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

Acquired perforating dermatosis (APD) is characterized by umbilicated 1- to 10-mm-measuring papulonodules with a central adherent oystershell-like keratotic plug, typically on the dorsa of the hands, forearms and over the knees. APD is associated with systemic diseases, especially diabetes mellitus and/or renal failure. Histologically the lesions show transepidermal elimination of altered dermal components into a cup-shaped epidermal depression. We present a 69-year-old man with coexisting APD and Poland syndrome (PS), an association not yet described. PS (OMIM 173800) is a rare congenital anomaly consisting of unilateral partial or total absence of the greater pectoralis muscle and ipsilateral symbrachydactyly. Most cases of PS are sporadic as it was in our case. Our patient had, in addition, an untreated diabetic condition, hyperuricaemia, dilated cardiomyopathy and a very recent pulmonary embolism. He responded to therapy with allopurinol.
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PMID:Acquired perforating dermatosis in a patient with Poland syndrome. 1465 33

Type 1 diabetes results from the destruction of insulin-producing pancreatic beta-cells by a beta-cell-specific autoimmune process. Although converting other cell types into insulin-producing cells may compensate for the loss of the beta-cell mass while evading beta-cell-specific T-cell responses, proof-of-principle of this approach in large animal models is lacking. This investigation was initiated to determine whether an insulin-producing human hepatocyte line can control diabetes when transplanted into totally pancreatectomized diabetic pigs. We established a reversibly immortalized human hepatocyte line, YOCK-13, by transferring a human telomerase reverse transcriptase cDNA and a drug-inducible Cre recombinase cassette, followed by cDNA for a modified insulin under the control of the L-type pyruvate kinase (L-PK) promoter. YOCK-13 cells produced small amounts of modified insulin and no detectable endogenous L-PK at low glucose concentrations, whereas they produced large amounts of both modified insulin and L-PK in response to high glucose concentrations. Xenotransplantation of YOCK-13 cells via the portal vein into immunosuppressed, totally pancreatectomized pigs decreased hyperglycemia and prolonged survival without adverse effects such as portal thrombosis, liver necrosis, pulmonary embolism, and tumor development. We suggest that this reversibly immortalized, insulin-secreting human hepatocyte line may overcome the shortage of donor pancreata for islet transplantation into patients with type 1 diabetes.
Diabetes 2004 Jan
PMID:Transplantation of reversibly immortalized insulin-secreting human hepatocytes controls diabetes in pancreatectomized pigs. 1469 4

A 73-year-old male in whom diabetes mellitus and benign prostatic hypertrophy had been diagnosed was hospitalized with a urinary tract infection (UTI) showing urinary retention and a high grade fever. His symptoms worsened although several antibiotics were administered after admission. A chest radiograph shows multiple nodular lesions and cavity formations in both lung fields. Arterial blood gas analysis showed hypoxia and hypocapnia. Pulmonary perfusion scintigraphy revealed perfusion defects corresponding to the nodular lesions observed on the chest radiograph. Enhanced abdominal CT demonstrated abscesses in the liver and kidney; and in urine and blood cultures, Klebsiella pneumoniae was isolated. We therefore diagnosed septic pulmonary embolism (SPE) occurring secondary to UTI. After diagnosis, the patient was given intravenous imipenem/cilastatin, minocycline and ciprofloxacin, and recovered. Although SPE occurring secondary to UTI is very rare, the incidence of SPE has recently increased in patients with DM. Therefore, we should consider the possibility of SPE in patients with DM who have respiratory symptoms.
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PMID:[A case of septic pulmonary embolism induced by urinary tract infection]. 1476 71

