TY - JOUR
AU - Chinnakotla, Bhavana
AB - Abstract Purpose The case of a transgender female who developed gallstone pancreatitis in the context of estrogen use for gender-affirming hormone therapy is reported. Summary A 24-year-old Caucasian transgender female presented to the emergency department for abdominal pain and vomiting after referral from urgent care for suspected pancreatitis. Her home medications included estradiol, medroxyprogesterone, and spironolactone for gender-affirming hormone therapy and omeprazole for reflux. The patient reported minimal alcohol intake, presented with mildly elevated triglyceride levels, and did not have a family history of pancreatitis or gallstone disease. She underwent a laparoscopic cholecystectomy on hospital day 4 and was given a postoperative diagnosis of chronic cholecystitis, cholelithiasis, and pancreatitis. Given her history and the present illness, the use of estrogen therapy is a likely risk factor for the development of gallstone pancreatitis. Conclusion Estrogen is a cornerstone of gender-affirming hormone therapy used by transgender women; however, in addition to its role in gender identity confirmation, estrogen can result in drug-induced pancreatitis. drug-induced diseases, gender-affirming hormone therapy, pancreatitis, pharmacy, surgery, transgender Key Points Use of gender-affirming hormone therapy in transgender females is not without risks of drug-induced disease. Systemic estrogen therapy is linked to pancreatitis and gallbladder disease, although specific mechanisms remain in question. Balancing the risks of drug-induced diseases from estrogens with the use of gender-affirming hormone therapy must be individualized. Estrogens are the mainstay of gender-affirming hormone therapy (GAHT) for transgender women (male to female), in which the goal in transgender women is to feminize the body’s appearance. While therapy goals are individualized to each patient, often there are 2 desired serum blood targets: estrogen levels of ≤200 pg/mL and testosterone levels of <49 ng/dL.1 When these targets are met, breast growth is induced and fat and muscle change to a composition consistent with a more feminine figure,1 while terminal hair growth (on the chin, cheeks, sternum, upper abdomen, and upper back), spontaneous erections, and penis size are reduced.1-3 While estrogens are the cornerstone of GAHT in transgender women, these medications come with risks. As with estrogen use for oral contraception, hormone replacement therapy, and embryo transfer during in vitro fertilization, transgender females on estrogen for GAHT are at an increased risk of venous thromboembolism events, certain hormonally mediated cancers, and adverse effects such as weight gain.4 An emerging risk of acute pancreatitis related to estrogen use is being documented. Reports of many cases in cisgender females and 3 previous cases in transgender females have shown that estrogen use can cause acute pancreatitis secondary to hypertriglyceridemia.5-7 There have also been reports of estrogen-induced pancreatitis in cisgender women with no concurrent hypertriglyceridemia.8 However, pancreatitis in the absence of hypertriglyceridemia as a result of estrogen use has not, to our knowledge, been documented before in transgender women. In this report, we discuss a case of estrogen-induced acute pancreatitis in a transgender female in the absence of hypertriglyceridemia. Case report The patient was a 24-year-old transgender Caucasian, non-Hispanic female who presented to the emergency department (ED) with complaints of abdominal pain and vomiting. She was previously seen at urgent care and was sent to the ED for further evaluation of pancreatitis. In the ED, the patient stated that the burning abdominal pain, rating a constant 7 out of 10 for pain, was present for 4 days before presentation. The pain worsened with positional changes. The patient was given a “GI cocktail” before discharge from urgent care. While in the ED, contrast-enhanced computed tomography (CT) of her abdomen/pelvis and an ultrasound of the abdomen were completed. Findings from these tests can be seen in Table 1. Upon admission, the patient stated that the pain had been sharp and intermittent, with radiation to her back when lying on her stomach. She reported bilious vomit but no blood in her stools or emesis. Further imaging indicated that her pancreas was mildly inflamed, likely owing to the gallstones and sludge seen on magnetic resonance imaging (MRI). General surgery was consulted to remove her gallbladder at the earliest opportunity, which occurred once her pain had decreased and her pancreatitis had resolved. This required waiting until hospital day 4. Table 1. Radiologic Imaging Findings Hospital Day . Diagnostic Test . Pertinent Findings . 0 CT of abdomen/pelvis with contrast The liver, spleen, gallbladder, pancreas, adrenal glands, and kidneys normal. Focal inflammation along the mesentery posterior to the descending colon, just below the splenic flexure. Small diverticulum present. Impressions: 1) Focal area of inflammation along the proximal descending colon consistent with a small focus of diverticulitis. No abscess formation identified. 2) Exam otherwise benign for age. 0 US of abdomen Limited evaluation of the pancreas unremarkable. No focal hepatic parenchymal lesion, although diffuse increase in echotexture present, most compatible with diffuse fatty infiltration. Stones and sludge within the gallbladder. 