No abstract

No abstract

Background: Immune thrombocytopenic purpura (ITP) in association with autoimmune thyroid diseases is a well-known entity. We report a case of Graves’ disease patient with coexisting ITP, where the control of ITP is in close relationship to control with Graves’ disease. Case Presentation: A 17-year-old female presented in 10/2014 with hyperthyroid symptoms for 4-5 months. Thyroid function tests (TFT’s) showed TSH 0.011 (0.45-4.5 mcIU/ml) and Total T4 (TT4) - 34.3 (4.5-12 ug/dl). Thyroid ultrasound showed thyromegaly without any discrete nodules. Thyroid uptake scan showed a homogeneous increased radiotracer uptake of 65% at 24 hours consistent with Graves’ disease and she was started on Methimazole (MMI) 20 mg PO daily. Over time, her hyperthyroidism remained well controlled on MMI 5 mg q other day, hence it was discontinued in 5/2016. She presented with multiple skin bruises in 12/2016 and her platelet count was noted to be 19 (150-400x10 3 /ml). TFT’s remained normal. Her presumptive diagnosis was ITP given another autoimmune condition - Graves’ disease and was started on Prednisone 80 mg daily. She followed with hematology and her platelet count was monitored regularly and prednisone dose was adjusted. In 7/2017 her platelet count dropped to 64 on prednisone 5 mg PO daily. Repeat TFT’s showed TSH 0.01 and free T4 3.31. MMI was resumed at 20 mg PO daily. Labs three months later show TSH 0.024, free T4 0.86, TT3 102 and platelets 186. Given the recurrence of Graves’ disease she underwent radioactive iodine (RAI) I131 therapy in 1/2018. Post RAI she required levothyroxine 50 mcg daily briefly. In 5/2018 her platelet count dropped again to 59 on prednisone. TFT’s showed TSH of 0.014, free T4 1.42 and TT3 117. Graves’ disease relapsed despite RAI therapy and MMI was started at 5 mg PO daily. Her thyroid function remains well controlled on MMI 5 mg PO daily. Her platelet count also returned to normal and remains stable on Prednisone 5 mg PO daily. Discussion: There are several case reports of Graves’ disease and ITP in the literature. Several mechanisms by which thrombocytopenia occurs have been postulated. Accelerated platelet turnover by an activated reticuloendothelial system, shortened platelet survival and consequently reduced platelet counts can occur in patients with hyperthyroidism. Platelet survival return to normal in patients maintained in euthyroid state for more than six months. Genetic predisposition to both Graves’ disease and ITP appears to be related to HLA B8 and DR3 haplotypes. In our patient, each time she had a low platelet count on prednisone therapy, thyroid function tests were suggestive of relapse of Graves’ disease. Treatment of Graves’ disease has resulted in improved response of ITP to glucocorticoid therapy and normalization of platelet count. In patients with ITP on glucocorticoid therapy, unexplained drop in platelet count should prompt checking for thyroid function abnormalities....

Background: Hepatitis C (Hep C) infection is one of the leading causes of end stage liver disease and hepatocellular carcinoma. Several advances have been made in the treatment of Hep C infection. Harvoni (ledipasvir and sofosbuvir) is one of the treatment options. There have been no case reports of hypocalcemia or hypoparathyroidism associated with Harvoni therapy. We report a case of hypocalcemia and permanent hypoparathyroidism that began after Harvoni therapy. Case Presentation: A 64-year old African American man presented with weight loss and was diagnosed to have Hep C. He was treated with 12 weeks course of Harvoni. He was first noted to have low calcium level at 8.4 (8.4 – 10.3 mg/dl), during the last week of Harvoni treatment. Several previous calcium levels were normal. Four months later, he presented to Emergency Department with numbness, palpitations, and muscle cramping. His calcium was then 6.6 mg/dl, albumin 4.3 (3.4 - 4.8 mg/dl), PTH 18 (15 - 65 pg/ml), 25-hydroxy vitamin D 11 (30 - 50 ng/ml), magnesium 2.2 (1.6 – 2.6 mg/dl), phosphorus 3.8 (2.3 - 4.7 mg/dl) and 24-hour urine calcium was less than 2. Oral calcitriol, ergocalciferol and calcium carbonate were initiated and his calcium normalized. His calcium remained normal on calcitriol and calcium carbonate, but twice he had to be treated in emergency department for symptomatic hypocalcemia after missing his medications. Recently, he began PTH (1-84) (NATPARA). He has been tolerating parathyroid hormone injections well. Discussion: Harvoni is a combination medication of Ledipasvir and Sofosbuvir. Ledipasvir is a NS5A inhibitor. NS5A is an RNA binding protein required for the activity of RNA polymerase of hepatitis C virus. Sofosbuvir is a viral RNA polymerase inhibitor. There have been no case reports of hypoparathyroidism occurring with Harvoni therapy in the literature. Hypoparathyroidism most commonly results after anterior neck surgery like thyroidectomy, parathyroidectomy, or anterior neck dissection. Other causes include neck irradiation, infections like HIV, infiltration of the glands by heavy metals such as iron or copper; genetic disorders of parathyroid gland development, parathyroid hormone synthesis and calcium sensing receptor mutations, and finally autoimmune etiologies. Our patient had none of the risk factors for developing hypoparathyroidism. Nevertheless, he developed permanent, symptomatic hypoparathyroidism towards the end of Harvoni treatment, making Harvoni as the most likely cause of his hypoparathyroidism. More long-term data on this drug is needed to assess the risk of hypoparathyroidism after Harvoni therapy. Conclusion: Hypoparathyroidism leading to hypocalcemia could be a potential complication of Harvoni treatment. Monitoring calcium and parathyroid hormone levels prior to initiation and periodically after completion of Harvoni treatment should be recommended for all patients.