The course of epicardial coronary arteries into a muscular tunnel under a bridge of myocardium is known as myocardial bridging (MB). This could be a benign anomaly, nevertheless, it could have a great impact on the quality of life in the setting of severe anginal symptoms. The clinical presentation and diagnosis could be challenging in those patients. The treatment options start from simple medical therapy to surgical intervention in refractory cases, the role of percutaneous coronary intervention (PCI) is limited in MB. We are describing a case of severe MB presenting as Wellens pattern with underlying left ventricular hypertrophy (LVH).

Introduction: Coronary Artery Disease (CAD) continues to be on the rise not only in the Western developed world but also affecting the South Asian race, particularly Bangladeshis. The objectives of this study were as follows: To determine whether or not risk factors of Bangladeshis differ from non-Bangladeshis, whether there is any difference in the extent of CAD for both groups, and if there are risk factors that can significantly affect the extent of CAD Methods: All patients with a diagnosis of CAD admitted to our 800-bed tertiary care hospital between January 2001 and December 2015 were retrospectively analyzed. We reviewed the age, sex, body-mass index (BMI), cardiac risk factors such as family history of CAD, dyslipidemia, hypertension, diabetes and smoking. We also reviewed coronary angiographic findings of these consecutive 150 Bangladeshis and a randomly selected group of 193 non-Bangladeshis. Results: A total of 343 medical records were evaluated, this included two groups: 193 non-Bangladeshis and 150 Bangladeshi subjects. The Bangladeshi group was older than the non-Bangladeshi group (63.49 vs 59.22, p-value=0.001), and included a larger proportion of males than the non-Bangladeshi group (28.7% vs 15.68%, p-value=0.0116). Bangladeshi subjects are more likely to be smokers than non-Bangladeshi (11.75% vs 6.67%, χ2=12.7, p-value=0.0004). Non-obstructive, 1-vessel, 2-vessel and 3-vessel accounts for 13.33%, 36.67%, 22%, and 28% for Bangladeshis, and 16.39%, 20.77% 34.43% and 28.42% for non-Bangladeshis, respectively. The difference of extent of CAD is significant between two groups (χ2 =12.397, p-value=0.0061). The findings suggest that Bangladeshi ethnicity has almost 2 times the likelihood of having 1-vessel CAD at coronary angiography (OR=2.361, 95% CI 1.452-3.839, p=0.0005). Conclusion: This study is a pivotal starting point for further evaluating the link between Bangladeshis and CAD. In our study we found that being Bangladeshi increases the risk of having CAD and may be an independent risk factor for multi-vessel CAD.

Introduction: Hypogonadotropic hypogonadism is a common disorder encountered in endocrine practice with a prevalence of 1 in 10,000 men (1). We describe a patient with possible mitochondrial mutation causing him to have concurrent central hypogonadism and NARP syndrome (neuropathy, ataxia, retinitis pigmentosa). Case: 65 year old male with central hypogonadism diagnosed at age 17 was on testosterone replacement therapy off and on since then. He was diagnosed with NARP at age 49. On exam, he was OX3, BP 147/83mmHg, HR 63 bpm, wt 185lbs. Pupils were sluggish to light. Unable to assess visual fields as patient is legally blind. No gynecomastia. Cardiac and pulmonary exam were normal. Testicles were soft and the volume was 12mL. Prostate was enlarged, non tender and without nodules. He had ataxic gait, abnormal finger to nose test and strength was normal. LH <0.2 mIU/ml (N 1.2 - 10.6 mIU/ml), FSH < 0.2 mIU/ml (N 0.7 - 10.8mIU), total testosterone as low as 12ng/dL when off and 260ng/dL (N 250-1110ng/dL) while on testosterone IM. CBC, CMP, prolactin, ACTH, cortisol, Igf-I, TSH and PSA wnl. MRI brain showed cerebellar atrophy and normal pituitary. Discussion: NARP is a mitochondrial disorder characterized by neuropathy, ataxia and retinitis pigmentosa primarily affecting the nervous system. NARP results from point mutation at base pair 8993 of the mitochondrial genome in the ATPase 6 gene. Symptoms typically consist of proximal neurogenic muscle weakness, sensory neuropathy, ataxia, and retinitis pigmentosa. According to Al-Gadi et al, hypogonadism has been reported in mitochondrial disease (2). RRM2B is a nuclear-encoded mitochondrial maintenance gene. Mitochondrial DNA depletion due to ar-RRM2B mutations have been reported in association with hypogonadism. A mutation of m.8561C>G in MT-ATP6/8 causing a mitochondrial syndrome with ataxia, peripheral neuropathy, diabetes mellitus, and hypergonadotrophic hypogonadism has also been reported in a case report of two patients (3). Upon literature review, no prior cases of hypogonadotropic hypogonadism in patients with NARP have been reported. The impairment of the hypothalamic-pituitary axis appears to manifest in severe mitochondrial phenotypes. For example, the association of central hypogonadism with Kearns Sayre Syndrome (KSS). Given that both disorders are related to mitochondrial dysfunction, we propose that the hypogonadism may be linked to NARP syndrome. References Rohayem, J.et al. (2016), Causes of hypogonadotropic hypogonadism predict response to gonadotropin substitution in adults. Andrology Al-Gadi.et al. (2018). Endocrine Disorders in Primary Mitochondrial Disease. JES Kytövuori, L. et al. (2016, August 8). A novel mutation m.8561C>G in MT- ATP6/8 causing a mitochondrial syndrome with ataxia, peripheral neuropathy, diabetes mellitus, and hypergonadotropic hypogonadism.

