Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

I have encountered 50 patients with clinical thrombophlebitis involving the lower extremites, with or without associated edema and pulmonary embolism, in whom longstanding self-medication with large amounts of vitamin E appeared to be a significant factor. The majority improved following cessation of vitamin E. In view of the epidemic nature of thrombophlebitis and deep vein thrombosis in the United States, the presumed innocuousness of vitamin E therapy requires reevaluation. Other clinical side effects also have been noted in patients receiving large doses of vitamin E. They include breast tenderness, elevation of blood pressure, a fatigue syndrome, myopathy, intestinal cramps, urticaria, and the possible aggravation of diabetes mellitus. The influence of concomitant metabolic, endocrine, and cardiovascular disorders on the thrombogenic potential of vitamin E is raised, and several possible mechanisms conducive to thrombophlebitis are reviewed.
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PMID:Thrombophlebitis associated with vitamin E therapy. With a commentary on other medical side effects. 43 74

Although it has long been known that both large and small blood vessels are abnormal in the tissues of diabetic patients, recent work has emphasized the widening of capillary basement membranes in diabetic tissues. Current views of the nature of this lesion and its relationship to diabetes are discussed and diabetic muscle and nerve lesions are emphasized. Other metabolic diseases with significant muscle pathology are types II, III and VII glycogen storage diseases. Myopathy with abnormal mitochondria is reviewed.
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PMID:Myopathies related to diabetes mellitus and other metabolic diseases. 105 68

1. 37 patients with pigmentary retinopathy, seeming otherwise healthy, were thoroughly examined for fine symptoms in other parts of the body, in particular for neuropathies and for blood chemistry peculiarities. 2. In 19 cases some constitutional pathology was discovered, in 4 cases hearing was affected by inner ear changes. 3. Clinically patients behaviour was changed and with electroencephalgraphy an encephalopathy was found in 7 cases. 4. Electroencephalograms were in more than 50% of cases slightly abnormal. 5. A myastenic reaction, confirmed by electromyography, occurred in one case (but not in its sibling who had also a pigmentary retinopathy.) 6. In 14 cases electromyogram was showing a neurogenic damage. Motor nerve conduction speed was lowered in 2 cases, in 5 cases it was at the lower limit of normal. In 6 cases very long distal latence times were noted. In 2 cases action potential was shortened but this could not be considered as a myopathy for certain. 7. In 6 cases a hyperlipoproteinaemia occurred. In 2 cases a mild diabetes mellitus, in 7 cases uric acid level in serum was raised. The number of cases was too small to give a statistical importance to those findings. 8. Cerebrospinal fluid was found normal in all cases. 9. This study should lead to further investigations. In spite of the small number of cases one can presume that pigmentary retinopathy is not an independent defect but is a phenomenon of a polygenetic entity.
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PMID:[Clinical-neurological and electromyographical studies of inpatients isolated with selective pigmentary retinopathy]. 112 79

The obstetrics histories of all the pregnances were studied, including the deliveries and abortions, the perinatal mortality of fetuses and the frequency of congenital malformations among newborns in 239 repeatedly pregnant women heterozygous for the gene of phenylketonuria (PKU), 40 women with the latent form of diabetes mellitus (LDM) and 96 women heterozygous for Dushenne's myopathy (MD). It was established that the frequency of women suffering from spontaneous abortions (SA) was increased as well as the SA frequency among all the pregnancies with natural results in heterozygotes for the PKU gene; it was also established that the frequency of stillborns and of the early mortality of newborns was considerably higher among women with LDM. In both these groups the frequency of congenital malformations among the newborns was also relatively high. In women heterozygous for the PKU gene the pathogenic effect was realized only during the first three months of pregnancy, while in women with LDM it was realized through all the period of pregnancy. The heterozygosity of women for MD proved not to be pathogenic for the progeny. Possible mechanisms realizing the effect of heterozygosity of women for the abovementioned recessive genes during pregnancy are discussed.
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PMID:[Effect of maternal genetic heterozygosity]. 124 Aug 17

