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

The pathologic aspects of an uncommon complication of diabetes mellitus, destructive arthropathy (Charcot's joint), were studied. The peripheral nerve demyelination resulting in clinically demonstrable deficits in perception of pain and vibration and in reflexes in the lower extremities reinforces the neurogenic role in this complication.
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PMID:Diabetic neuroarthropathy (Charcot's joint). 689 50

A practically complete destruction of both femoral heads including the femoral necks and acetabula was encountered in a 69-year-old patient with diabetes, which varied in intensity. This destruction, documented by radiographs which had been taken 8 years prior, had started as the typical picture of "idiopathic femoral head necrosis". In addition to diabetes, hyperuricemia and hyperlipoproteinemia were present at the time when the femoral head necrosis was first evidenced. One episode of gout was recorded. In recent years, following therapy, the hyperurecemia and hyperlipoproteinemia had normalized. The question is raised, as to whether or not the present radiological findings represent a complication of aseptic femoral head necrosis, combined with a diabetic arthropathy of the hip joints. Details of the angiographic findings and a spondylopathy, which have all the characteristics of a neuropathic spondylopathy, would favor this hypothesis. When associated with a diabetic condition, generalized osteoporosis and hypertrophic spondylosis of such a particular nature require special mention.
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PMID:Complete destruction of both femoral heads following idiopathic necrosis of the femoral heads in a diabetic patient with hyperuricemia and hyperlipoproteinemia. 699 Aug 94

Arthritis commonly accompanies clinical disturbances of metabolism, while diseases which are primarily articular may cause major general metabolic abnormalities. The relationship between diet, nutrition and joint diseases is complex and varies from simple mechanical factors (as in obesity) to complex metabolic processes. Current knowledge of these processes is extensive in some areas, such as in gout and hyperuricaemia, whereas in others, such as the arthropathy encountered after intestinal bypass surgery, it is very scant indeed. Joint disorders in hyperlipoproteinaemia and diabetes mellitus are varied and the pathogenesis of these articular problems is as yet ill understood. In view of the frequency with which these metabolic problems occur, these disorders offer no opportunities for the clinical study of the processes involved in joint inflammation and damage. In contrast, metabolic abnormalities such as hypergastrinaemia and elevated ionized calcium in rheumatoid arthritis are worthy of study, as they may offer clues to the underlying aetiology of the joint disease. This latter abnormality is suggestive of hyperparathyroidism, a condition which may present with polyarthritis and in which joint changes may be severe, although they are usually obscured by the more obvious bony problems in this disease. An illustrative historical vignette is included.
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PMID:Some metabolic aspects of arthritis. 703 19

The present article evaluates 26 cases with arterial occlusion and additional polyneuropathy in diabetes mellitus or chronic alcohol addiction. For comparison, a group of 30 patients with arterial occlusion without neurologically detectable polyneuropathy were also evaluated. It is pointed out that the osseous changes in the foot bone region are due to the additionally existing polyneuropathy and cannot be explained alone by an avascular bone necrosis in arterial vascular occlusion. Changes in the sense of an arthropathy occur in our group of patients even in case of unilateral arterial occlusion, these changes occurring bilaterally in the foot bones; after reconstruction measures in the arterial vascular system, these arthropathic changes in the foot bones continue to advance in case of persisting polyneuropathy.
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PMID:[Osseous changes in the foot bones in patients with arterial occlusion and simultaneous polyneuropathy (author's transl)]. 728 May 15

Diabetic arthropathy is a relatively rare manifestation of neuropathic disease, occurring in fewer than 5% of cases. Abnormalities of this type are confined largely to the small joints of the feet, although the larger joints of the lower limbs and the spine occasionally are affected. Some lesions, particularly in the feet, repair spontaneously, leaving radiological residua sufficiently characteristic to prompt suspicion of an unrecognised diabetic state. These include deformity of the head of the second metatarsal (akin to a Freiberg lesion), shortening of the great toe, painless deforming arthrosis of the knee, and ankylosis of interphalangeal joints. In the presence of these signs the patient should be interrogated concerning diabetes and blood sugar estimates, with provocation of necessary, obtained. Should such a diagnosis be sustained, appropriate protective measures may be undertaken to avoid a relapse of the arthropathy.
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PMID:The radiological residua of healed diabetic arthropathies. 733 Jun 72

We identified 35 homozygotes for hemochromatosis through pedigree studies. Thirteen were asymptomatic. Arthropathy was present in 20, hepatomegaly in 19, transaminasemia in 16, skin pigmentation in 15, splenomegaly in 14, cirrhosis in 14, hypogonadism in six, and diabetes in two. No homozygote was in congestive failure. Only one had the triad of hepatomegaly, hyperpigmentation, and diabetes. Serum iron was increased in 30 of 35, transferrin saturation was increased in all 35, serum ferritin in 23 of 32, urinary iron excretion after deferoxamine in 28 of 33, hepatic parenchymal cell stainable iron in 32 of 33, and hepatic iron in 27 of 27. Iron loading was 2.7 times greater in men than in women. No female had hepatic cirrhosis. Diagnosis of asymptomatic hemochromatosis is important because organ damage may be prevented by early therapy. Clinical diagnosis of early hemochromatosis is difficult. Persons with unexplained elevation of transferrin saturation should be studied for hemochromatosis.
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PMID:Homozygosity for hemochromatosis: clinical manifestations. 743 83

