Octreotide, a long-acting somatostatin analogue, in diabetic neuropathic pain.
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Aged↗
Biomedical subjects
A W Chan
Publications and source records attributed to A W Chan.
Contact thermography of painful diabetic neuropathic foot.
OBJECTIVE: To investigate regional differences in skin blood flow (measured by contact thermography) in the diabetic neuropathic foot and to examine the effect of foot temperature on the severity of neuropathic pain. RESEARCH DESIGN AND METHODS: Thirty-five diabetic patients with painful polyneuropathy (PPN) and 33 healthy age- and sex-matched control subjects comprised the study. Mean foot temperature (MFT) in PPN (mean +/- SE 28.3 +/- 0.3 degrees C) was significantly higher (P less than 0.001) than in the control subjects (25.9 +/- 0.5 degrees C), with the highest temperatures over the metatarsal areas and heel. Visual analogue scale pain score (mean +/- SD 5.3 +/- 1.9 cm) did not correlate with MFT (r = -0.14, P = 0.52). In 10 patients with PPN followed for 2-8 mo (mean 4.6), MFT fell by 1.6 degrees C (P = 0.05), but pain scores did not alter. CONCLUSIONS: Neuropathic pain is unaffected by alterations in skin temperature. Elevated skin temperatures at recognized sites of weight bearing (metatarsal heads and heels) are common in the diabetic neuropathic foot and may indicate tissue injury or inflammation induced by pressure trauma or increased arteriovenous shunting. Follow-up studies will determine whether thermographic hot spots are more susceptible to ulceration.
Diabetic Neuropathies↗
Longitudinal changes in serum fructosamine do not parallel those in glycated haemoglobin in young adults with insulin-dependent diabetes.
In 93 adolescent and young adult patients with type 1 diabetes (163 paired comparisons) changes in fructosamine concentration correlated poorly with changes in HbA1 (r = 0.53); this correlation was no better if fructosamine values were adjusted for serum albumin by calculating a fructosamine/albumin index, F.A.I. (155 pairs, r = 0.50). These correlation coefficients were lower than those for cross-sectional comparisons (HbA1 vs. fructosamine, r = 0.74; HbA1 vs. F.A.I., r = 0.80). One-way analysis of variance showed that values of HbA1, fructosamine and F.A.I. all tended to increase as glycaemic control, judged by the clinician, worsened (P less than 0.001). HbA1 correlated better with clinical assessment than did either uncorrected fructosamine or F.A.I. We conclude that changes in fructosamine from one clinic visit to the next do not provide a basis for changing therapy. Clinical assessments tend to agree with values for HbA1, which may be more reliable than fructosamine because of its longer biological half life.
Adolescent↗
Chronic treatment with ethanol or chlordiazepoxide alters the metabolism of chlordiazepoxide.
Although chronic ethanol administration in C57BL/6J mice did not cause an induction of ethanol metabolism, it altered the metabolism of chlordiazepoxide (CDP). Significantly lower blood levels of CDP, but higher levels of N-desmethyl CDP (NDCDP), were observed in ethanol-dependent mice compared to pair-fed controls during the first hour after CDP injection. Mice treated chronically with CDP showed significantly lower blood levels of CDP and NDCDP than pair-fed controls after a test dose of CDP. In response to an injection of ethanol, the CDP-dependent mice had lower blood alcohol levels (BAL) than the pair-fed controls, but the rate of fall of BAL was not different in the two groups. Thus, chronic CDP treatment affected the absorption and distribution of ethanol. These results provide a metabolic basis for the manifestations of CDP tolerance and ethanol cross-tolerance that have been reported in CDP-dependent mice.
Animals↗
Partial cross-dependence on ethanol in mice dependent on chlordiazepoxide.
Mice which had been fed chronically a liquid diet containing chlordiazepoxide (CDP) showed spontaneous and Ro15-1788-induced withdrawal signs upon CDP withdrawal. Ethanol (1.5 g/kg) injected 5 min before Ro15-1788 injection almost completely suppressed the withdrawal signs induced by the benzodiazepine receptor antagonist. However, neither ethanol injection nor ethanol diet administration could prevent the loss of appetite and weight loss on day 1 of CDP withdrawal. Likewise, the addition of saccharin in the ethanol diets did not prevent the loss of appetite. Mice which had been fed the CDP diet followed by 9 days of ethanol treatment (CDP/ethanol) showed more severe hypothermia during ethanol withdrawal compared to mice which had been fed the control/ethanol diets. The CDP/ethanol mice also retained the increase in runway activity attained from the prior CDP treatment. The data indicate that CDP-dependent mice showed partial rather than full cross-dependence on ethanol.
Animals↗
The assessment of thyroid status in rheumatic disease.
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Female↗
NADP+ reduction by human lymphocytes.
