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

Wolfram syndrome was originally described as a combination of familial juvenile-onset diabetes mellitus and optic atrophy. Other neurological features subsequently emerged, and "DIDMOAD" (diabetes insipidus, diabetes mellitus, optic atrophy, and deafness) became a commonly accepted acronym. Here, we describe 4 further cases from 2 families, in whom there occurred previously unrecognized neurological features, central apnea and neurogenic upper airway collapse, together precipitating primary respiratory failure (fatal in 1 case), startle myoclonus (in 2 unrelated cases), axial rigidity, and Parinaud's syndrome. Magnetic resonance images revealed striking brainstem atrophy affecting, in particular, the pons and midbrain. The mitochondrial DNA from 3 cases (and relatives) showed no evidence of any of the previously reported abnormalities. These neurological and neuroradiological features, in conjunction with (1) analyses showing the neurodegenerative origin of optic atrophy, deafness, diabetes insipidus, and incontinence, (2) other previously reported neurological complications (including anosmia, ataxia, epilepsy, and neuropsychiatric and cognitive abnormalities), and (3) the very small number of published postmortem studies, indicate that Wolfram syndrome should be reemphasized as a unique hereditary neurodegenerative disorder with prominent optic atrophy and diabetes mellitus.
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PMID:Wolfram syndrome: hereditary diabetes mellitus with brainstem and optic atrophy. 860 54

At first, we reviewed radiographic findings of primary pulmonary tuberculosis, secondary pulmonary tuberculosis, pulmonary M. avium complex (MAC) disease without predisposing conditions, and pulmonary tuberculosis in AIDS patient. Infiltrates in lower field, mediastinal lymphadenopathy, and pleural effusion were the characteristics for primary pulmonary tuberculosis, while multiple nodular shadow with/without cavitation in S1,2,6 were the characteristics for secondary pulmonary tuberculosis. In pulmonary MAC disease without predisposing conditions, lesions progressed slowly from a cluster of a small nodules to cystic bronchiectasis with collapse of the segment or the lobe, and it took usually more than 10-years for the whole process interval. The characteristics of pulmonary tuberculosis in AIDS patient were nearly the same as those of primary pulmonary tuberculosis. Secondly, we compared clinical characteristics between pulmonary tuberculosis and pulmonary MAC disease. We reviewed the medical records of hospitalized patients who were diagnosed as pulmonary tuberculosis or pulmonary MAC disease. Systemic compromised host defense, such as diabetes mellitus or malignancy, played a more important predisposing factors in the development of pulmonary MAC disease. The average age of patients with MAC disease was found to be older than those with tuberculosis. By gender women were predominant in MAC disease, while men were predominant in tuberculosis.
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PMID:[Clinical comparison of pulmonary tuberculosis with pulmonary M. avium complex disease]. 865 91

Neonatal hyperglycaemia may be permanent or, more often, transient. Transient hyperglycaemia occurs mainly in premature and low-birth-weight neonates, especially if they are stressed or receive endovenous glucose. There is no clinical or biological sign allowing to predict these children future at the time of diagnosis, even if the seriousness of hyperglycemia, the collapse of insulin secretion, and the association to complex pathologies is more usual in permanent diabetes. This explains why the treatment must be the same, namely precocious insulin therapy.
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PMID:[Neonatal hyperglycemia and diabetes mellitus]. 881 20

Obstructive sleep apnea (OSA) is a disorder in which there is repetitive collapse and closing of the pharynx during sleep. There is growing evidence to suggest that this disorder is a major cause of essential hypertension (EH) and that successful treatment of OSA can reduce the blood pressure (BP) significantly. In addition many other patients with EH have milder forms of sleep related breathing disorders (SRBD) like snoring, and upper airway resistance syndrome (UARS) which, while not as severe as OSA, may be severe enough to also cause systemic hypertension. We therefore propose a unifying hypothesis-that many patients with EH may have sleep related breathing disturbances (SRBD) and treatment of these disorders may improve the BP. SRBD could also explain many of the epidemiological, clinical, hereditary, biochemical, hematological and physiological characteristics seen in EH. In addition, many types of secondary hypertension (those caused by excessive alcohol intake, chronic renal failure, diabetes, hypothyroidism or acromegaly) have a higher than normal prevalence of OSA and OSA may contribute to the hypertension and organ damage found in these conditions as well. Thus SRBD may play an important role in the production of many cases of essential and secondary hypertension, and their early detection and treatment could reduce the hypertension and organ damage seen in these conditions.
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PMID:Essential and secondary hypertension and sleep-disordered breathing: a unifying hypothesis. 887 97