The prognosis of patients with myocardial infarction (MI) and normal coronary arteries (NCA) in the presence of an inherited coagulation disorder is unknown. The purpose of this study was to compare the clinical thrombosis outcome of patients with (GpI) or without (GpII), inherited coagulation disorders, who suffered from an acute MI with NCA. Eighty two consecutive patients (mean age 49 +/- 15 years; 29 females) with MI, but NCA, were recruited. Twelve patients (15%) had an inherited coagulation disorder. GpI and GpII were statistically similar regarding age (45 +/- 11 vs 50 +/- 16 years-old), gender (33 vs. 36% female), tobacco consumption (50 vs. 53%), diabetes mellitus (8 vs. 10%), hypertension (25 vs. 17%), obesity (8.3 vs. 14%), family history of coronary heart disease (33 vs. 19%), hypercholesterolemia (50 vs. 21%; p =.08), left ventricular ejection fraction (58 +/- 13 vs. 61 +/- 13%) and spasm (8.3% vs. 17%). All patients were initially treated with antiplatelet agents with the exception of one (8%) in GpI, and 6 (9%) in GpII who were taking oral anticoagulant therapy (ns). The mean follow-up was 57 +/- 26 (range from 2-91 months). During the outcome, 12/78 (15.4%) thrombosis events occurred, including venous thrombosis or pulmonary embolism (1/12 vs. 1/66), reinfarction (2/12 vs. 4/66), and stroke (2/12 vs. 2/66), with two events in one patient (GpI). Kaplan-Meier event-free survival, with combined end-point, defined as venous thrombo-embolic event, reinfarction, or stroke differed between the two groups: 4/12 (33.3%) in GpI and 7/66 (10.6%) in Gp II (p <.02). Patients with MI, NCA and congenital coagulation disorder present a high risk of thrombosis recurrence under antiplatelet agent.
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PMID:Long term prognosis of patients with myocardial infarction and normal coronary angiography: impact of inherited coagulation disorders. 1496 Nov 69

As for many cardiovascular events, pulmonary embolism (PE) is not randomly distributed over time, but shows rhythmic patterns. The purpose of this study was to investigate whether such temporal pattern of occurrence varied in subgroups of patients according to different risk comorbid conditions. All cases of PE observed at the Hospital of Ferrara, Italy, from 1998 to 2001, were considered. After determination of the day of onset, the population was grouped by gender and the most common underlying risk comorbid conditions, e.g., deep vein thrombosis (DVT), neoplasms, cardiomyopathies, traumas/surgical operations, diabetes mellitus, pulmonary diseases, hypertension, cerebrovascular diseases, heart failure, hematologic diseases. For statistical analysis, chi-square test for goodness of fit and partial Fourier series were used. A total of 784 cases (mean age 71 +/- 14 years) were included. Frequency of onset was higher in winter for total population (p = 0.002), men (p = 0.004), DVT (p = 0.001), pulmonary disease (p = 0.008), cardiomyopathies (p = 0.011), and major traumas/surgical operations (p = 0.049). Chronobiologic analysis identified a winter peak for total population (p = 0.008), men (p < 0.001), DVT (p = 0.006), pulmonary diseases (p = 0.017), and hypertension (p = 0.026). This study confirms the winter peak of PE and provides evidence that it is not influenced by the underlying clinical conditions, but probably by endogenous variations.
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PMID:Seasonal variation in onset of pulmonary embolism is independent of patients' underlying risk comorbid conditions. 1497 3

We hypothesize that the pathophysiology of many cardiovascular diseases reflects a maladaptation of the triad of trauma response: adrenergia, inflammation, and coagulation. During biologic evolution, trauma has likely been a prevailing factor in natural selection. Components of the trauma triad act to limit hemorrhage, defend wounds against microorganisms, and initiate reconstruction. Response pathways that enable survival after trauma confer obvious adaptive advantages especially if the individual goes on to reproduce. Modern humans have shaped their own ecologic environment in such a way that the incidence of trauma has waned and previously unseen pathologies have emerged. Manifestations of modern diet, changing lifestyles, and extended lifespan have suddenly created new pathologic challenges to our prehistoric physiologic system. During our evolutionary heritage, endothelial injury and end-organ hypoxia were likely exclusively associated with physical trauma and the responses of the trauma triad were appropriate. Today, endothelial injury is more often precipitated by distinctly modern stressors such as hypertension, smoking, diabetes, and dyslipidemia. The once-adaptive trauma response can maladaptively initiate dangerous, self-propelling cycles of adrenergia, inflammation, and coagulation. Acute coronary syndromes perhaps best exemplify this phenomenon. Congestive heart failure, which often ensues, can similarly be seen as a maladaptation of the trauma triad. Whereas end-organ hypoxia was once commonly associated with trauma, now hypoxia is more often attributable to distinctly modern stressors such as pump failure. The fluid conservation and inflammation that results from the trauma triad was clearly adaptive in our prehistoric past, but in congestive heart failure the response is maladaptive, engendering self-propelling exacerbations of pump failure and vascular disease. Our maladaptive trauma response hypothesis portends new diagnostic and therapeutic paradigms for cardiovascular diseases and has ramifications for many other conditions such as stroke, venous thrombosis, vasculitis, aortic disease, arterial disease, pulmonary embolism, and restenosis.
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PMID:Acute coronary syndromes and heart failure may reflect maladaptations of trauma physiology that was shaped during pre-modern evolution. 1514 37