1 MRI of abdomen without contrast (MRCP) Cholelithiasis with sludge in the gallbladder lumen. No evidence from current study of choledocolithiasis or biliary obstruction. Minimal peripancreatic ascites along the pancreatic tail with normal pancreatic duct. Findings likely indicative of mild pancreatitis. Hospital Day . Diagnostic Test . Pertinent Findings . 0 CT of abdomen/pelvis with contrast The liver, spleen, gallbladder, pancreas, adrenal glands, and kidneys normal. Focal inflammation along the mesentery posterior to the descending colon, just below the splenic flexure. Small diverticulum present. Impressions: 1) Focal area of inflammation along the proximal descending colon consistent with a small focus of diverticulitis. No abscess formation identified. 2) Exam otherwise benign for age. 0 US of abdomen Limited evaluation of the pancreas unremarkable. No focal hepatic parenchymal lesion, although diffuse increase in echotexture present, most compatible with diffuse fatty infiltration. Stones and sludge within the gallbladder. 1 MRI of abdomen without contrast (MRCP) Cholelithiasis with sludge in the gallbladder lumen. No evidence from current study of choledocolithiasis or biliary obstruction. Minimal peripancreatic ascites along the pancreatic tail with normal pancreatic duct. Findings likely indicative of mild pancreatitis. Abbreviations: CT, computed tomography; MRCP, magnetic resonance cholangiopancreatography; MRI, magnetic resonance imaging; US, ultrasound. Open in new tab Table 1. Radiologic Imaging Findings Hospital Day . Diagnostic Test . Pertinent Findings . 0 CT of abdomen/pelvis with contrast The liver, spleen, gallbladder, pancreas, adrenal glands, and kidneys normal. Focal inflammation along the mesentery posterior to the descending colon, just below the splenic flexure. Small diverticulum present. Impressions: 1) Focal area of inflammation along the proximal descending colon consistent with a small focus of diverticulitis. No abscess formation identified. 2) Exam otherwise benign for age. 0 US of abdomen Limited evaluation of the pancreas unremarkable. No focal hepatic parenchymal lesion, although diffuse increase in echotexture present, most compatible with diffuse fatty infiltration. Stones and sludge within the gallbladder. 1 MRI of abdomen without contrast (MRCP) Cholelithiasis with sludge in the gallbladder lumen. No evidence from current study of choledocolithiasis or biliary obstruction. Minimal peripancreatic ascites along the pancreatic tail with normal pancreatic duct. Findings likely indicative of mild pancreatitis. Hospital Day . Diagnostic Test . Pertinent Findings . 0 CT of abdomen/pelvis with contrast The liver, spleen, gallbladder, pancreas, adrenal glands, and kidneys normal. Focal inflammation along the mesentery posterior to the descending colon, just below the splenic flexure. Small diverticulum present. Impressions: 1) Focal area of inflammation along the proximal descending colon consistent with a small focus of diverticulitis. No abscess formation identified. 2) Exam otherwise benign for age. 0 US of abdomen Limited evaluation of the pancreas unremarkable. No focal hepatic parenchymal lesion, although diffuse increase in echotexture present, most compatible with diffuse fatty infiltration. Stones and sludge within the gallbladder. 1 MRI of abdomen without contrast (MRCP) Cholelithiasis with sludge in the gallbladder lumen. No evidence from current study of choledocolithiasis or biliary obstruction. Minimal peripancreatic ascites along the pancreatic tail with normal pancreatic duct. Findings likely indicative of mild pancreatitis. Abbreviations: CT, computed tomography; MRCP, magnetic resonance cholangiopancreatography; MRI, magnetic resonance imaging; US, ultrasound. Open in new tab The patient’s social history included moderate alcohol intake of 3 to 4 drinks (of unknown size or substance) per week, no illicit drug use, and no tobacco use. There was no family history of known pancreatitis or hypertriglyceridemia. She reported that her past medical history included reflux, with no new medications. Her home medications included estradiol 4 mg by mouth daily, medroxyprogesterone 10 mg by mouth daily, omeprazole 40-mg delayed-release capsule by mouth once daily, and spironolactone 100 mg by mouth daily. The specific manufacturers of the medications she received as an outpatient are unknown. The patient’s pertinent laboratory data and a list of all medications administered during her admission are in Tables 2 and 3, respectively. The patient was taken to the operating room on hospital day 4, where she underwent laparoscopic cholecystectomy. She was given a postoperative diagnosis of chronic cholecystitis, cholelithiasis, and pancreatitis. She had no complications from the surgery, with minimal blood loss documented. She was taken from the operating room to the recovery area in stable condition and was discharged from the hospital to establish care with a new primary care provider, as she was new to the area. She continued her GAHT, having filled her estradiol and spironolactone prescriptions the month following her cholecystectomy. Before her surgery, the patient provided informed consent for this case report to be written. Table 2. Pertinent Laboratory Findings Laboratory Test . Presentation to the ED . Hospital Day 1 . Hospital Day 2 . Hospital Day 3 . Hospital Day 4 (Day of Surgery and Discharge) . Reference Rangea . Glucose, mg/dL 100 88 78 78 – 70-99 Sodium, mEq/L 135 133 135 135 – 135-145 Potassium, mEq/L 3.3 3.2 3.9 4.1 – 3.4-5.0 Chloride, mEq/L 102 102 106 106 – 95-110 CO2, mEq/L 21 22 18 20 – 20-30 Calcium, mg/dL 8.9 8.4 8.3 8.5 – 8.5-10.5 BUN, mg/dL 9 10 9 7 – 6-25 Creatinine, mg/dL 0.8 0.8 0.6 0.7 – 0.5-1.2 eGFR (non–African