Neuroimaging In Tuberous Sclerosis

Tuberous sclerosis is a rare autosomal dominant neurocutaneous syndrome. The diagnosis is on the basis of diagnostic criteria applied to clinical findings classical triad of epilepsy, mental retardation, and adenoma sebaceum. Cardiac rhabdomyoma, renal angiomyolipoma, and neurologic involvement comprises of cortical or subependymal tubers and white matter abnormalities are the common radiologic findings, these will give strong evidence for suspecting tuberous sclerosis. accurate imaging differentiation of diagnosis and localization of tubers and is helpful for treatment.

Hyperhidrosis–Hypertension–Hypotension in Scorpion Envenoming Syndrome: Insulin–Glucose Infusion Reverses All the Clinical Manifestations Caused by Massive Release of Counter-Regulatory Hormones due to Killer Scorpion (Buthidae family) Stings

Death due to poisonous scorpion (Buthidae family) stings is common in many of the developing countries all over the world. Severe uncontrollable pain at the site of sting (without local oedema) results in autonomic storm, release massive quantities of catecholamines, angiotensin II, ACTH, glucocorticoids, glucagon, ADH, aldosterone, either suppressed insulin secretion/or hyperinsulinemia – insulin resistance causing hyperglycemia and a sudden increase in Free Fatty Acid levels (FFA). The increase in catecholamine and angiotensin II hormonal levels cause hyperhidrosis, initial transient hypertension, hyper salivation, hypotension, mydriasis, miosis, DIC, acute pancreatitis, and many other clinical manifestations. Suddenly increased FFA levels are toxic, produce inactivation of Na+–K+ATPase activities, arrhythmias, conduction defects, myocardial infarction, cardiogenic pulmonary oedema, Acute Respiratory Distress Syndrome (ARDS), multisystem organ failure and death. Hyperhidrosis is harmful and wasteful loss of fluid and electrolytes resulting in peripheral circulatory failure, hypotension and death. Based on our animal experimental studies and treating the scorpion sting victims with insulin glucose infusion, we consider that insulin has a primary metabolic role in preventing and reversing hyperhidrosis, hypertension, hypotension, cardiovascular changes, cardiogenic and non-cardiogenic pulmonary (ARDS) oedema. Treatment: Continuous infusion of regular crystalline insulin at the rate of 0.3 U/g glucose and glucose at the rate of 0.1 g/kg body weight/hour, for 48–72 hour, supplementation of potassium (if required), and maintenance of acid–base fluid and electrolyte balance.

Suppressed Insulin Secretion, Elevated Mediators of Inflammation, Hyper-Insulinemia-Insulin Resistance: Insulin Administration Reverses Cardiovascular, Metabolic Changes, Pulmonary Edema and All Other Clinical Manifestations in Scorpion Envenoming Syndrome

Death due to poisonous scorpion stings is common in many tropical and sub-tropical countries. Scorpion envenoming syndrome causes stimulation of neuro-endocrine axis resulting in autonomic storm, intense stimulation of sympathetic nervous system, massive release of catecholamines, angiotensin II, suppressed insulin secretion, glucagon, glucocorticoids, increased free fatty acid levels, hyperglycemia, hyper-insulinemia, insulin resistance, acute myocarditis, initial hypertension, hypotension, arrhythmias, conduction defects, ischemia, infarction, acute pancreatitis, CNS damage, motor aphasia, hemiplegia, mydriasis, hyperhidrosis, acute respiratory distress syndrome, disseminated intravascular coagulation, multi system organ failure, shock and death. The scorpion envenoming syndrome also causes stimulation of immuno-pathological axis, systemic and local inflammation, increase in production of proinflammatory cytokines IL-1α, IL-1β, IL-4, IL-6, IL-10, IL-12, TNF-α, IFN-γ and NO and contribute to immunological imbalance, hyperglycemia, hyper-insulinemia, insulin resistance, multi-system organ failure, shock and death. Elevated levels of TNF-α cause impaired glucose tolerance and induce insulin resistance for endogenously secreted insulin. Insulin administration reversed metabolic, respiratory changes, cardiogenic and non-cardiogenic pulmonary edema, electrocardiographic, cardiovascular changes and many other manifestations in our experimental animals and in our scorpion sting victims with scorpion envenoming syndrome. Treatment: Continuous infusion of regular crystalline insulin at the rate of 0.3 U/g glucose and glucose at the rate of 0.1g/kg body weight/h, for 48–72 h, with supplementation of potassium as needed, maintenance of fluid, electrolytes, acidbase balance.

