Assessing tophaceous spinal gout treatment response using dual-energy CT as a point-of-care imaging modality: case report.

We describe a case of chronic tophaceous gout affecting the spine, hands, elbows, feet, and knees in a 67-year-old man with serum urate levels at 549 µmol/L whose response to treatment was successfully mapped using dual-energy computed tomography (DECT). The patient presented with exacerbation of acute-on-chronic lumbar back pain. He had received a diagnosis of gout 3 years prior to this presentation yet was not on any urate-lowering therapy. The patient received febuxostat 80 mg and colchicine 0.3 mg once daily and underwent DECT to assess baseline monosodium urate (MSU) burden. At baseline, MSU deposits were seen in the hands, elbows, feet, knees, and lumbar spine including the left L5-S1 facet joint encroaching onto the neural foramen. After 2.5 years of treatment, serum urate level was within the target range (< 360 µmol/L), and the patient underwent a follow-up DECT that revealed almost full resolution of MSU deposition in the spine, including the MSU-burdened facet joint and neural foramen in the lumbar spine, in addition to all the affected peripheral joints. This case is the first report of radiological evidence of nearly complete resolution of MSU deposits in spinal gout on DECT after urate-lowering therapy treatment, which demonstrates the utility of this imaging modality as a non-invasive investigational point-of-care imaging modality for mapping treatment response and identifying the etiology of back pain in a patient with chronic tophaceous spinal gout.

Physiological role for nitrate-reducing oral bacteria in blood pressure control.

Circulating nitrate (NO(3)(-)), derived from dietary sources or endogenous nitric oxide production, is extracted from blood by the salivary glands, accumulates in saliva, and is then reduced to nitrite (NO(2)(-)) by the oral microflora. This process has historically been viewed as harmful, because nitrite can promote formation of potentially carcinogenic N-nitrosamines. More recent research, however, suggests that nitrite can also serve as a precursor for systemic generation of vasodilatory nitric oxide, and exogenous administration of nitrate reduces blood pressure in humans. However, whether oral nitrate-reducing bacteria participate in "setting" blood pressure is unknown. We investigated whether suppression of the oral microflora affects systemic nitrite levels and hence blood pressure in healthy individuals. We measured blood pressure (clinic, home, and 24-h ambulatory) in 19 healthy volunteers during an initial 7-day control period followed by a 7-day treatment period with a chlorhexidine-based antiseptic mouthwash. Oral nitrate-reducing capacity and nitrite levels were measured after each study period. Antiseptic mouthwash treatment reduced oral nitrite production by 90% (p < 0.001) and plasma nitrite levels by 25% (p = 0.001) compared to the control period. Systolic and diastolic blood pressure increased by 2-3 .5mmHg, increases correlated to a decrease in circulating nitrite concentrations (r(2) = 0.56, p = 0.002). The blood pressure effect appeared within 1 day of disruption of the oral microflora and was sustained during the 7-day mouthwash intervention. These results suggest that the recycling of endogenous nitrate by oral bacteria plays an important role in determination of plasma nitrite levels and thereby in the physiological control of blood pressure.