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)

Penile neuropathy is a common disease due to lesion of the sensory branch of the pudendal nerve, ie, the dorsal nerve of the penis. Sexual disorders (deterioration of erection) and sensory signs (hypoesthesia or paresthesia of the penis) are noted in patients with penile neuropathy. Electrophysiological recordings help guide the diagnosis (reduction of the sensory velocity of the dorsal nerve of the penis). Many etiologies can be found (traumatic, toxic, compressive), but the most common lesion is neuropathy related to diabetes.
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PMID:[Penile neuropathy: clinical and electrophysiologic study. Report of 186 cases]. 920 58

Diabetes mellitus associated with mitochondrial tRNA mutation at position 3243(DM-Mt3243) is a new disease. Patients have a distinctly different picture from MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes). During observations at the Saiseikai Central Hospital, the following findings were noted in DM-Mt3243 patients: DM-Mt3243 patients are diagnosed earlier with diabetes, compared to NIDDM (non-insulin dependent diabetes mellitus) controls without family history. DM-Mt3243 patients often need insulin more often than NIDDM controls without family history. Post-treatment neuropathy and insulin edema are often found in DM-Mt3243, and the two phenomena possibly have a similar pathophysiology related to mitochondrial dysfunction. Ambiguous psychiatric disorders of functional psychosis are observed frequently in DM-Mt3243. Mild headache is common in DM-Mt3243 cases. Ambiguous neuromuscular abnormalities such as sleep disturbance, paresthesia of the legs, edema of the legs, and palpitation may be symptoms associated with mitochondrial dysfunction in DM-Mt3243. Coenzyme Q may be effective in the relief of these neuromuscular symptoms.
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PMID:Diabetes mellitus associated with 3243 mitochondrial tRNA(Leu(UUR)) mutation: clinical features and coenzyme Q10 treatment. 926 20

Antioxidant treatment has been shown to prevent nerve dysfunction in experimental diabetes, providing a rationale for a potential therapeutic value in diabetic patients. The effects of the antioxidant alpha-lipoic acid (thioctic acid) were studied in two multicenter, randomized, double-blind placebo-controlled trials. In the Alpha-Lipoic Acid in Diabetic Neuropathy Study, 328 patients with NIDDM and symptomatic peripheral neuropathy were randomly assigned to treatment with intravenous infusion of alpha-lipoic acid using three doses (ALA 1,200 mg; 600 mg; 100 mg) or placebo (PLAC) over 3 weeks. The total symptom score (TSS) (pain, burning, paresthesia, and numbness) in the feet decreased significantly from baseline to day 19 in ALA 1,200 and ALA 600 vs. PLAC. Each of the four individual symptom scores was significantly lower in ALA 600 than in PLAC after 19 days (all P < 0.05). The total scale of the Hamburg Pain Adjective List (HPAL) was significantly reduced in ALA 1,200 and ALA 600 compared with PLAC after 19 days (both P < 0.05). In the Deutsche Kardiale Autonome Neuropathie Studie, patients with NIDDM and cardiac autonomic neuropathy diagnosed by reduced heart rate variability were randomly assigned to treatment with a daily oral dose of 800 mg alpha-lipoic acid (ALA) (n = 39) or placebo (n = 34) for 4 months. Two out of four parameters of heart rate variability at rest were significantly improved in ALA compared with placebo. A trend toward a favorable effect of ALA was noted for the remaining two indexes. In both studies, no significant adverse events were observed. In conclusion, intravenous treatment with alpha-lipoic acid (600 mg/day) over 3 weeks is safe and effective in reducing symptoms of diabetic peripheral neuropathy, and oral treatment with 800 mg/day for 4 months may improve cardiac autonomic dysfunction in NIDDM.
Diabetes 1997 Sep
PMID:Alpha-lipoic acid in the treatment of diabetic peripheral and cardiac autonomic neuropathy. 928 2

Myotonic dystrophy (DM) is the most common adult muscular dystrophy and follows an autosomal dominant pattern of inheritance. Up to now, the clinical diagnosis of DM was based on symptoms presented such as encephalopathy, facies myopathica, paresthesia, atrophy, myotonia, mental retardation, cataract, diabetes, cardiac conduction defects and electromyography. Since 1991 the specific molecular defect in DM is known and a respective diagnosis is possible. The mutation responsible for DM is the expansion of an unstable trinucleotide repeat, (CTG)n, in the 3'-untranslated region of the myotonin protein kinase gene. It is now generally accepted that the CTG repeat length correlates with the clinical category and the age at onset of the disease; therefore genetic tests are essential in monitoring and management of DM-patients and their family members. Based on the average incidence in Europe about 1000 affected individuals can be expected in Austria, a high percentage of whom is, however, not recognized as carries of the DM-mutation. After having established a genetic diagnosis in Austria allowing the detection of this mutation in DM-patients and their relatives, improvement of the diagnostic procedure should be possible.
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PMID:Myotonic dystrophy: molecular genetics and diagnosis. 949 72

Meralgia paresthetica may be associated with diabetes, trauma, infection, and use of self-retaining retractors. Our patient experienced left upper thigh paresthesia after undergoing laparoscopic myomectomy with extensive dissection of the left retroperitoneal space. Neurologic evaluation confirmed meralgia paresthetica. The patient was observed for 4 months, by which time the neuropathy resolved spontaneously.
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PMID:Laparoscopic myomectomy-an unusual cause of meralgia paresthetica. 966 57

