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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute magnesium (Mg) infusion decreases patathyroid hormone (PTH) secretion. However, the effect of chronic hypermagnesemia on PTH levels in dialysis patients is not well established. We studied 110 hemodialysis patients (mean age, 55 +/- 14 years; time on dialysis, 35 +/- 28 months) not receiving vitamin D and undergoing dialysis with an Mg dialysate concentration of 1.2 mg/dL. The primary phosphate binder was calcium carbonate, and 43% of the patients also needed aluminum hydroxide. During a 6-month period, calcium (Ca), phosphorus (P), and total serum Mg were measured every 2 months; intact PTH and aluminum (Al) were measured every 6 months. The mean value of each parameter was computed. Hypermagnesemia (serum Mg > 2.47 mg/dL) was observed in 73% of the patients. Mg and Ca were inversely correlated with PTH levels (r = -0.48; P < 0.001 and r = -0.21; P < 0.05, respectively). After adjusting for Ca and P (partial correlation analysis), Mg and PTH were inversely correlated (r = -0.58; P < 0.001). A stepwise multiple regression analysis showed that PTH levels were predicted by Mg (P < 0.001), alkaline phosphatase (P < 0.01), and P levels (P< 0.05; multiple R = 0.57; P < 0.001), whereas Ca level, sex (dummy variable), diabetes (dummy variable), time on dialysis, and Al level were not predictive. Patients with inadequately low PTH levels (relative hypoparathyroidism, PTH < 120 pg/mL; n = 52) showed greater serum Mg concentrations than the rest (n = 58; 3.01 +/- 0.33 v 2.63 +/- 0.38 mg/dL; P < 0.001). In conclusion, serum Mg concentrations in dialysis patients are independently associated with PTH levels, suggesting that chronic hypermagnesemia may decrease PTH secretion and/or synthesis. In addition, chronic hypermagnesemia of dialysis patients may have a role in the pathogenesis of adynamic bone disease.
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PMID:Relationship between serum magnesium and parathyroid hormone levels in hemodialysis patients. 1040 Oct 14

In the general population, blacks have higher parathyroid gland mass and circulating parathyroid hormone (PTH) levels than whites. This may predispose black patients to more severe parathyroid disease when renal failure develops. Therefore, racial differences in the severity of uremic hyperparathyroidism were examined in a population of patients with end-stage renal disease (ESRD). Among ESRD patients receiving hemodialysis or peritoneal dialysis, two or more values of intact PTH (immunoradiometric assay, pg/ml) obtained at least 90 d apart were available in 1270 prevalent cases (61.1% blacks, 51% males, and 31.1% diabetic), including 466 incident cases with onset of ESRD after 1993. Maximum PTH levels were analyzed as a function of race, gender, age, diabetic status, and levels of serum calcium, phosphorus, alkaline phosphatase, and aluminum. Using a stepwise multiple regression model, the determinants of maximum PTH in the order of their importance were black race, serum phosphorus, absence of diabetes, younger age, serum calcium, and female gender. The maximum PTH levels averaged 641.7 in blacks and 346.0 in whites after adjusting for age, gender, diabetic status, serum calcium, and phosphorus (P < 0.0001). In blacks compared with whites, the odds ratio (95% confidence interval) for adynamic bone disease (maximum PTH <150 pg/ml) was 0.26 (0.17 to 0.41), whereas the odds ratio for hyperparathyroid bone disease (mean PTH >500 pg/ml) was 4.4 (2.10 to 9.25). Race is a major independent determinant of uremic secondary hyperparathyroidism. Among ESRD patients, blacks may be at an increased risk for hyperparathyroid bone disease and whites for adynamic bone disease.
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PMID:Race is a major determinant of secondary hyperparathyroidism in uremic patients. 1066 40

