h.

The patient’s C reactive protein (CRP) level was 1.81 mg/dL.

The patient’s antinuclear antibody titer was 1:2560.

The patient’s antinuclear antibody titer had a nucleolar pattern.

The patient’s serum IgG4 level was 465 mg/dL.

Abdominal computed tomography (CT) showed intrahepatic duct (IHD) dilatation.

Abdominal CT showed intraductal soft tissue attenuation.

Abdominal CT showed periductal enhancement.

There was no definite obstructive lesion.

CT showed fibrotic enhancement around the infrarenal aorta.

The patient had a prominent itching sensation.

The patient showed obstructive-pattern jaundice.

The patient had infiltration of a large number of IgG4-positive cells in the ampulla of Vater.

The imaging findings included intrahepatic duct and common bile duct dilation.

The diagnosis was IgG4-SC compatible with the 2019 ACR/EULAR classification criteria.

The planned treatment was high-dose glucocorticoid followed by cyclophosphamide pulse therapy.

After treatment with high-dose GC and an immunosuppressant, imaging studies showed that intrahepatic duct dilatation had completely resolved.

The patient’s platelet count was 348000/L.

There was no definite obstructive lesion.


At age 28, she had elevated platelet counts (> 100 × 104/μL).

ET had been diagnosed based on bone marrow biopsy results.

She was prescribed aspirin (100 mg/day) and anagrelide (2.5 mg/day).

She had been prescribed ebastine for itching.

On admission, her ALT level was 82 IU/L.

Her ALT level had improved from that recorded previously.

Prothrombin time and activated partial thromboplastin time were normal.

Abdominal ultrasonography revealed a cecal tumor.

Colonoscopy revealed advanced cecal cancer.

The patient recovered from liver dysfunction without treatment.

She stopped taking oral aspirin 1 week prior to surgery.

She continued anagrelide until the day before surgery.

To prevent thrombosis, she wore elastic stockings.

Intermittent pneumatic compression was performed during surgery.

Laparoscopic-assisted ileocecal resection was performed.

From the first postoperative day, she started walking.

From the first postoperative day, she started drinking water.

From the first postoperative day, she resumed oral anagrelide intake.

She resumed oral aspirin intake on the fifth postoperative day.

Her perioperative platelet count was controlled to approximately 40–60 × 104/μL.

Prothrombin time and activated partial thromboplastin time did not show abnormal values during the perioperative period.

The postoperative course was uneventful.

She was discharged on the seventh postoperative day.

The tumor pathological stage was T3N1M0 (Stage IIIB).

She received intravenous oxaliplatin plus oral capecitabine as postoperative adjuvant chemotherapy.

After one course, she again experienced liver dysfunction (AST 388 IU/L; ALT 531 IU/L).

Her platelet count decreased to 17.8 × 104/μL.

She was asked to discontinue anagrelide and aspirin that day onwards.

Five days later, her platelet count recovered to 50 × 104/μL.

She resumed taking anagrelide and aspirin.

She refused to resume any adjuvant chemotherapy after this incident.

Her liver function normalized gradually in 4 months.

There were no clinical signs of thrombosis.

There was no appearance of a new thrombus on contrast-enhanced CT 6 months after the operation.

One-year post operation, she is well without tumor recurrence or new metastasis.

A 40-year-old woman was admitted to our hospital after presenting with liver dysfunction.

She had been previously diagnosed with ET.

Aspirin and anagrelide had been prescribed.

Subsequent examination at our hospital revealed cecal cancer.

Laparoscopic ileocecal resection was performed.

Anagrelide was discontinued only on the surgery day.

She was discharged on the seventh postoperative day without thrombosis or hemorrhage.

When capecitabine and oxaliplatin were administered as adjuvant chemotherapy with continued anagrelide administration, she experienced hepatic dysfunction and thrombocytopenia.

Five days later, her platelet count recovered.

Subsequently, anagrelide and aspirin administration was resumed, without any adjuvant chemotherapy.

She had been prescribed ebastine for itching.

On admission, her ALT level was 82 IU/L.

Colonoscopy revealed advanced cecal cancer.

The postoperative course was uneventful.

Her platelet count decreased to 17.8 × 104/μL.

She resumed taking anagrelide and aspirin.

There were no clinical signs of thrombosis.


The kidneys play a central role in maintaining homeostasis by filtering metabolic waste, excess ions, and fluid from the bloodstream via glomerular filtration, reabsorption, and secretion. Impaired renal function results in the accumulation of uremic toxins, dysregulation of electrolyte balance (e.g., potassium, phosphate), and fluid overload, which can lead to hypertension, metabolic acidosis, and progressive glomerulosclerosis. Chronic kidney disease (CKD) progression is influenced by factors including glomerular filtration rate (GFR), proteinuria, and comorbidities such as diabetes and hypertension. Early intervention with pharmacological agents, dietary modifications, and blood pressure control is critical to slow disease progression and preserve renal function.

The patient had a history of prolonged opium inhalation.

The patient was referred to Ghaem clinic in Mashhad.

The patient had occasional aspiration since last year.

The patient did not previously undergo any treatment.

In laryngoscopy, prior to surgery, left arytenoid was tumoral.

In laryngoscopy, prior to surgery, left aryepiglottic fold was tumoral.

In laryngoscopy, prior to surgery, left false vocal cord was tumoral.

In laryngoscopy, prior to surgery, left true vocal cord was tumoral.

In laryngoscopy, prior to surgery, anterior commissure was tumoral.

In laryngoscopy, prior to surgery, subglottic region was tumoral.

In laryngoscopy, prior to surgery, other parts of the larynx and hypopharynx were normal.

In the preoperative computed tomography scan, there was transglottic involvement on the left side.

In the preoperative computed tomography scan, cervical lymphadenopathy was not detected.

Laryngeal cartilage and hyoid bone were reported to be normal.

The right paraglottic space was involved.

The biopsy of the affected areas represented well-differentiated squamous cell carcinoma.

The patient was ultimately diagnosed with transglottic squamous cell carcinoma of the T3N0M0 stage.

Total laryngectomy with total thyroidectomy was performed.

Bilateral elective cervical lymph node dissection level I-IV was performed.

The surgical margin was checked with a frozen section for the presence of the tumor.

The neopharynx was closed with the suturing technique.

The patient was diagnosed with salivary fistula.

The patient was initially treated with conservative management.

Total parenteral nutrition was part of the conservative management.

Pressure dressing was part of the conservative management.

Broad-spectrum antibiotic therapy was part of the conservative management.

In spite of conservative treatment, the fistula was not recovered after 3 weeks.

Jejunostomy was inserted instead of gastrostomy.

There was no evidence of positive surgical margins on permanent specimen pathology.

A thoracic surgeon was consulted about gastric pull-up.

It was decided to perform fibrin glue injection into the fistula tract via the endoscopic approach.

Informed consent was obtained from the patient before the surgery.

The case underwent an endoscopy to locate internal fistula orifice.

In gastrointestinal endoscopy, a fistula was identified in the anterior wall of the neopharynx.

Fibrin glue was prepared from the patient’s blood sample.

The PCF tract was endoscopically localized.

An ERCP catheter passed through the fistula.

The de-epithelialization of fistula orifice was performed.

Fibrin glue was endoscopically injected into the fistula tract via the catheter.

A nasogastric tube was inserted under the endoscopic view.

Following the administration of fibrin glue, the patient underwent pressure dressing.

Two weeks later, the case was discharged with an NG tube and antibiotics.

One month after the fibrin glue injection, no evidence of contrast extravasation was observed on barium swallow test.

The fistula was completely closed one month after the fibrin glue injection.

The NG tube was drawn one month after the fibrin administration.

The patient returned to normal oral feeding without any problems.

Fibrin glue preparation required two components: fibrinogen and thrombin.

Fibrinogen is prepared after the extraction of blood from the patient's vein or blood bank.

Thrombin is produced as a ready-to-use commercial solution.

Thrombin is extractable from the plasma of the patient.

Thrombin is diluted in distilled water and combined with aminocaproic acid.

The first method of fibrinogen preparation is plasma.

The second method of fibrinogen preparation is plasma cryoprecipitate.

The third method of fibrinogen preparation is plasma cryoprecipitate.

In this study, the second method was used for the preparation of fibrin glue.

In this case, fibrin glue was injected by endoscopy.

Under intravenous sedation and left lateral decubitus position, the endoscope entered into neopharynx through the mouth.

