Tuberculosis of the right distal fibula bone case repot: An unusual T.B. case.

A 26-year-old Asian female was referred to on-call trauma services with 2 weeks history of swelling and pain of her right ankle. On laboratory evaluation, she only had an elevated CRP. Ankle roentgenogram showed a lytic lesion of the distal fibula bone with soft tissue swelling. Chest roentgenogram was abnormal along with clinical findings. Bacteriological report from right ankle specimen isolated Acid Fast Bacilli. Histological examination of the biopsy tissue showed granuloma and caseating necrosis of tuberculosis. She had incision and radical debridement of abscess and received anti-tuberculous therapy. During her follow-up in clinic, no residual or recurrent disease was established.

The amino bisphosphonate ibandronate prevents vitamin D toxicity and inhibits vitamin D-induced calcification of arteries, cartilage, lungs and kidneys in rats.

Experiments were carried out to determine whether the doses of the amino bisphosphonate ibandronate that inhibit bone resorption inhibit soft tissue calcification and death in rats treated with a toxic dose of vitamin D. These studies were prompted by the recent discovery that ibandronate doses that inhibit bone resorption potently inhibit artery calcification induced by treatment with the vitamin K antagonist warfarin. All 16 rats treated with the toxic dose of vitamin D (12.5 mg cholecalciferol x kg(-1)) died by d 6 after the first vitamin D injection (median survival: 4.5 d), whereas the 12 rats treated with vitamin D plus ibandronate (0.25 mg x kg(-1) x d(-1)) were alive and in good health at d 10. Rats treated with vitamin D alone and examined at d 4 had extensive Alizarin red staining for calcification in the aorta, the carotid, hepatic, mesenteric, renal and femoral arteries, kidneys and lungs, whereas rats treated with vitamin D plus ibandronate had no evidence for calcification at any of these tissues when examined at d 7 and 10. Ibandronate treatment also inhibited the dramatic increase in the levels of calcium and phosphate seen in the abdominal aorta, kidneys, lungs and trachea of the vitamin D-treated rats (P < 0.001). Serum calcium levels were, however, not different in rats treated with vitamin D alone (3.4 +/- 0.2 mmol x L(-1)) and in rats treated with vitamin D plus ibandronate (3.5 +/- 0.2 mmol x L(-1)). Treatment with vitamin D alone increased levels of matrix Gla protein, an inhibitor of soft tissue calcification, in the arteries, kidneys, lungs and trachea by 10- to 100-fold, and ibandronate treatment prevented this increase. The importance of these studies in the rat model is that they identify a class of drugs in current clinical use that can be used to treat patients with vitamin D toxicity and that they identify the dose of the drug that is predicted to be effective, namely the dose that inhibits bone resorption. Because there is no other known treatment for vitamin D toxicity, there would seem to be good reason to try bisphosphonates such as ibandronate in future studies aimed at treating patients who have been exposed to toxic levels of vitamin D.

Osteoprotegerin inhibits artery calcification induced by warfarin and by vitamin D.

The present experiments were carried out to test the hypothesis that arterial calcification is linked to bone resorption by determining whether the selective inhibition of bone resorption with osteoprotegerin will inhibit arterial calcification. In the first test, arterial calcification was induced by treating 22-day-old male rats with warfarin, a procedure that inhibits the gamma-carboxylation of matrix Gla protein and causes extensive calcification of the arterial media. Compared with rats treated for 1 week with warfarin alone, rats treated with warfarin plus osteoprotegerin at a dose of 1 mg/kg per day had dramatically reduced alizarin red staining for calcification in the aorta and in the carotid, hepatic, mesenteric, renal, and femoral arteries, and they had 90% lower levels of calcium and phosphate in the abdominal aorta (P<0.001) and in tracheal ring cartilage (P<0.01). More rapid arterial calcification was induced by treating 49-day-old male rats with toxic doses of vitamin D. Treatment for 96 hours with vitamin D caused widespread alizarin red staining for calcification in the aorta and the femoral, mesenteric, hepatic, renal, and carotid arteries, and osteoprotegerin completely prevented calcification in each of these arteries and reduced the levels of calcium and phosphate in the abdominal aorta to control levels (P<0.001). Treatment with vitamin D also caused extensive calcification in the lungs, trachea, kidneys, stomach, and small intestine, and treatment with osteoprotegerin reduced or prevented calcification in each of these sites. Measurement of serum levels of cross-linked N-teleopeptides showed that osteoprotegerin dramatically reduced bone resorption activity in each of these experiments (P<0.001). Therefore, we conclude that doses of osteoprotegerin that inhibit bone resorption are able to potently inhibit the calcification of arteries that is induced by warfarin treatment and by vitamin D treatment. These results support the hypothesis that arterial calcification is linked to bone resorption.

Intertrochanteric fractures of the femur: a randomized prospective trial comparing the Pugh nail with the dynamic hip screw.

Over a 14-month period, 100 consecutive cases of intertrochanteric fracture were randomly allocated to be treated by either Pugh nail-plate or Dynamic Hip Screw (DHS) fixation. Although there were 11 cases of malreduction and/or suboptimal positioning of the fixation device in the femoral head, only two of these gave long-term problems. Despite the difference in configuration of the devices and a considerable disparity in price, patient satisfaction and the incidence of untoward radiological features at an average of 6 months after surgery were similar in the two groups. A trifin-ended device would thus appear to be a reliable alternative to the more commonly used hip screw systems for intertrochanteric fracture.

Operative arthroscopy under local anaesthetic.

Forty-six patients requiring arthroscopic surgery following diagnostic arthroscopy under local anaesthetic infiltration had this tried under the same anaesthetic (four patients had to be converted to a general anaesthetic to complete the procedure). Local infiltration provides good anaesthesia for arthroscopic surgery, except in those with an acutely locked knee or a painful collateral ligament.

Arthroscopy under local anaesthesia.

Sixty patients underwent arthroscopy of the knee as day cases using a local anaesthetic technique. This provided satisfactory operating conditions and high patient acceptability.