American), mL/min/1.73m2 >90 >90 >90 >90 – >60 Alkaline phosphatase, IU/L 160 143 126 111 107 30-120 ALT, IU/L 455 368 272 211 171 5-55 Lipase, IU/L 355 168 – 42 48 0-60 AST, IU/L 153 112 74 54 50 5-45 Bilirubin total, mg/dL 3.3 1.9 1.6 1.2 0.7 0.2-1.5 Bilirubin direct, mg/dL – – – 0.4 0.4 0.0-0.3 Bilirubin indirect, mg/dL – – – 0.8 0.3 0.1-1.4 Magnesium, mg/dL – 2.1 – – – 1.8-2.4 Total protein, g/dL 7.7 7.0 6.8 6.5 7.0 5.7-8.2 Albumin, g/dL 4.0 3.7 3.4 3.3 3.5 3.5-4.8 Globulin, g/dL – – – 3.2 3.5 2.0-3.6 Triglycerides, mg/dL – 159 – – – <149 White blood cells, /μL 12,300 12,900 11,600 – – 4,500-11,000 HGB, g/dL 13.2 12.5 – – – 13.5-17.5 HCT, % 39.1 37.2 – – – 41.0-53.0 Platelets, /μL 350,000 322,000 – – – 150,000-450,000 Urinalysis Positive for ketones (40), bilirubin (present), bile (0.5) – – – – COVID-19 PCR Negative – – – – Temperature, range, ºC 37.2 36.8-37.2 36.9-37.2 36.7-36.9 –c Pulse rate, range, bpm 84 69-72 78-99 69-75 –c Respiratory rate, range, rpm 220b 16 16 16 –c Blood pressure, mm Hg 126/84 112-114/ 63-78 119-128/ 77-79 99-125/ 59-76 –c MAP, mm Hg 98 80-89 92-95 –c Oxygen saturation, % 97 97-100 97-100 99 –c Oxygen delivery Room air Room air Room air Room air –c Height, cm 193.04 193.04 – – – Weight, pounds and ounces 293, 0 293, 3 – – – Weight, kg 133.18 133.27 – – – BMI, kg/m2 35.7 35.8 – – – Laboratory Test . Presentation to the ED . Hospital Day 1 . Hospital Day 2 . Hospital Day 3 . Hospital Day 4 (Day of Surgery and Discharge) . Reference Rangea . Glucose, mg/dL 100 88 78 78 – 70-99 Sodium, mEq/L 135 133 135 135 – 135-145 Potassium, mEq/L 3.3 3.2 3.9 4.1 – 3.4-5.0 Chloride, mEq/L 102 102 106 106 – 95-110 CO2, mEq/L 21 22 18 20 – 20-30 Calcium, mg/dL 8.9 8.4 8.3 8.5 – 8.5-10.5 BUN, mg/dL 9 10 9 7 – 6-25 Creatinine, mg/dL 0.8 0.8 0.6 0.7 – 0.5-1.2 eGFR (non–African American), mL/min/1.73m2 >90 >90 >90 >90 – >60 Alkaline phosphatase, IU/L 160 143 126 111 107 30-120 ALT, IU/L 455 368 272 211 171 5-55 Lipase, IU/L 355 168 – 42 48 0-60 AST, IU/L 153 112 74 54 50 5-45 Bilirubin total, mg/dL 3.3 1.9 1.6 1.2 0.7 0.2-1.5 Bilirubin direct, mg/dL – – – 0.4 0.4 0.0-0.3 Bilirubin indirect, mg/dL – – – 0.8 0.3 0.1-1.4 Magnesium, mg/dL – 2.1 – – – 1.8-2.4 Total protein, g/dL 7.7 7.0 6.8 6.5 7.0 5.7-8.2 Albumin, g/dL 4.0 3.7 3.4 3.3 3.5 3.5-4.8 Globulin, g/dL – – – 3.2 3.5 2.0-3.6 Triglycerides, mg/dL – 159 – – – <149 White blood cells, /μL 12,300 12,900 11,600 – – 4,500-11,000 HGB, g/dL 13.2 12.5 – – – 13.5-17.5 HCT, % 39.1 37.2 – – – 41.0-53.0 Platelets, /μL 350,000 322,000 – – – 150,000-450,000 Urinalysis Positive for ketones (40), bilirubin (present), bile (0.5) – – – – COVID-19 PCR Negative – – – – Temperature, range, ºC 37.2 36.8-37.2 36.9-37.2 36.7-36.9 –c Pulse rate, range, bpm 84 69-72 78-99 69-75 –c Respiratory rate, range, rpm 220b 16 16 16 –c Blood pressure, mm Hg 126/84 112-114/ 63-78 119-128/ 77-79 99-125/ 59-76 –c MAP, mm Hg 98 80-89 92-95 –c Oxygen saturation, % 97 97-100 97-100 99 –c Oxygen delivery Room air Room air Room air Room air –c Height, cm 193.04 193.04 – – – Weight, pounds and ounces 293, 0 293, 3 – – – Weight, kg 133.18 133.27 – – – BMI, kg/m2 35.7 35.8 – – – Abbreviations: ALT, alanine aminotransferase; AST, aspartate aminotransferase; BMI, body mass index; bpm, beat per minute; BUN, blood urea nitrogen; ED, emergency department; eGFR, estimated glomerular filtration rate; HGB, hemoglobin; HCT, hematocrit; MAP, mean arterial pressure; PCR, polymerase chain reaction; rpm, respirations per minute. aReference ranges are institution specific. bCharted in error cIntentionally excluded because of the volatility of anesthesia during the time in the operating room. Open in new tab Table 2. Pertinent Laboratory Findings Laboratory Test . Presentation to the ED . Hospital Day 1 . Hospital Day 2 . Hospital Day 3 . Hospital Day 4 (Day of Surgery and Discharge) . Reference Rangea . Glucose, mg/dL 100 88 78 78 – 70-99 Sodium, mEq/L 135 133 135 135 – 135-145 Potassium, mEq/L 3.3 3.2 3.9 4.1 – 3.4-5.0 Chloride, mEq/L 102 102 106 106 – 95-110 CO2, mEq/L 21 22 18 20 – 20-30 Calcium, mg/dL 8.9 8.4 8.3 8.5 – 8.5-10.5 BUN, mg/dL 9 10 9 7 – 6-25 Creatinine, mg/dL 0.8 0.8 0.6 0.7 – 0.5-1.2 eGFR (non–African American), mL/min/1.73m2 >90 >90 >90 >90 – >60 Alkaline phosphatase, IU/L 160 143 126 111 107 30-120 ALT, IU/L 455 368 272 211 171 5-55 Lipase, IU/L 355 168 – 42 48 0-60 AST, IU/L 153 112 74 54 50 5-45 Bilirubin total, mg/dL 3.3 1.9 1.6 1.2 0.7 0.2-1.5 Bilirubin direct, mg/dL – – – 0.4 0.4 0.0-0.3 Bilirubin indirect, mg/dL – – – 0.8 0.3 0.1-1.4 Magnesium, mg/dL – 2.1 – – – 1.8-2.4 Total protein, g/dL 7.7 7.0 6.8 6.5 7.0 5.7-8.2 Albumin, g/dL 4.0 3.7 3.4 3.3 3.5 3.5-4.8 Globulin, g/dL – – – 3.2 3.5 2.0-3.6 Triglycerides, mg/dL – 159 – – – <149 White blood cells, /μL 12,300 12,900 11,600 – – 4,500-11,000 HGB, g/dL 13.2 12.5 – – – 13.5-17.5 HCT, % 39.1 37.2 – – – 41.0-53.0 Platelets, /μL 350,000 322,000 – – – 150,000-450,000 Urinalysis Positive for ketones (40), bilirubin (present), bile (0.5) – – – – COVID-19 PCR Negative – – – – Temperature, range, ºC 37.2 36.8-37.2 36.9-37.2 36.7-36.9 –c Pulse rate, range, bpm 84 69-72 78-99 69-75 –c Respiratory rate, range, rpm 220b 16 16 16 –c Blood pressure, mm Hg 126/84 112-114/ 63-78 119-128/ 77-79 99-125/ 59-76 –c MAP, mm Hg 98 80-89 92-95 –c Oxygen saturation, % 97 97-100 97-100 99 –c Oxygen delivery Room air Room air Room air Room air –c Height, cm 193.04 193.04 – – – Weight, pounds and ounces 293, 0 293, 3 – – – Weight, kg 133.18 133.27 – – – BMI, kg/m2 35.7 35.8 – – – Laboratory Test . Presentation to the ED . Hospital Day 1 . Hospital Day 2 . Hospital Day 3 . Hospital