Ankylosing spondylitis (AS) is a chronic inflammatory disorder primarily involving the sacroiliac joints and spine. It usually affects young people, and bone formation and resorption are implicated in the pathogenesis of AS. Non-steroidal anti-inflammatory drugs (NSAIDs) are the first line therapy and are very effective in most of patients who have inflammatory back pain. If NSAIDs are not effective, anti-TNF-alpha agents are strongly recommended in severe inflammatory back pain. Anti-TNF-alpha is very effective in most of AS patients. A study by Lee et al. showed that AS patients who were treated with anti-TNF-alpha have weight gain and improvement of osteoporosis. In this editorial, studies on the improvement of weight and osteoporosis with anti-TNF-alpha agents are reviewed.
Anti-Inflammatory Agents, Non-Steroidal ; Back Pain ; Humans ; Osteogenesis ; Osteoporosis* ; Sacroiliac Joint ; Spine ; Spondylitis, Ankylosing ; Weight Gain*

Ankylosing spondylitis (AS) is a chronic inflammatory disorder primarily involving the sacroiliac joints and spine. It usually affects young people, and bone formation and resorption are implicated in the pathogenesis of AS. Non-steroidal anti-inflammatory drugs (NSAIDs) are the first line therapy and are very effective in most of patients who have inflammatory back pain. If NSAIDs are not effective, anti-TNF-alpha agents are strongly recommended in severe inflammatory back pain. Anti-TNF-alpha is very effective in most of AS patients. A study by Lee et al. showed that AS patients who were treated with anti-TNF-alpha have weight gain and improvement of osteoporosis. In this editorial, studies on the improvement of weight and osteoporosis with anti-TNF-alpha agents are reviewed.
Anti-Inflammatory Agents, Non-Steroidal ; Back Pain ; Humans ; Osteogenesis ; Osteoporosis* ; Sacroiliac Joint ; Spine ; Spondylitis, Ankylosing ; Weight Gain*

Background: The pentadecapeptide BPC-157 has been shown to have anti-inflammatory and wound healing effects on multiple target tissues and organs. Peptides have potent anti-inflammatory effects on periodontal tissues in rats with periodontitis. Few studies have investigated the effect of BPC-157 on pain after dental procedures or oral surgeries. The purpose of the present study was to investigate the antinociceptive effects of BPC-157 on postoperative incisional pain in rats. Methods: Sprague–Dawley rats were randomly divided into five groups: control (saline with the same volume), BPC10 (10 μg/kg of BPC-157), BPC20 (20 μg/kg of BPC-157), BPC40 (40 μg/kg of BPC-157), and morphine (5 mg/kg of morphine). A 1-cm longitudinal incision was made through the skin, fascia, and muscle of the plantar aspect of the hind paw in isoflurane-anesthetised rats. Withdrawal responses were measured using von Frey filaments at 0, 2, 6 h and 4, 7 d after incision. The formalin test was also performed to differentiate its anti-nociceptive effect from an inflammatory reaction or central sensitization. Pain behavior was quantified periodically in phases 1 and 2 by counting the number of flinches in the ipsilateral paw after injection with 30 μL of 5% formalin. Results: The threshold of mechanical allodynia was significantly increased in the BPC10, BPC20, BPC40 and morphine groups compared with that in the control group at 2 h. These increasing thresholds then returned to the levels of the control group. The BPC-157 group showed a much higher threshold at 4 days after incision than the control group. The thresholds of the BPC groups, except the morphine group, were normalized 7 days after incision. The flinching numbers of the BPC10, BPC20, BPC40 and morphine groups were significantly decreased in phase 1, but there was no decrease in the BPC-157 groups except the morphine group in phase 2. Conclusions BPC-157 was effective only for a short period after incision. It was also effective during phase 1 but not during phase 2, as determined by the formalin test. BPC-157 might have a short antinociceptive effect, even though it has anti-inflammatory and wound healing effects.

Prolonged hypokalemia from chronic laxative abuse is recognized as the cause of chronic tubulointerstitial disease, known as "hypokalemic nephropathy," but it is not clear whether it contributes to acute kidney injury (AKI). A 42-year-old woman with a history of chronic kidney disease as a result of chronic laxative abuse from a purging type of anorexia nervosa (AN-P), developed an anuric AKI requiring hemodialysis and a mild AKI 2 months later. Both episodes of AKI involved severe to moderate hypokalemia (1.2 and 2.7 mmol/L, respectively), volume depletion, and mild rhabdomyolysis. The histologic findings of the first AKI revealed the remnants of acute tubular necrosis with advanced chronic tubulointerstitial nephritis and ischemic glomerular injury. Along with these observations, the intertwined relationship among precipitants of recurrent AKI in AN-P is discussed, and then we postulate a contributory role of hypokalemia involved in the pathophysiology of the renal ischemia-induced AKI.
Acute Kidney Injury* ; Adult ; Anorexia Nervosa ; Female ; Humans ; Hypokalemia* ; Necrosis ; Nephritis, Interstitial ; Renal Dialysis ; Renal Insufficiency, Chronic ; Rhabdomyolysis