Reversible atrioventricular blocks in thyroid storm.

Atrioventricular blocks or sinoatrial blocks are rarely described in patients with thyrotoxicosis or thyroid storm. The mechanism of these blocks remains obscure. Thyroid storm, being an emergency situation requires early diagnosis and management because if left untreated, it may prove fatal. Usually patients with AV blocks require pacing (temporary or permanent). Here we describe a case who developed AV blocks, did not undergo pacing, but recovered only on antithyroid treatment.

Evaluation of endothelial function and effect of glycemic control (excellent vs. poor / fair control) on endothelial function in uncontrolled type 2 diabetes mellitus.

OBJECTIVE: To evaluate the endothelial functions before and after glycemic control in type II diabetes mellitus. MATERIAL AND METHODS: It was an open, randomized and comparative study on 30 patients of type 2 diabetes mellitus. The study was of 12 weeks spread over 5 visits. The initial visit (visit 1) is for screening of patients. Other visits (visits 2 to 5) constituted the follow up of patients. The primary efficacy parameters included blood sugar (fasting and postprandial) done on each visit and glycosylated hemoglobin (HbA1c) done at visits 1 and 5. Based on glycosylated hemoglobin (HbA1c) only poorly controlled and fairly controlled patients were included in the study. Brachial artery flow mediated vasodilatation (FMD) was studied in all these patient at visits 1 and 5 to see the effect of glycemic control on endothelial functions. Results obtained were statistically analyzed with appropriate method. RESULTS: There was a significant improvement in endothelial functions in patients with fair, good and excellent control of diabetes. During uncontrolled state (HbA1c 10.08 +/- 0.48%) FMD was lowest, i.e., 2.88 +/- 0.53 at 1st week which improved to 11.94 +/- 3.33 at 12th week with control of diabetes (HbA1c 6.74 +/- 0.16%). The FMD in patients who had fair control (HbAlc 8.45 +/- 0.30%) in the beginning was 6.74 +/- 2.43% and after excellent control in these patients FMD rises to 12.81 +/- 3.16%. CONCLUSION: Our data showed that the endothelial functions improved sequentially with control of diabetes from fair to good to excellent glycemic control.

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.

Effect of glycemic control and vitamin E supplementation on total glutathione content in non-insulin-dependent diabetes mellitus.

Thirty patients with non-insulin-dependent diabetes mellitus were selected for the study. 15 age-matched healthy volunteers served as controls. Serum malonaldehyde, total glutathione, and vitamin E levels were estimated before and after glycemic control and after 4 weeks of vitamin E supplementation. Both total glutathione and vitamin E levels increased after glycemic control and showed an increase after vitamin E supplementation. Malonaldehyde levels lowered after glycemic control, but remained higher than controls. Since vitamin E supplementation significantly decreased oxidative stress in the present study, it may play a role in reducing free-radical-induced oxidant injury in diabetes mellitus.

Evaluation of oxidative stress before and after control of glycemia and after vitamin E supplementation in diabetic patients.

The present study evaluates the presence of oxidative stress in the uncontrolled diabetic state. Glycemic control reduced the oxidative stress, but total normalization of the parameters of oxidative stress was not achieved, indicating continued oxidant injury despite optimal control of the diabetes. Vitamin E supplementation for 4 weeks in these patients further reduced the oxidative stress, suggesting that vitamin E supplementation might be helpful in reducing free-radical-induced oxidant injury.

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.

Endosulfan poisoning in Northern India: a report of 18 cases.

Eighteen cases of endosulfan poisoning by accidental overexposure during spray, admitted between October 1995 to September 1997, were observed and analyzed. These accounted for approximately one third of the total number of poisoning cases admitted in our unit during this period. Nausea, vomiting abdominal discomfort, tonic and clonic convulsions, confusion, disorientation, and muscular twitchings were cardinal manifestations. None of the patients succumbed to their illness. Analysis of various incriminating factors revealed that accidental overexposure was due to failure to adhere to the instructions for spray either due to ignorance or due to illiteracy. All the patients avoided preventive measures and developed toxicity both due to inhalation and absorption through skin. Endosulfan (a chlordiene derivative) poisoning is gaining up momentum in this part of world and has become an important matter for public health in India.

