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PubMed1995

Management of unusual causes of ulcers of lower extremities.

Treatment of any wound begins with the correct diagnosis. The vast majority of chronic wounds can be classified as pressure ulcers, venous ulcers, insensate ulcers, or arterial insufficiency ulcers. This article focuses on wounds of unusual origin that must be considered in evaluation. All of these wounds are difficult to treat, are more likely to occur in specialized clinical settings, may provide clues to underlying systemic illnesses, and can be life-threatening. Unusual wounds discussed include atrophe blanche, calciphylaxis, leukocytoclastic vasculitis, necrobosis lipoidica, necrotizing fasciitis, and pyoderma gangrenosum.

Humans↗

PubMed2004

Vascular calcification mechanisms.

Vascular calcification is highly correlated with cardiovascular disease mortality, especially in patients with ESRD or diabetes. In addition to the devastating effects of inappropriate biomineralization seen in cardiac valvulopathies, calciphylaxis, and idiopathic arterial calcification, vascular calcification is now recognized as a marker of atherosclerotic plaque burden as well as a major contributor to loss of arterial compliance and increased pulse pressure seen with age, diabetes, and renal insufficiency. In recent years, several mechanisms to explain vascular calcification have been identified including (1) loss of inhibition, (2) induction of bone formation, (3) circulating nucleational complexes, and (4) cell death. Alterations in calcium (Ca) and phosphorus (P) balance as seen in patients with ESRD promotes vascular calcification via multiple mechanisms and may explain the alarmingly high levels of cardiovascular disease deaths in these patients. Strategies to control Ca and P levels in patients with ESRD have met with early success in preventing progression of vascular calcification. Whether or not vascular calcification can be reversed is not yet known, but exciting new studies suggest that this may be possible in the future.

Calcinosis↗

PubMed1995

Electron microscopic study of driving diaphragms in long-term survival with a total artificial heart.

A driving diaphragm in the long-term working total artificial heart (TAH) is under serious mechanical stress, and the long steady contact with blood causes changes to the diaphragm's surface. These changes can be influenced either by local or systemic interventions. In our study, we tried to follow the development of changes to the diaphragm's surface comparing the samples of diaphragms of long (over 30 days) and short (under 30 days) surviving calves and the effect of some preventive measures as well. We could confirm the presence of two types of calcification: a dystrophic calcification affecting primarily formed thrombi and necrotic tissue, and a primary type of calcification that begins in the form of calcifying nuclei on the protein layer of the polyurethane surface that is later on extensively covered with a fibrin network and blood cells. The calcified deposits caused mechanical damage or were the source of microembolization to the vital organs. A clotting mechanism occurs at the same time as the calcifying process from the beginning, often forming a fibrin network in and over the calcified deposits. An attempt at prevention was made by systemic administration of colloidal iron solution, Ferrum Lek (ferri saccharate in a stable colloidal form), based on the concept of the so-called reversed calciphylaxis.

Animals↗

PubMed2004

Osteogenic regulation of vascular calcification: an early perspective.

Cardiovascular calcification is a common consequence of aging, diabetes, hypercholesterolemia, mechanically abnormal valve function, and chronic renal insufficiency. Although vascular calcification may appear to be a uniform response to vascular insult, it is a heterogenous disorder, with overlapping yet distinct mechanisms of initiation and progression. A minimum of four histoanatomic variants-atherosclerotic (fibrotic) calcification, cardiac valve calcification, medial artery calcification, and vascular calciphylaxis-arise in response to metabolic, mechanical, infectious, and inflammatory injuries. Common to the first three variants is a variable degree of vascular infiltration by T cells and macrophages. Once thought benign, the deleterious clinical consequences of calcific vasculopathy are now becoming clear; stroke, amputation, ischemic heart disease, and increased mortality are portended by the anatomy and extent of calcific vasculopathy. Along with dystrophic calcium deposition in dying cells and lipoprotein deposits, active endochondral and intramembranous (nonendochondral) ossification processes contribute to vascular calcium load. Thus vascular calcification is subject to regulation by osteotropic hormones and skeletal morphogens in addition to key inhibitors of passive tissue mineralization. In response to oxidized lipids, inflammation, and mechanical injury, the microvascular smooth muscle cell becomes activated. Orthotopically, proliferating stromal myofibroblasts provide osteoprogenitors for skeletal growth and fracture repair; however, in valves and arteries, vascular myofibroblasts contribute to cardiovascular ossification. Current data suggest that paracrine signals are provided by bone morphogenetic protein-2, Wnts, parathyroid hormone-related polypeptide, osteopontin, osteoprotegerin, and matrix Gla protein, all entrained to endocrine, metabolic, inflammatory, and mechanical cues. In end-stage renal disease, a "perfect storm" of vascular calcification often occurs, with hyperglycemia, hyperphosphatemia, hypercholesterolemia, hypertension, parathyroid hormone resistance, and iatrogenic calcitriol excess contributing to severe calcific vasculopathy. This brief review recounts emerging themes in the pathobiology of vascular calcification and highlights some fundamental deficiencies in our understanding of vascular endocrinology and metabolism that are immediately relevant to human health and health care.

