Abstract. Sarcoidosis is a rare autoimmune disease resulting in formation of non-necrotizing “non-caseating” granulomas generally in the lung. The disease classically strikes African American females in their fourth and fifth decades. The resulting hypercalcemia is a result of 1-α hydroxylase overexpression in granulomas with increased 1,25-dihydroxy vitamin D levels. This phenomenon can also be observed in mycobacterial and fungal infections that produce granulomas in infected patients. Thus, chronic infectious diseases are part of differential diagnosis of granulomatous processes. We present an elderly Caucasian female who presented with hypercalcemia with serum calcium of 11 – 14 mg/dL and an elevated ionized calcium of 1.4 – 1.5 mmol/L. Initially cholecalciferol supplements were stopped, but hypercalcemia persisted for more than 2 months. 1,25-dihydroxy vitamin D levels were markedly elevated with low normal 25-hydroxy vitamin D levels, angiotensin-converting enzyme levels were also high, and chest computed tomography (CT) imaging was negative for any lymphadenopathy (including perihilar lymphadenopathy). Malignancy and infectious workups were negative for fungal and mycobacterial infections. Positron emission tomography revealed several small lymph nodes in right upper lobe of lung, and biopsy of bone marrow and lung lymph-nodes revealed non-caseating granulomata. We present an atypical case of occult sarcoidosis presenting mainly with biochemical findings without any definitive imaging findings, making diagnosis a clinical challenge.

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We thank Dr Haines for his interest in our article. As my mentor and a pioneer in radiofrequency catheter ablation, his insights carry much weight. At issue is the use of tetrazolium staining to define the acute radiofrequency lesion boundary. Specifically, the consideration is raised that for acute radiofrequency lesions, the tetrazolium staining method represents the isotherm for heat denaturation of cellular dehydrogenase enzymes rather than the boundary of cell death. If true, tetrazolium staining performed late after lesion formation would define a larger lesion size because of timedependent dissipation of enzymatic activity in a perimeter of devitalized tissue. The definition of the lethal isotherm for radiofrequency ablation is an important issue for evolving temperature monitoring technologies, and all possible sources of error should be examined. We believe, however, that latent enzymatic activity in otherwise devitalized tissue does not significantly distort the determination of the lethal isotherm for the following reasons. First, the issue of latent tetrazolium staining in thermally devitalized tissue has been addressed by direct experimentation. 1 The dimensions of tissue necrosis as determined by tetrazolium staining are the same when samples are studied 10 minutes, 24 hours, or 48 hours after laser-induced thermal injury. 1 Second, using glass microelectrode recordings, our laboratory has shown that electric activity is recorded 0.1 mm from the visible edge of an acute radiofrequency lesion. 2 This finding is consistent with the absence of a significant zone of stain-reactive but devitalized tissue about the lesion. Third, the studies that provide the lethal isotherm estimates of 50°C to 56°C also used the tetrazolium staining method to define acute lesion size. 3,4 These studies found the lethal isotherm to be less than the thermal inactivation temperature of dehydrogenase enzymes (62°C for porcine isoforms), suggesting that thermal enzymatic inactivation is not the limiting factor in determining lesion boundaries. 3,4 The discrepancy between these estimates and our work is likely due to the direct measurement of the temperature at the edge of the lesion in our study and estimation of that temperature by extrapolation in the prior studies. DisclosuresNone. (Circ Arrhythm Electrophysiol. 2011;4:e68.) Mark