Temporary lingual and labial paraesthesia are not uncommon following the removal of mandibular third molar teeth. In patients with insulin-treated diabetes circum-oral paraesthesia is a common and important sign of impending hypoglycaemia. This report highlights the case of a 17-year-old girl with Type 1 (insulin-dependent) diabetes who, following the extraction of her four wisdom teeth, experienced minor circum-oral sensory disturbances. These effectively masked her early warning signs of impending hypoglycaemia which had hitherto allowed her to have very good glycaemic control. Trembling, sweating and loss of concentration became the new presenting symptom complex, which she found both disabling and worrying. Fortunately, within six months the paraesthesia had subsided and the patient was once again able to appreciate her usual warning symptom of impending hypoglycaemia.
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PMID:Early warning signs of impending hypoglycaemia masked by post-extraction labial paraesthesia. 971 2

Diabetic neuropathy is a common complication in diabetes mellitus. Diabetic neuropathy is accompanied by alterations in axonal excitability, which can lead to either "positive" (paresthesia, dysesthesia, pain) and/or "negative" (hypesthesia, anesthesia) symptoms. The mechanisms underlying these alterations in axonal excitability are not well understood. Clinical tests reveal reduced nerve conduction velocity and axonal loss, but fail to explain nerve excitability. Many different factors have been suggested in relation to the pathophysiology of diabetic neuropathy. There are probably as many factors as there are different clinical pictures in diabetic neuropathy. Nevertheless, it seems that hyperglycemic hypoxia is mainly responsible for the electrophysiological changes seen in damaged diabetic nerves. This article summarizes experimental data indicating that a dysfunction of ion conductances, especially voltage-gated ion channels, could contribute to abnormalities in the generation and/or conduction of action potentials in diabetic neuropathy.
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PMID:The role of axonal ion conductances in diabetic neuropathy: a review. 973 52

Compared with control subjects, patients with amyotrophic lateral sclerosis (ALS) have been reported to experience less or no paresthesias during and after release of ischemic compression of the upper arm for 10 min. This is reminiscent of the resistance to ischemia of diabetic patients, in whom sensory and motor axons undergo less ischemic depolarization and less postischemic hyperpolarization than in control subjects. The present study compared the changes in axonal excitability produced by ischemia for 10 min in 21 patients with ALS and 14 age-matched control subjects. Fewer patients reported intraischemic or postischemic paresthesias and the intensity of paresthesias was less, but this was significant only for postischemic paresthesias. There were quantitatively similar changes in refractoriness, supernormality, and strength-duration time constant during ischemic compression, but the increase in excitability of motor axons was less during the second half of ischemia in the patients. After release of ischemia the postischemic hyperpolarization was greater in the ALS patients, the opposite of what occurs in diabetes. These changes could reflect reduced intraneural K+ accumulation due to loss of motor axons or an alteration in nerve metabolism or membrane properties. Either way, the present study has failed to confirm previous reports of "ischemic resistance" in ALS, and indicates that the changes in axonal properties in ALS are not analogous to those in diabetes mellitus.
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PMID:Ischemic resistance of cutaneous afferents and motor axons in patients with amyotrophic lateral sclerosis. 984 71

Between January/1989 and June/1996, 1,059 carpal tunnel syndrome hands (CTS) from 668 patients were studied. None had been previously operated and all had bilateral conduction studies; peripheral neuropathy was excluded. The patients were selected with sensory median/radial difference (MRD) > or = 1.0 ms that strongly supports electrodiagnosis of CTS (standard deviation > 6) after stimulation on wrist and recording on thumb. Normal MRD were obtained in 125 hands with upper limit of normality = 0.43 ms (mean + 2 SD). The age ranged from 17 to 83 years (mean 47.5) and 91.3% were female; the complaints were bilateral in 72% and nocturnal/awakening in 85.3%. Pain, numbness and paraesthesia occurred in 64.4%; pain as the only symptom was rare but proximal extension was frequent (39.4%). All fingers were symptomatic in 42.5%, followed by middle, middle-ring, thumb-index-middle and then index-middle-ring ones. There was no correlation with traumatic past history on wrist. The duration CTS symptoms ranged from 1 to > 120 months. Diabetes mellitus was present in 4.4% even after peripheral neuropathy exclusion.
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PMID:[Carpal tunnel syndrome: clinical and epidemiological study in 668 cases]. 1041 19

Ultimately traceable to neural glucose deprivation, symptoms of hypoglycemia include neurogenic (autonomic) and neuroglycopenic symptoms. Neurogenic symptoms (tremulousness, palpitations, anxiety, sweating, hunger, paresthesias) are the results of the perception of physiologic changes caused by the autonomic nervous system's response to hypoglycemia. Neuroglycopenic symptoms (confusion, sensation of warmth, weakness or fatigue, severe cognitive failure, seizure, coma) are the results of brain glucose deprivation itself. Glycemic thresholds for symptoms of hypoglycemia shift to lower plasma glucose concentrations following recent episodes of hypoglycemia, leading to the syndrome of hypoglycemia unawareness--loss of the warning symptoms of developing hypoglycemia. Thus, patients with recurrent hypoglycemia (e.g., those with tightly controlled diabetes or with an insulinoma) often tolerate abnormally low plasma glucose concentrations without symptoms.
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PMID:Symptoms of hypoglycemia, thresholds for their occurrence, and hypoglycemia unawareness. 1050 Sep 27


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