Differentiating between adenoid cystic carcinoma (AdCC) and polymorphous adenocarcinoma (PAC) can be difficult on small biopsies and cytologic specimens. As such, further characterization of their immunophenotype may aid in distinction. Previous studies have found AdCC to be SOX10+/GATA3 variable and PAC to be GATA3 negative. SOX10 expression in PAC has, as yet, not been established. We performed GATA3 and SOX10 immunohistochemistry on whole sections of 25 cases each of AdCC and PAC (including both classic PAC and the cribriform variant) to assess whether these markers are of diagnostic utility in distinguishing between these entities. SOX10 was found to be positive in 100% of PAC and AdCC whereas GATA 3 was immunoreactive in 45% of AdCCs and 20% of PAC. While this is the first series to compare SOX10 and GATA3 staining in these two tumor types, their frequent expression and similar staining patterns render them of limited value in discriminating between these neoplasms.
Primary amyloidosis (PA) is a protein deposition disorder that presents with localized or multisystemic disease. The incidence is low in the general public, ranging from three to eight cases per million, and with nonspecific presenting symptoms typically occurring later in life. Due to late presentation, substantial and irreversible damage has usually already occurred by the time of the diagnosis. However, if inadvertent diagnosis occurs before irreversible damage has taken place, as it did in the following case, some patients may benefit from the disease-arresting treatment. A 70-year-old female with a history of obstructive sleep apnea, hypertension, and arthritis presented with worsening dysphagia and biochemically confirmed primary hyperparathyroidism (PHPT). Further workup demonstrated multinodular goiter with compressive symptoms and substernal extension, osteopenia, and discrepant parathyroid localization on imaging. Intraoperatively, markedly difficult dissection and obliteration of tissue planes were encountered. Extensive, diffuse amyloid deposition in both the normal and pathologic parathyroid glands and thyroid tissue on surgical pathology leads to subsequent fibril typing by mass spectrometry and leads to the diagnostic of primary amyloid light-chain (AL) amyloidosis (PA; λ light chains). Subsequent workup for the underlying cause of the amyloid deposition revealed an immunoglobulin A monoclonal gammopathy of unknown significance. The surgical treatment of PHPT and compressive thyroid nodule unmasked an undiagnosed PA, allowing for early workup and monitoring of the progression of amyloidosis. The temporal comorbidity of PHPT and PA raises an interesting and, as yet, unanswered question regarding the pathophysiologic association between the two conditions.
INTRODUCTION: Eosinophilic myocarditis (EM) is a rare myocardial inflammation that can be potentially fatal if left untreated [1]. The causes of eosinophilia that underlie EM include parasitic infections, drug hypersensitivity, systemic vasculitis and idiopathic hypereosinophilic syndrome (HES) [3]. The present case report describes a biopsy-proven EM with a presentation of acute congestive heart failure. CASE PRESENTATION: The patient is a 68-year old man with history of HTN, asthma, paroxysmal atrial fibrillation (PAF), combined systolic and diastolic congestive heart failure (CHF) with left ventricular EF of w50% four weeks prior to admission. He presented with ataxia, proximal muscle weakness, and dyspnea. He denied any fevers, chills, night sweats, paroxysmal nocturnal dyspnea, orthopnea, and chest pain. MRI brain confirmed ischemic stroke. The patient reported missing some doses of dabigatran for his PAF. TTE showed a decrease in left ventricular EF to 25% with global hypokinesis. His initial lab work was notable for an elevated troponin of 28 ng/mL, BNP of 3041 pg/mL, and markedly elevated eosinophils of 20.46x10^3/mm3. TEE showed no thrombus but did show moderate plaque of the aorta. CT abdomen, chest and pelvis was unremarkable. Cardiac catheterization showed non obstructive coronary disease with very poor LV function consistent with acute onset CHF. Cardiac MRI showed patchy mid-myocardial scarring suggestive of a myopathic process. Bone marrow biopsy was deferred for later as patient was on anticoagulation. Endomyocardial biopsy (EMB) confirmed eosinophilic myocarditis (Figure A, Figure B, Figure C). There was no evidence of granulomas, multinucleated giant cells, parasites or vasculitis on biopsy. FISH revealed no evidence of PDGFR, FGFR1, or BCR-ABL1 rearrangement. He was started on high-dose oral steroids and discharged on a slow taper.
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