Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We conducted a double-blind, placebo-controlled, crossover study of the effectiveness of amitriptyline and fluphenazine in alleviating the pain of diabetic peripheral neuropathy in six diabetic patients. Pain was evaluated by the patients with a graphic rating scale. A placebo response was found, but no additional effect of amitriptyline and fluphenazine was seen. Although the statistical power of this study was low, these data, when combined with a reevaluation of previous trials of amitriptyline and fluphenazine in the treatment of painful diabetic neuropathy, indicate that there is no justification for the use of these agents in the treatment of painful neuropathy outside of large, controlled clinical trials. Depression as a possible cause of this condition should not go unnoted or untreated.
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PMID:A trial of amitriptyline and fluphenazine in the treatment of painful diabetic neuropathy. 351 12

Chickens given 15 to 45 ppm dietary corticosterone 1 day prior to and 5 days following subcutaneous administration of 1 mg/kg 0,0-diisopropyl phosphorofluoridate (DFP) were not protected from either clinical delayed neuropathy, depression of neurotoxic esterase activity or advanced degenerative peripheral nerve myelinated fiber damage.
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PMID:Absence of a protective effect of corticosterone on 0-0-diisopropyl phosphorofluoridate (DFP) induced delayed neurotoxicity in chickens. 387 40

Esophageal motility abnormalities, neuropathy, and psychiatric illness were independently determined in 30 patients with type 1 or type 2 diabetes mellitus to clarify the interrelationship of these findings in diabetics. Fifteen patients (50%) were found to have esophageal contraction abnormalities, a specific cluster of manometric derangements. Diagnoses of depression, dysthymia, or generalized anxiety disorder were made in 87% of those with contraction abnormalities but in only 21% of the patients with normal manometric patterns (p = 0.002). Log-linear analysis confirmed that this association was independent of neuropathy effects (p less than 0.001). Several changes in individual manometric parameters related to neuropathy alone were appreciated only when the patients with psychiatric illness were excluded from the analysis. These data indicate that some of the esophageal neuromuscular dysfunction observed in diabetics is independent of neuropathy yet is strongly associated with psychiatric disorder. Such findings help to clarify the discrepant relationship of motility disturbances to neuropathy noted in prior reports. We conclude that consideration should be given to psychiatric illness as well as to neuropathy when interpreting manometric features suggestive of autonomic dysfunction in diabetic patients.
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PMID:Correlation of esophageal motility abnormalities with neuropsychiatric status in diabetics. 395 33

80 patients with inoperable non-small cell bronchial carcinoma were treated, at an interval of 4 weeks between them, with ifosfamide (2 g/m2 on days 1-5) and cisplatin (75 mg/m2, day 1). All diagnoses had been confirmed histologically. The course of 72 patients (36 with squamous carcinoma, 25 with adenocarcinoma, two with alveolar-cell carcinoma and nine with large-cell carcinoma) could be evaluated. There were four complete and 21 partial remissions (response rate 35%). In a further 14 patients temporary arrest of tumor growth was registered. Median survival time of all patients was 8.3 months, for those with complete and partial remission 11.5 months. Patients in whom the tumor progressed lived on average 3.9 months. Age and general state of the patients, as well as histological tumor type, had no influence on the results of treatment. Patients in stage IV lived, at seven months, significantly less long than those with only loco-regional spread (11 months). Main side-effects were vomiting, bone-marrow depression and neuropathy. Urotoxicity was not significant, as a result of treatment with mesna. Remission rate and survival time of these patients corresponded with the results obtained with other cisplatin combinations.
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PMID:[Chemotherapy of the non-small cell carcinoma of the lung with ifosfamide and cisplatin]. 608 64

Applications of pulse-labeling techniques to the study of axonal transport have provided new insights into certain types of peripheral nerve disease. In normal neurons, many of the newly synthesized proteins that are rapidly transported to distal parts of the cell eventually undergo a process of "turnaround," after which they are carried back to the cell bodies for degradation. This turnaround is selectively impaired in rat nerves early in the course of streptozotocin-induced diabetes and of experimental neuropathies induced by exposure to acrylamide, zinc pyridinethione, or p-bromophenylacetylurea. In the neuropathy of p-bromo-phenylacetylurea, depression of turnaround precedes the clinical signs of neurologic dysfunction, is later proportional to the severity of the disability, and may account for the characteristic accumulation of debris in preterminal axons.
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PMID:Abnormalities of axonal transport: are they a cause of peripheral nerve disease? 618 27

Twenty-one patients with painful diabetic neuropathy were followed up for about 18 months by means of physical and psychological tests. Patients with painful diabetic neuropathy had significantly more neurotic, anxious and depressive traits than those with non-painful diabetic neuropathy. During the course of the study, 17 patients out of 21 were found to be relieved of their neuropathic symptoms with improved blood glucose control and medications. However, despite this improvement, diabetic retinopathy and nephropathy of the patients deteriorated. Patients with improved neuropathy had gained body weight, with a concomitant relief of depression, nervous tendency and anxiety. However, lack of extroversion was not changed at all. Patients with painful diabetic neuropathy were significantly less extroversive than those with non-painful diabetic neuropathy, even when their neuropathic symptoms might have improved. This study shows that although nervousness, anxiety and depressive tendencies may be secondary to the symptoms of painful diabetic neuropathy, lack of extroversion can be a primary characteristic trait which may easily induce painful diabetic neuropathy.
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PMID:A follow-up study of painful diabetic neuropathy: physical and psychological aspects. 667 Jan 2

