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M Sarli

Publications and source records attributed to M Sarli.

6 recordsLinked to original sources
PubMed2005

The vacuum cleft sign: an uncommon radiological sign.

The intravertebral vacuum cleft sign (VCS) is an uncommon radiological sign, characterized by a radiolucent zone in the vertebral body. It is composed of 95% nitrogen and small amounts of oxygen and carbon dioxide. Post-traumatic ischemic necrosis could be its physiopathological mechanism, along with other pathologies like osteoporosis, corticosteroid therapy, diabetes, arteriosclerosis, alcoholism, multiple myeloma, bone metastasis and osteomyelitis. The broad diagnosis is made by antero-posterior X-ray, but computed tomography scan (CT scan) and magnetic resonance imaging (MRI) may help with the differential diagnosis. The aims of this paper are, on one hand, to communicate the clinical case of a 73-year-old osteoporotic woman with traumatic vertebral fractures who developed this sign in her radiological survey. On the other hand, its secondary aims are to review the medical literature about this sign and to show the clinical and radiological evolution after a percutaneous vertebroplasty.

Aged↗
PubMed1999

[Post-transplantation osteoporosis].

In the last two decades organ transplantation has become an effective and established therapy for end-stage disease of various organs. The increase in survival has been due to the greater immunosuppressive capacity of regimens that include cyclosporin. During the first few months after transplantation cyclosporin is associated with high-dose steroids, which produce deleterious effects on bone and mineral metabolism. These effects are superimposed on the previous bone lesions produced by the underlying chronic diseases. Rapid bone loss occurs specially during the first 6 to 12 months after transplantation, when the incidence of fractures is greater. The majority of the fractures involve the spine. Fracture rates are lower after renal transplantation (7 to 11% in nondiabetic renal transplant recipients) and higher in the recipients of other organ transplants: 17.2 to 42% after liver transplantation, 18 to 50% after cardiac transplantation and 25 to 29% after lung transplantation. No pretransplant densitometric or biochemical parameter can adequately predict fracture risk in the individual patient. Despite this, patients with low bone mineral density at the hip, particularly in women, tend to have an increased risk of fracture. Patients can have vertebral fractures despite normal bone mineral density at the spine. Pathogenesis of bone loss is multifactorial. Patients with renal and liver diseases have either renal or hepatic osteodystrophy prior to transplantation that predispose to bone loss, and many patients awaiting pulmonary transplantation already have osteoporosis due to the use of corticosteroids for their lung disease. Rapid bone loss after transplantation depends, as suggested by prospective biochemical parameters, on a decrease in bone formation (reduction in osteocalcin levels) and an increase in bone resorption. Steroids seem to be the principal determinants of these derangements, although some role of cyclosporin cannot be excluded. Other factors that contribute to bone loss are secondary hyperparathyroidism and hypogonadism. Calcium supplementation and vitamin D administration as the only preventive measures do not seem to reduce fracture risk. The most promising regimens to prevent bone loss after transplantation seem to be the use of bisphosphonates immediately prior to and during the first year after transplantation.

Bone and Bones↗
PubMed1998

[Treatment of post menopausal osteoporosis with intravenous pamidronate in patients with esophagogastric pathology].

