Fatigue and diabetes mellitus: a prospective study

Background: Fatigue is a common complaint among patients with diabetes mellitus (DM) that can undermine the daily functional activities of a person. The objectives of the study were to assess the fatigue in patients of newly diagnosed type 2 DM and to relate fatigue with blood glucose parameters (BGP) and glycemic control.Methods: A total 50 patients of type 2 DM, diagnosed as per American Diabetes Association 2011 criteria, were enrolled in the study group. Each subject was evaluated two times for fatigue using Multidimensional Fatigue Symptom Inventory-Short Form (MFSI-SF) scale. 1st assessment was at the time of enrollment and 2nd was done after achieving target control of type 2 DM. Values of Fasting blood glucose (FBG), postprandial blood glucose (PPBG), blood glucose variability (BGV) and glycosylated hemoglobin (HbA1c) were obtained for each subject at each assessment. Data collected was analyzed statistically.Results: Mean age of study group was 50.7±8.9 years with male to female ratio of 1.17:1. Mean values of MFSI-SF score at 1st and 2nd assessment were 14.10±17.97 and 4.64±14.06, respectively indicating a statistically significant improvement in fatigue (p<0.05) after achieving target control. Overall fatigue, general fatigue, emotional fatigue, and vigor score correlated significantly with glycemic control (HbA1c) with correlation coefficient (r) of 0.337, 0.351, 0 .339, and - 0.281, respectively (all p <0.05).Conclusions: Fatigue had a positive correlation with FBG, PPBG and BGV and HbA1c. A significant improvement in all the parameters of fatigue was noted after control of diabetic status.

Glibenclamide vs gliclazide in reducing oxidative stress in patients of noninsulin dependent diabetes mellitus--a double blind randomized study.

OBJECTIVE: Parameters of oxidative stress were quantitated in 50 patients with type 2 diabetes mellitus in uncontrolled state and after control using oral glibenclamide or gliclazide. The estimates were further compared between the two groups irrespective of drug used to evaluate the difference, if any. METHODS: The study was a double blind, uncontrolled, noncrossover and randomized trial. Fifty patients of uncontrolled type 2 diabetes were divided in to two groups. Group I (25 patients) received capsule A (glibenclamide) while Group II (25 patients) received capsule B (gliclazide). The parameters studied were Superoxide dismutase (SOD), malonyl-dialdehyde (MDA) and reduced glutathione (GSH). They were done at (a) uncontrolled stage (FBS--165 +/- 16.7 mg/dl, PP--240 +/- 30.1 mg/dl and HbA1--10.5 +/- 0.9% in group I and FBS--150 +/- 15.8 mg/dl, PP--246 +/- 29.1 mg/dl HbA1 10.6 +/- 0.8% in group II) and during controlled stage at 12 weeks (FBS--120 +/- 18.5 mg/dl, PP--180 +/- 19.1 mg/dl and HbA1--8.4 +/- 0.29% in group I and FBS--118 +/- 17.6 mg/dl, PP--176 +/- 20.1 mg/dl and HbA1--8.5 +/- 0.39% in group II patients). RESULTS: The significantly raised levels of MDA and SOD, and decreased levels of reduced glutathione (GSH) during uncontrolled stage of diabetes indicated free radical stress induced lipid peroxidation. The significant fall of MDA and SOD and increased levels of GSH in blood in both groups after control revealed beneficial effects of glycemic control on oxidative stress. The levels were not normalized and stayed higher than those in controls. On intergroup comparison; the control of diabetes with gliclazide (group II) showed improvement in oxidative stress (MDA, GSH) better (p < 0.001) than glibenclamide (group I). CONCLUSION: Oxidative stress in uncontrolled diabetes is decreased with glycemic control. The control of diabetes with gliclazide reduced oxidative stress more than glibenclamide, indicating higher antioxidant properties of gliclazide. Normalization of oxidative stress was not achieved. Further studies are required to see long-term effect of drug therapy in combating oxidative stress after achieving acceptable control of diabetes.

Evaluation of oxidative stress before and after haemodialysis in chronic renal failure.

