Category Archives: Endocrinology and Metabolism

SFPC Ambulatory Report 2.21.18 – Funky Tongue and Secondary Amenorrhea

We had a mini case of Glossitis and Xerostoma.  Here are the key learning points:

  • Nutritional deficiencies that result in atrophic glossitis: B2, B6, and B12
  • Grace brought us back to our days of Step studying reminded us aboutPlummer-Vinson syndrome.  It is a rare disease that results in iron deficiency anemia, glossitis, esophageal webs.

    The goal of treating xerostomia is to alleviate symptoms and prevent complications such as dental caries, candidiasis, halitosis includes prevention: 1)hydration, avoid oral dessicants, avoid meds with anticholinergic side effects, and reduce mouth breathing; 2) treatment with sugar free gum or lozenges, artificial saliva, high strength fluoride toothpaste


Grace presented a great case of young woman with secondary amenorrhea likely due to stress.

  • Approach to amenorrhea
    • Step 1: Pregnant or not
    • Step 2: Primary vs. secondary – did the patient ever experience menses
    • Anatomic Approach to Secondary Amenorrhea – the HPO-axis
      • Hypothalamus
        • Hypothalamic hypogonadism
          • Functional: stress, excessive exercise, weight loss
          • Injury: infarct, tumor, infection
          • Systemic Illness
        • Hypothyroidism
        • Cushings
      • Pituitary
        • Increased prolactin
          • Prolactinoma
          • Breastfeeding
          • Meds such as antipsychotics
        • Injury: infarct, tumor, infection
      • Ovarian
        • Premature ovarian failure (can be due to chemo, radiation, autoimmune, adrenal insufficiency)
        • Menopause
        • PCOS
      • GU Structural Causes
        • Asherman’s syndrome
        • Cervical Stenosis
  • Check out an old blog post by Rabih for the hormone based approach to secondary amenorrhea.
  • What does the Progestin withdrawal bleeding test tell us?
    • If the patient bleeds after a progestin withdrawal challenge it signifies she is making estrogen but is anovulatory
    • If the patient does not bleed it means there are low estrogen levels or obstruction in the GU tract
  •  Functional Hypothalamic Hypogonadism
    • Due to decreased caloric intake, increased caloric expenditure due to excessive exercise, and stress
      • In the setting of stress high levels of cortisol and corticotroponin releasing hormone inhibit GnRH production
    • Is the cause of 25-35% of secondary amenorrhea

Evernote link:


Moffitt Pearls 2/9/18 – DKA and NSTEMI

Thank you to Katie Sullivan for presenting the case of an elderly woman with history of type 1 diabetes and CAD s/p CABG presenting after colonoscopy with severe nausea/vomiting and diarrhea. The patient was found to be in DKA likely 2/2 to an NSTEMI with EKG changes suggestive of ischemia and a troponin of 25!

Key Pearls

  • Complications after colonoscopy are rare (approximately 3 per 1000 screening colonoscopies) and include complications of sedation, complications related to the preparation, bleeding, and perforation.
  • Never forget that Ischemia – acute MI – can precipitate DKA!! See the rest of the “I’s” below brought to you by our wonderful interns Noa and Hayley.
  • Any patient with ACS regardless of intervention (stent or no stent) should be treated with DAPT for 12 months b/c of improved cardiovascular outcome. Bleeding risk needs to be balanced against benefits and shorter durations are sometimes used. (See graph from the study)
  • Troponin elevation in the setting on non-ACS related demand is associated with worse f/u cardiac mortality in both low and high risk patients. In one study incidence of cardiovascular death or heart failure after adjusting for conventional risk factors (hazard ratio 1.84, 95% CI 1.30-2.61) [1].
  • Patient with the flu are at a much higher risk of ACS during and in the week after illness. A recent Canadian study in the NEJM showed that MI admissions were 6x more likely to occur in the week after a positive flu test!!

Remember the I’s for causes of DKA reviewed!!

  • Infection
  • Ischemia
  • Infant/pregnancy
  • Ingestion/intoxication
  • In-adherence to medications
  • Iatrogenic
  • (I)Other: hypercortisol and sympathetic surge

CURE trial



  1. Prognostic value of cardiac troponin I measured with a highly sensitive assay in patients with stable coronary artery disease. Omland T, Pfeffer MA, Solomon SD, de Lemos JA, RøsjøH,ŠaltytėBenth J, Maggioni A, Domanski MJ, Rouleau JL, Sabatine MS, Braunwald E, PEACE Investigators. J Am Coll Cardiol. 2013 Mar;61(12):1240-9. Epub 2013 Feb 13.