Day 4 (Day of Surgery and Discharge) . Reference Rangea . Glucose, mg/dL 100 88 78 78 – 70-99 Sodium, mEq/L 135 133 135 135 – 135-145 Potassium, mEq/L 3.3 3.2 3.9 4.1 – 3.4-5.0 Chloride, mEq/L 102 102 106 106 – 95-110 CO2, mEq/L 21 22 18 20 – 20-30 Calcium, mg/dL 8.9 8.4 8.3 8.5 – 8.5-10.5 BUN, mg/dL 9 10 9 7 – 6-25 Creatinine, mg/dL 0.8 0.8 0.6 0.7 – 0.5-1.2 eGFR (non–African American), mL/min/1.73m2 >90 >90 >90 >90 – >60 Alkaline phosphatase, IU/L 160 143 126 111 107 30-120 ALT, IU/L 455 368 272 211 171 5-55 Lipase, IU/L 355 168 – 42 48 0-60 AST, IU/L 153 112 74 54 50 5-45 Bilirubin total, mg/dL 3.3 1.9 1.6 1.2 0.7 0.2-1.5 Bilirubin direct, mg/dL – – – 0.4 0.4 0.0-0.3 Bilirubin indirect, mg/dL – – – 0.8 0.3 0.1-1.4 Magnesium, mg/dL – 2.1 – – – 1.8-2.4 Total protein, g/dL 7.7 7.0 6.8 6.5 7.0 5.7-8.2 Albumin, g/dL 4.0 3.7 3.4 3.3 3.5 3.5-4.8 Globulin, g/dL – – – 3.2 3.5 2.0-3.6 Triglycerides, mg/dL – 159 – – – <149 White blood cells, /μL 12,300 12,900 11,600 – – 4,500-11,000 HGB, g/dL 13.2 12.5 – – – 13.5-17.5 HCT, % 39.1 37.2 – – – 41.0-53.0 Platelets, /μL 350,000 322,000 – – – 150,000-450,000 Urinalysis Positive for ketones (40), bilirubin (present), bile (0.5) – – – – COVID-19 PCR Negative – – – – Temperature, range, ºC 37.2 36.8-37.2 36.9-37.2 36.7-36.9 –c Pulse rate, range, bpm 84 69-72 78-99 69-75 –c Respiratory rate, range, rpm 220b 16 16 16 –c Blood pressure, mm Hg 126/84 112-114/ 63-78 119-128/ 77-79 99-125/ 59-76 –c MAP, mm Hg 98 80-89 92-95 –c Oxygen saturation, % 97 97-100 97-100 99 –c Oxygen delivery Room air Room air Room air Room air –c Height, cm 193.04 193.04 – – – Weight, pounds and ounces 293, 0 293, 3 – – – Weight, kg 133.18 133.27 – – – BMI, kg/m2 35.7 35.8 – – – Abbreviations: ALT, alanine aminotransferase; AST, aspartate aminotransferase; BMI, body mass index; bpm, beat per minute; BUN, blood urea nitrogen; ED, emergency department; eGFR, estimated glomerular filtration rate; HGB, hemoglobin; HCT, hematocrit; MAP, mean arterial pressure; PCR, polymerase chain reaction; rpm, respirations per minute. aReference ranges are institution specific. bCharted in error cIntentionally excluded because of the volatility of anesthesia during the time in the operating room. Open in new tab Table 3. Medications Administered During Hospitalization Medication, Dose, Route . Day of Admission . Hospital Day 1 . Hospital Day 2 . Hospital Day 3 . Hospital Day 4 (Day of Surgery and Discharge) . Scheduled medications Acetaminophen, 1,000 mg, oral 9:32 AM Ceftriaxone, 1 g, IVPB 9:50 PM Enoxaparin, 40 mg, subcutaneous 7:57 AM 7:56 AM Not given Not given Escitalopram, 5 mg, oral 2:04 PM Not given 5:28 PM Gabapentin, 600 mg, oral 9:32 AM Hydromorphone, 0.25 mg, IVP 11:42 AM Iopamidol, 150 mL, IVP 8:49 PM Levofloxacin, 750 mg, IVPB 1:57 AM 7:02 AM 6:32 AM 6:19 AM Medroxyprogesterone, 10 mg, oral 5:27 PM Metronidazole, 500 mg, IVPB 9:50 PM 4:06 AM, 2:25 PM, 8:55 PM 7:02 AM, 2:08 PM, 9:33 PM 4:57 AM, 1:14 PM, 8:12 PM 5:13 AM, 12:05 PM Midazolam, 1 mg, IVP 9:50 AM Morphine, 4 mg, IVP 9:50 PM Pantoprazole, 40 mg, IVP 7:57 AM 7:56 AM 7:30 AM 7:39 AM Sodium chloride 0.9%, 1,000 mL, intravenous 8:08 PM PRN medications Acetaminophen/hydrocodone (325 mg/5 mg), oral 1 tab 2:08 PM, 1 tab 9:33 PM 2 tabs 7:30 AM, 2 tabs 7:51 PM 2 tabs 12:05 PM, 2 tabs 5:27 PM Fentanyl, 25 μg, IVP (PACU order) 10:55 AM, 11:00 AM, 11:05 AM, 11:10 AM, 11:15 AM, 11:21 AM, 11:26 AM, 11:31 AM, 11:36 AM, 11:41 AM Lorazepam, 0.5 mg, IVP 11:15 AM 2:15 PM Lorazepam, 1 mg, IVP 5:27 PM Morphine, 2 mg, IVP 1:58 AM, 7:57 AM, 2:25 PM, 8:55 PM 4:50 AM, 7:56 AM Ondansetron, 4 mg, IVP 12:05 PM Continuous infusions Lactated Ringers, 1,000 mL, intravenous 8:50 AM Potassium chloride 40 mEq + sodium chloride 0.9%, 1,000 mL, intravenous 1:57 AM, 4:48 PM Medication, Dose, Route . Day of Admission . Hospital Day 1 . Hospital Day 2 . Hospital Day 3 . Hospital Day 4 (Day of Surgery and Discharge) . Scheduled medications Acetaminophen, 1,000 mg, oral 9:32 AM Ceftriaxone, 1 g, IVPB 9:50 PM Enoxaparin, 40 mg, subcutaneous 7:57 AM 7:56 AM Not given Not given Escitalopram, 5 mg, oral 2:04 PM Not given 5:28 PM Gabapentin, 600 mg, oral 9:32 AM Hydromorphone, 0.25 mg, IVP 11:42 AM Iopamidol, 150 mL, IVP 8:49 PM Levofloxacin, 750 mg, IVPB 1:57 AM 7:02 AM 6:32 AM 6:19 AM Medroxyprogesterone, 10 mg, oral 5:27 PM Metronidazole, 500 mg, IVPB 9:50 PM 4:06 AM, 2:25 PM, 8:55 PM 7:02 AM, 2:08 PM, 9:33 PM 4:57 AM, 1:14 PM, 8:12 PM 5:13 AM, 12:05 PM Midazolam, 1 mg, IVP 9:50 AM Morphine, 4 mg, IVP 9:50 PM Pantoprazole, 40 mg, IVP 7:57 AM 7:56 AM 7:30 AM 7:39 AM Sodium chloride 0.9%, 1,000 mL, intravenous 8:08 PM PRN medications Acetaminophen/hydrocodone (325 mg/5 mg), oral 1 tab 2:08 PM, 1 tab 9:33 PM 2 tabs 7:30 AM, 2 tabs 7:51 PM 2 tabs 12:05 PM, 2 tabs 5:27 PM Fentanyl, 25 μg, IVP (PACU order) 10:55 AM, 11:00 AM, 11:05 AM, 11:10 AM, 11:15 AM, 11:21 AM, 11:26 AM, 11:31 AM, 11:36 AM, 11:41 AM Lorazepam, 0.5 mg, IVP 11:15 AM 2:15 PM Lorazepam, 1 mg, IVP 5:27 PM Morphine, 2 mg, IVP 1:58 AM, 7:57 AM, 2:25 PM, 8:55 PM 4:50 AM, 7:56 AM Ondansetron, 4 mg, IVP 12:05 PM Continuous infusions Lactated Ringers, 1,000 mL, intravenous 8:50 AM Potassium chloride 40 mEq + sodium chloride 0.9%, 1,000 mL, intravenous 1:57 AM, 4:48 PM Abbreviations: IVP, intravenous push; IVPB, intravenous piggyback; PACU, postanesthesia care unit; PRN, as-needed. Open in new tab Table 3. Medications Administered During Hospitalization Medication, Dose, Route . Day of Admission . Hospital Day 1 . Hospital Day 2 . Hospital Day 3 . Hospital Day 4 (Day of Surgery and Discharge) . Scheduled medications Acetaminophen, 1,000 mg, oral 9:32 AM Ceftriaxone, 