Case 1, a 60-year-old man and case 2, a 70-year-old man had several year history of chronic renal failure with hypertension and hyperlipidemia due to diabetes mellitus. Treatment of hyperlipidemia was started by oral bezafibrate intake 1,200 mg per day in case 1 and 400 mg per day in case 2 respectively. Three to fourteen days later, both patients noticed symmetrical muscle pain and weakness. Then the symptoms worsened and they were hospitalized. At the time of admission, both patients revealed weakness in the proximal muscles of their upper and lower limbs and the serum creatine kinase and myoglobin levels were remarkably elevated. Myoglobinuria was also noted. Routine light microscopic examination of biopsied quadriceps femoris muscles of two patients showed scattered necrotic muscle fibers, some of which were under phagocytosis. The symptoms of the patients were immediately resolved after the drug was discontinued. Serum concentration of bezafibrate was remarkably elevated during treatment. Thus the diagnosis was established as having bezafibrate induced myopathy and, as far as we know, this is the first report of bezafibrate induced myopathy in Japan. On the basis of the above description, bezafibrate may induce muscle damage if dose is excess over the renal capacity. Extreme caution is warranted when the patient is placed on bezafibrate and has renal dysfunction. Strict dose adjustment is necessary in taking account of renal function to avoid muscle damage including rhabdomyolysis.
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PMID:[Bezafibrate myopathy in two patients with chronic renal failure]. 129 Nov 64

Although L-carnitine is not considered as an essential nutrient, endogenous synthesis may fail to ensure adequate L-carnitine levels in neonates, especially those born prematurely. Free L-carnitine is found in many foods, mainly those from animal sources. Absorption of free L-carnitine is virtually complete. Lysine and methionine are necessary ingredients for the biosynthesis of L-carnitine. All tissues in the body can produce deoxy-carnitine but, in humans, the enzyme that enables hydroxylation of deoxy-carnitine to carnitine is found only in the liver, brain and kidneys. Complex exchanges of carnitine and its precursors occur between tissues. Muscles take up carnitine from the bloodstream and contain most of the body carnitine stores. L-carnitine and L-carnitine esters are eliminated mainly through the kidneys, which may play a central role in the homeostasis of this compound. Thyroid hormones adrenocorticotrophin (ACTH), and diet all influence urinary excretion of L-carnitine. Free L-carnitine can be assayed in plasma and urine and is occasionally measured in muscle biopsy specimens. Plasma L-carnitine levels may not accurately reflect L-carnitine body stores. L-carnitine ensures transfer of fatty acids to the mitochondria where they undergo oxidation. This process is associated with production of short-chain acylcarnitine which exit from the mitochondria or peroxisomes. L-carnitine ensures regeneration of coenzyme A and is thus involved in energy metabolism. L-carnitine also ensures elimination of xenobiotic substances. Carnitine deficiencies are common. Currently, these deficiencies are classified into two groups. In deficiencies with myopathy, only the muscles are deficient in L-carnitine, perhaps as a result of a primary anomaly of the L-carnitine transport system in muscles. In systemic deficiencies, L-carnitine levels are low in the plasma and in all body tissues. Systemic L-carnitine deficiencies are usually the result of a variety of disease states including deficient intake in premature infants or long-term parenteral nutrition; renal failure; organic acidemias; and Reye's syndrome. Modifications in L-carnitine metabolism have also been reported in patients with diabetes mellitus, malignancies, myocardial ischemia, and alcohol abuse. A large number of supplementation trials have been carried out.
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PMID:[L-carnitine: metabolism, functions and value in pathology]. 129 65

The effects of the angiotensin converting enzyme inhibitor lisinopril on slow and fast twitch muscle contractile properties, nerve conduction and hypoxic resistance, and muscle and nerve capillary density were examined in streptozotocin-diabetic rats. Prolongation of soleus contraction and relaxation were partially prevented by treatment (p less than 0.01). A 22% deficit in fast twitch extensor digitorum longus tetanic tension production was also ameliorated (p less than 0.01). Sciatic motor and sensory conduction velocity, 25% and 12% reduced by diabetes respectively, were 75% normalized by lisinopril (p less than 0.01). There was a 47% increase in resistance to hypoxic conduction block with diabetes (p less than 0.01). Lisinopril treatment resulted in normal hypoxic resistance. Capillarization of nerve and muscle was little affected by diabetes; however, there was a 17% increase in capillary density in sciatic nerve, and a 40% increase in extensor digitorum longus muscle with lisinopril (p less than 0.01). For soleus, a smaller treatment-induced increase in capillary density led to an elevated capillary/muscle fibre ratio (p less than 0.01). These results suggest that lisinopril promoted angiogenesis. It was concluded that the beneficial effect of preventive lisinopril treatment is likely to depend upon a reduction of peripheral vascular resistance and improvement of tissue blood flow, which implicates relative hypoxia as an important factor in the development of myopathy and neuropathy in experimental diabetes.
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PMID:Angiotensin converting enzyme inhibition prevents development of muscle and nerve dysfunction and stimulates angiogenesis in streptozotocin-diabetic rats. 137 57