The hexose monophosphate shunt (HMPS) is known to be responsible for the reduction of NADP+ by lymphocytes. We tried to find other enzymatic systems that might provide the lymphocytes with NADPH. By measuring the absorbance at 340 nm we noted that the addition of NADP+ to a preparation of disrupted lymphocytes resulted in the formation of NADPH at a rate of 4 nmol/10(6) cells per min. This phenomenon could not be changed by negative feedback inhibition of HMPS, and could not be attributed to the low concentration of glucose, glucose-6-phosphate (G-6-P) and isocitrate found in the cell preparation (NADP(+)-dependent isocitrate dehydrogenase in addition to HMPS NADP+ reducing enzymes was found to be present in lymphocytes). Because of the activity of a NADP(+)-dependent lactate dehydrogenase, pyruvate oxidized the NADPH as it was being formed. Here we demonstrate the presence of an unknown NADP+ reducer in lymphocytes which seems to play an additional role to HMPS in NADP+ reduction by lymphocytes. NADP(+)-dependent lactate dehydrogenase may play a role in regulating the NADP+/NADPH ratio.
Humans↗
Clinical hyperthyroidism due to non-neoplastic inappropriate thyrotrophin secretion.
We report a case of hyperthyroidism due to inappropriate thyrotrophin (TSH) secretion in a patient with selective pituitary resistance to thyroid hormone action. Symptoms of hyperthyroidism in patients with this disorder are usually mild, implying some peripheral tissue resistance to the metabolic effects of thyroid hormone. Our patient had unusually severe symptoms, including marked weight loss and cardiac arrythmias which required carbimazole and beta-blocker therapy for control. Somatostatin was ineffective in suppressing TSH secretion. The introduction of sensitive thyrotrophin assays should facilitate the accurate diagnosis of TSH-induced hyperthyroidism and avoid inappropriate treatment.
Adult↗
Pituitary enlargement and hyperprolactinaemia due to primary hypothyroidism: errors and delays in diagnosis.
Two young women with pituitary gland enlargement and hyperprolactinaemia were referred for pituitary surgery. Both had received bromocriptine (one patient for 13 years) for presumed prolactinoma. Mild clinical signs of hypothyroidism were present and endocrine tests revealed primary autoimmune thyroid failure. Following thyroxine replacement treatment, the pituitary enlargement and hyperprolactinaemia completely resolved. In both patients the hyperprolactinaemia was relatively mild and menorrhagia had been present for many years. A third patient, a 61-year-old man presenting with bitemporal hemianopia due to pituitary enlargement underwent transphenoidal pituitary surgery. The results of thyroid function tests on admission were not available until after surgery. Although the patient was clinically euthyroid, these revealed primary hypothyroidism and his considerable pituitary enlargement may also have been secondary to thyroid failure. Urgent thyroid function tests should be performed in all patients with pituitary enlargement prior to surgery to exclude hypothyroid induced pituitary swelling.
Adult↗
Short term fluctuations in blood glucose concentrations do not alter pain perception in diabetic-patients with and without painful peripheral neuropathy.
Previous studies have suggested that acute hyperglycaemia may affect pain thresholds in non-diabetic subjects. We investigated the effects of acute fluctuations in blood glucose on the perception of pain in diabetic patients with and without painful diabetic neuropathy. Rapid swings in blood glucose concentration produced by IV glucose injection did not alter heat pain thresholds in diabetic patients without symptomatic neuropathy. Also, marked changes in neuropathic pain were not accompanied by significant alterations in blood glucose concentration in diabetic patients with painful neuropathy. Therefore, the alleged effects of acute hyperglycaemia on pain perception described in non-diabetic subjects are not reproduced in diabetic patients.
Adult↗
A liquid diet model of chlordiazepoxide dependence in mice.
Mice fed chronically (3 to 4 weeks) a liquid diet containing chlordiazepoxide (CDP) became physically dependent on the drug as demonstrated by the occurrence of withdrawal signs precipitated by injection of the benzodiazepine antagonist Ro15-1788 (5 to 25 mg/kg) or by omitting CDP from the diet (spontaneous withdrawal). Very low blood concentrations of CDP, but medium to high levels of the active metabolites N-desmethyl CDP and demoxepam were found during the period of CDP administration. The Ro15-1788-induced withdrawal signs appeared within 1 min after the injection of the antagonist and lasted for at least 10 min. Quantifiable withdrawal signs included tail lift, tremor, impaired movement and handling-induced seizures. Mice undergoing spontaneous withdrawal had milder withdrawal signs such as weight loss, in appetite and suppression of runway and head-dipping activities on day 1 or day 2 of withdrawal. These signs were also present in Ro15-1788-induced withdrawal. A long-lasting rebound increase in runway and head-dipping activities occurred several days after CDP withdrawal.
Animals↗
Transferrin and mitochondrial aspartate aminotransferase in young adult alcoholics.