1 g, IVPB 9:50 PM Enoxaparin, 40 mg, subcutaneous 7:57 AM 7:56 AM Not given Not given Escitalopram, 5 mg, oral 2:04 PM Not given 5:28 PM Gabapentin, 600 mg, oral 9:32 AM Hydromorphone, 0.25 mg, IVP 11:42 AM Iopamidol, 150 mL, IVP 8:49 PM Levofloxacin, 750 mg, IVPB 1:57 AM 7:02 AM 6:32 AM 6:19 AM Medroxyprogesterone, 10 mg, oral 5:27 PM Metronidazole, 500 mg, IVPB 9:50 PM 4:06 AM, 2:25 PM, 8:55 PM 7:02 AM, 2:08 PM, 9:33 PM 4:57 AM, 1:14 PM, 8:12 PM 5:13 AM, 12:05 PM Midazolam, 1 mg, IVP 9:50 AM Morphine, 4 mg, IVP 9:50 PM Pantoprazole, 40 mg, IVP 7:57 AM 7:56 AM 7:30 AM 7:39 AM Sodium chloride 0.9%, 1,000 mL, intravenous 8:08 PM PRN medications Acetaminophen/hydrocodone (325 mg/5 mg), oral 1 tab 2:08 PM, 1 tab 9:33 PM 2 tabs 7:30 AM, 2 tabs 7:51 PM 2 tabs 12:05 PM, 2 tabs 5:27 PM Fentanyl, 25 μg, IVP (PACU order) 10:55 AM, 11:00 AM, 11:05 AM, 11:10 AM, 11:15 AM, 11:21 AM, 11:26 AM, 11:31 AM, 11:36 AM, 11:41 AM Lorazepam, 0.5 mg, IVP 11:15 AM 2:15 PM Lorazepam, 1 mg, IVP 5:27 PM Morphine, 2 mg, IVP 1:58 AM, 7:57 AM, 2:25 PM, 8:55 PM 4:50 AM, 7:56 AM Ondansetron, 4 mg, IVP 12:05 PM Continuous infusions Lactated Ringers, 1,000 mL, intravenous 8:50 AM Potassium chloride 40 mEq + sodium chloride 0.9%, 1,000 mL, intravenous 1:57 AM, 4:48 PM Medication, Dose, Route . Day of Admission . Hospital Day 1 . Hospital Day 2 . Hospital Day 3 . Hospital Day 4 (Day of Surgery and Discharge) . Scheduled medications Acetaminophen, 1,000 mg, oral 9:32 AM Ceftriaxone, 1 g, IVPB 9:50 PM Enoxaparin, 40 mg, subcutaneous 7:57 AM 7:56 AM Not given Not given Escitalopram, 5 mg, oral 2:04 PM Not given 5:28 PM Gabapentin, 600 mg, oral 9:32 AM Hydromorphone, 0.25 mg, IVP 11:42 AM Iopamidol, 150 mL, IVP 8:49 PM Levofloxacin, 750 mg, IVPB 1:57 AM 7:02 AM 6:32 AM 6:19 AM Medroxyprogesterone, 10 mg, oral 5:27 PM Metronidazole, 500 mg, IVPB 9:50 PM 4:06 AM, 2:25 PM, 8:55 PM 7:02 AM, 2:08 PM, 9:33 PM 4:57 AM, 1:14 PM, 8:12 PM 5:13 AM, 12:05 PM Midazolam, 1 mg, IVP 9:50 AM Morphine, 4 mg, IVP 9:50 PM Pantoprazole, 40 mg, IVP 7:57 AM 7:56 AM 7:30 AM 7:39 AM Sodium chloride 0.9%, 1,000 mL, intravenous 8:08 PM PRN medications Acetaminophen/hydrocodone (325 mg/5 mg), oral 1 tab 2:08 PM, 1 tab 9:33 PM 2 tabs 7:30 AM, 2 tabs 7:51 PM 2 tabs 12:05 PM, 2 tabs 5:27 PM Fentanyl, 25 μg, IVP (PACU order) 10:55 AM, 11:00 AM, 11:05 AM, 11:10 AM, 11:15 AM, 11:21 AM, 11:26 AM, 11:31 AM, 11:36 AM, 11:41 AM Lorazepam, 0.5 mg, IVP 11:15 AM 2:15 PM Lorazepam, 1 mg, IVP 5:27 PM Morphine, 2 mg, IVP 1:58 AM, 7:57 AM, 2:25 PM, 8:55 PM 4:50 AM, 7:56 AM Ondansetron, 4 mg, IVP 12:05 PM Continuous infusions Lactated Ringers, 1,000 mL, intravenous 8:50 AM Potassium chloride 40 mEq + sodium chloride 0.9%, 1,000 mL, intravenous 1:57 AM, 4:48 PM Abbreviations: IVP, intravenous push; IVPB, intravenous piggyback; PACU, postanesthesia care unit; PRN, as-needed. Open in new tab The patient had a follow-up by telephone call with the surgery clinic 10 days after her surgery, owing to the prevalence of coronavirus disease 2019 (COVID-19) and the practices of the clinic at that time. She was doing well at follow-up, and no further surgical intervention or follow-up was indicated at that time. Discussion Systemic estrogens, in general, have been linked to pancreatitis in postmenopausal women using hormone replacement therapy.8 There are several proposed mechanisms for pancreatitis caused by estrogens; one of the best documented is pancreatitis secondary to hypertriglyceridemia. Increases in estrogen levels, such as during pregnancy, can decrease lipoprotein lipase activity, which in turn increases levels of very-low-density lipoprotein.9 When levels of very-low-density lipoprotein increase, serum chylomicron and triglyceride levels increase.9 As free fatty acids and chylomicrons increase in abundance, plasma viscosity is suspected to increase, leading to pancreatitis.9 In cases where triglyceride levels are greater than 1,000 mg/dL, pancreatic acinar cells can be injured and capillaries may plug, contributing to the development of pancreatitis.5 The first case report of a transgender woman with estrogen-induced pancreatitis described no history of alcohol use or evidence of gallstone disease but documented a marked increase in triglyceride levels at 5,174 mg/dL.5 This case enforced the link between estrogen use and pancreatitis in transgender women, whereas this link had only previously been documented in cisgender women. In the second and third published case reports of transgender females with pancreatitis, the patients had triglyceride levels of 2,073 mg/dL and greater than 7,000 mg/dL, respectively.6,7 Continuation of GAHT in these cases was mixed. In the first case, the patient was recommended to stop GAHT, but it is not known whether this recommendation was followed.5 It is also not known whether the patient continued therapy in the second case, but in the third case the patient was reported to not seek further treatment for transition therapy.6,7 In our patient’s case, she adamantly wished to continue GAHT upon discharge. Knowledge of the link between estrogens and pancreatitis should be weighed against the psychosocial benefits of GAHT for transgender women, and this link should continue to be evaluated on an individual basis.10 On the basis of these previous case reports, hypertriglyceridemia appears to be the most plausible link between estrogens and pancreatitis. While there is a strong link between the triglyceride-elevating properties of estrogens and pancreatitis, there are indications that other mechanisms exist, including gallstone disease8,11,12 and microlithiasis (ie, biliary sludge).13 