Multiple studies have documented reduction in peripheral bone mass in children with insulin dependent diabetes mellitus (IDDM). In this study, the bone mineral density (BMD) of the lumbar vertebrae (L2-L4) was measured by dual photon absorptiometry in 14 female and 16 male diabetic patients of age 11 to 16 years with varying clinical duration. Twenty three children between 11 to 16 years with normal anthropometric measurements between 10th and 97th percentile and no known history of metabolic bone disease served as a control group. BMD values, weight, height, body mass index, metabolic, biochemical and growth parameters of the study group were compared with those of the control group. BMD (L2 AP 0.732 +/- 0.15 gm/cm2, L2 lateral 0.534 +/- 0.09 gm/cm2 in the study group and 0.812 +/- 0.63 gm/cm2 and 0.619 +/- 0.20 gm/cm2 in the control group) and osteocalcin (10.10 +/- 3.40 ng/ml and 23.12 +/- 2.74 ng/ml in diabetes and control respectively) levels were significantly lower in diabetic patients (p < 0.05, p < 0.01 respectively). Within the study group BMD correlated positively with age but not with the duration of the disease nor with the level of metabolic control.
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PMID:Evaluation of bone mineral density in children with diabetes mellitus. 1079 85

The prevalence of low-turnover lesions in patients undergoing peritoneal dialysis (PD) is high. Our aims are to evaluate the prevalence of adynamic bone disease (ABD) in PD patients, analyze risk factors, and define the association of serum parathyroid hormone (PTH) levels measured under different plasma calcium concentrations with this lesion. Fifty-seven patients were studied by bone biopsy (BB). ABD was found in 63.2%, and 36.8% showed high-turnover bone disease (HTBD). Patients with HTBD had a lower prevalence of diabetes, younger age, lower accumulated oral calcium salt intake, and greater calcitriol doses, serum osteocalcin level, and ultrafiltration than patients with ABD. Both mean baseline PTH levels from the previous year and PTH level at time of BB were greater in patients with HTBD than those with ABD (357 +/- 267 pg/mL versus 89 +/- 67 pg/mL; 390 +/- 337 pg/mL versus 88 +/- 78 pg/mL, respectively; P < 0.05). However, the magnitude of the increase from baseline serum PTH levels in response to hypocalcemia was greater in patients with ABD than in those with HTBD (166.4% +/- 134% versus 83.5% +/- 73.6%; P < 0.05). We found that PTH levels less than 150 pg/mL in patients with ABD showed a sensitivity of 91. 6%, specificity of 95.2%, and positive predictive value (PPV) of 97%. In the HTBD group, PTH levels greater than 450 pg/mL had a specificity and PPV of 100%. Our data confirm that ABD is the most prevalent lesion in PD patients, and PTH secretion capacity is maintained in these patients. The definitive diagnosis and management strategies for many patients requires a BB, especially when HTBD is unlikely.
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PMID:Parathormone secretion in peritoneal dialysis patients with adynamic bone disease. 1105 51

For each individual, the genetic endowment at conception sets the limits on the capacity or metabolic function. The extent to which this capacity is achieved or constrained is determined by the environmental experience. The consequences of these experiences tend to be cumulative throughout life and express themselves phenotypically as achieved growth and body composition, hormonal status and the metabolic capacity for one or other function. At any time later in life the response to an environmental challenge, such as stress, infection or excess body weight is determined by an interaction amongst these factors. When the metabolic capacity to cope is exceeded, the limitation in function is exposed and expresses itself as overt disease. During early life and development the embryo, fetus and infant are relatively plastic in terms of metabolic function. The effect of any adverse environmental exposure is likely to be more marked than at later ages and the influence is more likely to exert a fundamental effect on the development of metabolic capacity. This has been characterised as "programming" and has come to be known as "the Barker hypothesis" or "the fetal origins hypothesis". Barker has shown that the size and shape of the infant at birth has considerable statistical power to predict the risk of chronic disease in later life. These relationships are graded and operate across a range of birth weight, which would generally be considered to be normal, and are not simply a feature of the extreme of growth retardation. The first evidence showed strong relations between birth weight and heart disease, the risk factors for heart disease, diabetes and hypertension, and the intermediary markers for heart disease, blood cholesterol and fibrinogen. Strong associations have also been found for bone disease, allergic disease and some aspects of brain function. In experimental studies in animals it is possible to reproduce all of the metabolic features predicted from this hypothesis by moderating the consumption of food, or its pattern during pregnancy, and determining metabolic behaviour in the offspring. It has been shown that aspects of maternal diet exert an influence on fetal growth, especially the dietary intake of carbohydrate, protein and some micronutrients. However, these relationships are less strong than might have been predicted, especially when compared with the associations which can be drawn with maternal shape, size and metabolic capacity. Maternal height, weight and body composition relate to the metabolic capacity of the mother and her ability to provide an environment in which the delivery of nutrients to the fetus is optimal. Current evidence suggests that the size of the mothers determines her ability to support protein synthesis, and that maternal protein synthesis, especially visceral protein synthesis, is very closely related to fetal growth and development. It is not clear the extent to which the effect of an adverse environment in utero can be reversed by improved conditions postnatally, but some care is needed in exploring this area, as the evidence suggests that "catch-up" growth imposes its own metabolic stress and may in itself exert a harmful effect.
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PMID:Nutrients, growth, and the development of programmed metabolic function. 1106 59