Animals↗

PubMedDate not supplied

Heparin-induced skin necrosis in a patient with end-stage renal failure and functional protein S deficiency.

Skin ulceration is a well-characterized thrombotic complication of the heparin-induced thrombocytopenia (HIT) syndrome. We present the case of a 73-year-old diabetic woman nearing end-stage renal failure who developed extensive upper thigh, abdominal and buttock ulceration following initiation of subcutaneous heparin for prophylaxis against deep vein thrombosis. A preliminary diagnosis of calciphylaxis was made based on the classical distribution and macroscopic appearance of the ulceration in a patient with end-stage renal failure and secondary hyperparathyroidism. However skin biopsy showed complete absence of calcium deposits in the dermal microvasculature. The presence of extensive microthrombi within dermal vessels prompted serologic testing to detect a prothrombotic state. We identified the combined presence of heparin-dependent platelet activating (HIT) antibodies and functional protein S deficiency. To our knowledge this is the first reported case of a dialysis patient presenting with skin ulceration induced by heparin and protein S deficiency. This case highlights the importance of a skin biopsy and testing for a hypercoaguable state in patients with end-stage renal disease and skin ulceration. We suggest that HIT antibodies should be requested in all dialysis patients presenting with skin ulceration.

Aged↗

PubMed1977

Sudden fatal pulmonary calcification following renal transplantation.

A 42-year-old male was hemodialyzed for 2 years with excellent control of calcium-phosphate metabolism. He received a cadaveric renal transplant but experienced a prolonged episode of acute tubular necrosis during which he could not tolerate phosphate-binding antacids. His calcium X phosphate product became markedly elevated for 20 days. Following a brief period of function, the homograft was removed on the 45th post-transplant day after severe rejection and subsequent infection. Chest X-ray was normal. Six days after graft nephrectomy, he became acutely dyspneic and markedly hypoxemic. Diffuse, flocculent pulmonary infiltrates appeared on the chest film. The patient expired 1 day later. At postmortem examination, there was severe, diffuse pulmonary alveolar calcification demonstrated by chemical and histologic examination. Although unlikely, the prolonged post-transplant period characterized by elevated calcium X phosphate product may have played a pathogenetic role. Calciphylaxis may have occurred, with hyperparathyroidism as the sensitizing agent and any of several drugs acting as challenger.

Adult↗

PubMed1996

Calcifying panniculitis with renal failure: a new management approach.

A 60-year-old woman with chronic renal failure, hyperphosphatemia, normocalcemia and hyperparathyroidism presented with skin and subcutaneous tissue necrosis over the upper lateral aspects of both thighs which became progressively worse with subsequent ulceration over the period of 1 week. A biopsy of the affected skin and subcutaneous tissues demonstrated discrete foci of calcification compatible with the diagnosis of calcifying panniculitis. While it was possible to control the patient's hyperphosphatemia using magnesium carbonate, local ulcer care, including daily whirlpool and repeated local surgical excision, failed to stop the progression of the surrounding skin and subcutaneous tissue necrosis with subsequent ulceration. A trial of oral prednisone for a total of 10 days followed by oral cimetidine for 3 months resulted in complete healing at the incision sites without recurrence after 9 months. In this case of calcifying panniculitis the conditions for calciphylaxis were present, and a new management approach was applied.

Anti-Inflammatory Agents↗

PubMed1996

Extensive necrotizing livedo reticularis in a patient with chronic renal failure, hyperparathyroidism and coagulation disorder: regression after subtotal parathyroidectomy.