Introduction: Pembrolizumab t is used to treat various cancers. It is associated with immune related adverse events (IRAEs) that can be life threatening [1,4]. We describe a patient who presented autoimmune Diabetes after the use of Pembrolizumab. Case: 64 y/o African American female PMHX of lung non-small cell lung cancer diagnosed in 2017 Clinical stage IV with gluteal metastasis, and dementia. Pt was referred by Oncology. The patient had a family history of Type 1 DM. and complained of dizziness, and unintentional weight loss (30 pounds) over a year. She had received 2 cycles of Pembrolizumab. The last cycle given 5 weeks before presentation to Endocrinology.Physical examination revealed cachectic female (weight 35 kg, height 147cm), dry mouth, BP 135/82, Plasma glucose 383mg%, A1c 7, negative Islet cell antibodies, positive anti-GAD, undetectableserum C-peptide. Cortisol 27, Acth 21 at 8 am and TSH 2.3. Discussion: In a systematic literature review, the early pattern of Diabetes onset with the use of checkpoint inhibitors was evaluated and on average after 4.5 treatment cycles [4].The incidence of immune checkpoint inhibitor-induced Type 1 Diabetes is estimated at 1% [3].This appeared to be earlier for the combination of anti-cytotoxic T-Lymphocyte associated antigen 4 monoclonal antibody and PD-1 therapy. The onset of β cell inflammation is often fulminant, suggested by the relatively low glycated hemoglobin levels, while C-peptide levels are usually low or undetectable at diagnosis and mostly positive GAD antibodies [5]. This side effect is predominantly found in patients exposed to blockade of the PD-1/PD-Ligand pathway. The IRAEs are primarily managed by immunosuppression with corticosteroids and discontinuation of immunotherapy except in autoimmune Diabetes which is irreversible. Physicians should be aware of and patients educated about the important multiorgan side effects since a growing number of patients are treated with checkpoint blockade.Azoury SC, Straughan DM, Shukla V. Immune checkpoint inhibitors for cancer therapy: clinical efficacy and safety. Curr Cancer Drug Targets 2015;15: 452-462Weber JS, Postow M, Lao CD, et al. Management of adverse events following treatment with anti-programmed death-1 agents. Oncologist 2016;21:1230-40Stamatouli AM, Quandt Z, Perdigoto AL, Clark PL, Kluger H,Weiss SA et al Collateral damage: insulin-dependent diabetes induced with checkpoint inhibitors. Diabetes 2018;67(8):1471-1480de Filette JMK, Pen JJ, Decoster L, et al. Immune checkpoint inhibitors and Type 1 Diabetes mellitus: a case report and systematic review. Eur J Endocrinol. 2019;181(3):363–374.Akturk HK, Kahramangil D, Sarwal A, Hoffecker L, Murad MH, Michels AW. Immune checkpoint inhibitor-induced Type 1 Diabetes: a systematic review and meta-analysis. Diabet Med. 2019;36(9):1075–1081.

Background: Oral tablets of levothyroxine (L-T4) are the standard of care for the treatment of Hypothyroidism and are recommended by current professional guidelines. However, patients with malabsorption syndromes, intolerance to excipients or dyes in tablets, or the intake of certain medications or foods may not be adequately controlled on these tablets. The use of liquid soft gel capsules (Tirosint) has been reported to be of value in such circumstances. Case Report: A 29 year old woman underwent total thyroidectomy followed by 124.5 mCi 131 I therapy at another facility for a right sided 3.7cm PTC with tall cell features. 12 ipsilateral central nodes were positive for cancer. Post therapy WBS was negative for evidence of distant metastases. She was placed onto branded L-T4 treatment but over the next 2 years, in spite of carefully documented adherence to her medication regimen, and with daily doses increasing from 0.1 to 0.3mg, TSH levels were unstable varying from 0.03 to 3.13μIU/ml and then 3 months later rose progressively further to 130μIU/ml. Her clinical Hypothyroidism became critical requiring emergent use of IV L-Thyroxine by her physicians who added L-T3 20μ/d to her L-T4 0.3mg but her TSH did not go below 98.54. She sought care at our institution. Issues of proper technique of medication administration were explained and emphasized with which the patient insisted she was fully compliant. Nevertheless, and in spite of a further increase in the daily L-T4 dose to 0.35mg, TSH remained excessive at 86.94. Treatment was then changed to Tirosint soft gel capsules alone starting at 0.3mg and then decreasing progressively to 0.2mg daily as her TSH reduced to 4.39 (6 months) and has remained in the range of 0.011 to 0.057 over the next 3 years. Other than Vitamin D and the temporary use of Depo-Provera, the patient denied the use of any other medications or supplements. Discussion: L-T4 tablets have long been the preferred and recommended treatment form for Hypothyroidism by professional societies. (1, 2) However, reports have appeared noting poor and inconstant response to this treatment in occasional patients such as those with malabsorption syndromes such as following bariatric surgery (3) or with gastroparesis (4), or with the concomitant intake of other medications such as proton pump inhibitors (5) or foods such as coffee (6). In such circumstances, it has been reported that use of liquid L-T4 or liquid soft gel capsules containing no excipients beyond glycerin and gelatin results in improved absorption of L-T4 with better and more stable control of thyroid biochemistry including TSH. (3, 4, 5, 6, 7) We present a case of a patient with Papillary Thyroid Cancer who, following total thyroidectomy and 131 I therapy, had variable and inadequate TSH suppression with development of clinical unresponsiveness to standard branded L-T4 treatment. Switching therapy to a soft gel product has enabled stable control of TSH