OBJECTIVE: To evaluate the oxidative stress before and after haemodialysis in chronic renal failure patients. METHODS: A prospective study comprising of 22 patients of CRF who have to receive their first haemodialysis. All patients were subjected to standard four hours haemodialysis. The parameters of oxidative stress i.e. erythrocyte malonaldehyde (MDA), reduced glutathione (GSH) and superoxide dismutase (SOD) were measured before and after haemodialysis. RESULTS: The value of mean erythrocyte MDA (9.40 +/- 3.36 mumol/L) and SOD (617 +/- 64.33 units/ml) were significantly higher in patients of CRF before haemodialysis than in controls (p < 0.001). The mean GSH levels were significantly lower (451 +/- 63.91 micrograms/ml) in patients than in controls before haemodialysis (p < 0.001). After haemodialysis MDA levels further increased (12.27 +/- 4.38 mumol/L), SOD levels decreased (458 +/- 69.58 EU/ml) and GSH levels further decreased (396 +/- 41.41 micrograms/ml) (p < 0.001). CONCLUSIONS: There was an evidence of oxidative stress in patients of CRF before haemodialysis which increased further after haemodialysis, the mechanisms of which is not delineated. The procedural factors may be contributing in the increased oxidative stress after haemodialysis.

An evaluation of oxidative stress in diabetes mellitus during uncontrolled and controlled state and after vitamin E supplementation.

OBJECTIVE: The study was conducted on 50 patients (10 insulin dependent diabetes mellitus (IDDM) and 40 non-insulin dependent diabetes mellitus (NIDDM) of recently diagnosed diabetes mellitus. The main objectives of the study were: 1. To evaluate oxidative stress at uncontrolled stage. 2. To evaluate the effect of optimal control on oxidative stress irrespective of type of drug therapy used. 3. To further evaluate the effect of vitamin E supplementation on oxidative stress after achieving optimal control. This was done in order to explore anti-oxidant effect of vitamin E. METHODS: Fifty patients of uncontrolled diabetes of less than 1 year duration and without any overt complications were studied. The parameters of oxidative stress included malonyl-di-aldehyde (MDA), reduced glutathione and vitamin E levels in the blood. They were done at three stages i.e. (a) In uncontrolled stage, (b) At controlled stage and (c) After 4 weeks of vitamin E supplementation in dosage of 400 mg daily. The parameters of control included fasting blood sugar < or = 140 mg%, post prandial < or = 200 mg and HbA1c < or = 7% (analysed by prepared kit). RESULTS: The significantly raised levels of MDA and decreased levels of reduced glutathione and vitamin E during uncontrolled stage of diabetes indicated free radical stress inducing lipid peroxidation. The significant fall of MDA and rise in reduced glutathione and vitamin E levels in blood after optimal control revealed its beneficial effect on oxidative stress. The levels were not normalised but still stayed higher than controls. After 4 weeks of vitamin E supplementation, further fall in MDA and rise in reduced glutathione suggested beneficial effect of vitamin E over and above the optimal control. Vitamin E estimation in blood at this stage did not constitute parameter of oxidative stress as it was provided from outside but was done to know the compliance of patients. Normalisation or near normalisation was not achieved with vitamin E therapy indicating persistence of oxidative stress. CONCLUSION: There was an evidence of oxidative stress in diabetes which decreased with optimal control and further declined after vitamin E supplementation indicating anti-oxidant effect of vitamin E alone. Normalisation of oxidative stress was not achieved. A further study is desired to study the effect of vitamin E for longer period at least 3-6 months before a definite conclusion is drawn.

Subcapsular tubercular liver abscess.

A young female married for the last 2 years but without any issue presented with lump in the right upper abdomen. This was proved to be a subcapsular liver abscess on USG and CT scan and proved to be tubercular on needle aspiration cytology. She was given four drugs antitubercular treatment (ATT). After four months of ATT she conceived and it was decided by both parents to continue the pregnancy. The three drug ATT was continued throughout the pregnancy and she delivered a perfectly healthy baby. Upto three months follow up the mother and baby were perfectly healthy. The subcapsular tubercular liver abscess is extremely rare and conception during treatment may be the first case in literature.

Free radical scavengers & lipid peroxidation in acute aluminium phosphide poisoning.

