In order to explore the distribution of hormone-responsive cells in skeletal tissues, we have examined the effects of synthetic bovine parathyroid hormone N-terminal peptide (bPTH 1-34) and salmon calcitonin (sCT) on cyclic AMP levels in periosteum-free rat calvaria, segments of periosteum, and in isolated cells dispersed from each tissue by collagenase digestion. Synthetic bovine PTH increased cyclic AMP levels to a greater degree in calvaria and in isolated bone cells than in the periosteal segments and cells, whereas sCT was more effective in the periosteal than in the bone systems. Primary cultures prepared from bone and periosteal cell populations exhibited progressive increases in their responsiveness to bPTH (1-34) and progressive decreases in responsiveness to sCT. After six days in the culture, bone cells failed to respond to sCT, and sCT did not modify their response simultaneously added bPTH (1-34). Six-day periosteal cell cultures exhibited residual sCT responsivity and an additive response upon simultaneous exposure to high concentrations of bPTH (1-34) and sCT suggesting separate sites of hormone action. Adenosine, a known stimulator of bone cell adenylyl cyclase, caused a greater increase in periosteal cell than in bone cell cyclic AMP. bPTH (1-34)-responsive cells which enrich periosteum-free bone may be osteoblasts, in view of their histological prominence in this tissue and in the bone cell isolates. Periosteal cells which responded to sCT and to adenosine preferentially are unidentified. Although periosteal segments contained numerous fibroblast-like cells, skin fibroblasts cultured from the same fetuses were sCT-insensitive. Growth in primary culture appears to alter the number of hormone-responsive cells or responsiveness of existing cells to each hormone, or both.

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Lithium treatment of humans and animals has been associated with adverse effects on bone and mineral metabolism. In order to determine whether lithium was altering the skeletal response to parathyroid hormone, we incubated bone rudiments for 5 days in the presence or absence of the drugs. Lithium had no effect on either parathyroid hormone-induced cyclic AMP generation or 45Ca release from the bone rudiments. The data are consistent with the hypothesis that the skeletal effects of lithium are not mediated via inhibition of the parathyroid hormone-adenyl cyclase-cyclic AMP system.

Adrenal incidentalomas are being increasingly found with the widespread use of thoracic and abdominal imaging. Clinicians must determine the nature of the mass to decide what treatment, if any, is needed. All patients should undergo biochemical testing to rule out hypercortisolism, pheochromocytoma and if hypertension is present, primary hyperaldosteronism. These patients should ideally be evaluated by endocrinologists as misdiagnosis can lead to complications. A 60-year-old African American female with a history of hypertension and type 2 diabetes, was admitted to the internal medicine ward with intractable vomiting, abdominal pain and hypotension. Two weeks prior to admission, she had undergone a left sided adrenalectomy for a diagnosis of primary hyperaldosteronism. An adrenal adenoma was incidentally found 1 year before surgery during abdominal imaging done for diverticulitis. She was immediately referred to a surgeon for further work up and evaluation. The work up done for the adrenal incidentaloma included renin, aldosterone and plasma fractionated metanephrines. Plasma renin was low (0.2 ng/mL/hr, n: 0.5-4.0 ng/mL/hr), and Aldosterone was normal (8.1 ng/dL, n<16 ng/dL) and the Aldosterone/ Renin ratio was elevated. No confirmatory test was done and no evaluation for hypercortisolism was done either. Plasma fractionated metanephrines were normal. During current hospitalization, an AM cortisol was 1.5 mcg/dL (n: 6-28 mcg/dL). An ACTH stimulation test was done which showed an inadequate response. She was subsequently started on stress dose steroids with rapid improvement in her symptoms. She was discharged with hydrocortisone and has been followed in our endocrinology clinic. She has yet to fully recover HPA axis but is currently on low dose Hydrocortisone and doing well. This patient was misdiagnosed with primary hyperaldosterenism when she most likely had subclinical hypercortisolism. Patients with primary hyperaldosteronism typically have plasma aldosterone > 15 ng/dL and low levels of plasma renin, with a ratio of plasma aldosterone to plasma renin activity > 20. Low levels of both plasma renin activity and aldosterone suggest nonaldosterone mineralocorticoid excess. Cushing syndrome can cause similar findings. Confirmatory tests should be done, and most patients require bilateral catheterization of the adrenal veins to measure cortisol and aldosterone levels to confirm whether the aldosterone excess is unilateral or bilateral. A 1 mg overnight dexamethasone suppression test is recommended for all adrenal incidentaloma patients to exclude asymptomatic hypercortisolism.

