|LETTER TO THE EDITOR
|Year : 2015 | Volume
| Issue : 1 | Page : 40-41
Pancytopenia due to Grave's disease: A rare scenario
Department of General Medicine, Institute of Post Graduate Medical Education and Research, Kolkata, West Bengal, India
|Date of Web Publication||18-Dec-2014|
Dr. Subrata Chakrabarti
Doctor Hostel, Institute of Post Graduate Medical Education, AJC Bose Road, Kolkata - 700 020, West Bengal
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Chakrabarti S. Pancytopenia due to Grave's disease: A rare scenario. Thyroid Res Pract 2015;12:40-1
Pancytopenia is a rare complication of Grave's disease with few case reports being available in literature. The author reports a case of Grave's disease complicated by pancytopenia.
A 38-year-old non-diabetic, non-hypertensive female presented with complaints of 'bulging eyes,' episodic palpitations and increased sweating for last one year. She also complained of progressive weight loss in presence of preserved appetite and easy fatigability and low grade irregular fever for same duration. Past history was insignificant and she was not on any drug therapy (including anti-thyroid drugs). General examination revealed tachycardia with a regular pulse rate of 116/min and water-hammer character. On ophthalmological examination, bilateral exophthalmos [Figure 1] with slightly decreased extraocular movement in upward gaze was found but vision was 6/6 bilaterally with equal and reactive pupils and normal fundi. Signs of thyroidophthalmopathy like Dalrymple's sign, Von graffe's sign were positive. Diffuse thyroid enlargement with suggestions of raised vascularity (bruit) was found [Figure 2]. Cardiovascular examination revealed loud S1. Other system examination showed no abnormality. Complete blood count showed trilineage depression-Hb-8.6 g/dl; Total white blood cell (WBC) count- 3100/cmm (N-67%; L-29%) and platelet - 78000/cmm. Red blood cell (RBC) indices were normal and peripheral smear revealed normal cellular morphology and no abnormal cell. Ferrokinetics and B12 assay were normal. Bone marrow aspirate and trephine biopsy showed normal cellular marrow with predominantly normoblasticery thropoiesis with maintained M: E ratio (2:1). Myelopoiesis and megakaryocytes were normal. Liver and renal function tests as well as serum electrolytes, abdominal ultrasound and chest X-ray were all normal. Sinus tachycardia was noted on electrocardiography (ECG) but transthoracic echocardiography was normal. Thyroid function test was performed, which showed increased thyroxine (T4) and triiodothyronine (T3) activities with depressed thyroid stimulating hormone (TSH). Triiodothyronine level was 517 ng/dl (normal 70-204 ng/dl), T4 level was 24.6 μg/dl (normal 5.2-12.5μg/dl) and TSH was 0.03 uIU/ml (normal 0.35-5.5 uIU/ml). Anti-thyroid peroxidase (TPO) was positive in high titers (1100 IU/ml). Thyroid ultrasound along with color Doppler revealed both lobes of thyroid to be diffusely enlarged with heterogeneous echo texture and increased vascularity. Thyroid scan with Technetium-99m ( 99m Tc) pertechnetate showed enlargement of both lobes of thyroid with increased homogenous tracer uptake. Based on the clinical features and laboratory parameters, a diagnosis of Graves' disease complicated by thyroid ophthalmopathy (Grave's associated ophthalmopathy) and pancytopenia was made. Patient was started on carbimazole (30 mg/day). As the pancytopenia was suspected to be due to the thyrotoxicosis state itself, micronutrient supplements for anemia and antibiotic cover for neutropenia were not given (moreover, absolute neutrophil count was >1000/cmm). Follow-up at 6 months revealed improvement of Grave's disease, both clinically and biochemically. Notably, return to euthyroid status was associated with marked improvement in hematological parameters, which reversed to normal range (Hb-11.7 g/dl; Total WBC count - 5700/cmm: N-71%; L-23%) and platelet - 152000/cmm).
Pancytopenia is a potentially life-threatening disorder that may be due to primary bone marrow failure or due to viral infection, radiation, drugs (NSAIDs, cytotoxic drugs). Thyrotoxicosis causing pancytopenia is extremely rare with scarce documentation regarding the entity. ,,,, Usually marrow depression in thyrotoxicosis is treatment related due to carbimazole or propylthiouracil, which may cause agranulocyosis. The index patient developed pancytopenia prior to administration of carbimazole. The causal effect of thyrotoxicosis in pancytopenia as in this patient is best exemplified by the normalization of blood counts following reversal of thyrotoxic state. The mechanism of pancytopenia in such patients is only speculative. As Grave's is an immune-mediated disorder, shared autoimmune mechanism may be responsible leading to reduced life span of blood cells. Disturbances in maturation and differentiation of the pluripotent stem cells may also be possible. Organ sequestration as in hypersplenism can contribute. ,, Single lineage abnormalities related to hyperthyroidism are more common than pancytopenia.  Thus, it is to be borne in mind by physicians that thyroid abnormalities may be the cause of unexplained pancytopenia and so routine hematologic evaluation should be performed before administration of anti-thyroid drugs to differentiate pancytopenia, which is related to the thyrotoxic state itself from the marrow depression induced by these drugs. In the former stage, pancytopenia reverses with use of these drugs, and in the later stage dose adjustment is mandatory.
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[Figure 1], [Figure 2]