Two recently proposed biochemical markers of alcoholism, namely, quantitation of plasma transferrin variant (Tf5.7) and the ratio of plasma mitochondrial aspartate aminotransferase (m-AspAT) to total AspAT (t-AspAT), were tested for their ability to detect young adult alcoholics. Another commonly used biochemical test, namely, activity of plasma gamma glutamyltransferase (GGT) was included as a comparison. Although mean values of GGT, TF5.7, total transferrin (Tftot), m-AspAT and t-AspAT in alcoholics were significantly higher than those in controls, there were too many overlapping values in each test between alcoholics and controls to render any of these tests suitable as a marker for young adult alcoholics. Depending on cut-off limits, the sensitivity of each test ranged from 0-52% and the specificity ranged from 80-97%. Moreover, the m-AspAT/t-AspAT and Tf5.7/Tftot ratios were not significantly different between alcoholics and controls. A stepwise linear discriminant function analysis of all the variables resulted in a slight increase in classification sensitivity (66%) but a decrease in specificity (77%). The relatively short duration (mean = 5.6 years) of heavy alcohol intake and the time elapsed (mean = 5.8 days) since the alcoholics last consumed alcohol very likely contributed to the low sensitivity. Young adults might also be more resilient with regard to the damaging biochemical effects of ethanol. Abnormal biochemical values might reverse to normal values much more quickly in young adult alcoholics than in those who are older and have more years of alcohol abuse.
Adolescent↗
Cryptosporidiosis as a cause of chronic diarrhoea in a patient with insulin-dependent diabetes mellitus.
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Adult↗
Differential effects of Ro15-1788 in actions of chlordiazepoxide and ethanol.
Three behavioral tests, namely, runway activity, horizontal dowel test and hypothermia, were used to compare the effects of Ro15-1788, a specific benzodiazepine antagonist, on the common neuropharmacological actions of chlordiazepoxide (CDP) and ethanol in C57BL/6J mice. Ro15-1788 completely reversed the CDP-induced inhibition of runway activity and incoordination on a horizontal dowel, but only partially antagonized the hypothermic effects of CDP. The latter phenomenon was likely to be due to the rapid elimination of Ro15-1788, but could also be due to the fact that hypothermia might not be a specific action of CDP. The sedative actions of ethanol were not antagonized at all by Ro15-1788. In fact, Ro15-1788 potentiated the incoordinating effect of ethanol as determined by the horizontal dowel test such that mice injected with Ro15-1788/ethanol had lower brain ethanol levels than mice injected with vehicle/ethanol when they fell off the dowel. In contrast, mice injected with Ro15-1788/CDP took longer to fall off and had significantly higher CDP levels at fall-off than mice injected with vehicle/CDP. The stimulatory effect of a low dose of ethanol on runway activity was reversed by Ro15-1788. These data are discussed in terms of the possible mechanisms of actions for CDP and ethanol.
Animals↗
Does chronic ethanol intake confer full cross-tolerance to chlordiazepoxide?
Four behavioral tests, namely, hypothermia, horizontal dowel, runway and head-dipping, were used to assess tolerance to ethanol and cross-tolerance to chlordiazepoxide (CDP) in mice chronically treated with an ethanol diet for 15 days. Mice were tested on day 3 of ethanol withdrawal, with some being retested on day 8. In terms of hypothermia and the horizontal dowel test, ethanol tolerance conferred full cross-tolerance to CDP, but the conclusion based on results of the latter test may be equivocal. Partial cross-tolerance to CDP was observed in the runway test, while no cross-tolerance to CDP was detected in the head-dipping test. For these latter two tests ethanol tolerance was present in the mice. Thus, the degree of equivalence between tolerance to ethanol and cross-tolerance to CDP in ethanol-dependent mice varied with the behavioral tests to assess tolerance. Possible mechanisms are discussed.
Alcoholism↗
Extranodal renal non-Hodgkin's lymphoma and severe hypercalcaemia.
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Female↗
Does acute hyperglycaemia influence heat pain thresholds?
The influence of acute hyperglycaemia on pain sensation was assessed in eight young adult non-diabetic subjects. Acute hyperglycaemia was induced with IV glucose in a double blind fashion, with IV saline as a control. Pain thresholds were assessed by a painful heat stimulus delivered by a Marstock thermode on the thenar eminence. Heat pain thresholds did not significantly alter during either acute hyperglycaemia or the control saline infusion. Previous work demonstrating a lowering of electrical pain thresholds by hyperglycaemia has therefore not been confirmed using a natural painful stimulus.
Adolescent↗
Factors affecting the drinking driver.
Although the relationship between alcohol and traffic safety has been the subject of numerous studies, much remains unknown about the mechanisms by which alcohol contributes to traffic accidents. A number of other factors, which are reviewed in this paper, also can contribute to car accidents. They may also interact with alcohol, perhaps in a complex manner. Therefore, multiple factors rather than one single factor may contribute to automobile accidents for those who drink and drive.
Accidents, Traffic↗