Page 215 - Abstract Book KONIKA 18

Gastroenterohepatology

P-GEH-011
Recurrent Pathological Fractures caused by Hepatic Osteodystrophy
in Chronic Cholestasis: A Case Report

1
2
1
Angela Kimberly Tjahjadi , Gryselda Hanafi , Antonius Hocky Pudjiadi , Fatima Safira Alatas 2
2
1
Faculty of Medicine and Department of Child Health , Faculty of Medicine, Universitas Indonesia/
Dr. Cipto Mangunkusumo Hospital, Jakarta, Indonesia
Abstract
Background Hepatic osteodystrophy (HO) is often found in children with chronic cholestasis which poses
them to higher risk of developing non-traumatic pathological fracture. Objective To emphasize the progressive
development of HO in chronic cholestasis patient. Case A 3-year-old girl with chronic cholestasis and
suspected with biliary atresia (BA) was brought to the emergency department with a complaint of loss of left
arm movement for the past 2 days without history of significant trauma. Two months prior, the patient had
similar complaint and multiple fractures were found in her right humerus and bilateral radius. No surgical
operation was conducted for the fractures. Musculoskeletal status of left upper arm revealed warm and
tender soft tissue swelling; limited range of movement due to pain, and dorsal angulation deformity in left
forearm. X-ray findings revealed new closed incomplete fracture on left proximal humerus with cortical
thinning and union fracture in distal radius and ulna, bilateral femoral bowing and incomplete pathological
fracture of the left femur diaphysis with osteopenia. Laboratory results showed hypocalcemia (8.2 mg/
dL), hypophosphatemia (3.2 mg/dL), and high total serum bilirubin (34.2 mg/dL). Measurement of serum
vitamin D was never performed due to financial limitation The patient was diagnosed with HO due to
chronic cholestasis. Immobilization using back-slab and plastic bandage was done; calcium carbonate and
paracetamol were given. Reluctance to move a limb despite having no trauma is a crucial symptom in the
early detection of pathological fracture related to HO in this case. Conclusions Long-term complication
of HO was inevitable in chronic cholestasis. Routine monitoring of vitamin D and bone mineral content is
essential to provide adequate treatment and prevent repeated fractures related to HO.
Keywords: fracture; hepatic osteodystrophy; chronic cholestasis

P-GEH-012
Case Report: Protein Losing Enteropathy in Chronic Diarrhea on Children

Marissa Leviani Hadiyanto, Intan Permata Sari, Rini Sulviani
Department of Pediatric, Syamsudin SH Hospital, Sukabumi, West Java, Indonesia
Abstract
Background Protein losing enteropathy (PLE) is an excessive loss of protein through the gastrointestinal tract,
along with anasarca edema as the most common clinical manifestation. A rare case of severe hypoalbuminemia
with anasarca edema associated with chronic diarrhea is elaborated on this report. Case A 12-year-old boy
complained about generalized edema since last week with a history of watery diarrhea for 3 weeks ago which
progressed into bloody diarrhea, urgency, and tenesmus for the last 2 days. He also mentioned abdominal
pain, nausea, lack of appetite, and low-grade fever. The physical examinations revealed anasarca edema and
ascites. Laboratory examinations showed leukocytosis and severe hypoalbuminemia. Urinalysis was normal
including negative protein and erythrocyte, normal cholesterol level, urea, creatinine, with normal chest
x-ray. Stool examination and fecal culture were not performed because the diarrhea had stopped after being
given therapy. Other causes of generalized edema can be removed from history, physical, and laboratory
examination. The patient was treated using albumin transfusions, furosemide, ceftriaxone, and metronidazole
alongside high protein diet. On the third days of treatment, the patient had clinical improvement followed
by weight loss, decrease abdominal circumference, loss of periorbital and legs edema. Discussion The
disorders causing PLE can be divided into those due to abnormality of the lymph system and those with
protein loss from intestinal mucosal. In developing countries, several gastrointestinal pathogens can impair
the enterocyte barrier function. In this patient, we believe that there is association between PLE and enteric
infection (Shigella, Entamoeba hystolitica or Giardia lamblia) observed from the clinical improvement
after antibiotic and antiparasite therapy. Conclusion The PLE is a rare complication of chronic diarrhea in
children which characterized by consequent hypoproteinemia and generalized edema. When treating severe
diarrhea and hypoalbuminemia, clinician should not only treat the main causes, but also administer albumin
and supportive therapy.
Keywords: protein losing enteropathy; hypoalbuminemia; chronic diarrhea; children

KONIKA XVIII Abstract Book 167