Objective:Rare disease Background:Fever of unknown origin (FUO) is a diagnosis that requires a demanding workup from physicians before confirming a diagnosis. Thyroid diseases are a rare cause of FUO. Subacute thyroiditis is an inflammatory disease that can lead to a wide spectrum of presentations. Case Report:We report a case of a previously healthy male who presented with persistent fever of 4 weeks following an upper respiratory tract infection associated with constitutional symptoms. His laboratory workup included complete blood counts (CBC), complete metabolic panel (blood urea and creatinine, liver function tests, and serum electrolytes), blood cultures, abdominal and pelvic ultrasound, and computed tomography abdomen and pelvis that were inconclusive. His thyroid function tests showed a hyperthyroid state and a thyroid scan confirmed a picture of thyroiditis. The patient was treated with Ibuprofen and then with prednisolone; he showed significant improvement over a few days and was discharged with treatment of tapering doses of prednisolone over 6 weeks. Two weeks after discharge the patient had a follow-up at an outpatient clinic and was found to be in good health with resolution of his symptoms. Conclusions:Thyroid disorders are not a common cause of FUO, and even if the clinical assessment of the patient is not suggestive of thyroid disease, we should consider it a possible cause. and thyroid function test should be performed to exclude thyroid problems.

Anemia constitutes a major global health burden, and iron deficiency is the most common cause of it. Iron deficiency and replacement affect not only hemoglobin (Hb) levels but also other hematological parameters such as platelet count. In this mini-review, we explore thrombocytopenia as a side effect of iron replacement therapy. We searched for relevant articles published in English, and all case reports/series of iron-induced thrombocytopenia were collected and analyzed. A total of 11 case reports and one case series were found relating to very low Hb at a baseline level of 5.25 +/-2.2 g/dl and variable platelet count at baseline that dropped in 9 +/-3 days to an average of 121 +/-112 x 10 9 /L, which in most of the cases was self-corrected. The parenteral route was more commonly reported to be associated with thrombocytopenia, and discontinuation of therapy was needed in two patients. The mechanisms, prevalence, and clinical significance of thrombocytopenia associated with iron replacement are unknown; several effects of iron on the primary hematopoietic cells and stromal cell lines have been proposed, such as influence on common progenitors, effects on cytokines, and thrombopoietic effect of erythropoietin, which is directly affected by iron levels. Iron replacement can lead to significant thrombocytopenia. Further research is needed to describe the exact incidence, mechanism, and clinical significance of thrombocytopenia associated with iron supplementation.

Introduction Severe IDA can cause many complications and impair the quality of life. Iron is an essential micronutrient required for catalysis, DNA synthesis, redox reactions and oxygen transport1. It is important for an early step in embryonic haematopoiesis, which is common for all developing blood cells. The link between IDA and leukopenia is not well recognized in the literature. Objectives To assess the prevalence and clinical significance of leukopenia in patients with IDA and effect of iron replacement and correction of anemia on the WBCs count. Materials and Methods We retrospectively reviewed the electronic medical records of all patients attended haematology clinic with the diagnosis of iron deficiency anemia (IDA) over 2 years in Hamad Medical Corporation, Qatar. All other causes of anemia and patients with systemic or chronic diseases were excluded. Age, nationality, BMI, Complete blood count and iron parameters were collected before and after treatment with IV iron therapy. Associated infections at the time of presentation (IDA and leukopenia) were noted including the course of the infection and response to treatment. Leukopenia was defined as WBCs count below 4000/microlitre. Statistical analysis was done using paired t test to compare variables after versus before iron therapy. Results Out of 1567 case of iron deficiency anemia, 80 case had leukopenia (5.105%) Their mean Leukocytes count was 3.35 +/- 0.48 ×103 before iron replacement. 7 patients had infections; 4 had upper respiratory tract infection, 1 urinary tract infection, 1 gastroenteritis, 1 lymphadenitis. Six of them received antibiotics and they had no complications. After iron therapy and correction of anemia the leukocyte count increased significantly to 4.38 +/- 1.82×103 (P < 0.05). There was no significant correlation between WBC count and iron parameters (Hb, TIBC, serum iron concentration). Discussion High level of erythropoietin in IDA is thought to cause down regulation of neutrophils in animal models. In our study leukopenia occurred in 5.1% of the big cohort with IDA. A previous study on 516 patients with IDA recorded leukopenia in 17.6% of them. Their cases with leukopenia occurred more in patients with severe anemia. The increase of WBC count with correction of anemia suggested a physiologic link between erythropoiesis and leukopoiesis. However, our study did not show correlation between WBC count and Hb or any of the iron parameters. In concert with our finding, a study in healthy children (n = 556) did not find associations between the measured iron markers and WBC In addition, the association between IDA and leukopenia did not significantly increase the risk of infections in our patients. The link between leukopenia and IDA needs to be addressed in more studies. Conclusions: The prevalence of leukopenia in this big cohort with IDA was 5.1%. This leukopenia was not associated with severe or complicated infections. There were no associations between the measured iron markers and white blood cell counts in healthy adults Figure Disclosures No relevant conflicts of interest to declare.

Primary hemochromatosis is an inherited disorder, and the homeostatic iron regulator (HFE) gene C282Y mutation is a common cause of hemochromatosis in Europe. We are reporting a case of a 56-year-old female known to have hemochromatosis with the HFE gene C282Y mutation with a serum ferritin level of 482 μg/L who underwent heart and liver T2* MRI which showed no evidence of iron overload-neither in the heart nor in the liver. This indicates that there is a discrepancy between serum ferritin and liver iron concentration by MRI and the superiority of T2* MRI in diagnosis and follow-up of iron overload in patients with hereditary hemochromatosis.