Necrotizing livedo reticularis is an infrequent, life-threatening complication of chronic renal failure. Since Selye's studies in 1962, calciphylaxis, i.e. acute calcium deposition in tissue, is considered the main pathomechanism, especially because hyperparathyroidism are very frequently present. However, other etiological and/or triggering factors, such as coagulation disorders, direct cellular toxicity of parathormone or calcium on endothelium, might be involved, acting perhaps in a cumulative way. We report a case with a circulating anticoagulant which supports this hypothesis.

Adult↗

PubMed1979

Generalized cutaneous calcinosis and mixed connective tissue disease.

A 49-year-old female patient with a history of fever episodes, muscular weakness, Raynaud's phenomenon, cardiac insufficiency and increasing cutaneous calcinosis over a period of 4 years is reported. Based upon clinical as well as histological and immunological findings, the disease is diagnosed as mixed connective tissue disease with generalized cutaneous calcinosis in an extent yet unpublished, to our knowledge, in this 'overlap syndrome'. The pathogenesis of cutaneous calcinosis is discussed with particular reference to the phenomenon of calciphylaxis, and some therapeutic implications are considered.

Calcinosis↗

PubMed2003

Leg ulcers of unusual causes.

In this review, unusual causes of leg ulcers are examined with an emphasis on pathophysiology, clinical presentation, and epidemiology. Cutaneous ulcers due to malignancy of unusual leg ulcers with hematologic disorders, vasculitis, sarcoidosis, calciphylaxis, Buerger's disease, and pyoderma gangrenosum are discussed.

Journal Article↗

PubMed2003

Secondary hyperparathyroidism in children with chronic renal failure: pathogenesis and treatment.

Despite advances in the management of patients with chronic renal failure, histologic features associated with secondary hyperparathyroidism remain the predominant skeletal findings; however, over the last decade the prevalence of adynamic bone has increased in both adult and pediatric patients with chronic renal failure. The management of children with secondary hyperparathyroidism and mild to moderate chronic renal failure should be started early, and should include correction of hypocalcemia and metabolic acidosis, maintenance of age-appropriate serum phosphorus levels, and institution of vitamin D therapy when serum intact parathyroid hormone (PTH) measurements are elevated to maintain the blood levels within normal limits; however, in children undergoing chronic dialysis therapy, the current recommendation is to maintain the serum intact PTH levels at least 2-4 times the upper limits of normal to prevent the development of low bone turnover disease. Serum calcium, phosphorus, alkaline phosphatase, and PTH levels should be monitored frequently, especially in infants and very young children. Discontinuation or reduction of vitamin D should be considered when there is a rapid decline in PTH levels, persistent elevation in serum calcium and serum phosphorus levels, and a significant diminution in alkaline phosphatase levels. In addition, a reduction in the calcium concentration of the dialysis fluid, and judicious use of calcium-containing salts as phosphate binding agents should also be performed in these patients. Although not yet extensively used in pediatric patients with secondary hyperparathyroidism, several therapeutic alternatives, such as the less calcemic vitamin D analogs, including paricalcitol [19-nor-1,25-(OH)(2)D(2)] and doxercalciferol [1-alpha-(OH)(2)D(2)], calcimimetics, and the availability of a calcium-free, aluminum-free phosphate binder such as sevelamer hydrochloride and lanthanum carbonate, may play significant roles in the future management of children with secondary hyperparathyroidism to promote linear growth, prevent parathyroid gland hyperplasia, avoid calciphylaxis and, in the long run, avert vascular calcifications.

Child↗

PubMedDate not supplied

Tracheopathia chondro-osteoplastica. A clinical study of thirty cases.

During the last 12 years, 30 cases of tracheopathia chondro-osteoplastica have been diagnosed at the Department of Otolaryngology of Kuopio University. Ten of these were accidentally revealed by bronchoscopy, 2 by autopsy, but 18 were revealed through a systematic examination. Ten of these 18 were preliminarily diagnosed by indirect laryngoscopy. The average age for women was 51 and for men 42, the youngest patient being 11 and the oldest 71 years of age. The characteristic symptoms were long-term recurrent cough, hoarseness and periodic expectoration. The sputum was frequently abundant and crusty, and sometimes contained streaks of blood. Shortness of breath was a common symptom, but there were often entirely asymptomatic periods. The disease begins with a persistent purulent tracheitis, which, probably owing to calciphylaxis, causes accumulation of calcium salts in the tracheal mucosa. Cartilage and bone later develop around these accumulations. In most of the cases of tracheopathia chondro-osteoplastica in the present series, the condition was associated with atrophic rhinitis or pharyngitis. As the nasal disease improves, some regression may occur, though hardly healing. Calcium and phosphorus metabolism was not disturbed, and no immunological aberrations were found in any of the patients in this series.

