bluuebunny/crossref_metadata_2025_split huggingface dataset:
PSAT303 Fecal Impaction as a Gastrointestinal Prodrome of Myxedema Coma in an Elderly Woman with Multiple Co-morbidities
Authors: Ahmad Mobeen , Song Rui , Elrod Sarah , Tejada Luis Arzeno 
Published: November 2022

Abstract

Introduction
Fecal impaction is a common occurrence in the elderly, with the most common risk factor being chronic constipation. A common cause of chronic constipation that can be overlooked in the elderly is hypothyroidism. If left untreated, hypothyroidism can have life-threatening manifestations including myxedema coma. In this case report, we describe a rare case of myxedema coma with prodromal fecal impaction.

Case description
An 87-year-old female with a past medical history of colon cancer status post partial colectomy, stroke, and end stage renal failure (ESRD) requiring hemodialysis, presented to the emergency department with extreme rectal pain. She was found to have fecal impaction on abdominal x-ray and was manually disimpacted and discharged home. Five days later, she presented with altered mental status in the setting of a new active herpes zoster infection and possible pneumonia. She was hypothermic (95F) and hypoxic, needing supplemental oxygen (2 L nasal cannula). Her labs showed hyponatremia (133 mg/dL), hypoglycemia (43 mg/dL), an elevated TSH level (100.0 mIU/ml) and decreased free T4 level (0.9 ng/L). Her EKG showed first-degree AV block with low voltage QRS complexes and her chest x-ray demonstrated bilateral pleural effusions. A CT scan of her head did not show hemorrhage or stroke. Given her classic clinical presentation and lab work findings, myxedema coma was diagnosed and the patient was treated with levothyroxine and hydrocortisone, though she was later transitioned to hospice as per her wishes.

Discussion
Chronic constipation is a known etiology of fecal impaction and can be caused by many chronic conditions in the elderly including ESRD, immobility, and hypothyroidism. Fecal impaction is easily identified but the investigation for the etiology is often overlooked. In this case, we argue that patients with an initial presentation of fecal impaction or with severe and unexplained constipation may warrant screening for hypothyroidism as a manageable risk factor for fecal impaction. By doing so, early recognition and treatment of hypothyroidism may prevent potentially fatal patient outcomes such as myxedema coma.
Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
PSAT342 Hypothyroidism After Use Of Immune Checkpoint Inhibitor Therapy In Patient With Graves’ Disease
Authors: Sharma Rajeev 
Published: November 2022

Abstract

Background
Immune checkpoint inhibitors (ICIs) are commonly used for many cancers. Thyroid gland involvement is the commonest endocrine toxicity seen with this class of drugs. Most common thyroid dysfunction is thyroiditis followed by hypothyroidism with some cases of recovery. There are rare case reports of Graves’ disease induced by ICIs. However, we report a patient with pre-existing Graves’ disease who developed hypothyroidism after immunotherapy.

Clinical Case
66-year-old man with metastatic squamous cell carcinoma of lung was referred to endocrine clinic for suppressed TSH. He was diagnosed with metastatic poorly differentiated lung cancer in September 2018. He received cheamotherapy with carboplatin and paclitaxel from October 2018 to January 2019. He was switched to immune checkpoint inhibitors with programmed cell death protein-1 (PD-1) inhibitor pembrolizumab every 3 weeks from February 2019. ICI therapy was stopped in until July 2019 due to immune mediated hepatitis. He was started on high dose steroids. Lung cancer findings remained stable even after stopping ICIs. Prior to starting ICIs his thyroid functions were consistent with hyperthyroidism. He continued to have suppressed TSH until his 6th cycle of pembrolizumab. TSH was found be significantly elevated prior to his 7th infusion. He was referred to endocrinology for further management. Clinically, patient was asymptomatic except for fatigue. Family history was positive for mother with Graves’ disease. Laboratory results on presentation showed significantly elevated TSH, low thyroxine (T4) and triiodothyronine (T3) consistent with diagnosis of primary hypothyroidism. Thyroid stimulating immunoglobulin (TSI) was positive suggesting autoimmune thyroid disease. Thyroid scan showed decreased 24-hour uptake (0.8%). A diagnosis of immune checkpoint inhibitor (ICI) related hypothyroidism was made. He was started on hormonal replacement with levothyroxine 50 mcg daily. Review of previous thyroid blood tests showed suppressed TSH since October 2016, but he was never treated. Thyroid peroxidase (TPO) antibodies were positive in the past. Thyroid sonogram in December 2016 showed a heterogeneous thyroid with no nodules. A radioactive scan in 1/2017 showed normal 24-hour uptake (12%) with no hot or cold nodules. (Fig 1). Since starting levothyroxine, the dose has been adjusted few times and patient has been doing well.