Free radicals scavengers superoxide dismuatase (SOD) and catalase and lipid peroxidation were studied in 45 patients of aluminium phosphide poisoning irrespective of age and sex admitted to a hospital in north India during the January 1992 to December 1993. Serial serum superoxide dismutase (SOD), catalase and MDA (malonyldialdehyde) were estimated on days 1, 2 and 5 post-admission depending on the survival of the patients. Serum SOD levels were significantly higher (P < 0.001) but serum catalase was significantly lower (P < 0.001) in patients than controls (patients of peripheral circulatory failure and normals) on days 1 and 2 which suggested stimulation of SOD and inhibition of catalase by phosphine resulting in excessive hydrogen peroxide (H2O2) load. Significantly higher levels of MDA (P < 0.001) in patients than controls on days 1 and 2 indicated enhanced lipid peroxidation in this poisoning. Twenty four patients died constituting a mortality rate of 53.3 per cent. The significantly high levels of SOD and MDA in non-survivors suggested their direct relation to mortality while catalase levels had an inverse relationship. Return of SOD and catalase and MDA to normal or near normal levels in survivors by day 5 suggested abolition of an oxidative stress due to elimination of phosphine.

Serial blood phosphine levels in acute aluminium phosphide poisoning.

Serial blood phosphine (PH3) levels were done in patients with severe (Group I, n = 30), mild (Group 2, n = 10) and minimal or nil toxicity due to aluminium phosphide compound. Blood phosphine levels were significantly higher (p < 0.001) in patients of Group I than other two groups. Phosphine was not detectable in Group 3 patients. Therefore, blood phosphine levels were positively correlated to clinical grades of toxicity and to dose of active pesticide consumed. Higher the blood phosphine, higher was the mortality. Patients having blood phosphine levels equal to or less than 1.067 +/- 0.16 mg% survived, hence, it appeared to be limit of phosphine toxicity.

Histopathological changes in aluminium phosphide poisoning.

A total of thirty cases of aluminium phosphide poisoning were studied for gross and microscopic changes in various organs of the body ie, lungs, liver, kidneys, heart, brain, stomach and adrenals. The histopathological changes revealed varying degrees of congestion, oedema and leucocytic infiltration, changes suggestive of cellular hypoxia. The most dramatic effects were produced in lungs, kidneys and adrenals.

Efficacy of magnesium sulphate in aluminium phosphide poisoning--comparison of two different dose schedules.

The results of an open randomised study on the efficacy of magnesium sulphate therapy in aluminium phosphide poisoning are presented. One hundred and fifty five patients divided in three groups and matched for age, sex, dose, duration and severity of poisoning constituted the subject matter. Significant hypomagnesemia was observed in patients who did not receive magnesium sulphate (group 1). Two dose schedules of MgSO4 therapy were tried. The dose schedule No.1 given to patients of group 2 did not raise the magnesium levels significantly as compared to controls (group 4). The difference in the mortality between groups 1 & 2 was also not significant. On the other hand, the dose schedule No.2 given to patients of group 3 raised the magnesium levels significantly and these remained above normal limits throughout the observed period. This dose schedule brought down the mortality significantly than dose schedule No.1 (p < 0.001). It was also found that dose schedule No.2 has been effective in reducing the mortality irrespective of dose of pesticide consumed and its efficacy was due to rapid rise in magnesium levels. It is suggested that hypomagnesemia might be responsible for high mortality of patients of aluminium phosphide poisoning and its correction has beneficial effect on the management and ultimate favourable outcome of the illness.

Toxicity of exposed aluminium phosphide.

Poisoning by the partially or fully exposed compound of aluminium phosphide (ALP) is becoming common, Fifty patients with history of ingestion of ALP either in the form of broken tablets or granular powder were included in this study for analysis of systemic effects and outcome. Forty patients (Gr. I) consumed broken or granular form of tablets. Ten patients (Gr. II) consumed only powder form of tablets from an old container. 30 patients in group-I developed mild hypotension (BP 80-90 mm Hg). 4 patients (10%) developed ECG changes and mild metabolic acidosis. One patient died constituting 2.5% mortality rate. The patients of group-II neither developed any systemic effects nor showed any mortality. The aim of the study is to differentiate these cases from patients who consume active, fresh compound where mortality rate will be much higher.