Myeloid Sarcoma of the Temporal Bone: A Unique Cause of Hearing Loss, Otalgia, and Facial Nerve Weakness.

OBJECTIVE: To characterize a clinical triad of symptoms associated with myeloid sarcomas of the temporal bone via a review of all previously reported cases. METHODS: Case report and Ovid MEDLINE database literature review. RESULTS: A literature search revealed that a clinical triad of hearing loss, otalgia, and facial nerve weakness are commonly associated with this rare presentation of myeloid sarcoma in the temporal bone. 44% (18/41) of patients presented with all three symptoms, while 76% (31/41) presented with at least two. The presence of t(8;21) was reported in nine patients with myeloid sarcomas of the temporal bone. CONCLUSIONS: Although myeloid sarcomas are exceedingly rare, it is necessary to consider them as part of the differential diagnosis for patients who might present with middle ear and mastoid opacification on computed tomography (CT) scan, hearing loss, otalgia, and facial nerve palsy. Physicians should maintain a high degree of suspicion in patients with a history of acute myelogenous leukemia (AML), especially if previous cytogenetic analysis revealed a t(8;21).

Microbiology, Histopathology, and Radiographic Findings in Silent Sinus Syndrome.

BACKGROUND: The histopathology and microbiology associated with silent sinus syndrome (SSS) have not been well described. OBJECTIVE: This study details the histopathological and microbiological characteristics in addition to radiographic findings of SSS in comparison to those of chronic maxillary sinusitis (CRS). METHODS: 42 patients diagnosed with SSS at Mayo Clinic Hospital in Arizona were identified. Paranasal computed tomography scans of the 42 SSS patients as well as 42 matched CRS patients were analyzed in order to assess differences in the prevalence of septal spurs/deviation. 20 of the SSS patients and 19 of the matched CRS patients also had histopathology and microbiology reports, which were compiled and summarized. Additionally, 19 SSS and 19 matched CRS patients were contacted via phone survey for a more complete patient history regarding maxillary dental disease/surgery. RESULTS: SSS patients have a significantly higher prevalence of septal spurs/deviation than CRS patients. The microbiomes of SSS patients more closely resemble those of healthy controls than those of CRS patients. Analysis of the histopathology of SSS reveals chronic, non-specific inflammation similar to that seen in non-eosinophilic CRS without polyps. SSS patients were significantly more likely to have a history of maxillary dental disease requiring surgery. CONCLUSION: These data support the hypothesis that the pathogenesis of SSS is more likely due to anatomical/mechanical factors than inflammatory/microbiological factors.

NADPH production by the oxidative pentose-phosphate pathway supports folate metabolism.

NADPH donates high energy electrons for antioxidant defense and reductive biosynthesis. Cytosolic NADP is recycled to NADPH by the oxidative pentose phosphate pathway (oxPPP), malic enzyme 1 (ME1) and isocitrate dehydrogenase 1 (IDH1). Here we show that any one of these routes can support cell growth, but the oxPPP is uniquely required to maintain a normal NADPH/NADP ratio, mammalian dihydrofolate reductase (DHFR) activity and folate metabolism. These findings are based on CRISPR deletions of glucose-6-phosphate dehydrogenase (G6PD, the committed oxPPP enzyme), ME1, IDH1, and combinations thereof in HCT116 colon cancer cells. Loss of G6PD results in high NADP, which induces compensatory increases in ME1 and IDH1 flux. But the high NADP inhibits dihydrofolate reductase (DHFR), resulting in impaired folate-mediated biosynthesis, which is reversed by recombinant expression of E. coli DHFR. Across different cancer cell lines, G6PD deletion produced consistent changes in folate-related metabolites, suggesting a general requirement for the oxPPP to support folate metabolism.