Conclusion
This is a unique case of patient with Graves’ disease who was cured because of immune related adverse event from use of immune-checkpoint inhibitor therapy.
Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
OR29-3 High-specific-activity Iodine 131 Metaiodobenzylguanidine for the Treatment of Advanced Pheochromocytoma and Paraganglioma: A Real-world Study
Authors: Al-ward Ruaa 
Published: November 2022

Abstract

Introduction
Metastatic pheochromocytomas/paragangliomas (mPPGLs) are rare tumors with limited treatment options. High-specific-activity 131I-meta-iodobenzylguanidine (HSA 131I-MIBG) is the only approved therapy for mPPGLs. We summarized the efficacy and safety profile of HSA 131I-MIBG in patients with mPPGL.

Methods
This is a retrospective cohort study in patients with mPPGL treated with HSA 131I-MIBG on label at a tertiary cancer center. The primary endpoint was radiographic treatment response determined with CT/MRI according to RECIST v1.1 and 123 I-MIBG scan. Secondary endpoints were blood pressure changes and HSA 131I-MIBG related adverse events. We correlated responses with the genetic background as an exploratory endpoint.

Results
Twenty-four patients were treated including 15 men (62%). Median age at the time of treatment was 44 years (range 18–82). Twenty-three patients had distant metastases and one patient had an unresectable primary tumor. Seventeen patients (70%) had hormonally active tumors and 17 patients (70%) were on antihypertensive medications before HSA 131I-MIBG therapy [7 patients on alpha-blockers only and 10 on combination antihypertensive therapy]. Thirteen patients (54%) previously received antineoplastic treatment. Eleven patients (46%) received one dose of HSA 131−I-MIBG, the remaining received two doses. Median duration of follow-up was 15 months (range 2–52). In 23 evaluable patients, radiographic responses included: 2 complete responses (CR), 10 partial responses (PR), 8 stable diseases (SD), 2 mixed responses (MR), and 1 progressive disease (PD) yielding disease control rate (DCR) of 87%. Median time to response was 12.5 months (95% CI, 4.6 to 25.1). Radiographic responses in patients with sporadic disease were [6/11 SD, 3/11 PR, 1/11 MR, 1/11 PR], while the response in patients with a genetic mutation (SDHB, VHL, RET) was [2/12 CR, 7/12 PR, 2/12 SD, 1/12 MR]. In 17 hormonally active tumors, plasma metanephrines normalized in 3(18%), improved by 50% in 5(29%), increased in 4(24%), 4 patients (24%) had no repeat levels and one had stable levels. Blood pressure was evaluable in 22 (92%) patients. Blood pressure normalized in 9 patients (41%) leading to discontinuation of antihypertensive therapy. One patient had an improvement in the blood pressure leading to a reduction of antihypertensive medications. The most common adverse events were grade I/II nausea/vomiting and transient bone marrow suppression. One patient developed premature ovarian failure. Grade III/IV myelosuppression was seen in 3/24 (12%) patients. One patient had fatal pneumonitis, and one patient developed fatal gastrointestinal bleeding a month after treatment with unclear attribution to HSA 131 −I-MIBG.

Conclusions
In mPPGL, HSA 131I-MIBG is associated with high DCR regardless of underlying genetic mutation. Severe adverse events are infrequent but can be fatal.
Presentation: Tuesday, June 14, 2022 10:15 a.m. - 10:30 a.m.
PSUN380 A Case of Sclerosing Epithelioid Fibrosarcoma With Metastases to the Thyroid
Authors: Bisquera Nichole Andrea , Villa Michael 
Published: November 2022

Abstract

Background
Sclerosing Epithelioid Fibrosarcoma (SEF) is a rare form of soft tissue sarcoma, often presenting in the soft tissues of the extremities. This tumor is characterized by slow growth, often with local recurrences and/or distant metastases. First described in 1995, subsequent case reports and case series have demonstrated that metastases are primarily to the lung, pleura and bone, but can occur anywhere. Treatment is primarily by wide excision and adjuvant chemotherapy or radiotherapy. However, treatment of this rare form of sarcoma is often unsatisfactory.