Zinc phosphide intoxication symptoms: analysis of 20 cases.

Twenty cases of zinc phosphide (Zn3P2) ingestion (self-poisoning) were seen during the last 5 years (January 1992-December 1996). Poisoning was rare before 1986. Profuse vomiting (100%), pain in abdomen (100%), palpitation and sweating (80%), dyspnea and tachypnea (75%), metabolic acidosis (60%), shock (40%), and hypotension (40%) were the most common presenting features. Five patients (25%) died. The toxic effects were due to liberation of toxic phosphine (PH3) gas which was detected by qualitative silver nitrate paper test in majority of cases.

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.

A critical evaluation of anti-peroxidant effect of intravenous magnesium in acute aluminium phosphide poisoning.

The anti-peroxidant effect of intravenous magnesium was evaluated in 50 patients with acute aluminium phosphide poisoning. The patients were divided into two groups, one who received magnesium sulphate therapy (Group I) and the other who did not (Group II). The clinical and biochemical parameters in both groups were comparable. Finding of increased mean malonyl-di-aldehyde (MDA) levels in group I (3.18 +/- 0.93 micromol/L) and group II (3.15 +/- 0.78 mmol/L) combined with low blood levels of reduced glutathione (18.5 +/- 1.6 mg/dl in group I) and (17.8 +/- 1.4 mg/dl in group II) indicated oxidative stress leading to accelerated lipid peroxidation in the early phase (0-6 h) of AlP poisoning. A significant fall in MDA levels was observed after 2 h in the magnesium treated group (group I) compared to the non-treated group (group II) and levels became normal between 48-72 h. Similarly reduced glutathione started recovering between 12-24 h which became significant after 24 h and full recovery took place between 48-72 h in the magnesium treated group (group I). Both these parameters suggested an anti-peroxidant effect of magnesium. There was also a slight fall in MDA levels and a rise in reduced glutathione in the non-treated group II patients. This could be due to elimination of phosphine (PH3). We hypothesize that oxidative stress in AlP poisoning buffered the magnesium leading to a transient fall in magnesium and magnesium dependent GSH, resulting in increased susceptibility of oxygen free radical injury and accelerated lipid peroxidation. The fall in MDA and slower rise in GSH in group I than in group II suggested magnesium combated free radical stress slowly and independent of elimination of phosphine. This hypothesis was further strengthened by similar observations when both these parameters were compared in survivors in both groups. Mortality was higher in group II than in group I (44 per cent vs 20 per cent) and was probably related directly to oxidative stress.

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.

Magnesium status and parenteral magnesium sulphate therapy in acute aluminum phosphide intoxication.

The results of an open randomized study on magnesium status and parenteral magnesium sulphate therapy in acute aluminium phosphide intoxication are presented. The study was conducted on 105 patients divided into two group (I & II). Patients of Group I did not receive parenteral magnesium and acted as blank. Magnesium levels were monitored every 6 h for 24 h. Patients of group II received magnesium sulphate therapy. It was administered as 1.0 g (8.1 mEq or 4.05 mmol) magnesium sulphate dissolved in 100 ml of 5 per cent dextrose intravenously as a bolus dose followed by 1.0 g every hour for three successive hours, then 1.0 g every 6 h as a maintenance dose for the next 24 h as intravenous infusion in 5 per cent dextrose. The total dose of magnesium sulphate infused was 30.0 mmol over a period of 24 h (initial dose), then 16.0 mmol (4.0 g) daily till final outcome or a maximum of five days. All the vital parameters were monitored. All the patients were followed till final outcome. The resuscitation methods used were the same in both groups. At the end of the study, mortality rates were calculated in both groups. Hypomagnesaemia was observed as the constant finding in patients of Group I. It was transient and reversed itself without MgSO4. The mortality rate was 52 per cent. On the other hand, magnesium levels rose immediately after parenteral MgSO4 administration in patients of group II and they remained persistently above normal during the observed period.(ABSTRACT TRUNCATED AT 250 WORDS)