The location of the fistula was observed in the anterior neopharyngeal wall.

The ERCP catheter passed through the endoscope into the fistula.

The de-epithelialization of fistula orifice was performed.

Five cc of the fibrin glue was endoscopically injected into the fistula tract via the catheter.

Some fibrin glue was percutaneously injected into the outer orifice of the fistula.

The patient follow-up showed that the fistula was completely closed three months after the administration.

Oral nutrition was successfully started.

The subsequent follow-up demonstrated that the patient tolerated a soft diet and fluids without any problems.

She had a transglottic squamous cell carcinoma of the T3N0M0 stage.

She had PCF development following total laryngectomy surgery.

She had total thyroidectomy and bilateral elective cervical lymph node dissection level I-IV.

The fistula was not recovered after 3 weeks of conservative treatment.

The patient had a history of prolonged opium inhalation.

The patient was referred to Ghaem clinic in Mashhad.

The patient had occasional aspiration since last year.

The patient did not previously undergo any treatment.

In laryngoscopy, prior to surgery, left arytenoid was tumoral.

In laryngoscopy, prior to surgery, left false vocal cord was tumoral.

In laryngoscopy, prior to surgery, left true vocal cord was tumoral.

In laryngoscopy, prior to surgery, anterior commissure was tumoral.

In laryngoscopy, prior to surgery, subglottic region was tumoral.

Laryngeal cartilage and hyoid bone were reported to be normal.

The right paraglottic space was involved.

Total laryngectomy with total thyroidectomy was performed.

The neopharynx was closed with the suturing technique.

The patient was diagnosed with salivary fistula.

The patient was initially treated with conservative management.

Total parenteral nutrition was part of the conservative management.

Pressure dressing was part of the conservative management.

Jejunostomy was inserted instead of gastrostomy.

A thoracic surgeon was consulted about gastric pull-up.

Informed consent was obtained from the patient before the surgery.

The case underwent an endoscopy to locate internal fistula orifice.

Fibrin glue was prepared from the patient’s blood sample.

The PCF tract was endoscopically localized.

An ERCP catheter passed through the fistula.

The de-epithelialization of fistula orifice was performed.

A nasogastric tube was inserted under the endoscopic view.

The NG tube was drawn one month after the fibrin administration.

The patient returned to normal oral feeding without any problems.

Thrombin is produced as a ready-to-use commercial solution.

Thrombin is extractable from the plasma of the patient.

The first method of fibrinogen preparation is plasma.

The third method of fibrinogen preparation is plasma cryoprecipitate.

In this case, fibrin glue was injected by endoscopy.

The ERCP catheter passed through the endoscope into the fistula.

The de-epithelialization of fistula orifice was performed.

Oral nutrition was successfully started.


He was born at 40 weeks’ gestational age.

He was delivered at term by episiotomy combined with forceps.

He was admitted to the Department of Neonatology of The Second Hospital of Jilin University due to dyspnea in February 2022.

Brain MRI showed a short T1 strip signal shadow (hemorrhage) under the cranial plate of the occipital region on both sides.

The right eye appeared normal in the routine retinal screening performed with RetCam 3.

A color fundus photograph of the left eye revealed a solitary yellowish-white flat mass with an approximate size of 1.5-disc diameters located in the nasal retina.

Fluorescein angiography showed diffuse hyperfluorescence with slight fluorescence leakage.

On B-scan ultrasound, the mass was inapparent, with no distinct foci of calcification.

Follow-up reexaminations were recommended.

Three months later, regression in the size of the retinal mass was observed.

Fluorescein angiography showed decreased vascularization of the lesion and slight mottled hyperfluorescence over its surface.

Seven months later, the fundus examination indicated no lesion in the left eye.

Fluorescein angiography showed mild tortuous vessels without leakage.

The clinical course suggested that the isolated RAH may undergo spontaneous regression.

An isolated retinal astrocytic hamartoma was detected in the nasal retina of the left eye of a 4-day-old male infant.

At the time of initial presentation, we detected a solitary yellowish-white flat mass with an approximate size of 1.5 disc diameters in the nasal retina.

Fluorescein angiography (FA) revealed a diffuse hyperfluorescence with slight fluorescence leakage.

Seven months later, the fundus examination showed no lesion in the left eye.

Fluorescein angiography revealed mild tortuous vessels without leakage.


A 27-year-old male involved in a motor vehicle accident was brought to Emergency Department room with respiratory distress.

He was intubated upon arrival due to low Glasgow Coma Scale (GCS) with extensive maxillofacial injuries.

Thoracic examination showed reduced air entry at right chest wall region.

Palpable crepitus on his right neck region was due to subcutaneous emphysema from the neck to the anterior chest wall.

A curvilinear transducer on the right second intercostal ribs showed the absence of sliding signs, suggestive of right pneumothorax.

On subxiphoid view of the heart, only the right ventricle was seen during diastole.

Part of the cardiac image was obscured by A-lines.

This raised a suspicion of pneumopericardium.

Only A-lines were visible on parasternal long axis (PLAX), parasternal short axis (PSAX), and apical four chamber (A4C) views.

The patient underwent head and chest CT scan.

The CT scan confirmed the diagnosis of Le Fort II facial bone injury.

The CT scan confirmed the diagnosis of right pneumothorax.

The CT scan confirmed the diagnosis of right pulmonary contusion.

The CT scan confirmed the diagnosis of pneumopericardium.

The pneumopericardium was treated conservatively.

A young man involved in a car accident and sustained blunt thoracic injuries, among others.

As part of primary survey, FAST scan was performed.

Subxiphoid view to look for evidence of pericardial effusion showed part of the cardiac image obscured by A-lines.

Other cardiac windows showed only A-lines, as well.

A suspicion of pneumopericardium was raised.


The patient was a 2 years and 5-month-old boy.

The patient was admitted for fever with onset 3 days before admission.

The fever was associated with abdominal pain and diarrhea within the last 24 hours.

The anamnesis did not reveal any possible exposure to COVID-19 infections.

The clinical exam at admission revealed bilateral palpebral edema.

The clinical exam at admission revealed conjunctivitis.

The clinical exam at admission revealed mucocutaneous signs of dehydration.

The clinical exam at admission revealed abdominal tenderness at palpation.

The laboratory test showed lymphopenia (1560/mm3).

The laboratory test showed thrombocytopenia (108x103/mm3).

The laboratory test showed anemia (hemoglobin – Hb 10.9 g/dL).

The laboratory test showed elevated C-reactive protein – CRP (162 mg/L).

The laboratory test showed elevated ferritin levels (389.3 ng/mL).

The laboratory test showed hyponatremia (132 mmol/L).

The laboratory test showed hypokalemia (3.94 mmol/L).

The laboratory test showed hypertriglyceridemia (476.3 mg/dL).

The laboratory test showed elevated D-dimer (>5 μg/ml).

The laboratory test showed increased troponin (16.6 ng/L).

The laboratory test showed increased NT-proBNP (19,831 pg/ml).

The chest X-ray showed no pathological findings.

The abdominal ultrasound showed no pathological findings.

The echocardiography showed no pathological findings.

We raised the suspicion of pediatric inflammatory multisystem syndrome possibly associated to COVID-19.

The RT-PCR test for SARS-CoV-2 infection was negative.

The serology (IgG anti-SARS-CoV-2) was positive.

We established the diagnosis of PIMS-TS.

We initiated intravenous immunoglobulin in a dose of 2 g/kg/day.

We initiated empirical antibiotic (ceftriaxone).

We initiated anticoagulation therapy (low-molecular weight heparin).

We administered symptomatic drugs (antipyretics, antiemetics, and antidiarrheics).

The fever persisted for the following 36 hours with no clinical improvement.

The laboratory test on the 3rd day showed an increase of the CRP value (216.65 mg/L).

The laboratory test on the 3rd day showed persistence of elevated NT-proBNP (9,884.2 pg/mL).

The laboratory test on the 3rd day showed persistence of elevated D-dimer (1,198 ng/mL).

The laboratory test on the 3rd day showed hypoalbuminemia (2.45 g/dL).

We initiated intravenous methylprednisolone (10 mg/kg/day) for 3 days.

We initiated substitutive treatment with human albumin.

The echocardiography showed minimal pericardial effusion.

The echocardiography showed slight dilation of the left cavities.

The echocardiography showed regional wall motion abnormalities with dyskinesia of the inferior and infero-septal basal segments of the LV.