Clinical case
A 36-year-old female, had for 30 years presented with a slowly enlarging mass on the left axilla. She had no constitutional symptoms and had previously been in good health. She was first diagnosed with SEF when she presented with abdominal pain where workup showed elevated Lipase 8,098 U/L (73-393 U/L) and Amylase 976 U/L (25-115 U/L). CT scans showed an ill-defined hypodense focus in the body of the pancreas, with incidental findings of a mixed intensity ovoid lesion in the left erector spinae, and heterogeneously enhancing ovoid masses in the left axilla, left lateral chest wall, left lower lung lobe, and the liver. Biopsy of the left axillary mass showed a round cell sarcoma consistent with Sclerosing Epithelioid Fibrosarcoma. PET scan confirmed widespread metastases to the lungs, pancreas, abdominal wall, left thigh and scalp. She underwent wide excision of the masses in the left axilla, thigh, and scalp. Adjuvant chemotherapy with Doxorubicin and Ifosfamide was then initiated. 6 months after starting treatment, she reported a rapidly enlarging anterior neck mass. She denied tremors, palpitations, any change in weight, heat/cold intolerance, changes in bowel movement, fatigue or muscle weakness. On physical examination there was a 2×2 cm, firm, non-tender, palpable nodule on the right thyroid lobe. Thyroid function tests were as follows: TSH 0.52 uIU/mL (0.55-4.78 uIU/mL), FT4 1.27 ng/dL (0.89-1.76 ng/dL), FT3 2.84 pg/mL (2.30–4.20 pg/mL). On thyroid ultrasound there was a 2.6×1.8×2.4 cm, mixed hypoechoic, solid, lobulated nodule in the upper to middle third of the right thyroid lobe, and a 0.3×0.2×0.3 cm hypoechoic solid nodule in the lower third of the left thyroid lobe. FNAB showed hypercellular smears with atypical round to spindle-shaped cells arranged in singly and loose to crowded clusters. She underwent total thyroidectomy, and histopathologic examination was consistent with a multifocal metastatic Sclerosing Epithelioid Fibrosarcoma. She was subsequently started on Levothyroxine replacement.

Conclusion
This case, to our knowledge, is the first reported case of Sclerosing Epithelioid Fibrosarcoma (SEF) metastatic to the thyroid.
Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
PSUN245 Non-ketotic Hyperglycemic Hemichorea-Hemiballismus Precipitated by Antipsychotics
Authors: Elsherif Ahmed , Jun John 
Published: November 2022

Abstract

Background
Non-ketotic hyperglycemic hemichorea-hemiballimus is a rare complication of uncontrolled diabetes mellitus characterized by sudden, unilateral and involuntary flailing movements. It is associated with basal ganglia lesions contralateral to the side of involuntary movements. We present a case with this complication after the initiation of olanzapine.

Clinical Case
A 44-year-old male with anxiety, depression and diabetes mellitus type 2 with a recent increase of glycohemoglobin from 8.0 to 14.6% over 4 months presented with a 2-week history of worsening involuntary jerky movements of his right upper extremity, which eventually progressed to his right lower extremity. He was on metformin monotherapy for his diabetes initially. Olanzapine had been prescribed in place of quetiapine 2 months prior and then he presented to a different hospital with diabetic ketoacidosis a month later. Insulin therapy was initiated at that time and olanzapine was discontinued about 2 weeks prior to the current presentation. Physical examination showed spontaneous, irregular and involuntary flailing movements in his right upper and lower extremities that subsided during sleep. Laboratory tests revealed a random plasma glucose of 124 mg/dL and a glycohemoglobin of 14.6% but otherwise diagnostic studies including heavy metal screening, C-reactive protein, cerebrospinal fluid analysis and electroencephalogram were unremarkable. A CT of brain showed increased attenuation of the left lateral basal ganglia and caudate nucleus, and an MRI of brain showed increased T1 and T2 signal within the left lateral basal ganglia, and decreased T2 signal in the left caudate nucleus. Along with a consistent carbohydrate diet, a basal-bolus insulin regimen was initiated and adjusted to optimize glycemic control between 80 to 150 mg/dL. Clonazepam and Quetiapine were prescribed for his motor symptoms. Over the span of 3 months, his motor symptoms gradually improved, his insulin requirements decreased, and eventually excellent glycemic control was achieved with metformin alone.