Since the introduction of oral contraceptives, their use has been associated with an increased risk of both venous and arterial thrombosis. Pulmonary embolism, myocardial infarction, and stroke are serious disorders with a considerable risk of mortality. Because worldwide over 100 million women use oral contraceptives, issues of drug safety are of great importance. The risk of venous thrombosis during low-dose oral contraceptive use is three- to sixfold increased compared with that of nonusers. The association is not only attributed to the estrogen component of the pill: the risk is twice as high for desogestrel and gestodene (third generation) containing oral contraceptives as for levonorgestrel (second generation) containing oral contraceptives. The risk of venous thrombosis is highest in the first year of use and in women with genetic or acquired risk factors for thrombosis. Both venous or arterial thrombosis are unrelated to duration of use or past use of combined oral contraceptives. The risk of myocardial infarction and stroke during low-dose oral contraceptive use is two- to fivefold increased relative to that of nonusers. The risk of arterial thrombosis induced by oral contraceptive use is more pronounced in smokers and women with hypertension, diabetes, and hypercholesterolemia. All types of thrombosis have strongly age-dependent incidences, and therefore in absolute figures the risks and effects of risk factors increase with age. The lowering of the estrogen dose in combined oral contraceptives from 50 microg to 20-30 microg in the last decade did not clearly reduce the risk of venous thrombosis, myocardial infarction, stroke, or peripheral arterial disease. For stroke and peripheral arterial disease no difference in risk was found between second and third generation oral contraceptives. For myocardial infarction study results are conflicting, and a small benefit of third- over second-generation oral contraceptives cannot be ruled out. However, this is unlikely to counterbalance the adverse effect of third generation contraceptives on venous thrombosis.
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PMID:Venous and arterial thrombosis during oral contraceptive use: risks and risk factors. 1519 94

MODALITIES FOR THE DIAGNOSIS OF VENOUS THROMBOEMBOLISM: Currently rely on the confrontation of the initial clinical data and the results of D-dimer measurements, a venous Doppler, although reliable, is not a first-line exploration. REGARDING TREATMENT: Indications for thrombolysis are currently limited to massive pulmonary oedema with shock. Alteplase added to heparin improves the progression of severe embolism; it spares the patients from heavy interventions of resuscitation but the mortality remains the same. Concerning anticoagulant treatments, prolonged antivitamin K at classical doses is more effective than low doses and for limited duration if phlebitis is an idiopathic one. FOR HEART FAILURE WITH PRESERVED EJECTION FRACTION: Treatment of these heart failures, formerly know as 'diastolic' is similar to that of the acute phase of systolic heart failure. However, care should be taken with vasodilatators. CONCERNING HEART FAILURE IN GENERAL: The brain natriuretic peptide (BNP) represents a remarkable progress for the aetiological diagnosis of dyspnoea (inferior to 80 pg/ml in the case of pulmonary origin, superior to 300 pg/ml in the case of cardiac origin or severe pulmonary embolism). Regarding treatment, for acute heart failure, it is still the association of nitrates and diuretics, with oxygen therapy and eventually inotropics. Beta-blockers, which have revolutionized the treatment of chronic heart failure, must be maintained whenever possible in the case of the onset of acute pulmonary oedema. Multisite pacing is increasingly used in refractory chronic heart failure. Implantable defibrillation has become common practice. Non-invasive ventilation (Bi or C-PAP) is interesting in acute cardiogenic pulmonary oedema. THE PREVENTIVE ROLE OF N ACETYL-CYSTEINE: N acetyl cysteine reduces the incidence of nephropathies induced by the radio contrast products in patients with chronic kidney failure. Combined with hydratation, it must be proposed the day before and on the day of the procedure in any patient with diabetes or kidney failure.
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PMID:[Diagnostic and therapeutic progress. Venous thromboembolism, cardiac insufficiency and radio contrast agents]. 1522 98