Fine structural changes in the Achilles tendons of patients with long-term diabetes mellitus were investigated. All patients had clinical and electrophysiological evidence of diabetic neuropathy and had ulceration and/or Charcot neuroarthropathy. Several differences between tendons of diabetic (n = 12) and nondiabetic (n = 5) individuals were observed by electron microscopy. In diabetics, these differences included increased packing density of collagen fibrils, decreases in fibrillar diameter, and abnormal fibril morphology. In one diabetic patient, individual collagen fibrils were tightly apposed so that many areas of tendon appeared as a single mass of closely adhering fibrillae. In addition, foci in which collagen fibrils appeared twisted, curved, overlapping and otherwise highly disorganized were common in specimens from most patients (11 of 12). These morphologic abnormalities in the Achilles tendons of diabetics appear to reflect a poorly known process of structural reorganization that may be the result of nonenzymatic glycation expressed over many years. Such structural changes could contribute to the tightening of the Achilles tendor a phenomenon consistent with clinical observations of extreme shortening of the Achilles tendon-gastrocnemius-soleus complex common in advanced diabetic neuropaths. In patients with diabetic neuropathy, tendon shortening causes severe equinus that may precipitate serious ulceration, stress fractures, and Charcot collapse of the foot. However, in nondiabetics, the fine structure of the Achilles tendon appears normal, consistent with the finding that the ultrastructural changes result from diabetes rather than neuropathy.
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PMID:Electron microscopic investigation of the effects of diabetes mellitus on the Achilles tendon. 929 42

The epidemic spread of tuberculosis after World War II and the deficiency of appropriate antituberculotic drugs led to a renaissance of surgical procedure such as plombage thoracoplasty, initiated in 1891 by Tuffier. Especially in Germany the insertion of paraffin and polyethylene was used in order to achieve an extrapleural pneumothorax in order to collapse the tuberculous cavities in the upper lobes. Due to a high rate of early complications and the assumed cancerogenicity, in a considerable number of cases the material was removed soon after its deployment. In some cases with the filling remaining in place, 30-40 years later infections and/or neoplasms occurred. From 1985 to 1996 in two centers of thoracic surgery 13 patients underwent procedures for removal of filling material. The patients suffered from infections (n = 11), malignant lymphoma associated with infection of the plombage (n = 1) and bronchial carcinoma (n = 1). Technically, we performed the thoracoplasty described by Schede (n = 9). Schede's thoracoplasty in combination with a muscle flap repair (n = 1) or partial resection of the thoracic wall (n = 1), an empyemectomy (n = 1), and an en-bloc pleuropneumonectomy (n = 1). All patients suffered from multiple underlying diseases (COPD, coronary heart disease, diabetes mellitus). However, apart from beside two procedure related deaths (pulmonary embolism n = 1, pneumonia complicated by multi-organ failure n = 1) no other major complications were observed. The plombage material in the case of malignant lymphoma is probably carcinogenic in relation to the time of exposure and should be removed in all cases.
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PMID:[Delayed complications after extrapleural pneumonolysis for lung tuberculosis]. 941 Jun 83

Twenty-seven feet with neuroarthropathic fracture resulting in significant deformity were treated with surgical reconstruction. The average age of the patients was 57 years with 21 patients having diabetes mellitus an average of 24 years. Five patterns of midfoot collapse were identified. The most common patterns involved abduction and dorsal displacement of the forefoot with equinus of the hindfoot. Preoperative evaluation included a medical assessment, adequate control of blood sugar, and a comprehensive vascular evaluation. Five patients presented for surgical consultation with open plantar ulcers. Four were healed with total contact casting alone whereas one patient required an exostectomy to heal the ulcer before surgery. After reconstruction, all feet had improvement in their weightbearing posture. For feet with midfoot involvement, the average anteroposterior talo-first metatarsal angle increased 5 degrees, and the average lateral talo-first metatarsal angle decreased 6.5 degrees. There was no significant loss of correction at long term follow-up. The average time in a cast postoperatively was 5.7 months, and the time to unrestricted weightbearing was 7 months. All patients were able to wear over-the-counter footwear postoperatively. Significant complications included six nonunions and two feet with extension of the neuroarthropathic process. One nonunion required revision surgery, and the feet with extension of their neuroarthropathic fractures required conversion of a triple arthrodesis to a pantalar fusion and the addition of a triple arthrodesis after a successful midfoot fusion. No infections or amputations occurred as a result of the surgery. Function increased and pain decreased as a result of successful arthrodesis. Surgical reconstruction of midfoot, hindfoot, and ankle neuroarthropathic deformity is a viable alternative to amputation for patients who fail nonoperative care. Proper preoperative evaluation and assessment will result in a rate of complications comparable to foot surgery in nondiabetic patients.
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PMID:Surgical treatment of neuroarthropathic foot deformity. 949 83

Although diabetes and peripheral neuropathy are perhaps the most important risk factors for neuropathic osteoarthropathy, we hypothesized that peak plantar pressures may also be higher in patients who have this condition. We are unaware of any reports in the medical literature that have specifically addressed this hypothesis. We obtained data from the medical records of 164 diabetic patients who had been managed in a multidisciplinary tertiary-care diabetic foot-specialty clinic. We then divided the patients into four groups: those who had acute Charcot arthropathy, those who had neuropathic ulceration, those who had neuropathy without ulceration, and those who had neither neuropathy nor ulceration. The peak plantar pressures were significantly higher in the patients who had acute Charcot arthropathy and those who had a neuropathic ulcer (p < 0.001 for both) compared with the pressures in those who had no history of arthropathy and those who had neuropathy without ulceration. With the numbers available, we could not detect a significant difference in the peak pressure between the affected and the unaffected foot in the patients who had Charcot arthropathy (mean [and standard deviation], 100+/-8.5 compared with 101+/-9.6 newtons per square centimeter; p > 0.05). However, the mean peak pressure was significantly higher on the ulcerated side than on the contralateral side in the patients who had a neuropathic ulcer (90+/-18.8 compared with 86+/-20.7 newtons per square centimeter; p < 0.02). Although the midfoot was the site of maximum involvement in all patients who had Charcot arthropathy, the peak plantar pressure was on the forefoot, suggesting that the forefoot may function as a lever, forcing collapse in the midfoot.
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PMID:Elevated peak plantar pressures in patients who have Charcot arthropathy. 987 50

