Calcineurin-inhibitor-induced pain syndrome after bone marrow transplantation.

Calcineurin-inhibitor-induced pain syndrome (CIPS), a rare complication seen in patients with organ transplants, is associated with the use of calcineurin inhibitors (CIs) such as cyclosporine (CSP) and tacrolimus (FK). Patients with this syndrome usually present with severe leg pain. This case report demonstrates the successful pain control of this pain syndrome in a 42-year-old female patient who had been given CIs (FK and CSP) as an immunosuppressive agent after a bone marrow transplant. Twenty-one days after the transplantation, she complained of severe pain in her bilateral lower extremities; this lasted several weeks, and was resistant to ordinary analgesics such as intramuscular pentazocine, intravenous morphine, and even oral nifedipine, which is generally accepted as an effective analgesic agent for the pain in this syndrome. Due to the presence of allodynia, our patient's pain had neuropathic pain-like characteristics, unlike the pain in previously reported patients with other organ transplants. Her pain was successfully relieved by the administration of oral amytriptyline, clonazepam, oxycodone, and intravenous lidocaine, all of which ordinarily have an analgesic effect on neuropathic pain. CIPS in patients with hematopoietic stem cell transplants treated with FK may have a mechanism by which neuropathic pain may develop that is different from that in patients with other organ transplants.

Persistent hypertension does not alter the cerebral blood flow and glucose utilization in young-adult Dahl salt-sensitive rats.

The Dahl- Iwai salt-sensitive (DS) rat develops hypertension due to a high-salt diet without any structural alterations of the brain arteries and arterioles. We investigated the effect of persistent hypertension on the regional cerebral blood flow (rCBF) and regional cerebral glucose utilization (rCGU) in the DS rats. The rats were fed either a high-salt diet (HSD; 8% NaCl, n = 5) or a low-salt diet (LSD; 0.3% NaCl, n = 6) from 8 to 16 weeks of age, and the HSD group developed hypertension lasting for 1 month. At 16 weeks of age, the rCBF was measured in the sensorimotor and visual cortices using the hydrogen clearance method, and the rCGU was measured in 26 different brain structures using the [(14)C]deoxyglucose method. The mean arterial pressure was significantly higher in the HSD group (168+/-7 mm Hg) than in the LSD group (139+/-3 mm Hg) (P < 0.01). The mean rCBF and the rCGU values tended to be lower in the HSD group than in the LSD group; however, there were no statistically significant differences except for the reduced rCGU value in the nucleus accumbens. These results suggest that hypertension itself does not alter either the rCBF or the rCGU in young-adult DS rats. This indicates that the functional / structural changes of the cerebral arteries and arterioles that are associated with hypertension appear to be responsible for altered rCBF and rCGU in other animal models of hypertension.