Thromboembolism is considered the inciting cause of many vascular disorders including acute coronary syndrome (ACS), ischemic stroke, pulmonary embolism (PE), deep vein thrombosis (DVT), and mesenteric ischemia. Adrenergia and inflammation are known to accompany these conditions, particularly among arterial thromboembolic disorders, but the teleologic basis of these associations remains poorly understood. We argue that thromboembolism may sometimes be the result, rather than the cause, of acute vascular events, and may be precipitated by underlying adrenergia. Thromboembolic events are most prone to occur during parts of the circadian, seasonal, lifespan, and reproductive cycles with sympathetic dominance, as well as during behavioral, exertional, physiologic, and iatrogenic activation of sympathetic stress. Molecular evidence suggests that adrenergia and inflammation can promote coagulation and lead to co-activation of the pathways. Acute vascular events that occur without angiographic evidence of occlusion suggest that some infarcts may be attributable to adrenergia alone. "Embolic" disorders may represent asynchronous systemic phenomena rather than clot migration. During acute thromboembolism, downstream tissue hypoxia can activate maladaptive self-propelling cycles of sympathetic bias, inflammation, and coagulation. The counterproductive co-activation of these pathways may reflect a maladaptive interlink forged during the primordial evolution of trauma physiology. Their rapid co-mobilization enables rapid control of hemorrhage, microbial defense, and perfusion maintenance during trauma, but the pathways may behave maladaptively in the setting of modern diseases where endothelial injury may be more often precipitated by smoking, diabetes, dyslipidemia, or hypertension. Sympathetic blockade is already employed in ACS, and beta-blockers are used as antihypertensives to prevent stroke. Our hypothesis suggests that the benefits of beta-blockers in stroke may be independent of antihypertensive effects, and that adrenergia may represent a target for managing all thromboembolic disorders, independent of anti-coagulative and thrombolytic therapies. Perhaps reducing adrenergia, rather than maintaining high cerebral perfusion pressure, may represent a counterintuitive strategy for treating stroke and for reducing reperfusion injury. Plausible mechanisms by which autonomic dysfunction may induce venous thrombosis are discussed, especially in those with baroreceptor dysfunction, immobilization, or dehydration. Unexplained hypercoagulability of cancer may also operate through tumor-induced adrenergia and inflammation.
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PMID:Can thromboembolism be the result, rather than the inciting cause, of acute vascular events such as stroke, pulmonary embolism, mesenteric ischemia, and venous thrombosis?: a maladaptation of the prehistoric trauma response. 1569 86

The adverse and beneficial effects of postmenopausal hormone replacement therapy include: ischemic heart disease, stroke, pulmonary embolism, breast cancer, an increased rate of onset of asthma as well as reductions in the incidence of diabetes in women with known coronary artery disease and osteoporotic fractures. These varied effects can be explained by the down regulation of 11beta-hydroxysteroid dehydrogenase by estradiol, which results in a reduction of tissue specific cortisol production. The reduction in local cortisol production which diminishes the endogenous anti-inflammatory effects, also allows for the progression of both vascular and pulmonary inflammation. The decrease in cortisol activation reduces insulin resistance and anti-proliferative effects thereby reducing the potential for diabetes but allowing for the emergence of malignancy. Furthermore, the decreased local tissue availability of cortisol reduces the tendency for the development of osteoporosis. New techniques and drugs are being developed to evaluate the modulation of 11beta-HSD1 activity. Further study should result in new ways to control both inflammation and metabolism.
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PMID:Estradiol induced inhibition of 11beta-hydroxysteroid dehydrogenase 1: an explanation for the postmenopausal hormone replacement therapy effects. 1595 Mar 94


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