MRL-lpr/lpr mice spontaneously develop various manifestations of autoimmunity including an inflammatory arthropathy and immune complex glomerulonephritis. This study examines the role of nitric oxide, a molecule with proinflammatory actions, in the pathogenesis of MRL-lpr/lpr autoimmune disease. MRL-lpr/lpr mice excreted more urinary nitrite/nitrate (an in vivo marker of nitric oxide production) than did mice of normal strains and MRL-(+/+) and B6-lpr/lpr congenic strains. In addition, MRL-lpr/lpr peritoneal macrophages had an enhanced capacity to produce nitric oxide in vitro as well as increased nitric oxide synthase activity, and certain tissues from MRL-lpr/lpr mice had increased expression of inducible nitric oxide synthase (NOS) mRNA and increased amounts of material immunoreactive for inducible NOS. Oral administration of NG-monomethyl-L-arginine, a nitric oxide synthase inhibitor, prevented the development of glomerulonephritis and reduced the intensity of inflammatory arthritis in MRL-lpr/lpr mice. By using interspecific backcross mice, the gene for inducible NOS (Nosi) was mapped to mouse chromosome 11. This chromosomal localization was different from those loci that we have previously demonstrated to be linked to enhanced susceptibility to renal disease in an MRL-lpr/lpr cross. However, the chromosomal location of the NOS gene was consistent with an insulin-dependent diabetes locus identified in an analysis of nonobese diabetic (NOD) mice. These results suggest that elevated nitric oxide production could be important in the pathogenesis of autoimmunity, and that treatments to block the production of nitric oxide or block its effects might be valuable therapeutically.
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PMID:The role of nitric oxide in the pathogenesis of spontaneous murine autoimmune disease: increased nitric oxide production and nitric oxide synthase expression in MRL-lpr/lpr mice, and reduction of spontaneous glomerulonephritis and arthritis by orally administered NG-monomethyl-L-arginine. 750 9

Diabetic neuropathy (DN) is chronic complication which occurs in 50% of long standing diabetes mellitus. DN is a consequence of hyperglycemia probably through the following mechanisms: a) activation of aldose-reductase, intracellular sorbitol accumulation and myoinositol depletion, reduced activity of Na+/K+ATPase, loss of Na+ channels and demyelination; b) proteins glycation; c) microangiopathy; the first mechanism being the best known and the most reliable. DN may be subclinical or clinical. The main clinical picture is a peripheral, bilateral, symmetric polyneuropathy with a "socks and gloves" sensory impairment, muscular weakness, hyporeflexia, plantar ulcers and arthropathy. Less frequent syndromes are proximal motor neuropathy and mononeuropathy of cranial nerves or thoraco-abdominal roots. Diagnosis is based on clinical data, and may be sustained on impaired nerve conduction velocity, abnormal evoked somatosensory potentials, or sural nerve biopsy. These methods are highly sensitive but unspecific. Etiopathogenic treatment is based on glycemic control and aldose reductase inhibitors. Improvement in clinical, electrophysiologic and histopathologic data have been obtained with the latter. Symptomatic treatment includes carbamazepin, phenytoin, tricyclic antidepressives and a phenotiazin. Mononeuropathies tend to complete recovery in less than 6 months. Polyneuropathy is thought to be irreversible and progressive; however, with excellent glycemic control or with aldose reductase inhibitors nerve damage may be stabilized or even reversed.
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PMID:[Diabetic neuropathy. Current concepts on etiopathogenesis, diagnosis, and treatment]. 755 46

Because of degenerative joint diseases and the reduced resistance in older patients the correct diagnoses of joint-empyema is difficult. In 29 pat (> 60 y) the mean delay of diagnoses was 5.1 months. First location of the infection have been: urinary tract 12, pneumonia 6, skin infection 10, and decubitus 3. Risk factors have been diabetes 4, polyarthritis 3, gout 3 and tuberculosis 3. The species were: s. aureus 12, s. albus 2, streptococcus 2, diphtheroid 2, e.coli 2, pseudomonas 2, proteus 4, enterobacter 3 and salmonella 1. 8 patients demonstrated mixed infections. The high mortality (3 pat.) and the frequent general sepsis (5 pat.) underline the importance of a missed joint-empyema in the elderly.
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PMID:[Joint destruction and infection in advanced age]. 783 47

Hereditary hemochromatosis is a common disorder of iron metabolism with a prevalence as high as 8 per 1000. Affected individuals absorb excessive amounts of dietary iron and over time, tissue iron deposition results in skin discoloration, arthropathy, hepatic cirrhosis, heart failure, diabetes mellitus and impotence. Early diagnosis and institution of phlebotomy treatments will prevent these manifestations and normalize life expectancy. Once organ damage is established many of the manifestations are irreversible. Since the early manifestations of the disease are subtle, a case can be made for routine screening. This conclusion is supported by cost-effectiveness analysis based on available data. A reasonable screening strategy would start with a serum transferrin saturation. A value > or = 55% should trigger a repeat transferrin saturation in a fasting state and a serum ferritin level. If both these tests are abnormal, a liver biopsy with quantitative iron determination is the currently accepted confirmatory test.
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PMID:Management of hereditary hemochromatosis. 788 27


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