Correspondence

H. pylori : Association with Megaloblastic Anaemia

Sir,

The article by Desai and Gupte¹ entitled “Helicobacter pylori link to pernicious anaemia” is very interesting and timely. Megaloblastic anaemia is a common problem both in outdoor as well as in indoor patients, where they are admitted for anaemia related complications. We have also noticed that the usual causes of nutritional or systemic disorders are absent in a great majority of these patients and at time it is extremely difficult to pin-point a probable etiology. Gastrointestinal symptoms are usually neglected unless they point towards definitive malabsorption features. We report below a young patient with megaloblastic anaemia in whom a diagnostic work-up was done as the anaemia had developed over a few weeks without a definitive etiology both systemic as well as nutritional.

A 23 years old male presented with generalised weakness for 4 weeks, blurring of vision, nausea and vomiting for 15 days. There was no history of addiction, especially alcohol intake/prolonged drug intake such as antiepileptic drugs. He came from a good family background and nutritional intake was absolutely normal. On examination patient was conscious, oriented to time, place and person, BP was 114/70 mmHg, pulse rate 126/min regular, respiratory rate 20/min and he was severely pale. CVS – loud S1 and soft systolic murmur at apex was present. Respiratory system, abdominal and nervous system examination were normal. Investigations revealed Hb of 4.0 gm%, TLC 3400/mm³, DLC – P₇₀L₂₈M₁E₁, platelet count 134000/mm³, reticulocyte count 3.2%, PCV 11.9%, RBC 1.27x10⁶/mm³, MCV 104.7 fl, MCH 31.5 pg/cell and MCHC was 33.2 g/l. Peripheral smear showed anisocytosis, microcytosis, macrocytosis, poikilocytosis and neutrophil hypersegmentation. Kidney function test, serum electrolytes, blood sugar and urine examination were normal. In liver function tests serum bilirubin (T) was 1.6 mg/dl (direct 0.03 mg/dl), SGPT 23 U/l, SGOT 64 U/l, alkaline phosphatase 36 KAU/l and total protein was 6 gm/dl (albumin 4 gm/dl). X-ray chest PA view and ultrasound abdomen were within normal limits. Stool for occult blood was positive. Iron study was normal and serum vitamin B12 level was 146 (normal 200-800 pg/ml). Fundus examination showed anemic retinopathy. Upper GI endoscopy revealed gastric erosions and rapid urease test was positive for H. pylori. Gastric and duodenal biopsies were taken to rule out atrophic gastritis and sprue. Report revealed chronic gastritis with activity and Giemsa stain was positive for H. pylori. Duodenal biopsy was suggestive of non-specific inflammation. Anti-gastric parietal cell antibodies was 49.0 U/ml (normal <10 U/ml). IFA could not be done due to cost factor. Patient was put on H. pylori kit (two Cap. Omeprazole 20 mg, two Tab. Amoxycillin 750 mg and two Tab. Tinidazole 500 mg) 1 OD for 10 days and inj. Vitcofol once a week for 4 weeks. Patient showed dramatic response to the treatment.

Our case illustrates that GI symptoms should be sought carefully and minutely in all patients with megaloblastic anaemia especially when profile indicates absence of usual causes. Upper GI endoscopy combined with investigations for H. pylori both in serum and biopsy become mandatory as indicated by these authors¹ as well as Kaptan et al,² who suggested H. pylori as novel causative agent in vitamin B12 deficiency. Similar observations have also been reported elsewhere.³ We agree with the view that the work-up as suggested in this article will establish diagnosis of pernicious anaemia / atrophic gastritis in a cost effective manner.

R Avasthi*, SC Chaudhary**

*Professor; **Senior Resident, Department of Medicine, UCMS (University of Delhi) and GTB Hospital, Delhi -110095.

Received : 27.12.2007; Accepted : 3.1.2008

References

1.    Desai HG, Gupte PA. Helicobacter pylori link to pernicious anaemia. J Assoc Physicians India 2007;55:857-59.

2.    Kaptan K, Beyan C, Ural AU, Cetin T, Avcu F, Gulsen M, et al. Helicobacter pylori – is it a novel causative agent in vitamin B₁₂ deficiency? Arch Intern Med 2000;160:1349-53.

3.    Annibale B, Negrini R, Caruana P, et al. Two-thirds of atrophic body gastritis patients have evidence of Helicobacter pylori infection. Helicobacter 2001;6:225-33.