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

A 40-year-old man presented with hardening of the skin of his hands and upper back, which had slowly worsened with time. His medical history included insulin-dependent diabetes mellitus since childhood. Histopathologic features of a biopsy specimen from the skin of his back showed a thick reticular dermis with collagen bundles in a haphazard array, which were separated by increased deposits of connective-tissue mucin. Scleredema and diabetic sclerodactyly are both well recognized skin findings that may occur in patients with diabetes mellitus. It is important to differentiate this condition from scleroderma. Treatment is difficult, and therefore many modalities have been used. This patient has improved with aminobenzoate, colchicine, and DMSO gel.
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PMID:Scleredema and diabetic sclerodactyly. 1640 75

Amifostine is a broad-spectrum cytoprotective agent approved for protection against cisplatin toxicities and radiation-induced xerostomia; strong clinical evidence exists that amifostine protects normal mucosa and lung from radiation damage. Hypotension, nausea/vomiting, fatigue and fever/rash are the main side-effects associated with amifostine administration. The present study summarizes our experience on daily amifostine administration to cancer patients with various coexisting medical conditions and diseases. The tolerance and the eventual interference of amifostine with the course of the coexisting diseases is reported, providing a core list of medical conditions met in radiotherapy practice, their compatibility with amifostine administration and recommendations on how to deal with these patients. This list comprises genetic diseases (xeroderma pigmentosum, glucose-6-phosphate dehydrogenase deficiency), autoimmune disorders (vitiligo, scleroderma, thyroiditis, perforating collagenosis), metabolic diseases (diabetes mellitus), cardiovascular diseases, neuro/psychiatric diseases and other medical conditions (hypoglycemia, hepatic cirrhosis, alcoholism). A high incidence of fever/rash was noted in patients with autoimmune diseases, while all other conditions did not alter the patterns of side-effects expected following amifostine administration.
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PMID:Amifostine administration during radiotherapy for cancer patients with genetic, autoimmune, metabolic and other diseases. 1642 30

Gastroparesis refers to chronically abnormal gastric motility characterized by symptoms suggestive of mechanical obstruction and delayed gastric emptying in the absence of mechanical obstruction. It may be idiopathic or attributable to neuropathic or myopathic abnormalities, such as diabetes mellitus, postvagotomy, postviral infection, and scleroderma. Dietary and behavioral modification, prokinetic drugs, and surgical interventions have been used in managing patients with gastroparesis. Although mild gastroparesis is usually well managed with these treatment options, severe gastroparesis may be very difficult to control and may require referral to a specialist center if symptoms are intractable despite pharmacological therapy and dietetic support. New advances in drug therapy, botulinum toxin injection, and gastric electrical stimulation techniques have been introduced and might provide new hope to patients with refractory gastroparesis. This article critically reviews the advances in the field from the perspective of the clinician.
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PMID:Gastroparesis: clinical update. 1669 89

Free radical-mediated oxidative damage and consequent protein modification by the end products of oxidative damage are important mediators of cell toxicity and disease pathogenesis. Aldehydic products, mainly the 4-hydroxy-2-alkenals, form adducts with proteins and make them highly immunogenic. Oxidative modification of proteins has been shown to elicit antibodies in a variety of diseases including systemic lupus erythematosus (SLE), alcoholic liver disease, diabetes mellitus (DM), and rheumatoid arthritis (RA). Oxidatively modified DNA (8-oxodeoxyguanine) and low-density lipoproteins (LDL) occur in SLE, a disease in which premature atherosclerosis is a serious problem. In addition, immunization with 4-hydroxy-2-nonenal (HNE)-modified 60-kDa Ro autoantigen elicits an accelerated epitope spreading in an animal model of SLE. Advanced glycation end product (AGE) pentosidine and AGE-modified IgG have been shown to correlate with RA disease activity. Oxidatively modified glutamic acid decarboxylase is important in type 1 DM, while autoantibodies against oxidized LDL are prevalent in Behcet's disease. The fragmentation of scleroderma-specific autoantigens occurs as a result of oxidative modification and is thought to be responsible for the production of autoantibodies through the release of cryptic epitopes. In the face of overwhelming evidence for the involvement of oxidative damage in autoimmunity the administration of antioxidants is a viable untried alternative for preventing or ameliorating autoimmune disease, although results in cardiovascular disease are disappointing.
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PMID:Oxidatively modified autoantigens in autoimmune diseases. 1686 87