The drugs used to treat diabetes mellitus are diverse and involve several classes. However, these drugs can be roughly separated into hypoglycaemic agents, such as insulin and the sulphonylureas, and antihyperglycaemic agents, such as the biguanides, the alpha-glucosidase inhibitors and troglitazone. Reports of insulin overdose are rare. The major effects of insulin overdose are secondary to the insult to the CNS produced by hypoglycaemia. The mainstay of insulin overdose management is glucose replacement therapy. Sulphonylureas are the most commonly used oral antihyperglycaemic agents in the management of type 2 (non-insulin-dependent; NIDDM) diabetes mellitus. Sulphonylureas primarily cause serum glucose reduction by stimulating the release of preformed insulin from the pancreatic islets. The mainstay of sulphonylurea overdose management is glucose replacement therapy, and in severe cases, reduction of insulin release. In the large majority of patients intravenous glucose supplementation will be sufficient to maintain euglycaemia. Repaglinide, a meglitinide analogue, is a new nonsulphonylurea oral hypoglycaemic agent. In overdose, this drug may produce prolonged hypoglycaemia similar to the sulphonylureas. The primary problem with biguanide overdose is the potential for lactic acidosis. The management of biguanide overdose is largely supportive and directed at correcting the metabolic acidosis along with associated complications. The alpha-glucosidase inhibitors, acarbose, voglibose and miglitol competitively and reversibly inhibit the alpha-glucosidase enzymes (glucoamylase, sucrase, maltase and isomaltase) in the brush border in the small intestine, which delays the hydrolysis of complex carbohydrates. They appear unlikely to produce hypoglycaemia in overdose, but abdominal discomfort and diarrhoea may occur. Troglitazone is the first thiazolidinedione antidiabetic drug available. There are no data on overdose, probably because of its very recent introduction. Overdoses with antidiabetic drugs produce major morbidity, with many cases requiring intensive care medicine and prolonged hospital stays. However, fatalities are rare when treatment is initiated early. The management of the hypoglycaemic drugs (insulin and sulphonylureas) is based primarily on restoring and maintaining euglycaemia via intravenous dextrose supplementation. In the case of the sulphonylureas, reduction of insulin secretion via pharmacological intervention may also be necessary. With biguanides the main risk appears to be cardiovascular collapse secondary to profound acidosis. The management focus is on restoring acid-base balance with hyperventilation and the use of insulin to shift the utilisation of glucose from the nonoxidative pathway to the oxidative pathway. Use of haemodialysis has shown equivocal results but may be valuable in metformin overdose.
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PMID:Management of antidiabetic medications in overdose. 982 53

Apopotic cell death is reported to be prominent in the stable tissues of the failing heart, in cardiomyopathies (CM), in the sinus node of complete heart block, in B cells of diabetes mellitus, and in neurodegenerative diseases. Recently, mitochondrial (mt) control of nuclear apoptosis was demonstrated in the cell-free system. The mt bioenergetic crisis induced by exogenously added factors such as respiratory inhibitors leads to the collapse of mt transmembrane potential, to the opening of the inner membrane pore, to the release of the apoptotic protease activating factors into cytosol, and subsequently to nuclear DNA fragmentation. However, the endogenous factor for the mt bioenegertic crisis in naturally occurring cell death under the physiological conditions without vascular involvement has remained unknown. Recently devised, the total detection system for deletion demonstrates the extreme fragmentation of mtDNA in the cardiac myocytes of senescence, and mt CM harboring maternally inherited point mutations in mtDNA and on the cultured cell line with or without mtDNA disclosed that mtDNA is unexpectedly fragile to hydroxyl radial damage and hence to oxygen stress. The great majority of wild-type mtDNA fragmented into over two hundreds types of deleted mtDNA related to oxidative damage, resulting in pleioplasmic defects in the mt energy transducing system. The mtDNA fragmentation to this level is demonstrated in cardiac myocytes of normal subjects over age 80, of an mtCM patient who died at age 20 and one who died at age 19, of a recipient of heart transplantation at age 7 with severe mtCM, and in mtDNA of a cultured cell line under hyperbaric oxygen stress for two days, leading a majority of cells to apoptotic death on the third day. The extreme fragility of mtDNA could be the missing link in the apoptosis cascade that is the physiological basis of aging and geriatrics of such stable tissues as nerve and muscle.
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PMID:Mitochondrial DNA mutations and age. 992 26


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