Pamidronate is an effective inhibitor of bone resorption; for this reason it is used in the treatment of high bone turnover diseases and osteoporosis. Because of potential gastric and esophagic side effects their oral use is limited in patients with active pathology in these organs. With the aim to evaluate the usefulness and to establish the ideal schedule of treatment of intravenous pamidronate, we assayed pamidronate infusions (APDIV) in 20 postmenopausal women with active gastroesophagical diseases. Ten of these patients received 30 or 45 mg weekly until they achieved an average dose of 157.50 +/- 9.28 mg/year in one month (range: 120-180 mg) (Group A). Another comparable ten women's group received 30 or 45 mg every three months or 90 mg every six months; the achieved average dose in this group was 166.50 +/- 6.87 mg/year (range: 120-180 mg) (Group B). All patients received 1,000 mg elemental calcium daily. Bone mineral density in lumbar spine significantly increased in both groups, but this increment (delta DMO%) was higher in group B. Bone mineral density in femoral neck was only increased in group A. Parathyroid hormone (iPTH) significantly increased at the third month but returned to basal values at the end of the year in both groups. Parameters of bone remodeling such as osteocalcin (BGP), pyridinoline and deoxipyridinolin decreased progressively and remained low at the end of the year. The treatment was well tolerated: only two patients in group A and one in Group B experienced fever and pseudoflu syndrome; phlebitis was present in one patient in the second group. In conclusion, intravenous Pamidronate is an effective and safe treatment for postmenopausal osteoporosis specially in these patients with esophagicor gastric disorders. Future trials are needed to clarify the ideal dose and schedule of treatment.

Aged↗
PubMed1997

[Extended use, up to 6 years, of an oral amino-bisphosphonate in patients with established osteoporosis].

In osteoporotic women (n:163), 63.8 (+/- 8.1) years old and 15.2 (+/- 8.3) years since menopause, oral (200 mg/day) pamidronate was administered during protracted periods, up to 6 years. During the first 4 years of therapy significant increases from basal in both, lumbar spine and femoral neck were reported (p < 0.01). Patients who underwent to 5-6 years of treatment also showed positive results in both skeletal sites. Whole body mineral content estimated a 23.8 g/year mean gain during a 4-year period. Biochemical bone markers of resorption and formation reflected a variable degree of bone turnover decrease. Such changes were more pronounced at the beginning, and remained steady after the first year of continuous therapy. Calcemia remained between normal range without any hypocalcemic episode being reported. Phosphatemia, within normal range, showed a smooth trend to increase. PTH remained within normal range and vitamin D tended to slightly increase. The total number of new bone fractures and total number of patients with new fractures were less frequent during the pamidronate treatment period than before (p < 0.01). Indeed, the relative risk (RR) of fracture was estimated comparing the treatment lapse, 495 patient/year, vs a pretreatment period of 1,814 patient/year. Overall RR resulted less than 1 (RR = 0.83; CI 95% = 0.53-1.26). In total, hip, forearm and "other" fractures, RR was also less than 1 and remained over 1 in vertebral fractures. The latter can be explained because our sample started its treatment probably in a period of increased spine crushing. Overall fracture results, in a sample of patients as own controls and in spite of differences in ages, suggested that during treatment, patients improved their skeletal biomechanical competence, mainly in sites where cortical bone plays a meaningful role, as in femoral neck. It is concluded that pamidronate is an effective tool to ameliorate the skeletal conditions of postmenopausal osteoporotic women.

Administration, Oral↗
PubMed1994

[Alcoholic osteopathy].

Alcohol intake is one of the multiple risk factors for developing osteoporosis. Alcohol has direct toxic effects on osteoblasts which determines lower osteocalcin levels at an early stage, and histomorphometric changes later on. Some authors found not only diminished bone formation in alcoholics, but also increased bone resorption. The effect of alcoholism on calciotropic hormones includes fall of PTH serum levels after an acute or moderate alcohol intake, causing transient hypoparathyroidism. In chronic alcoholism, serum levels of vitamin D and its metabolites are decreased independently of any liver disease, probably related to alcohol influence on enzymatic systems. The mineral homeostasis of alcoholics is affected: hypocalcemia is found in acute intoxication, with hypo or hypermagnesemia. In chronic alcoholism the serum calcium values tend to be normal. Alcohol intake causes multiple endocrine changes that lead to hypogonadism in both sexes. The stimulation of hypothalamus-hypophyseal-adrenal axis contributes to the alcoholic bone disease, because of the adverse effects of corticoids on bone. Caloric and protein malnutrition, in addition to a dissipated life style are additional risk factors for the development of osteoporosis.

Alcoholism↗