The purpose of this work is to report soft tissue calcifications in severely diabetic patients that simulate venous stasis or scleroderma, without other stigmata of these diseases. Findings from lower extremity radiographs were reviewed on two patients with severe diabetes mellitus and abnormal soft tissue calcifications. Findings were correlated with clinical history, physical exam findings, and laboratory values. Both patients in this study demonstrate radiographic findings of lower extremity soft tissue calcifications similar to those seen in venous stasis or scleroderma. Clinical history, physical examination, and laboratory values support severe diabetes mellitus, with no evidence of these other disease entities. Patients with severe diabetes mellitus may exhibit soft tissue calcifications of their lower extremities that may simulate the changes of venous stasis or scleroderma. This association has not been previously described.
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PMID:Soft tissue calcifications in the lower extremities of severely diabetic patients simulating venous stasis or collagen vascular disease. 1703 8

Diabetes mellitus is the commonest endocrine disease in all populations and all age groups. It is a syndrome of disturbed intermediary metabolism caused by inadequate insulin secretion or impaired insulin action, or both. Anemia is a common accompaniment of diabetes, particularly in those with albuminuria justifying tubulointestitial injury or reduced renal function. There are other additional factors present in diabetes, which may contribute to the development of an increased risk of anemia. Cord blood, because of its rich mix of fetal and adult hemoglobin, high platelet and WBC counts, hypo-antigenic nature, altered metabolic profile and high affinity for oxygen, may be an ideal choice for cases of diabetes with severe anemia necessitating blood transfusion. This article presents my team's experience with 78 units of placental umbilical cord whole blood (from 1 April 1999 to April 2005), collected after lower uterine cesarean section (LUCS) from consenting mothers (56 ml-138, ml mean 82 ml +/- 5.6 ml SD, median 84 ml, mean packed cell volume 49.7 +/- 4.2 SD, mean percent hemoglobin concentration 16.6 g/dl +/- 1.5 g/dl SD) and transfused to diabetes patients with microalbuminuria and severe anemia necessitating transfusion. After collection, the blood was transfused, in most cases immediately after completion of the essential norms of transfusion. In rare cases, it was kept in the refrigerator and transfused within 72 hours of collection to a suitable recipient. For inclusion in this study, the patient's percent plasma hemoglobin had to be 8 g/dl or less (the pretransfusion hemoglobin in this series varied from 5.2 g/dl to 7.8 g/dl) in the background of type two diabetes (fasting sugar 200 mg or more), along with features of microalbuminuria (albumin excretion 30-299 mg/g creatinine). This study included 39 informed consenting patients (22 males + 17 females, aged 48-74 yrs, mean 59.6 yrs). The patients were randomized into two groups: Group A (control cases N = 15, males = 8 and females = 7) and Group B (study group N = 24, males = 14 and females = 10). In Group A the rise of hemoglobin (Hgb) after two units of adult blood transfusion was 1.5 to 1.8 g/dl, as seen after a 72-hour blood sample assessment. The rise of Hgb as noted after 72 hours of two units of freshly collected cord blood transfusion was .6 g/dl to 1.5 g/dl. Each patient received two of four units of freshly collected cord blood transfusion (two units at a time), depending on availability and compatibility. Microalbuminuria was assessed in both groups after one month of treatment with transfusion and other identical support. The mean result was 152 +/- 18 m SD of albumin per gram of creatinine excreted through 24-hour urine (pre-transfusion mean excretion was 189 +/- 16 mg) in Group A and 103 +/- 16 mg SD of albumin excretion per gram of creatinine in 24-hour excretion of urine in Group B (pretransfusion mean excretion was 193 +/- 21 mg). Univariate analysis using Fisher's exact test was performed for the results of Groups A and B. The difference between Group A and B values and its comparison with the pre-transfusion microalbuminuria appeared to be statistically significant (p < less than .003). We have not encountered any clinical, immunological or non-immunological reaction so far in either group. Fetomaternal cell traffic has been implicated as the cause of scleroderma in mothers delivering male babies. In the present series, we did not see any such rare and unusual complication due to neonatal blood transfusion in the adult system in Group B patients in the six years from the initiation of the study.
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PMID:Placental umbilical cord blood transfusion: a new method of treatment of patients with diabetes and microalbuminuria in the background of anemia. 1708 81