VA Ambulatory Report 9.13.17 – Vitiligo, Hashimoto’s, and Pernicious Anemia

Thank you to Rabih for presenting this interested case of a young man presenting to clinic with fatigue, weight gain, hypopigmented skin lesions found to have pernicious anemia, hashimoto’s and possible vitiligo.

Key Learning Points

  • For skin hypopigmentation try to determine if there is complete depigmentation vs. hypopigmentation to narrow your differential
  • Decision to treat subclinical hypothyroidism is based on level of TSH elevation, age, CV risk factors, and symptoms
  • Consider pernicious anemia as a cause of B12 deficiency especially in patients with other autoimmune diseases


Hypopigmentation of the skin

  • First try to determine if it is complete depigmentation or hypopigmentation.  This can be difficult especially in lighter skin individuals.
    • Degpimentation
      • Vitiligo – most frequent cause of depigmentation
        • Loss of epidermal melanocytes
        • Etiology not known, but associated with autoimmune diseases
        • No racial or ethnic propensity but often causing more impact on darker skin individuals due to is being more disfiguring
      • Consider exposures to chemicals (such as those found in hair dyes, insecticides, adhesives) or meds (topical steroids, imatinib, pegylated interferon)
    • Hypopigmentation
      • Commonly seen after an inflammatory skin process
      • Infections – pityriasis versicolor, leprosy, syphilis, non-syphilis treponema, onchocerciasis
      • Atopic – pityriasis alba
      • Rheumatologic causes – scleroderma, discoid lupus
      • Acquired
        • idiopathic guttate hypomelanosis – seen with aging
        • progressive macular hypomelanosis – unknown cause, possibly related to infection, typically seen in young adults, more common in darker skin individuals
      • Nutritional deficiencies – B12, copper, iron, kwashiorkor
      • Endocrinopathies – hypopituitarism, Cushing syndrome,


Subclinical Hypothyroidism

  • Definition: Elevated TSH with Normal T4
    • Always recheck after 2-3 months given these are numbers are dynamic to confirm subclinical hypothyroidism
  • When should we treat subclinical hypothyroidism? Based on TSH level, age, symptoms, TPO antibody status, and CV risk factors
    • TSH >10
      • Treat all patients <70
      • For patients >70 only treat if symptoms are present or have +TPO antibody
    • TSH 7-10
      • If symptoms are present
      • If patient is <70 and has cardiac risk factors or has +TPO
        • Patients who are younger and have +TPO antibodies are more likely to progress to overt hypothyroidism
    • TSH 4-7 AND
      • Symptoms of hypothyroidism: consider 6 month trial of treatment but stop therapy is symptoms do not improve with treatment
  • See this discussion in NEJM for more review of subclinical hypothyroidism
  • Recent study in NEJM showed no benefit to treating subclinical hypothyroidism in adult s> 65 years


Pernicious Anemia Fun Facts

  • What is pernicious anemia? Anemia due to autoimmune atrophic gastritis.
    • Autoanitbodies to intrinsic factor and parietal cells –> Loss of parietal cell mass –> hypochlorhydria and inadequate production of intrinsic factor –> B12 malabsorption –> anemia
  • It is called pernicious anemia because when it was described patients symptoms would progress gradually over time without available treatment
  • Diagnosis
    • Macrocytic anemia, low B12
    • Autoantibodies to parietal cells and intrinsic factor
      • Antibodies to IF are specific but not sensitive
      • Antibodies to parietal cells have better sensitivity, but only ~80%
      • If high enough concern and negative antibodies, may need EGD with biopsy demonstrating atrophic gastritis in the gastric body
    • Can also check serum gastrin which will be elevated
  • 40% of patients will have autoimmune thyroid disease
  • There is a theory that H. pylori infection may trigger the autoimmune destruction of parietal cells. However patients with pernicious anemia are less likely than age matched controls to have h. pylori. Associated with H. pylori infection thought possibly due to active infection gradually replaced by an autoimmune process
  • Increased risk of gastric neuroendocrine tumors and adenocarcinoma