Many liver transplant recipients are now reaching survival beyond 5 years from the liver transplant procedure, and many others are alive more than a decade from acquiring their new liver. Orthotopic liver transplant recipients enjoy the benefits of normal liver function, but a variety of metabolic and other medical problems often develop that require diagnosis and adequate management. These problems include hyperlipidemia, obesity, diabetes mellitus, renal disfunction, arterial hypertension, bone disease and neuropsychiatric syndromes. The gastroenterologist, internist, or local family physician is frequently called on to identify and treat these postoperative complications in conjunction with physicians at the transplant center.
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PMID:Long-term care of the liver transplant recipient. 1123 68

Despite our best efforts, chronic wounds continue to confound us. Cases of patients with diabetes who have wounds are particularly perplexing and challenging to manage. The diagnosis and treatment of osteomyelitis in this population are of great interest to clinicians. Much of wound care is based on tradition and expert opinion. The current focus is on evidence-based practice. The purpose of this critical literature review is to determine the best evidence for diagnosing osteomyelitis as a basis for providing appropriate therapy to patients with diabetes and foot ulcers. Treatments vary greatly in terms of time, cost, and invasiveness depending on the accuracy of the diagnosis. The choice of oral versus parenteral antibiotics, the length of the treatment, and decisions about surgical intervention or aggressive debridement are based on correctly differentiating osteomyelitis from soft tissue infection, osteoarthropathy, and other conditions. It is difficult to differentiate soft tissue infection from bone infection in the patient with diabetes and neuropathic bone disease. The precision of available tools for diagnosing osteomyelitis in patients with diabetes and foot ulcers is widely debated. A gold standard as a reference test for clinical trials and treatment decisions has not been consistently used in published research studies. Without a reference test that is reliable and valid, the conclusions regarding effectiveness of diagnostic modalities and antibiotic treatment regimens are questionable.
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PMID:A critical review of the literature: part I: diagnosing osteomyelitis in patients with diabetes and foot ulcers. 1124 28

