Graves' disease mimicking beta-thalassemia trait

Akasheh, Marwan

doi:10.1136/pgmj.70.822.300

Cited by 4 publications

(7 citation statements)

References 5 publications

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“…In GD anemia the mean corpuscular volume (MCV) could be normal [ 8 ] or, probably more commonly, low [ 4 , 9 ]. Generally the anemia that coexists with GD is observed to be mild and is commoner with severe disease [ 5 ] When GD anemia is microcytic, iron indices are normal and hereditary hemoglobinopathies are readily excluded [ 10 ]. Anemia may be the sole haematological abnormality, or it may be combined with thrombocytopenia, or leucopenia; and occasionally it may be present as a part of a GD-associated pancytopenia [ 9 , 11 , 12 ].…”

Section: Anemiamentioning

confidence: 99%

“…Erythropoietin levels are within normal reference ranges [ 4 ] and bone marrow, if examined, is hypercellular or, less commonly, normocellular; with normal iron stores [ 9 , 13 ]. The exact pathogenesis of GD anemia remains unclear [ 8 ]; however an effect of the excess thyroid hormones has been postulated [ 10 ]. The hypercellular marrow may indicate that erythropoiesis is enhanced due to hyperthyroidism, but in the same time it is ineffective, hence the finding of anemia with low MCV [ 10 ].…”

Section: Anemiamentioning

confidence: 99%

“…The exact pathogenesis of GD anemia remains unclear [ 8 ]; however an effect of the excess thyroid hormones has been postulated [ 10 ]. The hypercellular marrow may indicate that erythropoiesis is enhanced due to hyperthyroidism, but in the same time it is ineffective, hence the finding of anemia with low MCV [ 10 ]. Hematologically, anemia in the presence of hypercellular marrow could be related to either organ sequestration such as observed in hypersplenism, an enhanced removal of circulating red blood cells by an immune or toxic mechanism, or a hemopoietic stem cell dysfunction such as myelodysplasia [ 9 ].…”

Section: Anemiamentioning

confidence: 99%

“…Hematologically, anemia in the presence of hypercellular marrow could be related to either organ sequestration such as observed in hypersplenism, an enhanced removal of circulating red blood cells by an immune or toxic mechanism, or a hemopoietic stem cell dysfunction such as myelodysplasia [ 9 ]. One or both of the latter 2 mechanisms could be responsible for the GD anemia, with myelodysplasia being the most widely accepted explanation [ 9 , 10 , 13 ]. The finding that thyroid-stimulating hormone (TSH) receptor antibodies nonspecifically attach to the surface of the red blood cells, may suggest an autoimmune basis for GD anemia [ 14 ].…”

Section: Anemiamentioning

confidence: 99%

“…Generally, GD anemia resembles anemia of chronic disease in many aspects including red cell morphology, iron status, erythropoietin levels, and association with markers of inflammation [ 4 ]. GD anemia was observed to correct promptly with return to the euthyroid state following hyperthyroidism treatment [ 4 , 9 , 10 , 12 , 13 ]. Correction included normalisation of the haemoglobin concentration and also of the MCV [ 4 , 9 , 10 ].…”

Section: Anemiamentioning

confidence: 99%

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Atypical Clinical Manifestations of Graves' Disease: An Analysis in Depth

Hegazi

Ahmed

2012

Journal of Thyroid Research

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Over the past few decades, there has been an increase in the number of reports about newly recognized (atypical or unusual) manifestations of Graves' disease (GD), that are related to various body systems. One of these manifestations is sometimes the main presenting feature of GD. Some of the atypical manifestations are specifically related to GD, while others are also similarly seen in patients with other forms of hyperthyroidism. Lack of knowledge of the association between these findings and GD may lead to delay in diagnosis, misdiagnosis, or unnecessary investigations. The atypical clinical presentations of GD include anemia, vomiting, jaundice, and right heart failure. There is one type of anemia that is not explained by any of the known etiological factors and responds well to hyperthyroidism treatment. This type of anemia resembles anemia of chronic disease and may be termed GD anemia. Other forms of anemia that are associated with GD include pernicious anemia, iron deficiency anemia of celiac disease, and autoimmune hemolytic anemia. Vomiting has been reported as a presenting feature of Graves' disease. Some cases had the typical findings of hyperthyroidism initially masked, and the vomiting did not improve until hyperthyroidism has been detected and treated. Hyperthyroidism may present with jaundice, and on the other hand, deep jaundice may develop with the onset of overt hyperthyroidism in previously compensated chronic liver disease patients. Pulmonary hypertension is reported to be associated with GD and to respond to its treatment. GD-related pulmonary hypertension may be so severe to produce isolated right-sided heart failure that is occasionally found as the presenting manifestation of GD.

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