IJRCI. 2015;3(1):CS2 CASE STUDIES GAVE: An interesting cause of iron deficiency anemia

A 55-year-old female presented to the OPD clinic with dyspnea on exertion, easy fatigability, and melena. She was referred from hematology department due to the occurrence of persistent anemia. No history of hematemesis, abdominal pain or chronic drug intake was reported. She had difficulty in getting up from sitting position, multiple joint pain, and Raynaud’s phenomenon. She had been transfused twice for anemia in the last one year. She had attained menopause and had normal bowel habits. Physical examination revealed that the patient was severely pale with sclerodactyly and facial skin tightening. Her BP was 160/100 mm Hg. She had symmetrical proximal muscle weakness of both lower and upper limbs (power of 3/5). No skin lesions suggestive of dermatomyositis were reported. Other systems examinations were within normal limits. Her hemoglobin was 5.6 g/dl with normal total count and platelets. Peripheral smear showed microcytic hypochromic anemia and the stool examination was positive for occult blood. Results of upper gastrointestinal (UGI) endoscopy showed hyperemic streaks alternating with normal mucosa (watermelon stomach) (Fig. 1 and 2), suggestive of gastric antral vascular ectasia (GAVE). Her creatine phosphokinase (CPK) was 126 IU/L and the levels of other enzymes such as LDH, SGOT, and SGPT were normal. The findings of electromyography (EMG) were normal with no feature suggestive of inflammatory myositis or myopathy. She was positive for ANA by ELISA and for CENP-B (Anti Centromere Ab) by immunoblot. The patient had undergone Argon laser photocoagulation (Fig. 3 and 4) and packed cells transfusion, and the treatment had contributed to symptomatic improvement. Based on the clinical investigations and history, she was diagnosed to have limited cutaneous systemic sclerosis with GAVE. The initial presentation of severe iron deficiency anemia was due to intermittent GI bleeding. Discussion GAVE is a rare cause for upper GI loss and subsequent iron deficiency anemia. The syndrome was first described by Ryder et al. in 1953 and the term ‘watermelon stomach’ (endoscopic appearance) was first coined by Jabbari et al.