Gallstones are a mechanism by which estrogen can cause acute pancreatitis in the absence of hypertriglyceridemia, and the link between estrogen and gallstone development is known in menopausal cisgender women and is dose dependent.12 Estrogens are also known to increase risk of gallbladder disease by increasing hepatic secretion of biliary cholesterol 11,12; this promotion of gallstone formation may be the mediator of estrogen-induced pancreatitis.8 While gallstones are mostly composed of cholesterol, other risk factors remain for gallstone development, such as female sex at birth.11 Cisgender females are approximately 2 to 3 times more likely to develop gallstones than cisgender males, and this link is due to sex hormones.11 Higher doses of estrogen, similar to those used by our patient, are likely the culprit, as a link with low-dose estrogens in oral contraceptives is absent.11 Gallstone pancreatitis is caused by blockage of the common bile duct at the ampulla of Vater, which promotes retrograde flow of pancreatic enzymes into the pancreas where they accumulate and irritate the pancreatic tissue, rather than allowing normal transit of the enzymes into the duodenum.14 However, these instances may still not explain all mechanisms of estrogen-induced pancreatitis, as there is one case report of a cisgender woman on estrogen for menopausal hormone replacement over 7 years with recurrent acute pancreatitis despite normal levels of plasma lipids and no evidence of gallstones.15 Obesity has been shown to cause an increase in cholesterol turnover that is related to total body fat.16 As cholesterol spills into the bile, causing a higher abundance of cholesterol relative to bile acids (supersaturation)17 and phospholipids, the likelihood of precipitation and gallstone formation increases.16 In this case report, the patient also had a body mass index (BMI) of <36, which could be another risk factor for gallstone development. The patient’s weight and classification as obese (BMI cutoff of 35.7) have been linked to an increased risk of pancreatitis and gallstone formation.17-19 Obesity is also a known risk factor for cholesterol gallstone development17,19 and adverse effects on the pancreas20, although our patient’s gallstones did not undergo diagnostic pathology to determine their origin. The pathology report indicated that the patient’s gallstones were a dark green color, suggesting that the stone composition included bile, rather than these being pure cholesterol gallstones.19 Our case lacked some of the classic risk factors for acute pancreatitis, with triglyceride levels within normal limits and alcohol intake that was not excessive. The patient also did not have a family history of either pancreatitis or gallstone disease. Instead, her high doses of estrogen (4 mg daily) and the presence of gallstones possibly suggest an estrogen-induced mechanism for acute pancreatitis. In the Naranjo assessment (Table 4), the patient scored a 4, showing that gallstone pancreatitis could possibly be explained by her estrogen use. This low score is primarily due to many unknown factors, such as adverse event reappearance when reinitiating the medication, adverse event occurrence with a placebo, and whether the event would be less severe with a lower dose. These are unknowns because (1) the patient’s gallbladder has been removed, thus removing her ability to develop gallstones within the gallbladder; (2) provision of placebo GAHT to a transgender woman is unethical and would be apparent when the expected results were not achieved; and (3) doses of agents within GAHT are specifically targeted to and individualized for patients. As it was not necessary to treat this patient’s gallstone pancreatitis, the patient’s plasma concentrations of estrogen were not determined; it is therefore not known whether they were significantly higher than the target of ≤200 pg/mL.1 However, these “unknowns” could be an area for further study on the topic of estrogens and pancreatitis. Table 4. Naranjo Assessment Question . Yes . No . Do Not Know . Patient’s Scorea . 1. Are there previous conclusive reports on this reaction? +1 0 0 +1 2. Did the adverse reaction appear after the suspected drug was administered? +2 –1 0 +2 3. Did the adverse reaction improve when the drug was discontinued or a specific antagonist was administered? +1 0 0 +1 4. Did the adverse event reappear when the drug was readministered? +2 –1 0 0 5. Are there alternative causes (other than a drug) that could on their own have caused the reaction? –1 +2 0 –1 6. Did the reaction appear when a placebo was given? –1 +1 0 0 7. Was the drug detected in the blood (or other fluids) in concentrations known to be toxic? +1 0 0 0 8. Was the reaction more severe when the dose was increased or less severe when the dose was decreased? +1 0 0 0 9. Did the patient have a similar reaction to the same or similar drugs in any previous exposure? +1 0 0 0 10. Was the adverse event confirmed by any objective evidence? +1 0 0 +1 Total +4a Question . Yes . No . Do Not Know . Patient’s Scorea . 