Anthracosis is an environmental lung disease caused by carbon deposition and pigmentation in the airways. However, in rare instances, it can also have systemic involvement. We present a patient with B-symptoms and diffuse lymphadenopathy who was diagnosed with the infrequently described nodal anthracosis. A 64year-old Vietnamese gentleman with a 50-pack-year smoking history who was recently diagnosed with prostate cancer post-radical prostatectomy and awaiting radiation therapy presented with generalized weakness, low-grade fever, night sweats, and unquantifiable weight loss for a month. He was hemodynamically stable, and examination revealed bilateral inguinal and axillary lymphadenopathy. Computed tomography (CT) showed diffuse lymphadenopathy involving the mediastinum, hilar, axillary, mesenteric, retroperitoneal, and bilateral iliac chains with multiple diffuse pulmonary nodules. Laboratories disclosed anemia, thrombocytopenia, elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), albumin-globulin (A-G) reversal, and sterile blood cultures. The disseminated intravascular coagulation panel was negative with normal fibrinogen and mildly elevated D-dimer. Autoimmune workup, including antinuclear antibody (ANA), was negative. Infectious workup included Babesia, Ehrlichia, Anaplasma, Lyme serology, QuantiFERON-TB Gold, HIV, and hepatitis panel, and all were negative. He was managed with broad-spectrum antibiotics, which were discontinued after a negative infectious workup. He also complained of a new-onset holocranial headache with no features of meningitis; an MRI with contrast revealed focal occipital leptomeningeal involvement and cerebral edema with occipital lymphadenopathy. A lumbar puncture was planned but deferred at the patient's request. An excisional lymph node biopsy of the left axillary lymph node revealed reactive follicular hyperplasia with no evidence of malignancy, with flow cytometry negative for any evidence of B-or T-cell malignancies. He continued to have persistent low-grade fevers. A bone marrow biopsy showed 70% cellularity with paratrabecular interstitial lymphoid aggregates composed of both T and B cells, which was nonspecific, and flow cytometry could not be done due to dry tap. An F-18-fluorodeoxyglucose positron emission tomography (FDG PET) scan showed extensive hypermetabolic disease both above and below the diaphragm with bulky mediastinal adenopathy and splenomegaly. Subsequently, he underwent a mediastinoscopy and biopsy of the mediastinal lymph nodes, which demonstrated reactive hyperplasia and abundant anthracitic pigment on microscopic examination, consistent with the diagnosis of nodal anthracosis. He was managed conservatively, discharged, and found to have spontaneously resolved symptoms at a six-week follow-up. Nodal anthracosis with PET-positive mediastinal and hilar lymphadenopathy is a rare presentation of anthracosis that mimics infectious conditions, granulomatous diseases, and malignancies. The pigment deposition can cause persistent inflammatory...

No abstract

Discussion: Atrioventricular reciprocating tachycardia (AVRT) is a type of Supraventricular tachycardia (SVT) caused by an accessory pathway can result in symptomatic and also life-threatening arrhythmias. Supraventricular tachycardias are less commonly seen in hypothyroidism than hyperthyroidism. We present a case of a 41 year old gentleman who presented with chest pain and SVT was found to have severe hypothyroidism with pre-excitation pattern on his EKG. Case: 41-year-old Caucasian gentleman with history of untreated Hashimoto’s thyroiditis presented with palpitations and acute onset left-sided chest pain. His symptoms were aggravated with movement and improved with rest. When EMS found him, his vitals were significant for tachycardia with a heart rate (HR) of 200 beats per minute (bpm). EKG showed supraventricular tachycardia. Vagal maneuvers were attempted followed by adenosine. This resulted in conversion to sinus rhythm and improvement in HR to 88 bpm. His chest pain completely resolved. He was then brought to the emergency room where he had normal vitals. Examination revealed thyroid gland was palpable and noted to be diffusely enlarged. Laboratory data was significant for an elevated thyroid-stimulating hormone (TSH) of 373 mIU/ml and undetectable free thyroxine (fT4) levels. His creatinine kinase (CK) was high at 16260, and troponin was elevated at 0.220 ng/ml (reference:<0.04 ng/ml). TPO antibodies were >600 IU/ml. EKG demonstrated sinus rhythm with pre-excitation and incomplete left bundle-branch block. He had normal chest x-ray. An echocardiogram showed an ejection fraction of 55% with mild LV diastolic dysfunction. He later underwent a stress myocardial perfusion scan which showed no definite evidence of inducible ischemia. Follow up: He was started on thyroxine replacement therapy. He is due for an EP study to evaluate for an accessory pathway causing pre-excitation with repolarization pattern on his ECG. Conclusion: This case suggests that severe hypothyroidism can also cause supraventricular tachycardias (SVT) by metabolic and conduction derangements revealing concealed bypass tracts in patients with accessory pathways. In most cases these arrhythmias are reversible once the underlying thyroid disorder is treated.