The effects of up to 4 months dietary supplementation with 40% galactose on muscle and nerve function were examined in rats. Galactitol, a polyol pathway metabolite, accumulated to high levels in both tissues. This led to changes similar to those found in experimental diabetes, which were largely prevented by treatment with an inhibitor of the first enzyme in the pathway, aldose reductase. For fast twitch extensor digitorum longus muscle there was weight loss, fibre damage, slowing of twitch time to peak, increased twitch tension, and reduced tetanic tension. There were no relaxation deficits. For slow twitch soleus there were no changes in tension production. However, contraction and relaxation for both twitch and tetanus were prolonged. Fatigue resistance was reduced after 1 week. Damage in soleus led to a reduction in mean fibre area after 2 months, which largely recovered by 4 months. There was a selective loss of fast oxidative glycolytic fibres. Histochemical staining for succinic dehydrogenase was normal in galactosaemic soleus, in contrast to the marked reduction seen in diabetes. Sciatic nerve conduction velocity was reduced after 2 months, particularly in normally fast conducting motor and sensory fibres. Resistance to hypoxic conduction block was increased in galactosaemic nerves to diabetic levels. It was concluded that polyol pathway hyperactivity is likely to contribute to the aetiology of diabetic myopathy and neuropathy, and that experimental galactosaemia provides a good model in which to study pathway effects without the complicated hormonal changes found in diabetes.
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PMID:Muscle and nerve dysfunction in rats with experimental galactosaemia. 153 21

The response of rat quadriceps muscle fibers to chronic streptozotocin (STZ) diabetes was studied. Transverse sections of rectus femoris muscle from diabetic and weight-matched control rats were assayed for myofibrilar adenosine triphosphatase (ATPase) and nicotinamide adenine dinucleotide-tetrazolium reductase (NADH-TR). A quantitative analysis was carried out by an automatic interactive analysis system focused on the fiber type size and distribution. STZ-induced diabetes caused important effects in this muscle, with changes in the distribution of oxidative enzyme reactions, type I fiber hypertrophy, and type II fiber atrophy, which was greater in type IIB than in type IIA. It is concluded that hypoinsulinism produces morphological alterations in proximal skeletal muscle fibers that are similar to those of neurogenic myopathy. Thus the pathological changes in these mammalian muscle fibers could explain the clinical syndrome seen in diabetic patients called "diabetic symmetrical proximal motor neuropathy," perhaps the least understood of the major neuropathic complications of diabetes.
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PMID:Proximal skeletal muscle alterations in streptozotocin-diabetic rats: a histochemical and morphometric analysis. 182 78

Cavernous electrical activity was recorded in 214 patients with erectile dysfunction and in 39 normal patients. In 34 of the 39 normal patients potentials of a uniform shape were recorded during flaccidity. At cutoff frequencies of 0.5 to 500 Hz. the duration was 8 to 18 seconds (mean 12.8 +/- 2.8, seconds, standard deviation), the amplitude was 250 to 750 microv. (mean 444 +/- 109 microv.) and the polyphasity was 8 to 22 (mean 13.8 +/- 3.3). With increasing tumescence and rigidity during audiovisual sexual stimulation, high frequency potentials of low amplitude and short duration were found in the normal patients. In impotent patients with an upper motor neuron or peripheral lesion specific types of potentials were observed. In 11 of 14 impotent patients with insulin-dependent diabetes for more than 20 years and with clinical findings of cavernous myopathy the potentials showed low amplitude, irregular shape and slow depolarizations. Abnormal findings of cavernous electrical activity were recorded in 51.6% of the consecutive impotent patients. Our clinical study suggests that single potential analysis of cavernous electrical activity may be useful in the diagnosis of cavernous autonomic neuropathy and cavernous smooth muscle myopathy.
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PMID:Single potential analysis of cavernous electrical activity in impotent patients: a possible diagnostic method for autonomic cavernous dysfunction and cavernous smooth muscle degeneration. 187 91


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