1. Are there previous conclusive reports on this reaction? +1 0 0 +1 2. Did the adverse reaction appear after the suspected drug was administered? +2 –1 0 +2 3. Did the adverse reaction improve when the drug was discontinued or a specific antagonist was administered? +1 0 0 +1 4. Did the adverse event reappear when the drug was readministered? +2 –1 0 0 5. Are there alternative causes (other than a drug) that could on their own have caused the reaction? –1 +2 0 –1 6. Did the reaction appear when a placebo was given? –1 +1 0 0 7. Was the drug detected in the blood (or other fluids) in concentrations known to be toxic? +1 0 0 0 8. Was the reaction more severe when the dose was increased or less severe when the dose was decreased? +1 0 0 0 9. Did the patient have a similar reaction to the same or similar drugs in any previous exposure? +1 0 0 0 10. Was the adverse event confirmed by any objective evidence? +1 0 0 +1 Total +4a aScore interpretations: ≤0, doubtful; 1 to 4, possible; 5 to 8, probable; ≥9, definite. Open in new tab Table 4. Naranjo Assessment Question . Yes . No . Do Not Know . Patient’s Scorea . 1. Are there previous conclusive reports on this reaction? +1 0 0 +1 2. Did the adverse reaction appear after the suspected drug was administered? +2 –1 0 +2 3. Did the adverse reaction improve when the drug was discontinued or a specific antagonist was administered? +1 0 0 +1 4. Did the adverse event reappear when the drug was readministered? +2 –1 0 0 5. Are there alternative causes (other than a drug) that could on their own have caused the reaction? –1 +2 0 –1 6. Did the reaction appear when a placebo was given? –1 +1 0 0 7. Was the drug detected in the blood (or other fluids) in concentrations known to be toxic? +1 0 0 0 8. Was the reaction more severe when the dose was increased or less severe when the dose was decreased? +1 0 0 0 9. Did the patient have a similar reaction to the same or similar drugs in any previous exposure? +1 0 0 0 10. Was the adverse event confirmed by any objective evidence? +1 0 0 +1 Total +4a Question . Yes . No . Do Not Know . Patient’s Scorea . 1. Are there previous conclusive reports on this reaction? +1 0 0 +1 2. Did the adverse reaction appear after the suspected drug was administered? +2 –1 0 +2 3. Did the adverse reaction improve when the drug was discontinued or a specific antagonist was administered? +1 0 0 +1 4. Did the adverse event reappear when the drug was readministered? +2 –1 0 0 5. Are there alternative causes (other than a drug) that could on their own have caused the reaction? –1 +2 0 –1 6. Did the reaction appear when a placebo was given? –1 +1 0 0 7. Was the drug detected in the blood (or other fluids) in concentrations known to be toxic? +1 0 0 0 8. Was the reaction more severe when the dose was increased or less severe when the dose was decreased? +1 0 0 0 9. Did the patient have a similar reaction to the same or similar drugs in any previous exposure? +1 0 0 0 10. Was the adverse event confirmed by any objective evidence? +1 0 0 +1 Total +4a aScore interpretations: ≤0, doubtful; 1 to 4, possible; 5 to 8, probable; ≥9, definite. Open in new tab Guidelines for transgender health care recommend routine monitoring of sex hormone levels, cardiovascular risk screening, such as with a lipid panel, and monitoring for diabetes in patients using GAHT.21 These recommendations indicate that the potential effects of estrogens in the transgender population are known and should be closely monitored. The Endocrine Society21 also recommends that transgender females receiving GAHT be evaluated every 3 months in the first year of therapy and 1 to 2 times per year thereafter, to monitor for both signs of feminization and adverse reactions to therapy. Serum testosterone and estradiol levels should be measured every 3 months to ensure that the goal levels of <50 ng/dL testosterone and 100 to 200 pg/mL estradiol are met.21 Additionally, periodic monitoring of prolactin levels in transgender females is recommended, as well as bone mineral density screening, especially in those who stop GAHT after gonadectomy.21 The University of California San Francisco (UCSF) guidelines for transgender care22 have similar recommendations on estrogen and testosterone levels (monitoring every 3 months until goal concentrations are reached and yearly or as needed thereafter) but specifically state that lipids have “no evidence to support monitoring at any time; use clinical discretion based on USPSTF [US Preventive Services Task Force] guidelines.” On the basis of growing data, at a minimum, transgender females with significant risk factors such as high doses of estrogens, obesity, familial history of hyperlipidemia/hypertriglyceridemia, and familial history of gallstone disease should have routine lipid monitoring as well as evaluation at baseline. Conclusion Several mechanisms have been proposed in relation to estrogen use and the development of pancreatitis, including pancreatitis secondary to hypertriglyceridemia, gallstones, and microlithiasis. Obesity must also be considered as a potential mechanism. Transgender medicine is still evolving, and, as patients explore the benefits of GAHT, providers must become familiar with the potential adverse effects of high doses of estrogen therapy. Emerging case reports linking estrogen therapy to pancreatitis in transgender women must be scrutinized, especially as multiple mechanisms appear to contribute. In this case, the transgender woman experienced symptomatic cholelithiasis in addition to pancreatitis, which we propose was caused by estrogen use. GAHT provides transgender women confidence and satisfaction as gender-associated anxiety and stress improve.10 Providers have the responsibility to ensure that patients are aware of the risks of estrogen therapy, such as pancreatitis, and the symptoms to watch for. Most transgender women choose to proceed with therapy after weighing the risks. However, with the paucity of documented scientific evidence, there are more opportunities to research the correlation between exogenous estrogen use and pancreatitis. Inclusion of individuals using GAHT into prospective or retrospective trials will further the medical community’s understanding of this correlation, although this research aim must be fully explained and flushed out to avoid any individual feeling targeted or at risk of losing access to GAHT. Acknowledgments The authors would like to thank and recognize the patient for her contribution to the medical evidence on GAHT and drug-induced diseases. Disclosures The authors have declared no potential conflicts of interest. References 1. Safer JD , Tangpricha V. Care of the transgender patient . Ann Intern Med . 