The echocardiography showed LV systolic dysfunction with LV ejection fraction of 40%.

The echocardiography showed mild mitral regurgitation.

The echocardiography showed no coronary impairment.

We associated angiotensin converting enzyme inhibitors (Lisinopril).

Serial echocardiography showed resorption of the pericardial effusion.

Serial echocardiography showed improvement of LV function.

Serial echocardiography showed decreased serum levels of NT-proBNP (123.1 pg/mL).

Serial echocardiography showed decreased serum levels of troponin (5.2 pg/mL).

The patient was discharged on the 11th day of admission.

The patient was discharged without any complaints.

Most of the laboratory parameters were within normal ranges at discharge.

D-dimer was not within normal ranges at discharge.

We recommended continuation of anticoagulant therapy for another week.

We recommended continuation of Lisinopril for the following 2 weeks.

We recommended continuation of Spironolactone for the following 2 weeks.

We recommended continuation of Hydrochlorothiazide for the following 2 weeks.

The patient was a 2 years and 5-month-old boy.

The patient was admitted for fever, abdominal pain, and diarrhea.

The clinical exam at admission revealed influenced general status.

The clinical exam at admission revealed bilateral palpebral edema.

The clinical exam at admission revealed conjunctivitis.

The laboratory tests showed lymphopenia.

The laboratory tests showed thrombocytopenia.

The laboratory tests showed elevated C-reactive protein.

The laboratory tests showed elevated erythrocyte sedimentation rate.

The laboratory tests showed elevated ferritin levels.

The laboratory tests showed hyponatremia.

The laboratory tests showed hypokalemia.

The laboratory tests showed hypertriglyceridemia.

The laboratory tests showed elevated D-dimer.

The laboratory tests showed increased troponin.

The laboratory tests showed increased NT-proBNP.

The RT-PCR test for SARS-CoV-2 infection was negative.

The serology for SARS-CoV-2 was positive.

The diagnosis of PIMS-TS was established.

Intravenous immunoglobulin was initiated.

Empirical antibiotic therapy was initiated.

The clinical course and laboratory parameters worsened.

The 2nd echocardiography showed minimal pericardial effusion.

The 2nd echocardiography showed slight dilation of the left cavities.

The 2nd echocardiography showed dyskinesia of the inferior and septal basal segments of the left ventricle.

The 2nd echocardiography showed left ventricular systolic dysfunction.

Intravenous methylprednisolone was added.

Angiotensin converting enzyme inhibitors were added.

The clinical evolution was outstandingly favorable.

The patient was a 2 years and 5-month-old boy.

The clinical exam at admission revealed bilateral palpebral edema.

The clinical exam at admission revealed conjunctivitis.

The laboratory test showed lymphopenia (1560/mm3).

The laboratory test showed thrombocytopenia (108x103/mm3).

The laboratory test showed anemia (hemoglobin – Hb 10.9 g/dL).

The laboratory test showed elevated ferritin levels (389.3 ng/mL).

The laboratory test showed hyponatremia (132 mmol/L).

The laboratory test showed hypokalemia (3.94 mmol/L).

The laboratory test showed hypertriglyceridemia (476.3 mg/dL).

The laboratory test showed elevated D-dimer (>5 μg/ml).

The laboratory test showed increased troponin (16.6 ng/L).

The laboratory test showed increased NT-proBNP (19,831 pg/ml).

The chest X-ray showed no pathological findings.

The abdominal ultrasound showed no pathological findings.

The echocardiography showed no pathological findings.

The RT-PCR test for SARS-CoV-2 infection was negative.

The serology (IgG anti-SARS-CoV-2) was positive.

We established the diagnosis of PIMS-TS.

We initiated intravenous immunoglobulin in a dose of 2 g/kg/day.

We initiated empirical antibiotic (ceftriaxone).

We initiated substitutive treatment with human albumin.

The echocardiography showed minimal pericardial effusion.

The echocardiography showed slight dilation of the left cavities.

The echocardiography showed mild mitral regurgitation.

The echocardiography showed no coronary impairment.

Serial echocardiography showed improvement of LV function.

The patient was discharged on the 11th day of admission.

The patient was discharged without any complaints.

D-dimer was not within normal ranges at discharge.

The patient was a 2 years and 5-month-old boy.

The patient was admitted for fever, abdominal pain, and diarrhea.

The clinical exam at admission revealed influenced general status.

The clinical exam at admission revealed bilateral palpebral edema.

The clinical exam at admission revealed conjunctivitis.

The laboratory tests showed lymphopenia.

The laboratory tests showed thrombocytopenia.

The laboratory tests showed elevated C-reactive protein.

The laboratory tests showed elevated ferritin levels.

The laboratory tests showed hyponatremia.

The laboratory tests showed hypokalemia.

The laboratory tests showed hypertriglyceridemia.

The laboratory tests showed elevated D-dimer.

The laboratory tests showed increased troponin.

The laboratory tests showed increased NT-proBNP.

The RT-PCR test for SARS-CoV-2 infection was negative.

The serology for SARS-CoV-2 was positive.

The diagnosis of PIMS-TS was established.

Intravenous immunoglobulin was initiated.

Empirical antibiotic therapy was initiated.

The clinical course and laboratory parameters worsened.

The 2nd echocardiography showed minimal pericardial effusion.

Intravenous methylprednisolone was added.

Angiotensin converting enzyme inhibitors were added.

The clinical evolution was outstandingly favorable.


The patient is a 3.7-kg, 1-month-old male.

He presented at day 24 of life with severe aortic stenosis and coarctation of the aorta.

He was born at term following an uncomplicated pregnancy.

On day 5 of life, he was noted to be jaundiced and have a murmur.

His jaundice resolved, and he was discharged home with cardiac follow-up.

He had progressive increase in his work of breathing.

An echocardiogram on day 24 of life showed a thickened and dysplastic bicuspid aortic valve with doming of the valve leaflets.

The flow across the valve was measured on continuous wave doppler at 4 m/s.

He was found to have a discrete juxta ductal coarctation of the aorta with continuous doppler flow of 2.5 m/s with diastolic tail.

His ventricular function remained preserved.

He was started on intravenous prostaglandin.

The best course of action was felt to be a hybrid approach with surgical end-to-end anastomosis of the aortic arch via a thoracotomy followed by surgical carotid cut down for AoVP.

The patient was taken to the hybrid catheter laboratory theater.

He underwent the surgical end-to-end anastomosis via the thoracotomy via the third intercostal space.

The arch, patent ductus arteriosus, and descending aorta were dissected out.

Clamps were applied to the arch and descending aorta.

The patent ductus arteriosus was ligated.

An end to side anastomosis was performed between the aortic arch and the descending aorta.

The pleura and chest were closed in layers.

The patient was assessed and felt to be stable to proceed with the planned aortic balloon.

A 5/0 purse string suture was applied to the right common carotid artery.

A 4-Fr sheath was inserted in the right common carotid artery.

Ascending aortic pressure was measured at 61/42 mmHg.

The aortic valve annulus measured 7.5 mm.

The pressure in the left ventricle was recorded at 110/13 mmHg.

A peak to peak gradient of 49 mmHg was calculated.

A 0.014 ChoICE PT extra support coronary wire was placed in the left ventricle.

A NuMED Tyshak II 6 mm × 2 cm percutaneous transluminal valvuloplasty balloon catheter was delivered over the ChoICE wire to the aortic valve.

The balloon was inflated to burst pressure of 4 atmospheres.

A waist was seen within the balloon and dewaisting occurred.

The pressure was measured at 100/10 mmHg.

Repeat angiogram at the aortic root did not demonstrate any significant aortic incompetence.

A 7 mm × 2 cm NuMED Tyshak II percutaneous transluminal valvuloplasty balloon catheter was delivered over the coronary guidewire in position.

A waist was again seen and dewaisting occurred.

The pressure within the left ventricle was now 90/10 mmHg.

The pullback peak to peak gradient between the left ventricle and ascending aorta measured 30 mmHg.

The vessel was repaired by tightening the pursestring suture.

An echocardiogram performed post procedure showed qualitatively normal ventricular function with no pericardial effusion.

The arch was unobstructed with doppler flow velocity of 1.6 m/s.

The aortic valve was bicuspid and obviously dysplastic.

There was mild flow acceleration across the valve using continuous wave doppler of 3 m/s.

There was a mean doppler gradient of 15 mmHg.

There was no obvious aortic incompetency seen.