SFPC Ambulatory Report 7.13.17 Post-pancreatectomy diabetes

Thanks to Alicia for presenting a challenging management case of a patient with ESRD s/p transplant and traumatic pancreatectomy resulting in brittle diabetes.
Learning Pearls
  • Post-pancreatectomy considerations
    • Reasons people lose pancreatic function
      • Diseases: CF, chronic pancreatitis
      • Surgical resection due to malignancy, trauma, chronic pancreatitis
    • Endocrine replacement
      • Insulin: Patients should be treated similar to those with Type 1 Diabetes
      • Patients also lose their endogenous glucagon production
    • Exocrine replacement
      • Pancreatic enzymes
      • Vitamin supplementation: Should also supplement with the fat soluble vitamins (Vitamins A, D, E, K) due to fat malabsorption
  • Insulin pump Criteria
    • American Association of Clinical Endocrinologist recommendations for the Ideal candidates in adult patients:
      • DM type 1 or DM type 2 who is insulin dependent and intensively managed
      • Performing >= 4 insulin injections and >=4 glucose checks daily
      • Motivated
      • Willing and able to carry out the necessary tasks to manage the pump
      • Willing to maintain frequent contact with the healthcare team
        • Multidisciplinary team follow-up including pump trainer, educator, and endocrinologist
        • Monthly specialist f/u until on stable regimen
  • Islet cell/pancreas transplant
    • Can isolate islet cells from a resected pancreas or transplant full pancreas
    • ~30% of patients are insulin free after islet cell transplant.  Success depends on the mass and quantity of islet cells transplanted
    • Require lifelong immunosuppression therefore you will need to balance the risk of immunosuppressive medications with the benefits
    • ADA criteria for transplant:
      • Patients with ESRD who have had or will have a kidney transplant.  Most often perform simultaneous pancreas-kidney transplant
      • Patients without renal disease who have a history of severe metabolic complications from DM and consistent failure of insulin therapy to prevent acute complications
  • New Onset Diabetes after Transplant (NODAT)
    • Incidence is not known due to varying study methodology
    • Risk factors
      • Patient factors: Older age, obesity, African American race, hispanic ethnicity, family hx of DM, hx of gestational DM
      • Transplant factors: Meds (steroids, calcineurin inhibitors, mTOR inhibitors)
      • Other: HCV, preoperative hyperglycemia, hypomagnesemia
    • All patients should have post-op glucose checks weekly for first four weeks, then at 3 and 6 months and then yearly. A1c should be checked 3 months post-op

Evernote link to Ambulatory Report Pearls:

MOFFITT ENDOCRINE REPORT PEARLS 5/17/17: Hypercalcemia of Malignancy and PTHrP!

Hey Everyone! Thanks to Vaibhav for presenting the case of an older woman with newly diagnosed bladder cancer who presented with weight loss and failure to thrive, found to have severe hypercalcemia with workup pending. We suspected she might have PTHrP-mediated hypercalcemia, a known association with urothelial carcinomas. Pearls on PTHrP below!


Top Pearls:

  1. PTHrP is the most common cause of hypercalcemia in non-metastatic solid tumors
  2. PTHrP-related hypercalcemia is typically a finding in advanced disease with poor prognosis
  3. PTHrP acts primarily on bone and kidneys to cause hypercalcemia, not the GI tract


For those who want more info:

Check out Myung’s pearls on hypercalcemia:

*Important general pearls on hypercalcemia of malignancy: 1) It occurs in 10-30% of patients with advanced tumors. 2) It is the most common cause of hypercalcemia in the inpatient setting. 3) Prognosis is poor (up to 50% 30-day mortality).

Now some more specific info on PTHrP!

What is PTHrP?

  • Normal gene product expressed in several tissues
  • Also called humoral hypercalcemia of malignancy (HHM)
  • The most common cause of hypercalcemia in patients with non-metastatic solid tumors
  • Most often in patients with advanced disease and poor prognosis (not usually an early finding)
  • Solid tumor associations: SCC, renal/bladder, breast, ovarian
  • Liquid tumor associations: NHL, CML (blast phase), T-cell leukemia/lymphoma

How is PTHrP related to PTH?

  • First 13 N-terminal amino acids are homologous to PTH (PTH = 84 AAs, PTHrP =139-173 AAs)
  • Binds to same PTH-1 receptor as PTH: bone resorption, renal Ca reabsorption/phos wasting
  • Structural divergence after first 13 amino acids: less likely to stimulate 1,25 vit D production, does not increase intestinal Ca absorption
  • Thus, PTHrP hyperCa is from bone/renal only, while PTH hyperCa is also from GI
  • Lab findings in PTHrP hyperCa: 1) elevated PTHrP, 2) low PTH, 3) normal/low 1,25-vit D

How is measurement of PTHrP useful (aside from diagnosis)?