Conclusion
This case highlights a unique presentation of hemichorea-hemiballismus as a rare complication of uncontrolled diabetes mellitus precipitated by olanzapine, an atypical antipsychotic with a higher risk of metabolic adverse effects.
Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
PSUN247 Unique Presentation of MODY Type 5
Authors: Bella Sama , Elhamdani Rawan , Benhamed Nesreen 
Published: November 2022

Abstract
A 46-year-old female with a past medical history significant for a blind vaginal birth defect that required vaginal reconstructive surgery with a partial hysterectomy at 15 years old and Type 2 Diabetes diagnosed at 44 years old. The patient was started on Sitagliptin, metformin 500 mg BID, and glimepiride 2 mg, but she remained poorly controlled with A1C 12.5%. Liver enzymes were elevated with the following values on the liver panel: AST 63 U/L Alt113 U/L bilirubin total 1.0 U/L direct bilirubin 0.3 U/L Alkaline phosphatase 642 U/L. Abdominal ultrasound and serology for chronic liver disease were unremarkable; enhanced MRI of the abdomen showed no abnormalities in the liver and pancreas. CT-guided liver biopsy was performed and pathology revealed diabetic hepatosclerosis. Ultimately, the patient was referred for endocrinology evaluation for poorly controlled diabetes mellites. Blood work was negative for GAD antibodies 65 and anti-pancreatic islet cell antibodies. C peptide level was within normal limits. The patient was not compliant with medications; her A1C continues to range between 11.5 and 8.5 so she was started on subcutaneous insulin.
A few years later, the patient presented to the ED for generalized weakness, anorexia, and unintentional weight loss of approximately 40 pounds with a BMI of 17 kg/m2. Bloodwork revealed glucose was 222 mg/dl, and glycated hemoglobin (A1C) was 15.4%, with no acute metabolic disorder (no ketosis). Biochemical analysis reported triglycerides of 174 mg/dL, total cholesterol of 280 mg/dL, HDL of 82 mg/dL, aspartate aminotransferase of 75 U/L, alanine aminotransferase of 117 U/L. alkaline phosphatases 190U/L, Potassium 3.1mEq/L, and magnesium 1.3mEq/L
Her electrolytes failed to correct despite adequate replacement; hence nephrology evaluation was warranted. As a result, 24h urine collection was obtained and revealed a Gitelman pattern with salt wasting, K+ wasting, Mg2+ wasting, and no calcinuria. This raised suspicion for MODY type 5. An enhanced MRI of the abdomen revealed her pancreas was missing the distal body and tail as well as bilateral cystic kidney disease. Genetic testing was pursued and demonstrated mutations in the hepatic nuclear factor 1B (HNF1B) gene which confirmed the MODY type 5 diagnosis.
The patient was discharged on 11 units of insulin degludec at bedtime in addition to insulin aspart 2 units TID; her A1c improved to 8.3% on her most recent follow-up.
Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
PSUN282 Sertraline-Induced Hypoglycemia in a Non-Diabetic Patient
Authors: Zahedpour Anaraki Sara , Vasudev Magaji 
Published: November 2022

Abstract

Background
Sertraline is one of selective serotonin reuptake inhibitors (SSRIs) commonly prescribed for depression. Irrespective of diabetes status, SSRIs can cause glycemic dysregulation.

Clinical Case
74-year-old man with depression was evaluated for hypoglycemia. His depression was managed with sertraline for more than 10 years. He did not have diabetes. Non fasting, laboratory studies done during annual evaluation showed blood glucose of 29 mg/dL but he didn't have any symptom of hunger, sweating, shaking or dizziness. Lab report was initially considered to be an error. Repeat blood glucose was 102 mg/dl. Subsequent labs done 6 months later also reported blood glucose of 27mg/dl. He suffered from a bicycle accident with head laceration in May 2021, his blood glucose on presentation to ED was 38 mg/dL). Follow up labs showed a fasting glucose 86 mg/dL, insulin level 4.2 IU/ml (1.9-23. 0 IU/ml), c-peptide 1.3 ng/ml (0.8-3.5 ng/ml), AM cortisol 22.6 mcg/dL (6.7-22.6 mcg/dl) and hemoglobin A1C 5.3%. Thyroid function test was normal. Sertraline was discontinued and he was on continuous glucose monitoring for 6 months during which there were no hypoglycemic episodes. The exact mechanism of sertraline-induced hypoglycemia remains unclear.
Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
PSUN296 Impact of Diabetes Mellitus on Outcomes of Hospitalizations for SIADH
Authors: Awoyomi Moyosoluwa , Ojemolon Pius , Shaka Hafeez , Koshbin Katayoun , Kwei-Nsoro Robert , Olafimihan Ayobami 
Published: November 2022