The patient was transferred from the hybrid catheter laboratory to the pediatric intensive care unit.

He remained cardiovascularly stable during his PICU admission.

He was extubated but had to be reintubated within a few hours due to upper airway issues.

He was successfully extubated on day 3 post procedure.

His admission on the ward was uncomplicated.

He was discharged on day 6 post intervention.

At 4 months of age, he was reviewed in the outpatient clinic.

He was clinically asymptomatic with steady growth.

His echocardiogram demonstrated qualitatively normal ventricular function.

The aortic valve stenosis was mild to moderate with flow of 3.7 m/s on continuous wave doppler.

There was evidence of mild aortic incompetence.

The aortic arch remained unobstructed with flow velocity of 1.4 m/s.

His most recent follow-up was at 8 months of age.

He remained asymptomatic and well with his weight increasing to 9 kg.

His echocardiogram again demonstrated qualitatively normal ventricular function.

The bicuspid aortic valve had flow of 3.2 m/s across the valve.

There were no issues with his carotid artery access.

There were no ongoing neurological issues.

The decision was made to perform a hybrid surgical procedure.

The patient underwent a lateral thoracotomy for repair of the CoA.

The patient underwent carotid cutdown for aortic balloon valvuloplasty.

The patient is a 3.7-kg, 1-month-old male.

He was born at term following an uncomplicated pregnancy.

He had progressive increase in his work of breathing.

His ventricular function remained preserved.

He was started on intravenous prostaglandin.

Clamps were applied to the arch and descending aorta.

The patent ductus arteriosus was ligated.

The pleura and chest were closed in layers.

A 4-Fr sheath was inserted in the right common carotid artery.

Ascending aortic pressure was measured at 61/42 mmHg.

The aortic valve annulus measured 7.5 mm.

A peak to peak gradient of 49 mmHg was calculated.

The balloon was inflated to burst pressure of 4 atmospheres.

A waist was seen within the balloon and dewaisting occurred.

The pressure was measured at 100/10 mmHg.

A waist was again seen and dewaisting occurred.

The pressure within the left ventricle was now 90/10 mmHg.

The vessel was repaired by tightening the pursestring suture.

The aortic valve was bicuspid and obviously dysplastic.

There was a mean doppler gradient of 15 mmHg.

There was no obvious aortic incompetency seen.

He remained cardiovascularly stable during his PICU admission.

He was successfully extubated on day 3 post procedure.

His admission on the ward was uncomplicated.

He was discharged on day 6 post intervention.

At 4 months of age, he was reviewed in the outpatient clinic.

He was clinically asymptomatic with steady growth.

There was evidence of mild aortic incompetence.

His most recent follow-up was at 8 months of age.

There were no issues with his carotid artery access.

There were no ongoing neurological issues.


An 84-year-old man was admitted to our hospital complaining of muscular weakness while rising up from a chair that led to a fall.

His head CT and MRI did not report any abnormal structural findings.

He reported a significant 10% weight loss in the past 6 months.

The weight loss was associated with decreased appetite and diminished mobility.

The weight loss was associated with progressive muscular weakness and difficulty rising from chair.

The physical examination was remarkable for muscular weakness with 3/5 muscle strength in the lower extremities.

The physical examination showed 4/5 muscle strength in the upper extremities.

Muscle weakness was confined to the proximal muscles.

The tone examination revealed mild bilateral quadriceps hypotonia and atrophy.

There were no other clinical findings on the physical examination.

The patient reported a medical history of stage G4 chronic kidney disease.

The patient reported a medical history of erythroid and megakaryocyte-predominant myelodysplastic syndrome.

The patient reported a medical history of high blood pressure.

The patient was receiving medication with azacytidine.

The patient was receiving medication with diltiazem.

The patient was receiving medication with darbepoetin.

The family history was negative for neuromuscular diseases.

During the present admission, laboratory investigation showed an elevated creatine kinase level of up to 78,924 U/L.

The creatine kinase level was more than 50 times the normal reference range.

Elevated serum creatinine was found (4.4 mg/dl).

Mild hypocalcemia (7.2 mg/dl) was found.

Mild hyponatremia (130 mg/dl) was found.

Coprologic examination revealed positive testing for rotavirus.

Antibody testing reported negative results for antinuclear antibodies (ANAs).

Antibody testing reported negative results for anti-Jo1.

Antibody testing reported negative results for anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR).

Antibody testing reported negative results for anti-Mi-2.

Antibody testing reported negative results for antiganglioside antibodies.

The electromyography (EMG) of the upper and lower limbs showed myopathic changes in proximal muscle.

The EMG showed short duration, low-amplitude polyphasic potential.

The EMG showed no spontaneous electrical activity.

An FDG-PET/CT scan was performed searching for neoplasia.

The FDG-PET/CT scan revealed increased FDG uptake in bilateral quadriceps.

There was no posterior compartment muscle uptake.

There was no increased metabolism in any other region of the body.

An open biopsy of the left vastus lateralis muscle was performed.

Light microscopy showed 50% myonecrosis.

There were mild fiber atrophy and lymphocytic infiltrate with CD8+ predominance.

There were no immune deposits in the skin microscopic examination.

The patient started on intravenous hydration with medium saline solution/bicarbonate for rhabdomyolysis.

The patient started on prednisone 0.5 mg/kg/day.

The patient received intravenous immunoglobulin with a total dose of 2 g/kg distributed in 5 days.

The patient received calcium supplementation.

Steroid-sparing drugs such as azathioprine or methotrexate were not considered.

The renal function of the patient improved within 5 days.

There was partial recovery of lower limb strength.

The patient was discharged for external consultation follow-up.

After 2 months from discharge, the patient had increased muscle strength.

After 2 months from discharge, the patient had diminished CPK levels.

The patient received low-dose prednisone as maintenance therapy.

The patient had difficulty rising from a chair.

Laboratory results showed increased creatine kinase levels of more than 50 times the normal reference values.

Electromyography showed myopathic changes.

FDG-PET/CT scan showed increased FDG uptake in bilateral quadriceps.

A biopsy revealed lymphocytic predominant infiltrates.

Intravenous immunoglobulin was administered.

The patient was discharged for further follow-up.

Muscle weakness was confined to the proximal muscles.

The patient reported a medical history of high blood pressure.

The patient was receiving medication with azacytidine.

The patient was receiving medication with diltiazem.

The patient was receiving medication with darbepoetin.

The family history was negative for neuromuscular diseases.

Elevated serum creatinine was found (4.4 mg/dl).

Mild hypocalcemia (7.2 mg/dl) was found.

Mild hyponatremia (130 mg/dl) was found.

Antibody testing reported negative results for anti-Jo1.

Antibody testing reported negative results for anti-Mi-2.

The EMG showed no spontaneous electrical activity.

An FDG-PET/CT scan was performed searching for neoplasia.

There was no posterior compartment muscle uptake.

Light microscopy showed 50% myonecrosis.

The patient started on prednisone 0.5 mg/kg/day.

The patient received calcium supplementation.

The renal function of the patient improved within 5 days.

There was partial recovery of lower limb strength.


She presented with a polyp on top of a red plaque in the left side mons pubis for 1 year.

The plaque was slightly bulgy without pressing pain.

The lesion was covered with a thick yellow-white crust.

There were no other systemic abnormalities.

Ultrasound B was applied to evaluate the superficial inguinal lymph nodes.

She had no significant history of medicine, surgery, irritation, and trauma.

Before the lesion appearance, the patient had no discomfort.

She did not use other external medicines.

Until nearly a month, she found that the lesion was prone to bleed after friction.

Histopathologic examination was performed.

The possibility of skin tumor was considered through dermoscopy.

The skin biopsy was made on December 31, 2019.

The immunohistochemical reports were done on January 17, 2020.

Dermoscopic images showed a dark red background.

The dermoscopic images showed a thick yellow-and-white crust.

The dermoscopic images showed spot-shaped and polymorphic vascular structures.

The dermoscopic images showed white homogeneous structures.

The dermoscopic images showed dark red clumps.

The skin lesions were considered as the diagnosis of skin tumors using dermoscopy.

The specimen tissue was fixed in formalin.

The histological examination showed the skin lesion at the left side of mons pubis was spindle-shaped.

The polyps were lined by melanocytes with pale cytoplasm.

The polyps showed atypical cells and heteromorphic nuclei.

Each slide was reviewed by 3 different pathologists.

The diagnosis was made as the melanocyte tumor.