Celiac disease (CD) is an immune-mediated enteropathy caused by a reaction to gliadin which responds to a restriction to dietary gluten. It has been traditionally recognized in children and young adults, although, recently, detection in the elderly population has increased. CD occurs in 2–5% of patients with autoimmune hypothyroidism, and is more prevalent in this group than in the general population An 82-year-old Caucasian woman with primary hypothyroidism and a BMI of 16 is referred to our endocrinology clinic for help with the management of hypothyroidism. She had a history of well controlled hypothyroidism on weight-dosed levothyroxine for many years until several months prior when she developed sudden onset of diarrhea and weight loss. Since then, her thyroid function tests showed an elevated TSH despite medication adherence. Her levothyroxine dose was steadily increased to 300 mcg daily and yet, her TSH still remained elevated. Laboratory work up was done which revealed elevated transglutaminase antibodies, suggesting the diagnosis of CD. The patient refused an endoscopy for a tissue diagnosis. Even though the patient has been diagnosed with CD, she has trouble following a gluten free diet and still has intermittent diarrhea and high levothyroxine requirements. Although lack of medication adherence is common, it is important to exclude gastric or intestinal causes of malabsorption in patients with high thyroid replacement requirements. Elderly patients often have paucity of symptoms, so high clinical suspicion is necessary to diagnose these patients.

Background: Diabetic myonecrosis is a rare complication of diabetes mellitus with less than 200 cases reported in the literature since initial description in 19651. Diabetic myonecrosis most commonly affects the thigh and usually presents with acute muscle pain, edema, and erythema in the absence of trauma or fever1. The pathogenesis has yet to be elucidated—atherosclerosis, microangiopathy, vasculitis, and ischemia-reperfusion injury have been theorized. Laboratory findings are relatively nonspecific—of the findings reported in a systematic review, CRP was elevated in 90%, ESR elevated in 83.3%, WBC elevated in 42.5%, and CK elevated in 31.6%1. Definitive diagnosis can be made by muscle biopsy which demonstrates muscle necrosis and edema; however, it is not routinely recommended due to procedural complications. MRI is the diagnostic modality of choice for diabetic myonecrosis which is both sensitive and specific for the diagnosis2. Clinical Case: 76-year-old male with T2DM presented to regional hospital with severe right lower leg pain in the absence of fever, tachycardia, hypotension, or recent trauma. Physical exam demonstrated discrete erythema of distal 2/3 of posterior right lower leg extending to the ankle distally. Labs demonstrated normal CK, elevated ESR, HgbA1c 8.2%, and negative blood cultures. MRI of the right lower extremity demonstrated abnormal prolongation of T2 relaxation time involving posterior muscle compartment including soleus and gastrocnemius with associated perifacial and subcutaneous edema. These findings were consistent with diabetic myonecrosis without evidence of osteomyelitis or abscess. Rest, optimal glycemic control, and aspirin were recommended and patient improved gradually with complete clinical resolution on outpatient follow-up. Conclusions: Diabetic myonecrosis is a rare complication of diabetes and should be considered in patients presenting with acute muscle pain. Among cases described in literature, 5.7% have affected the soleus and 5% have affected the gastrocnemius respectively1. The diagnostic modality of choice is contrast enhanced MRI with typical findings including hyperintense signal on T2 weighted images with associated muscular, perifascial, and/or subcutaneous edema3. The optimal treatment is yet unknown, but reasonable strategies based on case series include rest, glycemic control, and NSAID therapy1. References: 1. Horton WB, Taylor JS, Ragland TJ, Subauste AR. Diabetic muscle infarction: a systematic review. BMJ Open Diabetes Res Care. 2015;3(1):e000082. doi:10.1136/bmjdrc-2015-000082 2. Morcuende JA, Dobbs MB, Crawford H, Buckwalter JA. Diabetic muscle infarction. Iowa Orthop J. 2000;20:65–74. 3. Goswami P, Baruah MP. The Role of MRI in Diagnosis of Diabetic Muscle Infarction : an Underdiagnosed Entity. Int J Endocrinol Metab. 2012;9(2):353–355. doi:10.5812/kowsar.1726913X.1886

Late dumping syndrome manifesting with hypoglycemia should be considered in the workup of patients with a history of gastric surgery and unusual postprandial symptoms. This case highlights the importance of an appropriate workup that can lead to avoidance of unnecessary testing in such patients.