  • Tumor marker: helps to assess treatment response
  • Prognostic marker: worse survival if PTHrP level > 12 pmol/L, which predicts less robust response of hyperCa to bisphosphonate therapy

HyperCa Malignancy



Have a great day everyone!


Moffitt Endocrinology Report 4/19/17: Hypophysitis and Cavitary Lung Nodules

Hello Everyone!

Thank you Chloe, for presenting the case of a young woman with a history of granulomatous hypophysitis who presented with fevers and cavitary lung lesions. We discussed various entities on the ddx, including ANCA-vasculitis and lymphomatoid granulomatosis! Best,



  • Hypophysitis (or pituitary inflammation) is most frequently associated with ACTH and TSH deficiency.
  • Check out the paper on cavitary lung nodules: PMID18400799


Approach to Hypophysitis  (Inflammation of Pituitary)

  • Hypophysitis is often classified by histologic findings: lymphocytic, granulomatous, plasmacytic, and xanthomatous
  • Clinical manifestations : headache out of proportion to size of lesion, hypopituitarism : preferential hypofunction of ACTH and TSH-secreting cells have been described, but DI, hyperprolactinemia, GH excess, and autoimmune thyroiditis can also occur.
  • Eventually, progressive pituitary atrophy can occur with fibrosis.
Lymphocytic Hypophysitis Most common form; often occurs in late pregnancy or post-partum period
Granulomatous Hypophysitis Majority are idiopathic, but known causative entities include GPA and TB
Plasmacytic (IgG4-associated) Hypophysitis Often associated with infiltration of other organs, such as the pancreas
Xanthomatous Most rare, characterized by foamy histiocytes


Approach to Cavitary Lung Lesions


    • Bacteria
      • Common bacterial infections: septic pulmonary emboli, necrotizing pneumonias, lung abscess
      • Uncommon bacterial infections: actino, nocardia
    • Mycobacteria: TB and NTB
    • Fungal: aspergillosis, zygomycosis, histo, blasto, cocci, paracocci, crypto, PCP
    • Parasites: echinococcus, paragonimiasis


    • Rheum: vasculitis
    • Malignancy
    • Other: PE with infarct, bullae/cysts, pulmonary sequestration


Evernote Link:

MOFFITT AM REPORT PEARLS 3/29/17: Eosinophilia and Hypertriglyceridemia!

Hey everyone! Thanks to Evan for presenting an interesting conundrum of a young woman with abdominal symptoms who was found to have eosinophilia. We touched on a few different topics including creating a differential diagnosis for GI symptoms with eosinophilia, as well as some manifestations of hypertriglyceridemia. Pearls below!


Top Pearls:

  1. The ddx for eosinophilia and GI symptoms includes parasites, vasculitis, eosinophilic GI disease, malignancy, IBD, and primary/idiopathic hypereosinophilic syndromes.
  2. Apheresis is often indicated for triglyceride-induced acute pancreatitis. Insulin drip is 2nd line treatment.


For those who want more info:

See prior pearls below on eosinophilia definitions, ddx, and workup:

In addition, we constructed a differential for eosinophilia with GI symptoms:

  • Parasites: Strongyloides most common
  • Vasculitis: EGPA and PAN
  • Eosinophilic GI disease: esophagitis, gastroenteritis, colitis
  • Malignancy: GI lymphoma, gastric cancer, colon cancer
  • IBD: Crohn disease is a rare cause of eosinophilia
  • Primary and idiopathic hypereosinophilic syndromes: may rarely have GI symptoms


Some interesting points about hypertriglyceridemia:

Remember severe hypertriglyceridemia (TG>500) as a cause of acute pancreatitis! The risk really goes up when TG>1000.

Many patients with triglyceride-induced acute pancreatitis benefit from apheresis! If apheresis is not possible, insulin drip is recommended (with D5 infusion as needed to prevent hypoglycemia).

Hypertriglyceridemia can be caused by primary inherited disorders or by common conditions such as DM2, alcohol, hypothyroidism, pregnancy, obesity, nephrotic syndrome, renal failure, multiple myeloma, lupus, or medications. (See table below)

*HH Pearl: Hypertriglyceridemia can cause eruptive xanthomata involving tendons!




Have a great day everyone!