The immunohistochemistry studies revealed positive staining for S-100.

The immunohistochemistry studies revealed positive staining for HMB-45.

The immunohistochemistry studies revealed positive staining for Melan A.

The immunohistochemistry studies revealed positive staining for Cyclin D1.

The final histopathological diagnosis was melanocyte nevus malignancy, nodular malignant melanoma.

The patient underwent a complete local excision.

The patient was required to re-examined regularly after surgery.

Recent follow-ups showed that she recovered well.

There was no sign of recurrence till now.

The lesion was a solitary polypoid nodule without apparent pigmentation on her vulvar skin.

Dermatoscopy was indicated a possible tumorous change.

The final diagnosis was nodular malignant melanoma (NM).

She did not use other external medicines.

Histopathologic examination was performed.

The specimen tissue was fixed in formalin.

There was no sign of recurrence till now.


The patient is a 16-year-old Persian man.

The patient's mother was diagnosed with aggressive MTC.

The patient's mother had a mass in the thyroid gland and cervical lymphadenopathy for six years.

The patient's mother underwent thyroidectomy a year earlier.

The patient had no history of lymphadenopathy.

The patient had no history of weight loss.

The patient had no history of café au lait spots.

The patient had no history of ocular problems.

The patient had no history of gastrointestinal problems.

The patient had no history of thyroid nodule.

The patient had no history of hoarseness.

On physical examination, the patient's face was symmetric.

There was no sign of high arched palate.

There was no sign of mandibular prognathism.

The patient had several neuromas on his upper and lower eyelids, lips, and tongue.

The neuromas were characteristic of MEN2B.

There were no other remarkable findings in the physical examination.

There were no signs of marfanoid habitus.

The patient had increased calcitonin levels.

The patient had increased carcinoembryonic antigen (CEA) levels.

Tests for RET proto-oncogene on exon 10, 11, and 16 were negative.

The results of an ophthalmology examination showed several mucosal neuromas on inner eyelids and conjunctivae.

The ophthalmology examination showed prominent perilimbal conjunctival blood vessels.

The ophthalmology examination showed enlarged corneal nerves.

The patient's intra-ocular pressure (IOP) was normal.

The upper gastrointestinal and small bowel series were normal.

Pheochromocytoma was ruled out based on the laboratory test results.

The results of pathological tests revealed a small (0.5cm) medullary thyroid carcinoma in the right lobe.

The surgical margins were free of tumor.

Post-operative evaluation included cervical ultrasound.

Post-operative evaluation included cervical, thoracic, and abdominal computed tomography.

The post-operative evaluations were normal.

The patient's calcitonin and CEA levels were assessed periodically.

All the family members had signed an informed consent.

The family members provided the authors with an authorization to publish their information.

The patient is a 16-year-old Persian man.

The patient was diagnosed as having a non-invasive form of multiple endocrine neoplasia 2B.

The patient has medullary thyroid cancer.

The patient has mucosal neuroma of the tongue.

The patient has mucosal neuroma of the lips.

The patient has mucosal neuroma of the inner eyelids.

The patient had a positive family history of medullary thyroid cancer.

The patient had no signs of marfanoid habitus.

The patient is a 16-year-old Persian man.

The patient had no history of weight loss.

The patient had no history of hoarseness.

There was no sign of high arched palate.

The neuromas were characteristic of MEN2B.

There were no signs of marfanoid habitus.

The surgical margins were free of tumor.


The patient was a 39-year-old Chinese woman.

She had delivered a second live full-term infant through an uncomplicated cesarean section in 2011.

She had a first cesarean section in 2005.

In December 2014, she noticed a purple, nontender swelling appearing as an anterior abdominal wall mass around her cesarean scar.

The mass was not accompanied by any abdominal pain.

The mass was not accompanied by any abnormal vaginal bleeding.

There were no notable findings in her past medical history.

There were no notable findings in her family history.

There were no notable findings in her psychosocial history.

The abdominal wall mass had progressively enlarged.

She had undergone tumor resection of the abdominal wall in June 2015.

The resection might be interpreted as the abdominal wall endometriosis malignancy.

She had visited a regional tertiary hospital for a consultation regarding the pathologic diagnosis of a CC.

Her physical examination showed no abnormalities except for the scar from the local excision on the abdominal wall.

The first excised specimen from the previous hospital was reviewed by our pathologists.

The pathologists confirmed the characteristic of CC coexisting with minor ETT.

Her Ki-67 proliferative index was approximately 50%.

Laboratory analysis revealed normal serum levels of β-human chorionic gonadotropin (β-hCG; < 1.2 IU/L).

Laboratory analysis revealed normal tumor markers, including CA 125, CEA, CA 19-9, CA 15-3, and α-fetoprotein.

Positron emission tomography was performed.

No residual tumor and suspicious malignant lesions were observed.

The results of endometrial curettage revealed normal menstrual phase endometrium.

The patient received two courses of chemotherapy with a regimen of etoposide and cisplatin (EP) over a 2-month period.

During chemotherapy, her serum β-hCG levels remained negative (< 1.2 IU/L).

A recurrent nodule was found on the same abdominal wall scar site in January 2017.

The nodule was found approximately 17 months after the last chemotherapy.

Her serum β-hCG had increased to 6.17 IU/L.

Two oval hypoechoic masses were visualized by ultrasonography in the subcutaneous soft tissue of the lower abdomen wall scar.

Chest CT and head MRI showed no abnormality.

She underwent a second notable mass excision by ultrasound interventional localization.

The nodule was in the fat layer next to the superficial fascia.

Her serum β-hCG level was decreased to 3.4 IU/L on the second postoperative day.

The result of pathological examination was initially in line with CC metastasis to the abdominal wall.

The patient’s pathological sections were sent to the Fudan University Obstetrics and Gynecology Hospital for further consultation.

The patient was encouraged to maintain close follow-up.

Her serum β-hCG level had gradually decreased.

In the follow-up visits, the patient’s serum β-hCG level was elevated to the highest level of 10.68 IU/L again 4 months later.

A pelvic CT scan showed several nodules on the abdominal wall midline fascia.

The largest nodule was approximately 21 × 15 mm in size.

The nodules were less uniform in internal echoes.

Test results for tumor markers such as CA 125, CA 19-9, CEA, and HE4 were negative.

The results of routine blood sampling tests were normal.

We suggested a third resection of the mass to the patient.

She opted for a hysterectomy due to fear of malignancy and further relapse.

She finally underwent exploratory laparotomy with removal of the abdominal wall lesion, subtotal hysterectomy, bilateral salpingectomy, left ovarian cyst resection, and right inguinal lymph node biopsy in July 2017.

Intraoperative exploration revealed that the abdominal wall lesion was located on the anterior wall fascia.

Histopathological observations suggested that hyperplasia of fatty fibrous tissue was visible with cancer infiltration and necrosis around the cancer tissue.

The histopathological findings were consistent with trophoblastic tumor.

The trophoblastic tumor was constituted primarily by major epidermoid trophoblastic tumors (approximately 90%).

The trophoblastic tumor was constituted by CC components (approximately 10%).

Immunohistochemistry showed β-hCG (focal positive).

Immunohistochemistry showed inhibin-α (epithelial trophoblast negative, CC positive).

Immunohistochemistry showed p63 (epidermoid trophoblast positive, CC positive).

There was no tumor involvement in other tissues, including uterine, left ovarian cyst, and the right inguinal lymph nodes.

The patient’s postoperative recovery was uneventful.

Two weeks after hysterectomy, her serum β-hCG level had returned to normal (low 1.2 IU/L).

Two years later, there was no evidence of recurrence according to serum β-hCG and imaging studies.

The patient was a 39-year-old Chinese woman.

She had a history of two cesarean sections.

She had a recurrent anterior abdominal wall mass around her cesarean scar.

The mass was initially suspected of being choriocarcinoma of unknown origin.

The patient had negative or mildly increased serum β-human chorionic gonadotropin at follow-up.

She had two courses of chemotherapy with an etoposide and cisplatin regimen.

She finally opted for exploratory laparotomy with abdominal wall lesion removal.

The abdominal wall lesion was revealed by microscopy and immunohistochemical staining to be approximately 90% epithelioid trophoblastic tumors.

The abdominal wall lesion was revealed by microscopy and immunohistochemical staining to be 10% choriocarcinomas.

The lesion was from a solely extrauterine mixed gestational trophoblastic neoplasm around an abdominal wall cesarean scar.