Localized lesions at the foot skeleton are a serious and well recognized complication of diabetes mellitus which may impair the clinical outcome of the patients remarkably. In contrast, the presence of a generalized bone disease or osteoporosis related to diabetes mellitus is less acknowledged and its clinical relevance is less obvious. This paper is a clinically focused review of the literature on osteoporosis related to diabetes mellitus. Due to the different pathogenesis of diabetes mellitus type 1 and type 2 it is not surprising that there is no uniform entity of diabetic osteopathy. The majority of clinical studies in subjects with diabetes mellitus type 1 showed a moderately decreased bone mass at the forearm, while bone mass at the femur or lumbar spine was either decreased or not different from non-diabetic controls. In patients with diabetes mellitus type 2 the risk of osteopenia is not as clear as in type 1 diabetes. Bone mineral density at the forearm in patients with type 2 diabetes mellitus was decreased, unchanged or even increased in comparison to controls, while bone mineral density at the vertebrae or femoral neck was either not significantly different or increased, but rarely decreased. The underlying mechanisms triggering changes in bone mass in patients with diabetes mellitus type 1 and type 2 are not well known. In most studies there was no consistent relationship between the metabolic control of diabetes and bone mineral density. Biochemical parameters of the calcium and bone metabolism showed no clear relationship to the bone mineral density measurements. From few bone histology studies in humans and experimental studies there is evidence that a decreased bone formation is one major mechanism leading to reduced bone mass in diabetics. Microangiopathy at the bone tissue was also discussed as a possible reason for diabetic osteopenia. It was shown that insulin and insulin like growth factors (IGF-1, IGF-2) have an influence on bone metabolism itself and other growth factors, cytokines and hormones may determine changes in diabetic bone metabolism. Recent findings suggest that leptin is involved in the regulation of osteoblast function and bone mass, which is of special interest in diabetes mellitus type 2. The clinical relevance of osteoporosis or osteopenia is determined by the increased risk for insufficiency fractures. Few studies found an increased fracture risk, especially in older women with type 1 diabetes mellitus, while others did not show an increased risk for fractures or even found a decreased rate of fractures in women with diabetes mellitus type 2. There is a need for further longitudinal studies, including the incidence and risk factors for osteoporotic fractures. In clinical routine the extent of diagnostic and therapeutic activities in patients with type 1 or type 2 diabetes mellitus in respect to generalized bone disease or diabetic osteopenia should be based on individual conditions and risk profile for osteoporosis.
Exp Clin Endocrinol Diabetes 2001
PMID:Diabetes mellitus a risk for osteoporosis? 1146 May 94

Diabetic bone disease is characterized by low bone turnover resulting from impaired secretion of parathyroid hormone (PTH). However, it was suggested that the difference in duration of hemodialysis (HD) therapy and age of patients between HD patients with and without diabetes mellitus (DM) may be responsible for a significant reduction in serum intact PTH (iPTH) level in HD patients with DM. The present study showed that although such major factors affecting PTH secretion as age, sex, HD duration, and serum calcium, phosphate, and magnesium levels did not differ significantly between HD patients with and without DM, serum iPTH levels were still significantly lower in HD patients with than without DM. Among biochemical markers for bone metabolism, serum levels of intact osteocalcin (iOC) and deoxypyridinoline (DPD) were significantly lower in HD patients with than without DM, whereas serum bone-specific alkaline phosphatase, pyridinoline, and beta-crosslaps did not differ significantly between the two groups of patients. In summary, our findings indicate that PTH secretion may be significantly impaired in HD patients with DM compared with those without DM, and serum iOC and DPD are bone markers sensitive enough to detect low bone turnover in HD patients with DM.
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PMID:Impaired secretion of parathyroid hormone is coherent to diabetic hemodialyzed patients. 1157 40

1. Forty percent of transplant centers expect the primary care physician to be the primary physician; 40% have both a primary care physician and a hepatologist manage the patient. 2. Transplant centers expect primary care physicians to provide general preventive medicine, physical examinations, vaccinations, and, rarely, management of hypertension, renal dysfunction, and diabetes. 3. A high percentage of primary care physicians feel comfortable caring and managing the overall health care of a long-term liver transplant patient. 4. Primary care physicians feel at most ease managing preventive care, annual physical examinations, hypertension, diabetes mellitus, hyperlipidemia, bone disease, and vaccinations. 5. Primary care physicians should be aware of the common medical conditions of the liver transplant patient of hypertension, diabetes, obesity, hyperlipidemia, and recurrent disease. 6. Common medical conditions for both the transplant centers and primary care physicians are hypertension, dyslipidemia, diabetes mellitus, malignancy, bone disease, pregnancy, vaccination, infectious prophylaxis, and headaches.
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PMID:Posttransplantation care: role of the primary care physician versus transplant center. 1168 71


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