Abstract

Introduction
Diabetes mellitus (DM) is known to cause hyponatremia via multiple mechanisms and is often a confounder in the diagnosis of the syndrome of inappropriate anti-diuretic hormone secretion (SIADH). However, not much is known about the prevalence of DM in patients with SIADH or the effect it has on outcomes of hospitalizations for SIADH.
Method: Data was extracted from the US Nationwide Inpatient Sample (NIS) for 2019. The NIS contains hospital discharge information estimating yearly US hospitalizations. We included hospitalizations with a principal discharge diagnostic code for SIADH using the ICD-10-CM code (E22.2). We excluded hospitalizations of patients less than 18 years. This cohort was divided based on the secondary diagnosis of diabetes mellitus (DM).
We compared inpatient mortality rates, mean length of hospital stay (LOS), mean hospitalization cost (THC), and rates of septic shock, acute myocardial infarction (AMI), acute respiratory failure (ARF), acute renal failure (AKI), and acute pulmonary edema (PE) between the subgroups. Adjustments were made for age, sex, race, primary payer, median household income by zip code, Charlson Comorbidity Index (CCI), hospital location, bed-size, and teaching status using multivariate regression analysis. Statistical significance was set at a p-value &lt; 0.05.

Results
In 2019, there were 39,110 hospitalizations with SIADH as the reason for the admission. Comorbid DM was prevalent in 25.4% of these admissions. A higher proportion of hospitalizations involved females, with no significant difference between both cohorts (62.3 vs 60.1%, p=0.084). Patients with DM had a higher mean age (73.3±12 vs 72.4±13.8 years, p=0.005), a higher proportion of CCI &gt;2, and a higher proportion of ethnic minorities.
In patients with SIADH, DM was associated with no mortality difference (1.2% vs 0.9%, p=0.317) and no difference in LOS (4.9 vs 5.1 days, p=0.328) despite increased THC (10,873 vs 10,641 US$, p =0.03). Comorbid DM was associated with lower odds of AMI (0.4 vs 0.8%, aOR: 0.315, p=0.002), PE (0.15 vs 0.4%, aOR: 0.22, p=0.012) and ARF (6.8% vs 7.5%, aOR: 0.77, p=0.016), higher odds of AKI (15.9 vs 10.7, aOR: 1.23, p=0.008), with no significant difference in odds of septic shock or CVA.

Conclusions
Comorbid DM was associated with no difference in mortality or LOS despite an association with increased THC and AKI in hospitalizations of patients with SIADH. Notably, DM also appeared to lower the odds of AMI, PE, and ARF in this cohort of patients.
Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.
PSUN315 Elevated Serum B12 Levels are Associated with Diabetes
Authors: Anwaar Neelum , Chang Villacreses Maria M , Chiu Ken 
Published: November 2022

Abstract

Background
Vitamin B12 is an essential nutrient found in diverse food sources. Prokaryotic beings are capable of production through de novo aerobic and anaerobic biochemical reactions. It is common wisdom that diabetics, especially those receiving metformin, have vitamin B12 deficiency. However, little is known about the relationship between B12 levels and glucose tolerance.

Methods
A retrospective analysis of vitamin B12 levels and glucose tolerance in a representative U.S. population was performed. Records from the 2011-2014 National Health and Nutrition Examination Survey were reviewed. Individuals over the age of 20 were grouped according to a history of diabetes, Hb A1c levels, and fasting or 2-hour glucose tolerance test results into normal glucose (NG), abnormal glucose tolerance (AGT), and diabetes. A total of 19, 931 individuals were identified. Sample weighted analyses were performed with adjustment for the covariates of age, gender, body mass index, race/ethnicity, education, poverty index, current smoking, current alcohol consumption, family history of diabetes, vitamin B12 intake, and metformin use.

Results
Serum vitamin B12 levels were significantly higher among individuals with diabetes compared to those defined as AGT and NGT patients (496±14, 453±6, and 443±8 pmol/L, mean ± SE respectively, P=0.004). Diabetic individuals taking metformin had significantly lower serum vitamin B12 levels than diabetics not using metformin (445±16 vs. 518±13 pmol/L, P=0.0005). After exclusion of metformin users, diabetic subjects still had significantly higher serum vitamin B12 levels than NGT and AGT individuals (498±15, 456±6, and 445±8 pmol/L, respectively, P=0.006). The frequency of vitamin B12 supplement use was similar among diabetic, NGT, and AGT subjects (31%, 33%, and 31%, respectively, P=0.30). Likewise, the quantity of vitamin B12 supplementation was similar among the groups (233±34, 189±18, 192±24 mcg/day, respectively, P=0.50).

Summary
Retrospective analysis found higher serum B12 levels in diabetics compared to individuals with abnormal and normal glucose homeostasis. This novel finding was not secondary to exogenous B12 supplementation in diabetic individuals. Not unexpectedly, in individuals with diabetes, metformin exerted a negative effect on B12 levels. While the causes of elevated B12 in these individuals remain unknown, analysis of the intestinal bacterial flora and metabolome may be warranted.
Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.