Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Persistent or recurrent hyperparathyroidism after total parathyroidectomy with forearm implant may be caused by hyperplastic grafted tissue, residual parathyroid tissue left in the neck or the presence of a supernumerary gland not found during surgery. A correct assessment of graft function is needed to localize the source of hormone excess and to avoid an unnecessary neck reoperation in cases of graft dependent hyperparathyroidism. In 12 patients with relapsing hyperparathyroidism after total parathyroidectomy with forearm implant, total ischemic blockade of the arm bearing the parathyroid graft produced a "transitory implantectomy" with a significant reduction of serum levels of intact PTH in those with graft hyperfunction. In 6 patients with proved supernumerary glands, total ischemia of the graft was not followed by significant changes in intact PTH. Hyperparathyroidism was reversed after surgical resection of the parathyroid implants in the 6 patients with positive responses to the ischemic maneuver. A repeat neck reoperation removing cervical or mediastinal supernumerary glands was followed by control of recurrent hyperparathyroidism in the 6 patients with a negative response to the ischemic blockade. Total ischemic blockade of the arm bearing the parathyroid graft is a valuable method for a correct assessment of graft function after total parathyroidectomy with forearm autotransplantation.
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PMID:Secondary hyperparathyroidism: diagnosis of site of recurrence. 189 42

Four cases of secondary hyperparathyroidism were treated by total parathyroidectomy with autotransplantation into the sternocleidomastoid muscle. These total parathyroidectomy patients are presented to demonstrate the reliability of parathyroid autotransplantation into the sternocleidomastoid muscle. Our technique is described in detail, and all procedures were successful. In one case, the patient was found, in retrospect, to have an adenoma in the transplanted parathyroid tissue. When the patient developed graft-dependent hypercalcemia, a portion of the graft was easily excised under local anesthesia and the patient became normocalcemic. Parathyroid tissue should be transplanted into the sternocleidomastoid muscle rather than other sites because of easy accessibility, one operative site, less graft ischemia, a low incidence of infection, and a high success rate due to excellent blood supply.
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PMID:Autotransplantation of parathyroid tissue into sternocleidomastoid muscle. 335 95

Progressive vascular calcification with ischemia and gangrene of the extremities occurs rarely in uremic patients, patients undergoing maintenance dialysis, and following renal transplantation. In this paper we present two additional patients on chronic hemodialysis who developed this syndrome in association with severe secondary hyperparathyroidism. Fulminant gangrene led to the death of the first patient, while in the second, multiple amputations had to be performed after parathyroidectomy. In both patients, evidence of iron overload due to multiple blood transfusions was present and iron was histologically demonstrated in a calcification area in one case. The possibility of iron overload as a "challenger" for systemic calciphylaxis is discussed.
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PMID:Progressive vascular calcification with necrosis of extremities in hemodialysis patients: a possible role of iron overload. 394 13

Chronic renal failure and its sequelae, particularly secondary hyperparathyroidism, may be associated with spontaneous quadriceps tendon ruptures. This is a report of two cases of bilateral spontaneous simultaneous quadriceps tendon ruptures in uremia and a review of the literature. The level at which the tendon ruptures is inconstant. Light microscopy reveals nonspecific changes of degeneration and calcification. Under electron microscopy, the structure and maturity of collagen fibers are normal. The ruptures occur in patients younger than 40 years of age who reject medical treatment (i.e. oral phosphate binder) and have long-standing renal disease (mean = 12.3 years). The predisposing causes of rupture are unknown. An abnormality of collagen metabolism, ischemia, direct effects of parathormone, and dystrophic calcification are some of the possible contributory factors.
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PMID:Quadriceps tendon ruptures in uremia. 397 53

A 31-year-old woman with systemic lupus erythematosus (SLE), diabetes mellitus, and chronic renal failure developed digital ischemia, myocardial dysfunction, abnormal ECG, and elevated CPK levels. Radiographic studies revealed calcification of the peripheral vasculature although coronary angiography was unremarkable. An endomyocardial biopsy demonstrated intra and extracellular myocardial calcification without evidence of vasculitis or primary myocarditis. A diagnosis of calciphylaxis, as a result of secondary hyperparathyroidism, was made. This case demonstrates that calciphylaxis can mimic the cardiovascular manifestations of SLE. Early differentiation of these disparate diseases is important because treatment strategies employed in SLE may exacerbate calciphylaxis.
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PMID:Systemic lupus erythematosus: calciphylaxis induced cardiomyopathy. 769 81

Systemic calciphylaxis is a rare, poorly understood syndrome of progressive ischemic necrosis, usually associated with hyperparathyroidism. The combination of hyperparathyroidism, usually secondary or tertiary, and chronic renal failure seems to produce a particular biochemical environment conducive to the development of an unusual progressive form of ischemia. Early recognition and diagnosis, appropriate therapy including wound care, and expeditious parathyroidectomy often will halt the progression of the disease, minimize limb loss, and prevent subsequent sepsis and death.
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PMID:Systemic calciphylaxis. 811 2