Acute Pancreatitis in Scorpion Envenoming Syndrome: Insulin-Glucose Administration Reverses Haemodynamic Changes, Pulmonary Edema and Other Clinical Manifestations Due to Scorpion (Mesobuthus tamulus Concanesis, Pocock [Buthidae family]) Stings

Death due to poisonous scorpion (Buthidae family) stings is a common event in the developing countries. Scorpion envenoming syndrome results in autonomic storm, release of catecholamines, angiotensin II, glucagon, glucocorticoids, either suppressed insulin secretion or hyperinsulinemia; hyperglycemia, lipolysis – sudden increase in free fatty acids (FFA), acute myocarditis, disseminated intravascular coagulation, cardiovascular disturbances, pulmonary oedema, acute pancreatitis, and many clinical manifestations. Under these altered hormonal mileu, insulin administration reversed the metabolic and ECG changes induced by scorpion envenoming in the experimental animals and in scorpion sting victims. Insulin has a primary metabolic role in preventing, counter-acting and reversing the metabolic, cardiovascular, haemodynamic, and neurological manifestations and pulmonary oedema induced by scorpion envenoming and reversing all the deleterious effects of FFA by inhibiting the catecholamine induced lipolysis, and increase intra-cellular K+, facilitating glucose transport to the myocardium and glucose metabolism through different pathways. Profuse sweating, excessive salivation and abdominal pain are the triad of symptoms of ominous significance in scorpion sting victims with acute pancreatitis. Laryngeal spasm and respiratory failure are more common with acute pancreatitis. Continuous infusion of regular crystalline insulin should be given at the rate of 0.3 U/g glucose and glucose at the rate of 0.1 g/kg body weight/hour, for 48–72 hours, with supplementation of potassium as needed and maintenance of fluid, electrolytes and acid-base balance.

Laryngeal Spasm in Scorpion Envenoming Syndrome

Death due to scorpion envenoming syndrome is a common event all over the world in tropical and sub-tropical countries. Scorpion envenoming syndrome results in a severe autonomic storm with a massive release of catecholamines, increased levels of angiotensin II, glucagon, cortisol, thyroid hormones, either hypoinsulinemia or hyperinsulinemia, hyperglycemia and increased free fatty acid levels. Under these conditions, scorpion envenoming syndrome with laryngeal spasm, fasciculations, clonus and tetany like skeletal muscle contractions, myocardial damage, disseminated intravascular coagulation, cardiovascular disturbances, peripheral circulatory failure, cardiac pulmonary oedema, adult respiratory distress syndrome, and many other clinical manifestations cause multi-systemorgan-failure and death. Under these altered conditions, scorpion envenoming essentially results in a syndrome of fuel – energy deficits and an inability to use the existing metabolic substrates by vital organs causing MSOF and death. Based on our animal experiments in which insulin administration reversed the metabolic and ECG changes induced by scorpion envenoming and treating the poisonous scorpion sting victims with insulin, we consider that insulin has a primary metabolic role in preventing and reversing laryngeal spasm, fasciculations, clonus and tetany like contractions, the cardiovascular, neurological manifestations and pulmonary oedema. Administration of insulinglucose infusion to scorpion sting victims is the physiological basis for the control of the metabolic response when that has become a determinant to survival. Continuous infusion of regular crystalline insulin at the rate of 0.3 U/g glucose and glucose at the rate of 0.1 g/kg body weight/hour, for 48–72 hours, potassium supplementation and maintenance of fluid, electrolytes and acid–base balance.

Predictors of Significant Jaundice in Late Preterm Infants.

Objectives: To study (i) the incidence and course of jaundice, and (ii) the predictors of ‘significant jaundice’ in late preterm infants. Design: Prospective analytical study. Setting: Urban perinatal center. Patients: Inborn late preterm infants (post menstrual age of 34 0/ 7 to 36 6/7 weeks). Methods: Infants were followed till day 14 of life or till onset of significant jaundice. Relevant maternal, perinatal and neonatal variables were prospectively recorded. Transcutaneous bilirubin (TcB) was measured in each infant twice daily for the first 48 hours of life. Outcomes: Significant jaundice defined as requirement of phototherapy/exchange transfusion as per hour specific total serum bilirubin (TSB) nomogram of AAP guidelines. Results: 216 infants were enrolled, of which 123 (57%) had significant jaundice. 36% of the jaundiced infants had TSB greater than 15 mg/dL. The mean duration of onset of significant jaundice was 61 ± 32 hours. The mean duration of phototherapy was 49 ± 26 hours. Large for gestation, lower gestational age, birth trauma and previous sibling with jaundice predicted severe jaundice. TcB measured at 24-48 hrs was a better predictor of ‘significant jaundice with onset after 48 hrs’ than clinical risk factors. Conclusion: There is a high incidence of significant jaundice in late preterm infants. TcB measured at 24-48 hrs of life better predicts ‘significant jaundice after 48 hours of life’, in comparison with clinical risk factors.