The patient was a 39-year-old Chinese woman.

She had a first cesarean section in 2005.

The mass was not accompanied by any abdominal pain.

The mass was not accompanied by any abnormal vaginal bleeding.

There were no notable findings in her past medical history.

There were no notable findings in her family history.

There were no notable findings in her psychosocial history.

The abdominal wall mass had progressively enlarged.

She had undergone tumor resection of the abdominal wall in June 2015.

Her Ki-67 proliferative index was approximately 50%.

Positron emission tomography was performed.

No residual tumor and suspicious malignant lesions were observed.

During chemotherapy, her serum β-hCG levels remained negative (< 1.2 IU/L).

The nodule was found approximately 17 months after the last chemotherapy.

Her serum β-hCG had increased to 6.17 IU/L.

Chest CT and head MRI showed no abnormality.

The nodule was in the fat layer next to the superficial fascia.

The patient was encouraged to maintain close follow-up.

Her serum β-hCG level had gradually decreased.

The largest nodule was approximately 21 × 15 mm in size.

The nodules were less uniform in internal echoes.

The results of routine blood sampling tests were normal.

We suggested a third resection of the mass to the patient.

She opted for a hysterectomy due to fear of malignancy and further relapse.

The histopathological findings were consistent with trophoblastic tumor.

The trophoblastic tumor was constituted by CC components (approximately 10%).

Immunohistochemistry showed β-hCG (focal positive).

The patient’s postoperative recovery was uneventful.


The patient was admitted for recurrent lower extremity edema for 9 mo, abdominal distension for 7 mo, and aggravation for half a month.

A 53-year-old rural Chinese woman visited Dafang County People’s Hospital.

Symptoms began to appear nine months ago.

Edema and abdominal distension of both lower extremities recurred.

These symptoms gradually worsened during the previous two months.

Initial liver function examination showed elevated alanine transaminase (ALT).

Initial liver function examination showed elevated aspartate aminotransferase (AST).

Initial liver function examination showed elevated total bilirubin (TBIL).

Initial liver function examination showed elevated direct bilirubin (DBIL).

Initial liver function examination showed decreased albumin/globulin (ALB/GLO) ratio.

Examination of blood cells indicated decreased white blood cells (WBCs).

Examination of blood cells indicated decreased red blood cells (RBCs).

Examination of blood cells indicated decreased hemoglobin (HB).

Examination of blood cells indicated decreased platelets (PLTs).

Examination of coagulation function indicated an increased international normalized ratio (INR).

Examination of coagulation function indicated prolonged prothrombin time (PT).

Examination of coagulation function indicated prolonged activated partial thromboplastin time (APTT).

Examination of coagulation function indicated decreased fibrinogen (FIB).

An upper abdominal computed tomography (CT) showed liver cirrhosis.

Examination of thyroid function showed an elevated level of thyroid stimulating hormone (TSH).

Examination of thyroid function showed a decreased level of free triiodothyronine (FT3).

The initial diagnosis was “decompensated stage of cirrhosis and subclinical hypothyroidism.”

She tested negative for hepatitis viruses.

She tested negative for autoimmune hepatitis.

She was hospitalized twice for abdominal distension with yellow staining of the sclera.

These symptoms resolved after administration of a liver protectant and a diuretic to reduce swelling.

After discharge, she still reported repeated abdominal distension and discomfort.

These symptoms gradually became worse from 2020 Oct 1.

Since the initial presentation, her liver function indexes have fluctuated.

Thyroid function tests indicated a decreasing level of triiodothyronine (T3).

Thyroid function tests indicated an increasing level of TSH.

This indicated progression from subclinical hypothyroidism to clinical hypothyroidism.

She reported loss of vision 30 years ago.

She had no history of long-term heavy drinking.

She had no history of taking a Chinese medicine.

She had no history of exposure to toxic substances.

We designated the index patient as proband II-1.

She had five siblings (3 sisters, 2 brothers).

Her parents had no night blindness or impaired vision.

We performed serum biochemical examinations of the father (I-1) and all siblings.

The mother (I-2) was too old to travel to our institution for testing.

The AST level was elevated in all 7 individuals.

Fasting blood glucose was decreased in the father and 4 siblings.

Two siblings had elevated levels of high density lipoprotein cholesterol (HDL-C).

The TSH level was high in three siblings.

Some of the siblings also had elevated levels of TBIL.

Some of the siblings also had elevated levels of apolipoprotein A-I (APOA1).

CT examinations showed that neither the father (I-1) nor the mother (I-2) had cirrhosis.

Siblings II-3, II-5, and II-6 did not have cirrhosis.

Abdominal color ultrasound indicated that sibling II-4 had a fatty liver.

A physical examination indicated she had a BMI of 22.22.

There was evidence of chronic liver disease.

A cardiopulmonary examination showed no obvious abnormalities.

Her abdomen was positive for shifting dullness.

There was moderate pitting edema in both lower limbs.

2020 Oct 14: Blood lipid analysis indicated an HDL of 1.42 mmol/L.

2020 Oct 14: Hepatitis A virus, hepatitis B virus, and hepatitis C virus related tests were all negative.

2021 Jan 17: All antibody tests for autoimmune liver diseases were negative.

2021 Jul 16: Examination of ascites indicated the Rivalta test was negative.

2021 Jul 16: Ascites WBC count was 50 × 106/L.

2021 Jul 16: Ascites total protein (TP) was 5.50 g/L.

2021 Jul 16: Ascites adenosine deaminase (ADA) was 3.4 U/L.

2021 Jul 16: Ascites glucose (GLU) was 8.71 mmol/L.

2021 Jul 16: Ascites lactate dehydrogenase (LDH) was 48.8 U/L.

2020 Oct 15: Color Doppler ultrasonography of the thyroid showed bilateral thyroid cysts.

2020 Oct 23: A plain CT scan of the upper abdomen with enhancement showed cirrhotic ascites with splenomegaly.

We suggested more extensive examination of a liver biopsy to clarify the cause of cirrhosis.

This was not possible because the patient did not consent.

The index patient was one of 6 siblings.

Sibling II-2 was similar (night blindness complicated with cirrhosis and hypothyroidism).

Sibling II-5 was completely blind in both eyes.

The other three siblings had obvious night blindness.

We suggested molecular genetic analysis.

After receiving informed consent, we collected peripheral blood samples for whole-exome sequencing.

The results indicated the presence of the deletion/insertion mutation C.802-8_810delinsGC (homozygous) in the cytochrome P450 4V2 (CYP4V2) gene.

The results indicated the presence of the transcoding mutation C.413dupA (heterozygous) in the dual oxidase activator 2 (DUOXA2) gene.

The same CYP4V2 mutation was present in I-1, I-2, II-2, II-3, II-5, II-6.

Patient II-4 did not receive genetic testing because he lived in Tianjin.

The patient is a 53-year-old female from a rural area in China.

She was hospitalized for lower limb edema, abdominal distension, cirrhosis, and hypothyroidism.

Common causes of liver disease were excluded.

The patient had night-blindness since age 23 that worsened to complete blindness.

The patient's parents were first cousins.

All 5 siblings had night blindness and impaired vision.

Another sister had night-blindness complicated with cirrhosis and subclinical hypothyroidism.

Entire exome sequencing showed mutations in the CYP4V2 gene in the patient, parents, and siblings.

The CYP4V2 mutations of the parents and two sisters were heterozygous.

The CYP4V2 mutations of the other siblings were homozygous.

Two siblings also had heterozygous DUOXA2 mutations.

A 53-year-old rural Chinese woman visited Dafang County People’s Hospital.

Symptoms began to appear nine months ago.

Edema and abdominal distension of both lower extremities recurred.

These symptoms gradually worsened during the previous two months.

Initial liver function examination showed elevated total bilirubin (TBIL).

Initial liver function examination showed elevated direct bilirubin (DBIL).

Examination of blood cells indicated decreased white blood cells (WBCs).

Examination of blood cells indicated decreased red blood cells (RBCs).

Examination of blood cells indicated decreased hemoglobin (HB).

Examination of blood cells indicated decreased platelets (PLTs).

Examination of coagulation function indicated decreased fibrinogen (FIB).

An upper abdominal computed tomography (CT) showed liver cirrhosis.

She tested negative for hepatitis viruses.

She tested negative for autoimmune hepatitis.

These symptoms gradually became worse from 2020 Oct 1.

Since the initial presentation, her liver function indexes have fluctuated.