NKT cells are a subset of regulatory lymphocytes characterized by co-expression of the NK cell receptor-CD161 and an invariant TCR-alpha chain (Valpha14-Jalpha28). They are most abundant in the liver, spleen, and bone marrow. NKT lymphocytes have been implicated in the regulation of autoimmune processes in both mice and humans. Activation of NKT lymphocytes leads to rapid amplification of either IFNgamma or IL4, endowing these cells with the capability to mediate both pro-inflammatory and anti-inflammatory immune responses. Activation of this subset of cells is associated with significant liver damage in the Concanavalin A immune mediated hepatitis model. Administration of CD1d ligand has a protective role in collagen-induced arthritis in mice. Disease amelioration was associated with a shift in the immune balance from a pathological Th1 type response towards a protective Th2 type response. In humans, patients with SLE, scleroderma, diabetes, multiple sclerosis, and rheumatoid arthritis have lower numbers of peripheral NKT cells. NKT lymphocytes promote tumor rejection in experimental models of tumor immunotherapy. In contrast, NKT lymphocyte-related anti-tumor activity is associated with pro-inflammatory Th1-type immune responses. NKT cells were shown to have a role in suppression of hepatocellular carcinoma (HCC) via immune regulation towards tumor derived antigens, and adoptive transfer of dendritic cells pulsed ex vivo with the same antigens. NKT lymphocytes are activated by interaction of their TCR with glycolipids presented by CD1d, a nonpolymorphic, MHC class I-like molecule expressed by antigen presenting cells, and also by hepatocytes. Several possible ligands for NKT cells have recently been suggested including CD1d bound Glucocerebroside. Glucocerebroside (GC, beta-glucosylceramide), a naturally occurring glycolipid, is a metabolic intermediate in the anabolic and catabolic pathways of complex glycosphingolipids. Its synthesis from ceramide is catalyzed by the enzyme glucosylceramide synthase. Inherited deficiency of glucocerebrosidase, a lysosomal hydrolase, results in Gaucher's disease. Patients with Gaucher's disease have altered humoral and cellular immune profiles and increased peripheral blood NKT lymphocytes. CD1d-bound glucocerebroside does not activate NKT cells directly, and may inhibit activation of NKT cells by alpha-GalCer. On the other hand, glucosylceramide-synthase deficiency was shown to lead to defective ligand presentation by CD1d, with secondary inhibition of NKT cell activation. Recent studies have suggested that a number of glycolipids, including GC, have an immune modulatory effect in several immune mediated disorders. The ability to alter NKT lymphocyte function in various settings and the potential application of natural glycolipids for treatment are discussed.
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PMID:Glycolipids as immune modulatory tools. 1710 Jun 36

Werner's syndrome (WS) is a rare hereditary disorder which is characterized by clinical signs of premature aging. A 31-year-old man presented with a 12-year history of hoarseness. Also noted were diabetes mellitus, cataracts, scleroderma-like skin atrophy, osteoporosis, and hypogonadism. A clinical diagnosis of WS was made. Laryngoscopy revealed bowed vocal folds resulting in a spindle-shaped closure with glottal incompetence during phonation. We used Gortex for medialization of the middle part of vocal fold to correct the glottal gap in this patient. Despite correction of glottal incompetence in patients with WS, quality of voice could not be improved to that of age-matched normal individuals.
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PMID:Werner's syndrome: a rare cause of hoarseness. 1724 70

Gastroparesis is a chronic alteration of gastric motility characterized by symptoms suggestive of mechanical obstruction and delayed gastric emptying in the absence of obstruction. Gastroparesis can be idiopathic or attributable to neuropathy or myopathy as in diabetes mellitus and scleroderma or can occur after vagotomy. Diagnosis is based on symptoms (nausea, vomiting, abdominal distension and early satiety), physical examination (capotement) and on complementary investigations, the procedure of choice being isotope gastric emptying tests. Treatment depends on the clinical repercussions. In most patients, gastroparesis can be controlled by prokinetic drugs, dietary measures, exclusion of drugs that alter gastric emptying, and exhaustive control of blood glucose levels. In patients with severe gastroparesis, hospital nutritional measures (intravenous and/or enteral), gastric decompression and intravenous antiemetic and prokinetic agents are required. Aggressive nutritional therapies (parenteral or enteral nasojejunal nutrition), intrapyloric injection of botulinum toxin, implantation of a gastric stimulation device, or gastrectomy should only be used in patients unresponsive to conservative treatment or if there is selective alteration of gastric motility.
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PMID:[Diagnostic and therapeutic approach to patients with gastroparesis]. 1766 20

The ocular manifestations are described in autoimmune disease, being most common associated with systemic lupus erythematosus, scleroderma, rheumatoid arthritis, insulin-dependent diabetes mellitus, and dermatomyositis. Nonetheless, the antiphospholipid syndrome is a relatively newly recognized autoimmune disorder. Ocular conditions in which to consider antiphospholipid syndrome include amaurosis fugax, transient ischemic attack, retinal haemorrhages and cotton wool spots, central retinal vein and artery occlusion, anterior ischemic optic neuropathy, ophthalmic and cilioretinal artery occlusions. Ocular features due to antiphospholipid antibodies - induced thrombosis should be treated with anticoagulant drugs. In opposition, for the treatment of ocular features due to immunological mechanisms such as vasculitis, immunosuppressants seem to be more suitable. The aim of this article is to underline the mainly ocular features of Hughes' syndrome and for the most part attention should be paid to the patients with central retinal vascular occlusion with no cause but most likely caused by lupus anticoagulant.
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PMID:Ocular manifestations of antiphospholipid (Hughes)' syndrome--minor features? 1806 49


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