A case of pneumatosis cystoides intestinalis attributed
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A case of pneumatosis cystoides intestinalis attributed to an α- glucosidase inhibitor. Case: A 70-year old female Past history: Right knee osteoarthritis, autoimmune anemia (oral steroid administration), diabetes, angina Current history :

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A case of pneumatosis cystoides intestinalis attributed to an α- glucosidase inhibitor

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A case of pneumatosis cystoides intestinalis attributed to an glucosidase inhibitor

A case of pneumatosis cystoides intestinalis attributed

to an α-glucosidaseinhibitor

Case: A 70-year old female

Past history:

Right knee osteoarthritis, autoimmune anemia (oral steroid administration), diabetes, angina

Current history:

Aug Year X:The patient was suspected to be suffering from inferior myocardial infarction due to a complaint of anterior chest pain, and was placed on conservative treatment after being hospitalized. Rapid progress of anemia was observed with hemoglobin of 6.3 during hospitalization, and the patient was diagnosed with autoimmune anemia, and was given treatment.

Oct Year X: The patient starting having walking difficulties due to the onset of right knee pain during hospitalization. Prominent swelling was observed in the right lower limb, with imaging showing gas within the muscle layer. Since the CRP was 24.6, the patient was diagnosed with gas gangrene, and right femoral amputation was performed. Thereafter, amputation stump plastic was performed on the right femur.

Jan Year X+1: The patient was transferred to our hospital for the purpose of rehabilitation.

Introduction

Pneumatosis cystoides intestinalis (PCI) is a rare disease in which multiple cysts (gas tumors) develop filled with gasses under the mucosal membrane of the intestinal tract or under the serous membrane. The present report is on a case of PCI considered to be caused by an α-glucosidase inhibitor (α-GI).

Progress

PCI improvement

Onset of PCI

PCI diagnosis and treatment

10 days

Treatment complete

Start of treatment

Discontinuation of oral antidiabetic agents, administration of O2, maintenance transfusion, glutamine fiber oligosaccharide (GFO) therapy

19

Day

50

40

30

At the time of onset(Day30)

At the time of onset(Day 37)

At the time of onset(Day 40)

Glimepiride 1mg

Sitagliptin 50mg

Pioglitazone 30mg

Oral hypoglycemic agent

Glimepiride 2mg

Sitagliptin 50mg

Oral administration

discontinued

・Constipation (+)→ (-)

(lienteric stool)

・Lower abdominal discomfort (+)

・ Weakened peristaltic movement

・Abdominal bloating (+)

・Vomiting (+)

・Inflammation observed(-)

・Constipation (±)

・ Lower abdominal discomfort (±)

・Peristaltic movement - Weak/ good

・Abdominal bloating (±)

・Vomiting (-)

・Inflammation observed(-)

・Constipation (±)

・ Lower abdominal discomfort (-)

・Peristaltic movement - Good

・Abdominal bloating (-)

・Vomiting (-)

・Inflammation observed(-)

Pioglitazone 30mg

Voglibose 0.9mg

Intra-transfusion insulin dosage21 unit

Insulin

Long-acting insulin4 units/ day

Rapid-acting insulin( units/ day)

Long-acting insulin8 units/ day

Discontinuation

10

10

6

8

12

16

6

14

18

・Free air within intestinal wall (-)

・Free air within intestinal wall (+)

Change in blood glucose level

150- 250

180- 400

150- 300

150- 350

Summary

The present case suggested that α-GI, an antidiabetic agent, can cause PCI.

It is believed that the mechanism of onset is that α-GI increases the internal pressure of the intestinal tract when the patient has decreased peristaltic movement due to autonomic nerve dysfunction accompanying diabetes, and that reduced glucose absorption causes the breakdown of glucose through intestinal bacteria, leading to an increase in gas generation.

The present case suggests that it is recommended to continue treatment keeping in mind that α-GI may have caused PCI when the patient suffers from gastric symptoms with non-inflammatory reactions, and when they are suspected to be suffering from PCI based on imaging examinations.

Discussion

Since the onset of and improvement of PCI was observed from the commencement of α-GI administration to its discontinuation, and since there was no increase or change in CRP in examination data, we believe it is highly likely that α-GI affected the onset of the present PCI.


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