Observations have been made on nine cases of painful diabetic neuropathy of acute onset. All cases were male and all were associated with and preceded by precipitous and severe weight loss. The pain was of a continuous burning quality and experienced mainly in the legs, especially distally. Contact discomfort of the skin was often a troublesome feature, but sensory loss was mild or absent, and reflex loss or depression not invariable. There were no accompanying motor signs. Depression and impotence were constant features. The weight loss responded to adequate control of the diabetes with insulin and was followed by improvement in the neuropathy. The severe manifestations subsided in all cases within 10 months, and in most cases within 6 months, and later resolved completely in all except one. No recurrences were observed after follow-up periods of up to 6 years. Abnormalities of nerve conduction were mild or even lacking. Sural nerve biopsies from three cases taken in the acute stage showed evidence of active degeneration of myelinated nerve fibres of all diameters and also degeneration of unmyelinated axons. There was a mild degree of demyelination. It is concluded that acute painful diabetic neuropathy is a distinct syndrome, occurring in insulin or noninsulin dependent patients of any duration, and unrelated to other diabetic complications. It is separable from other types of painful diabetic sensory polyneuropathy that have been described.
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PMID:The natural history of acute painful neuropathy in diabetes mellitus. 687 82

The toxic effects of chronic ethanol abuse on cerebral and hepatic function have long been recognized. The role of ethanol abuse as an etiologic factor in heart disease is less clear and is often attributed to coexistent malnutrition. However, malnutrition has been dissociated from ethanol use in many patients with congestive cardiomyopathy. Studies in various animals provide major support for the role of ethanol as a toxic agent when used in large amounts for a prolonged period. Abnormalities that result from ethanol in test animals include depression of left ventricular performance and metabolic and morphologic changes that parallel the changes in human alcoholics with subclinical mechanical dysfunction of the heart, such as symptomatic cardiac arrhythmias, particularly during intensive alcohol ingestion. What causes the progression to heart failure or arrhythmias is not known, but several factors may be involved. These include, particularly in males, the cumulative effects of ethanol alone or after intensified drinking episodes, excessive exposure to trace metals or superimposed infection. The low prevalence of clinical nutritional deficiency in patients with alcoholic cardiomyopathy and the apparent infrequency of heart failure in patients with cirrhosis or neuropathy supports the view that the cardiac abnormality is often not dependent on malnutrition. Clinical data indicate that the cessation of alcohol intake may reverse the disease or interrupt its progression in many patients. However, the pathogenetic process may continued unabated in some who become abstinent.
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PMID:Ethanol abuse and heart disease. 702 Sep 81

The authors treated 51 patients with solid tumours with vindesine 4 mg/m2, generally every third week, in combination chemotherapy protocols scheduled according to diurnal variability of kinetics. No dose-related sensory disorders were observed: On the contrary, motor toxicity appeared cumulative: 1) Early depression of osteotendinous reflexes from the first course onward, with progressive deterioration. No more normal reflexes could be evoked after 55 mg; 2) Early appearance of neurogenic pattern in the electromyograph after 5-10 mg. Progressive alteration with no normal detection recordings after 45 mg; 3) Late slowing down of conduction speeds (normal in 50% of cases up to 55-60 mg). Improvement or even complete recovery of neuropathy was documented following reduction of the unit dose, increased time interval between doses, or discontinuation of the treatment. The drug had to be withheld in only three patients: in two cases a low dosage related to individual sensitivity was being used.
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PMID:Neurological toxicity of vindesine used in combination chemotherapy of 51 human solid tumors. 730 35

1. Baroreflex sensitivity was evaluated in 22 non-dialysed patients with chronic renal failure secondary to chronic glomerulonephritis. Baroreflex sensitivity was judged by the slope of the linear regression of the pulse interval on the rise in systolic blood pressure with injection of phenylephrine or reduction by amyl nitrite inhalation. 2. Baroreflex sensitivity was reduced in these patients as compared with normal controls. Reduction of baroreflex sensitivity was significantly greater in nine hypertensive than 13 normotensive patients with chronic renal failure. 3. A significant positive correlation was found between baroreflex sensitivity and motor nerve conduction velocity measured on ulnar nerve in 13 patients examined. 4. Saline was given with high dietary salt intake to seven normotensive patients with chronic renal failure for 2 or 5 days in order to determine whether the severe depression of baroreflex sensitivity can be an initiating factor for hypertension. Blood pressure was raised to hypertensive levels within 5 days in two patients in whom baroreflex sensitivity was nearly as low as that of hypertensive patients, but not in five cases whose baroreflex sensitivity was normal or only mildly depressed. Plasma volume increased to the same degree in both groups. Baroreflex sensitivity did not change in the former two cases despite blood pressure elevation. 5. It is concluded that reduced baroreflex sensitivity in chronic renal failure correlated with the prescence ofhypertension, as well as uraemic neuropathy, and may be one of the pathogenetic mechanisms of hypertension in end-stage chronic glomerulonephritis.
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PMID:Baroreflex sensitivity in renal failure. 735 50


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