Thyroid function tests indicated an increasing level of TSH.

She reported loss of vision 30 years ago.

She had no history of long-term heavy drinking.

She had no history of taking a Chinese medicine.

She had no history of exposure to toxic substances.

We designated the index patient as proband II-1.

She had five siblings (3 sisters, 2 brothers).

Her parents had no night blindness or impaired vision.

The mother (I-2) was too old to travel to our institution for testing.

The AST level was elevated in all 7 individuals.

Fasting blood glucose was decreased in the father and 4 siblings.

The TSH level was high in three siblings.

Some of the siblings also had elevated levels of TBIL.

Siblings II-3, II-5, and II-6 did not have cirrhosis.

Abdominal color ultrasound indicated that sibling II-4 had a fatty liver.

A physical examination indicated she had a BMI of 22.22.

There was evidence of chronic liver disease.

A cardiopulmonary examination showed no obvious abnormalities.

Her abdomen was positive for shifting dullness.

There was moderate pitting edema in both lower limbs.

2020 Oct 14: Blood lipid analysis indicated an HDL of 1.42 mmol/L.

2021 Jul 16: Ascites WBC count was 50 × 106/L.

2021 Jul 16: Ascites total protein (TP) was 5.50 g/L.

2021 Jul 16: Ascites adenosine deaminase (ADA) was 3.4 U/L.

2021 Jul 16: Ascites glucose (GLU) was 8.71 mmol/L.

2021 Jul 16: Ascites lactate dehydrogenase (LDH) was 48.8 U/L.

This was not possible because the patient did not consent.

The index patient was one of 6 siblings.

Sibling II-5 was completely blind in both eyes.

The other three siblings had obvious night blindness.

We suggested molecular genetic analysis.

The same CYP4V2 mutation was present in I-1, I-2, II-2, II-3, II-5, II-6.

Patient II-4 did not receive genetic testing because he lived in Tianjin.


A 39-year-old woman visited our hospital complaining of worsened right low back pain and fever in 1 month before her first visit.

She had an experience of pyelonephritis 10 years ago.

Her initial laboratory data had no abnormal findings.

Ultrasound imaging revealed right gross hydronephrosis.

CECT also detected right gross hydronephrosis.

CECT was reconstructed to 3D imaging with Osirix®.

3D imaging found an aberrant blood vessel contacting with the right ureteropelvic junction.

UPJO was preoperatively diagnosed due to the aberrant blood vessel.

Tc-99m MAG3 renal scan confirmed that the right kidney exhibited obstructive pattern.

The right kidney had poor diuretic response.

The T1/2 of the right kidney was 21.07 min.

The right kidney function was similarly preserved to the left kidney function.

MAG3 clearance of the right kidney was 163.7 ml/min/1.73 m2.

Surgical treatment was indicated because of the symptomatic disease.

Preoperative RP showed that the right ureter shifted inward compared with the normal position.

Preoperative RP suggested the coexistence of retrocaval ureter.

RALP was conducted by a three-port transperitoneal approach.

Port position was more medial than usual.

The swollen right renal pelvis and the aberrant blood vessel were identified.

The right ureter was confirmed to be positioned behind the IVC.

The ureter was repositioned anterior to the IVC.

The strictured ureteropelvic junction was removed.

The ureter and the renal pelvis were spatulated.

The ureter and the renal pelvis were reanastomosed in a tension-free fashion.

The anastomosis was sutured with interrupted 5-0 sutures.

A 10-Fr BLAKE Silicon drain was put into the anastomosis place.

The urethral catheter was removed 5 days after surgery.

The drain was removed 6 days after surgery.

No perioperative adverse events were found.

The double-J stent was removed 2 months after surgery.

No recurrence of the symptoms was observed.

Her right hydronephrosis improved in 2 years after surgery.

She visited the hospital complaining of worsened right low back pain and fever.

Contrast-enhanced computed tomography diagnosed right hydronephrosis due to ureteropelvic junction obstruction.

Retrograde pyelography before robot-assisted laparoscopic pyeloplasty revealed concomitant ipsilateral retrocaval ureter.

Laparoscopically, ureteropelvic junction obstruction due to aberrant blood vessel and coexisting retrocaval ureter was confirmed.

Transposition of the ureter from posterior to anterior of the inferior vena cava and following dismembered pyeloplasty was performed.

Two years after surgery, her right hydronephrosis improved.

She had no complain of any symptom two years after surgery.

The T1/2 of the right kidney was 21.07 min.

Port position was more medial than usual.

The drain was removed 6 days after surgery.

No perioperative adverse events were found.

No recurrence of the symptoms was observed.


The patient is a 62-year-old previously healthy Sri Lankan native male from Gampaha, in the Western Province of Sri Lanka.

He presented with high fever associated with chills and rigors for 17 days.

He also complained of malaise, myalgia and arthralgia for the same duration.

He denied any urinary, respiratory or abdominal symptoms.

He had obtained treatment from a local hospital for the illness with no clinical improvement.

He had received co-amoxyclav, clarythromicin and paracetamol for 4 days.

He had not been consuming any medication prior to the illness.

He had not received any drug that would result in extrapyramidal features.

Around the 5th day of the clinical illness he had developed intermittent resting tremor in his right arm and leg.

By the time he presented to us he had stiffness and very frequent intermittent resting tremor.

This resulted in difficulty to carry out normal work with the right hand.

He also found it difficult to walk due to unusual stiffness and heaviness of the right leg.

He found it difficult to smile with others and felt very distressed.

There was no associated hearing impairment, seizures, or altered level of consciousness.

There were no symptoms to suggest involvement of cerebellar system or autonomic nervous system.

There was no family history of movement disorders.

He had been working in his garden 7 days prior to the onset of fever.

Examination revealed intermittent high amplitude low frequency resting tremor in his right hand.

He had a mask like face where he found difficult to smile or show his teeth.

He also had increased muscle tone limited to the right side with normal tendon reflexes.

The rest of the central nervous system was unremarkable.

His blood pressure was 140/90 mmHg in both supine and standing positions.

The respiratory system revealed few basal crackles.

The abdominal examination was unremarkable except for a superficial crater like lesion suggestive of an eschar.

He did not have lymphadenopathy or a rash.

His full blood count was 13.4 × 109/L (Neutrophils 43 %, Lymphocytes 56 %).

Erythrocyte sedimentation rate was 80 mm/1st h.

He was positive for Immunofluoresence Assay (IFA)-IgM and IgG for O. tsutsugamushi on the 17th day of illness.

The IFA-IgG titre using Orientia Karp antigen was 1:1024 which rose up to 1:16,384 after 2 weeks.

His fever settled with oral doxycycline and azithromycin within 48 h.

He demonstrated some improvement in his Parkinsonism features prior to discharge from hospital in 4 days.

He visited for review 2 weeks after discharge.

By this time he showed complete improvement and was happy with a smiling face.

The patient is a 62-year-old previously healthy Sri Lankan native male from the Western province of Sri Lanka.

He presented with high fever with malaise, myalgia and arthralgia for 17 days.

On the 5th day of illness he developed intermittent resting tremor in his right arm and leg.

Clinical examination revealed a high amplitude low frequency resting tremor in his right hand.

There was a mask-like face and increased muscle tone limited to the right side.

The rest of the system examination was normal except for an eschar over the abdomen.

Immunofluorescence assay-IgM and IgG against Orientia tsutsugamushi Karp antigen were positive with rising titers.

With oral doxycycline and azithromycin his fever settled within 48 h.

A complete recovery of Parkinson's features was observed within 2 weeks.

There was no family history of movement disorders.

The rest of the central nervous system was unremarkable.

The respiratory system revealed few basal crackles.

He did not have lymphadenopathy or a rash.

Erythrocyte sedimentation rate was 80 mm/1st h.

He visited for review 2 weeks after discharge.


He presented with frequent bloody stool.

Five years earlier, his symptoms began with intermittent vague abdominal pain.

Five years earlier, his symptoms began with bloody stool.

Progressive deterioration of symptoms included increased blood in the stool.

Progressive deterioration of symptoms included new onset of mucoid discharge.

Progressive deterioration of symptoms included new onset of constipation.

He complained of straining during defecation.

He complained of difficulty passing hard and narrowed stool.

He complained of a sense of incomplete defecation.

He had no previous history of prescription medication.

He had no previous history of any other medical condition.

He experienced no significant weight loss.