Post-transplant cure tubular necrosis (ATN) represents the most frequent cause of delayed graft function in the immediate post-transplant period. Several causes have been associated with the development of post-transplant ATN such as donor and recipient ages, cold-warm ischemia times, HLA mismatches, and postoperative hypotension. In the present study, we retrospectively evaluated the role of secondary hyperparathyroidism and high parathyroid hormone (PTHi) blood levels in the development of post-transplant ATN. One hundred patients submitted to cadaveric renal transplant between January 1992 and March 1993 in our unit were included. Twenty-seven patients (27%) developed post-transplant ATN and seventy-three (73%) did not. Post-transplant ATN was significantly associated with gender (p < 0.01), recipient age (p < 0.01), number of transplantations (p < 0.01), time on hemodialysis (p < 0.001), cold ischemic time (p < 0.05) and PTHi levels (p < 0.001). The bivariate and multivariate statistical analyses demonstrated that the development of post-transplant ATN was significantly more frequent in females; retransplanted patients, patients with a time on dialysis of more than 5 years, recipients over 60 years old, patients with a PTHi blood level higher than 240 pg/ml (4 times normal level) and a cold ischemia time of more than 18 h. Based on these results, we conclude that high PTHi blood levels in the renal transplant recipients represent a relevant factor in the development of post-transplant ATN. The administration of intravenous pulsed of 1,25(OH)2D3 and/or a calcium channel blocker in the perioperative period could be useful to decrease the incidence and severity of post-transplant ATN in these patients.
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PMID:Role of secondary hyperparathyroidism in the development of post-transplant acute tubular necrosis. 874 60

A certain number of elements suggest a link between arteriosclerosis and osteoporosis. Generally, osteoporosis in women is considered to result from altered secretion of sexual hormones after menopause and in elderly subjects from hyperparathyroidism secondary to calcium and vitamin D deficiency. As for the heart, the brain, the kidney or muscle, bone tissue could also be altered by vascular aging and arteriosclerosis. Large epidemiological studies have demonstrated a relationship between bone mineral density, measured by monophotonic absorptiometry and mortality due to cerebral vascular events. Several hypotheses have been proposed to explain this relationship including lower endogenous estrogen levels and arteriosclerosis of the renal vessels favoring perturbed vitamin D metabolism. Arteriosclerosis could also have a direct effect on bone tissue via an ischemic mechanism. The pathophysiolojical mechanisms are not fully understood, but could involve hormone and cytokine-dependent bone remodeling and the complementary actions of bone tissue and the hematopoietic bone marrow functioning as an unit. Further epidemiological studies would be useful to confirm the relationship between arteriosclerosis and osteoporosis. The efficacy of vasodilator drugs on osteoporosis could be tested and histology and immunochemical studies could help in our understanding of the effect of ischemia on bone metabolism.
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PMID:[Arteriosclerosis and osteoporosis]. 874 17

Patients with end-stage renal disease often demonstrate retarded healing of surgical wounds, but the basis for spontaneous wound formation in these patients is less well understood. We report our experience with four patients with a unique clinical entity previously described as the uremic gangrene syndrome (also known as calciphylaxis) that involves spontaneously forming and insidiously progressive wounds of the skin and soft tissue in uremic patients with hyperparathyroidism. The importance of recognizing this phenomenon relates to the potential benefit to wound-healing efforts resulting from subtotal parathyroidectomy and adjustment of serum calcium and phosphate levels when severe hyperparathyroidism is present. Disrupted parathyroid homeostasis as a mechanism for soft-tissue ischemia and subsequent infarction is supported by wound biopsies demonstrating microarterial calcification. As experts in factors resulting in refractory wounds, plastic surgeons need be aware of this peculiar vulnerability for spontaneously forming wounds in uremic patients. Clinical and laboratory findings, success with wound treatment in four patients, and currently popular pathophysiologic mechanisms are discussed.
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PMID:The uremic gangrene syndrome: improved healing in spontaneously forming wounds following subtotal parathyroidectomy. 877 89

99mTc-MIBI (Sestamibi) was originally developed for myocardial perfusion studies. The agent also may be used for the depiction and characterization of tumors. Performing such examinations has shown uptake in skeletal structures in several patients suggesting bone engagement of the disease which later was excluded. Retrospective evaluation of 44 examinations with 99mTc-MIBI performed in order to localize diseased parathyroid in patients with suspected hyperparathyroidism showed skeletal activity in 21 (48%) patients. Although these patients represent a selected group, the observation indicates a mechanism for skeletal accumulation of this radiopharmaceutical. Evaluation of another 13 normocalcemic patients undergoing whole-body registration for malignancy staging or to assess lower extremity ischemia with 99mTc-MIBI showed skeletal activity in 6 (46%) patients. Complementary mouse experiments confirmed skeletal uptake of 99mTc-MIBI, where most of the activity is taken up by the red bone marrow. It is concluded that homogeneous, diffuse weak skeletal activity at examination with 99mTc-MIBI is a normal finding and does not indicate malignancy.
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PMID:Accumulation of 99mTc-MIBI in bone marrow. 888 2


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