The late diagnosis of hemochromatosis in the patient with chronic hepatitis B and kidney damage Clinical Case Report

O.V. Skosireva

doi:10.37547/tajmspr/volume03issue04-09

Abstract

A late diagnosis of secondary hemochromatosis was made to a 38-year-old man with chronic hepatitis B, who after poisoning with alcohol surrogate (which was a year ago) had episodes of macrohematuria with signs of acute kidney damage, which required treatment in the ICU and hemodialysis sessions, after which kidney function was restored. In August 2020, the patient had a contact with a COVID-19 patient, but upon admission to the hospital, the results of tests for COVID-19 were negative. During the examination in our department, after the exclusion of the urological disease, the diagnosis of interstitial nephritis of toxic etiology, hemolytic anemia, chronic viral hepatitis B was made. Then in-depth study of iron metabolism, bone marrow, and MRI of parenchymal organs revealed secondary hemochromatosis.

Highlights

Primary or secondary excessive accumulation of iron in a human body can be genetic or acquired
According to the clinical diagnosis the patient was referred to the Research Institute for Hematology and Blood Transfusion for further treatment with the recommendation to continue the treatment with the following drugs for one month: 5 mg prednisolone, 14 tablets according to the protocol, 25 mg dipyridamole, 2 tablets 3 times a day, Ursodeoxycholic acid, 1000 mg/day, Alpha-tocopheryl acetate, 200 mg/day, Iron sulfate with vitamins, 1 capsule twice a day, The therapy should be followed by one more examination by a nephrologist and acomplete analysis of urine, urea and creatinine. This clinical case is of interest in terms of late diagnosis of hemochromatosis, that, most likely, was associated with the manifestation of the disease by symptoms generated by the kidneys and urinary tract in the form of episodes of macrohematuria and the signs of acute kidney damage which required hemodialysis sessions
An increase in the level of transaminases, LDH, total bilirubin owing to its indirect fraction, serum iron, and ferritin levels with a simultaneous decrease in total protein, haptoglobin, transferrin, serum iron-binding capacity, as well as the characteristic picture of the bone marrow, i.e. erythroid germ hyperplasia in normoblastic type of hematopoiesis, indicated clearly the hemolytic nature of anemia

Summary

INTRODUCTION

Primary or secondary excessive accumulation of iron in a human body can be genetic or acquired. Both these conditions are known to result in organ damage with clinical symptoms. Excessive iron is primarily deposited in the parenchymal cells, whereas in hemochromatosis associated with blood transfusion, it is primarily accumulated in the reticuloendothelial cells. The abnormal amount of iron is deposited in the cells as hemosiderin. This inevitably results in the cell death and replacement of these cells by a fibrous deposition that leads to destruction and/or impairment of organ function [3]. It is not easy to diagnose hemochromatosis because the disease is rare and manifests itself by various symptoms

CASE PRESENTATION

PHYSICAL EXAMINATION

Casts Mucus Bacteria

DISCUSSION