The use of midazolam and haloperidol in cancer patients at the end of life

<p><b>INTRODUCTION</b>This study aimed to describe the patterns of sedative use among terminally ill cancer patients who were referred to a hospital-based specialist palliative care service for symptom management. It also aimed to examine whether sedative use among terminally ill cancer patients during the last two days of life had any impact on their survival.</p><p><b>METHODS</b>A retrospective review of case notes was carried out for patients with a diagnosis of terminal cancer, who died in a 95-bedded oncology ward between September 2006 and September 2007. Data was collected on patient characteristics, duration of palliative care, indications and doses of sedatives used at 48 hours and 24 hours before death.</p><p><b>RESULTS</b>A total of 238 patients died while receiving specialist palliative care, 132 of whom (55.5%) were female. At 48 hours and 24 hours before death, 22.6% and 24.8% of patients, respectively, were on sedatives like midazolam, haloperidol or both. The median dose of midazolam was 5 mg/day while the haloperidol dose at 48 hours and 24 hours before death was 3 mg/day and 4 mg/day, respectively. The indications for midazolam were anxiety, breathlessness and stiffness, while those for haloperidol were confusion agitation and nausea. Survival analysis showed no significant difference in survival between patients who were on sedatives and those who were not. The p-value for log-rank test was 0.78.</p><p><b>CONCLUSION</b>The results showed that the doses and overall frequency of sedative use in this patient population tended to be low and that usage of sedatives had no deleterious influence on survival.</p>

Leukocyte protein-bound carbohydrate components in diabetes mellitus

The protein bound components [hexose, hexosamine and sialic acid] in the leukocytes of type I type II diabetic patients and age and sex matched non-diabetic subjects were determined. The mean values of plasma glucose and glycated hemoglobin of type I patients were 201 +/- 39 mg/d1 and 11.7 +/- 2.48% respectively. The repective values of type II patients were 176 +/- 39 mg/dl and 11.34 +/- 2.1%. The levels of hexose, hexosamine and sialic acid were significantly higher in diabetic patients than those of age and sex matched non-diabetic control subjects. The increased protein bound carbohydrate components may cause an increase in the levels of glycoprotein material which might result in the thickening of the basement membranes characteristic of diabetes mellitus

Leukocyte lipids in diabetes mellitus

The lipid composition and the activities of cholesterol ester hydrolase [CEH] and cholesterol ester synthetic [CES] in the leukocytes of type I and type II diabetic patients and age and sex matched non diabetic healthy subjects were determined. The mean values of fasting plasma glucose and glycated hemoglobin of type I patients were 201 +/- 39mg/dl and 11.7 +/- 2.48% respectively. The respective values of the type II patients were 176 +/- 39 mg/dl and 11.34 +/- 2.1%. The levels of cholesterol, phospholipids and triglycerides in the plasma as well as in the leukocytes of the diabetic patients were significantly higher than those of the age and sex matched non-diabetic subjects [p <0.001]. In the diabetic patients, the activity of leukocyte CEH decreased significantly [p <0.001], while the activity of CES increase significantly [p <0.001] as compared with the non-diabetic counterparts. As expected, this resulted in a decrease in the ratio CEH/CES in diabetic patients. The increased levels of lipid components and a decrease in the CEH/CES ratio of the leukocytes might be considered as an important step in the genesis of atherosclerosis and coronary heart disease in diabetes mellitus

In vitro effect of prostaglandins, prostaglandin endoperoxides and thromboxane on rat intestinal alkaline phosphatase and (Ca2+ – Mg2+) adenosine triphosphatase.

The activity of alkaline phosphate and Ca2+–Mg2+ adenosine triphosphatase, two of the enzymes involved in limpid and calcium uptake across the intestinal membrane, were increased in experimental atherosclerosis. Administration of Annapavala sindhooram, an antiatherosclerotic drug, lowers these enzyme levels to near normal values. Prostaglandin E2 stimulated the enzyme activities in vitro, while prostaglandin endoperoxide inhibited the activity. Thromboxane and other prostaglandins had no effect on the enzyme activities. Addition of the antiatherosclerotic drug to the in vitro assay system reversed the effect of both prostaglandin E2 and prostaglandin endoperoxide.