Adolescent↗

PubMed2000

Considerations for the global assessment and treatment of patients with recalcitrant wounds.

Many factors, both intrinsic and extrinsic, may contribute to wound recalcitrance. For example, arterial circulation may be impaired by atherosclerosis, vasospastic disorders, microemboli, thromboangiitis obliterans, vasculitis, sickle cell anemia, and antiphospholipid syndrome, all of which may impair healing. Inflammatory disorders that may lead to recalcitrance include pyoderma gangrenosum and necrobiosis lipoidica. Chronic venous insufficiency, infection, diabetes mellitus, systemic malignancy, malnutrition, and exposure to pressure and shear prolong the healing process. Wounds secondary to primary skin carcinoma will not heal. Calciphylaxis, a life-threatening metabolic disorder, leads to multiple ulcerations that are especially difficult to heal. Knowledge of common factors that lead to wound recalcitrance is essential to the wound care clinician, as accurate diagnosis results in appropriate treatment. To arrive at the diagnosis, the wound care clinician must perform a thorough history and physical examination and order relevant investigative studies. Treatment is based on correction of the identified underlying condition. By utilizing a systematic approach in the management of each patient with a chronic wound, the wound care clinician increases the probability of achieving wound closure.

Bandages↗

PubMedDate not supplied

[Rheumatological calcinoses].

The different types of calcinosis observed in rheumatic patients are described : those most frequently found are periatricular and tendinous ; others that are less frequent are subcutaneous and result from tissue attack (filariasis, repeated microtraumatisms) ; diffuse dystrophic calcinoses of the Thibierge and Weissenbach syndrome ; and lasty, in contrast to the preceding examples, diffuse, dystrophic, and metabolic articular chondrocalcinosis. The etiopathogenesis of these calcinoses remains obscure, but the phenomenon of calciphylaxis seems to be involved.

Bursitis↗

PubMed2000

Prevalence and clinical consequences of elevated Ca x P product in hemodialysis patients.

Control of serum phosphorus (P) levels is a central goal of managing patients with chronic renal failure (CRF). Hyperphosphatemia develops invariably with kidney failure, and inadequate control of serum P leads to an elevated calcium-phosphorus (Ca x P) product. Further contributing to an elevated Ca x P product is the fact that hemodialysis patients are generally in a net positive calcium balance-dietary intake of calcium, ingestion of calcium-based phosphate binders, calcium absorption from dialysate, and abnormalities in bone buffering and turnover all contribute to the calcium burden in hemodialysis patients. In addition, treatment with calcitriol to manage secondary hyperparathyroidism increases intestinal absorption of both calcium and P. These abnormalities in divalent ion metabolism can result in a number of harmful conditions in CRF patients, including vascular calcification, cardiovascular disease, calciphylaxis, and death. We are now beginning to realize that our current therapeutic approaches to CRF management may not only be ineffective in controlling P and Ca x P product, but may actually contribute to serious calcific and cardiovascular hazards in these patients. Elevated P and Ca x P product are both significant predictors of cardiovascular mortality in hemodialysis patients. These effects are observed at P and Ca x P product levels that were considered safe until recently. Based on current national studies, we now recommend that serum P levels and Ca x P product of patients with CRF be maintained between 3.0-5.0 mg/dl and less than 55 mg2/dl2, respectively. Achieving these more rigorous treatment goals will require a shift in our therapeutic management strategies to incorporate aggressive use of calcium-free phosphate binders and, when necessary, use of less calcemic vitamin D analogs.

Calcium↗

PubMed2001

Refractory renal hyperparathyroidism: clinical features and outcome of surgical therapy.