2019 ; 171 ( 1 ): ITC1 - ITC16 . Google Scholar Crossref Search ADS PubMed WorldCat 2. Randolph JF . Gender-affirming hormone therapy for transgender females . Clin Obstet Gynecol . 2018 ; 61 ( 4 ): 705 - 721 . Google Scholar Crossref Search ADS PubMed WorldCat 3. Cunha FS , Domenice S, Sircili MHP, et al. Low estrogen doses normalize testosterone and estradiol levels to the female range in transgender women . Clinics (Sao Paulo) . 2018 ; 73 . Google Scholar OpenURL Placeholder Text WorldCat 4. Tangpricha V , Heijer MD. Oestrogen and anti-androgen therapy for transgender women . Lancet Diabetes Endocrinol . 2017 ; 5 ( 4 ): 291 - 300 . Google Scholar Crossref Search ADS PubMed WorldCat 5. Perego E , Scaini A, Romano F, et al. Estrogen-induced severe acute pancreatitis in a male . JOP . 2004 ; 5 ( 5 ): 353 - 356 . Google Scholar PubMed OpenURL Placeholder Text WorldCat 6. Goodwin N , Nolan N, Chinnakotla B. Estrogen-induced pancreatitis: transgender females at risk . Am J Hosp Med. Published online October 2018 . doi:10.24150/ajhm/2018.023 Google Scholar OpenURL Placeholder Text WorldCat 7. Shipley LC , Steele DT, Wilcox CM, Burski CM. A rare cause of acute pancreatitis in a transgender female . J Investig Med High Impact Case Rep . 2020 ; 8 : 2324709620921333 . Google Scholar PubMed OpenURL Placeholder Text WorldCat 8. Jones MR , Hall OM, Kaye AM, Kay AD. Drug-induced acute pancreatitis: a review . Ochsner J . 2015 ; 15 ( 1 ): 45 - 51 . Google Scholar PubMed OpenURL Placeholder Text WorldCat 9. De Pretis N , Amodio A, Frulloni L. Hypertriglyceridemic pancreatitis: epidemiology, pathophysiology and clinical management . United European Gastroenterol J . 2018 ; 6 ( 5 ): 649 - 655 . Google Scholar Crossref Search ADS PubMed WorldCat 10. Nguyen HB , Chavez AM, Lipner E, et al. Gender-affirming hormone use in transgender individuals: impact on behavioral health and cognition . Curr Psychiatry Rep. 2018 ; 20 ( 12 ): 110 . Google Scholar Crossref Search ADS PubMed WorldCat 11. Novacek G . Gender and gallstone disease . Wien Med Wochenschr. 2006 ; 156 : 527 - 533 . Google Scholar Crossref Search ADS PubMed WorldCat 12. Simonsen MH , Erichsen R, Froslev T, et al. Postmenopausal estrogen therapy and risk of gallstone disease: a population-based case-control study . Drug Saf . 2013 ; 36 ( 12 ): 1189 - 1197 . Google Scholar Crossref Search ADS PubMed WorldCat 13. Lee SP , Nicholls JF, Park HZ. Biliary sludge as a cause of acute pancreatitis . N Engl J Med . 1992 ; 326 ( 9 ): 589 - 593 . Google Scholar Crossref Search ADS PubMed WorldCat 14. Wang GJ , Gao CF, Wei D, et al. Acute pancreatitis: etiology and common pathogenesis . World J Gastroenterol . 2009 ; 15 ( 12 ): 1427 - 1430 . Google Scholar Crossref Search ADS PubMed WorldCat 15. Blake WE , Pitcher ME. Estrogen-related pancreatitis in the setting of normal plasma lipids: case report . Menopause . 2003 ; 10 ( 1 ): 99 - 101 . Google Scholar PubMed OpenURL Placeholder Text WorldCat 16. Bray GA . Medical consequences of obesity . J Clin Endocinol Metab. 2004 ; 89 ( 6 ): 2583 - 2589 . Google Scholar Crossref Search ADS WorldCat 17. Bonfrate L , Wang DQH, Garruti G, Portincasa P. Obesity and the risk and prognosis of gallstone disease and pancreatitis . Best Pract Res Clin Gastroenterol. 2014 ; 28 ( 4 ): 623 - 635 . doi:10.1016/j.bpg.2014.07.013 Google Scholar Crossref Search ADS PubMed WorldCat 18. Khatua B , El-Kurdi B, Singh VP. Obesity and pancreatitis . Curr Opin Gastroenterol. 2017 ; 33 ( 5 ): 374 - 382 . Google Scholar Crossref Search ADS PubMed WorldCat 19. Lammert F , Gurusamy K, Ko CW, et al. Gallstones . Nat Rev Dis Primers. 2016 ; 2 : 16024 . doi:10.1038/nrdp.2016.24 Google Scholar Crossref Search ADS PubMed WorldCat 20. Cruz-Monserrate Z , Conwell DL, Krishna SG. The impact of obesity on gallstone disease, acute pancreatitis, and pancreatic cancer . Gastroenterol Clin North Am. 2016 ; 45 ( 4 ): 625 - 637 . Google Scholar Crossref Search ADS PubMed WorldCat 21. Hembree WC , Cohen-Kettenis PT, Gooren L, et al. Endocrine treatment of gender-dysphoric/gender-incongruent persons: an Endocrine Society clinical practice guideline . J Clin Endocrinol Metab. 2017 ; 102 ( 11 ): 3869 - 3903 . Google Scholar Crossref Search ADS PubMed WorldCat 22. UCSF Transgender Care, Department of Family and Community Medicine, University of California San Francisco . Guidelines for the Primary and Gender-Affirming Care of Transgender and Gender Nonbinary People. 2nd ed. Published June 2016 . Accessed November 4, 2020. http://transcare.ucsf.edu/guidelines Google Scholar Google Preview OpenURL Placeholder Text WorldCat COPAC © American Society of Health-System Pharmacists 2021. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)
TI - Estrogen-induced gallstone pancreatitis in a transgender female
JF - American Journal of Health-System Pharmacy
DO - 10.1093/ajhp/zxab190
DA - 2021-05-05
UR - https://www.deepdyve.com/lp/oxford-university-press/estrogen-induced-gallstone-pancreatitis-in-a-transgender-female-uodSB6VyTf
SP - 1
EP - 1
VL - Advance Article
IS - 
DP - DeepDyve
ER -