His family history was negative for gastrointestinal disorders.

His family history was negative for malignancies.

His family history was negative for IBD.

His family history was negative for FAP.

He had his first colonoscopy approximately four years prior.

The first colonoscopy revealed a solitary ulcer in the rectum.

The initial histologic examination revealed regenerative crypts in the lamina propria.

The initial histologic examination revealed fibrosis.

The initial histologic examination revealed smooth muscle proliferation.

The initial histologic examination confirmed the diagnosis of SRU.

A previous laboratory evaluation revealed a WBC of 8100 × 109 cells/liter.

A previous laboratory evaluation revealed an Hb of 13.2 g/dL.

A previous laboratory evaluation revealed an MCV of 79.8 FL.

A previous laboratory evaluation revealed platelets of 251,000 × 1010/unit.

A previous laboratory evaluation revealed an FBS of 85 mg/dL.

A previous laboratory evaluation revealed a TSH of 3.49 mIU/liter.

A previous laboratory evaluation revealed an AST of 12 units/liter.

A previous laboratory evaluation revealed an ALT of 16 units/liter.

A previous laboratory evaluation revealed an ALP of 391 units/liter.

A previous laboratory evaluation revealed a ferritin of 22.2 mcg/liter.

A previous stool exam was negative for occult blood.

A previous stool exam was negative for ova of parasites.

A previous stool exam was negative for protozoa cyst.

On physical examination, his vital signs were stable.

There were no abnormal findings in his head.

There were no abnormal findings in his neck.

There were no abnormal findings in his chest.

There were no abnormal findings in his abdomen.

A perineal examination revealed no skin tags.

A perineal examination revealed no fissures.

A perineal examination revealed no visible prolapse.

A perineal examination revealed no other indications of child abuse.

Multiple irregular mass-like lesions were detected during the digital rectal examination.

The colonoscopy revealed multiple diffuse polyposes ranging in shape and size from 5 to 15 mm.

The polyposes extended from the rectum’s middle section to the rectosigmoid junction.

Multiple biopsies were taken and sent for histopathologic evaluation.

The histopathologic evaluation revealed a polypoid structure with a cap of ulcerated granulation tissue.

The histopathologic evaluation revealed inflammatory exudates on the surface.

The histopathologic evaluation revealed tortuous non-dysplastic crypts.

The histopathologic evaluation revealed mucin spillage in the inflamed stroma.

The histopathologic evaluation revealed smooth muscle fibers.

The histopathologic evaluation revealed congested vessels.

The diagnosis of CP was confirmed based on these new findings.

Until histopathologic confirmation of CP is obtained, conservative measures such as a high-fiber diet are recommended.

Until histopathologic confirmation of CP is obtained, the use of laxative agents is recommended.

Until histopathologic confirmation of CP is obtained, avoidance of manual stool evacuation is recommended.

After histopathologic confirmation, we decided to perform endoscopic mucosal resection (EMR).

We resected as many polyps as possible during the first session.

The patient underwent two additional colonoscopy sessions during the 3-month follow-up.

The majority of the remaining polyps were removed using EMR.

Complete eradication of polyps was not possible.

The patient was previously diagnosed with SRU.

The patient presented with rectal bleeding.

The patient presented with mucoid discharge.

The patient presented with abdominal pain.

Additional colonoscopy evaluation revealed multiple polyposes varying in size and shape limited to the rectum.

Histologic examination revealed a characteristic cap of granulation tissue covering tortuous nondysplastic crypts in the inflamed stroma.

The histologic findings indicated that SRU had transformed into CP.

The plan was to perform endoscopic mucosal resection of the lesions in multiple sessions.

He presented with frequent bloody stool.

Five years earlier, his symptoms began with bloody stool.

He complained of straining during defecation.

He complained of difficulty passing hard and narrowed stool.

He complained of a sense of incomplete defecation.

He had no previous history of prescription medication.

He had no previous history of any other medical condition.

He experienced no significant weight loss.

His family history was negative for malignancies.

His family history was negative for IBD.

His family history was negative for FAP.

He had his first colonoscopy approximately four years prior.

The first colonoscopy revealed a solitary ulcer in the rectum.

The initial histologic examination revealed fibrosis.

A previous laboratory evaluation revealed an Hb of 13.2 g/dL.

A previous laboratory evaluation revealed an MCV of 79.8 FL.

A previous laboratory evaluation revealed an FBS of 85 mg/dL.

A previous stool exam was negative for occult blood.

A previous stool exam was negative for ova of parasites.

A previous stool exam was negative for protozoa cyst.

On physical examination, his vital signs were stable.

There were no abnormal findings in his head.

There were no abnormal findings in his neck.

There were no abnormal findings in his chest.

There were no abnormal findings in his abdomen.

A perineal examination revealed no skin tags.

A perineal examination revealed no fissures.

A perineal examination revealed no visible prolapse.

The histopathologic evaluation revealed smooth muscle fibers.

The histopathologic evaluation revealed congested vessels.

The diagnosis of CP was confirmed based on these new findings.

The majority of the remaining polyps were removed using EMR.

Complete eradication of polyps was not possible.


She had been undergoing oral treatment for diabetes with canagliflozin 100 mg/day, metformin 1,000 mg/day, and saxagliptin 5 mg/day.

She noticed general malaise a month before her emergency department visit.

Two weeks before her emergency department visit, her oral intake decreased because of reduced appetite.

She continued oral medications at their initial dose.

The day prior to her emergency department visit, her malaise worsened.

She developed nausea and abdominal pain.

A local doctor discovered notable metabolic acidosis (pH, 6.860; CO2, 8 mmHg; HCO3, −1.0 mEq/L; base excess measurement, below sensitivity).

She was urgently transferred to Kurume University Hospital Advanced Emergency Medical Service Center.

On admission, her body temperature was 35.0 °C.

On admission, her respiratory rate was 28/min.

On admission, her blood pressure was 111/75 mmHg.

The findings on consultation included notable dryness inside the oral cavity.

The findings on consultation included a cold sensation on distal regions of the limbs.

Chest auscultation revealed no significant findings.

There was mild tenderness in the lower abdominal region.

Blood gases demonstrated notable metabolic acidosis (pH, 6.89; CO2, 11.4 mmHg; HCO3, 1.9 mEq/L; base excess, −31.3 mmol/L).

Lactic acid was mildly elevated at 3.3 mmol/L.

Blood sugar was mildly elevated at 259 mg/dL.

Hyperkalemia was observed accompanying the acidosis.

No significant kidney function impairment was observed.

A diagnosis of lactic acidosis secondary to metformin was considered.

The patient had not recently been exposed to a contrast agent.

Point-of-care urine testing showed strongly positive urinary ketones.

Point-of-care urine testing showed strongly positive urinary glucose.

Plasma 3-hydroxybutyric acid was markedly high (>10,000 μmol/L).

An injection of 0.45% sodium chloride was given as an intravenous drip at 800 mL/h.

Blood sugar dropped to 180 mg/dL after using two units of short-acting insulin.

An intravenous drip of glucose was started.

Around 6 units/day of insulin were used as appropriate.

Sodium bicarbonate was given as an intravenous drip.

Continuous renal replacement therapy (CRRT) was started from day 2 after hospital admission.

The acidosis improved because of CRRT over 3 days.

Hyperketonemia reduced notably after a few days.

Osmotic diuresis set in with urinary glucose as the cause.

Fluid replacement was carried out using Ringer’s solution.

Urinary sugar turned negative on day 16 after admission.

She was discharged on day 18 after admission.

She was being treated for type 2 diabetes.

She was taking canagliflozin, metformin, and saxagliptin orally.

She presented to the ED for evaluation of reduced oral intake, malaise, nausea, and abdominal pain.

The 3-hydroxybutyric acid was > 10,000 μmol/L.

The uncontrolled acidosis improved following 3 days of continuous renal replacement therapy.

Elevated urinary glucose continued for more than 10 days.

Ringer's lactated fluid supplementation was continued for management of polyurea and glucosuria.

Urinary glucose turned negative on day 16.

There was improvement in the patient's overall state.

She developed nausea and abdominal pain.

On admission, her body temperature was 35.0 °C.

On admission, her respiratory rate was 28/min.

Lactic acid was mildly elevated at 3.3 mmol/L.

Blood sugar was mildly elevated at 259 mg/dL.

An intravenous drip of glucose was started.

Hyperketonemia reduced notably after a few days.

She was discharged on day 18 after admission.