Despite improvements in medical management parathyroidectomy has an important role in treatment of refractory renal hyperparathyroidism (HPT). The medical records of all patients who underwent parathyroidectomy from 1991 through 2000 were reviewed to determine the clinical and laboratory features and outcomes of treatment in patients with renal versus primary HPT. Twenty-one of 92 patients who underwent parathyroidectomy had renal HPT with a mean age of 47+/-3 years compared with 56+/-2 years for patients with primary HPT (P < 0.05). Clinical manifestations included osteodystrophy (19), pruritus (six), extraosseous calcification (three), and calciphylaxis (one). Parathyroid hormone, phosphorus, and alkaline phosphatase levels and weights of excised glands were higher in renal versus primary HPT (P < 0.05). Supernumerary glands were found in three patients (14%) with renal HPT and none of nine patients with primary parathyroid hyperplasia. After surgical therapy persistent or recurrent HPT occurred in three (14%) patients with renal and one (1.4%) patient with primary HPT (P < 0.05). Postoperative hypocalcemia occurred in 20 (95%) patients with renal HPT all of whom required intravenous calcium, compared with 25 (35%) patients with primary HPT (P < 0.05) of whom only three (4%) required intravenous calcium (P < 0.05). In contrast to those with primary HPT patients with renal HPT are younger and more likely to have severe osteodystrophy, postoperative hypocalcemia, and persistent or recurrent HPT.

Adult↗

PubMed2001

Outcome of percutaneous endoscopic gastrostomy feeding in patients on peritoneal dialysis.

Protein malnutrition is now well established as an important contributory factor to the high mortality in peritoneal dialysis (PD) patients. Low dietary protein calorie intake is one of the factors leading to protein malnutrition. If PD patients develop difficulty eating, percutaneous endoscopic gastrostomy (PEG) feeding may prove beneficial in providing adequate nutrition. Studies on the effectiveness of PEG feeding in PD patients are limited to pediatric patients. The objective of the present study was to assess the outcome of PEG feeding in adult patients with end-stage renal disease (ESRD) on PD. We retrospectively reviewed charts from May 1992 to February 2000 of 10 consecutive patients in our center who had had feeding tubes inserted. The patients' ages ranged from 37 to 81 years, with mean age of 65. Of the 10 patients, 7 were male, 5 were diabetic, and 1 was infected with the human immunodeficiency virus. Two patients had cerebrovascular accident (CVA) with dysphagia, 3 had multi-infarct dementia, 2 had anoxic encephalopathy, 2 had dementia, and 1 had calciphylaxis with anorexia. Of the 10 patients, 9 failed to eat because of neurologic disorders. Two patients who had functioning PEG feedings before starting PD had no complications. Only 2 of 8 patients already on PD continued with long-term PD after a PEG was inserted. Both patients whose PD was not interrupted at the time of PEG placement immediately developed peritonitis. Of the 6 patients who were maintained on hemodialysis (HD), 2 developed peritonitis within one week of starting PEG feedings. The other 4 had no complications from PEG feedings while being maintained on HD, but 1 developed peritonitis when PD was resumed. Of the 5 patients who developed peritonitis, 3 experienced fungal peritonitis. In PD patients, PEG feeding is associated with frequent complications. However, PEG placement prior to PD initiation appears to be safe. Maintaining patients on HD for at least 6 weeks appears to decrease the incidence of peritonitis, but does not eliminate it. Use of anti-fungal prophylaxis and maintenance of the patient on HD for longer than 6 weeks may produce better results.

Adult↗

PubMed2002

[Skin manifestations with internal diseases. Finding the origin].

Inspection of the skin in its entirety often turns up initial and orientating symptoms allowing the early detection of internal disorders. For example, the painful ulcerations of pyoderma gangrenosum can provide clues as to the presence of underlying inflammatory bowel or joint or hematologic disturbances. Extremely painful ulcerations with livedoid bleeding located on the lower limbs are indicative of calciphylaxis as a serious complication of terminal renal failure. Periorificial and migratory necrolytic erythema may signal a glucagon-producing carcinoma of the pancreatic islet cells. Pasty, whitish-yellow papules on the face associated with a tendency for developing petechiae may be a manifestation of amyloidosis in a plasmacytoma. Numerous diffuse angiomas covering the body of a younger patient should prompt the physician to consider the genetic enzyme defect of alpha-galactosidase (Fabry's disease). In the case of pacemaker- or defibrillator-associated erythema, unnecessary revision of the device can be avoided if such possibilities are considered. In consultation with the dermatologist, the exact classification of symptoms, an accurate diagnostic work-up, and differential-diagnostic considerations should be undertaken with the aim of enabling early initiation of causal or stabilizing treatments.

Biopsy↗