Publications by authors named "Anuradha Aggarwal"

Imatinib results in growth retardation in children with chronic myeloid leukemia (CML). The study was planned to assess the GHRH-GH-IGF1 axis in children with CML, receiving Imatinib and to evaluate the efficacy of human growth hormone (hGH) therapy. Twenty children with CML, receiving Imatinib for a period exceeding 6 months, with resultant growth retardation were included.

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Unlabelled: Spontaneous diabetic muscle infarction (DMI) is a rare and under diagnosed complication of diabetes mellitus. Clinically it presents with acute to subacute onset swelling, pain and tenderness of muscle(s) without systemic manifestations. MRI is helpful in diagnosis, exclusion of other causes and for localization of affected muscle for biopsy in atypical cases.

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Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is one of the most common causes of hyponatremia. The usual causes are malignancies, central nervous system, pulmonary disorders, and drugs. Amiodarone is a broad spectrum antiarrhythmic agent widely used in the management of arrhythmias.

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Disseminated cryptococcosis is rare in immunocompetent hosts and hepatic manifestations as the presenting feature is further rare. We report a case of disseminated cryptococcosis with hepatic involvement as an initial manifestation in a previously healthy, immunocompetent adult. A young married female presented with progressive jaundice, anorexia, weightloss, cough with expectoration, and hepatosplenomegaly.

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Unlabelled: We describe the clinical presentation, diagnostic and management issues in five cases of non-islet cell tumor hypoglycemia (NICTH), diagnosed at a tertiary care institute over a period of 15 years. The clinical, laboratory, and histopathological findings of these patients along with diagnostic utility of IGF2:IGF1 ratio are discussed. The mean age of presentation was 52 years, with a male predominance (3:2).

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Background: Haemodialysis results in a left ventricular hypertrophic response. It is unclear whether tight blood pressure control or particular medications might attenuate this response. We sought to determine, in a pre-dialysis cohort on atenolol, whether Losartan might attenuate left ventricular hypertrophy post arteriovenous fistula creation in end stage kidney disease.

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Background: We have previously shown that the angiotensin-converting enzyme (ACE) inhibitor perindopril reduced aortic diameter by 3-7mm in Marfan syndrome (MFS) patients. Excessive signalling by the transforming growth factor-beta (TGF-beta) has been implicated in the development of aortic dilatation. We hypothesised that reduction in aortic diameter would correlate with reduction in plasma TGF-beta and matrix metalloproteinase (MMP) levels.

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Fabry's disease (FD) is a genetic disorder leading to deficiency of alpha-galactosidase A. Enzymatic replacement therapy has recently become available. Patients with classical FD develop multi-system involvement; however, there is an increasingly recognized cardiac variant that presents as unexplained left ventricular hypertrophy.

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Marantic endocarditis is a non-infective cause of valvular masses. It is most commonly associated with advanced malignancy. We report a case of rapidly progressive marantic endocarditis, complicated by valve destruction and recurrent systemic embolisation, in a patient whose cancer was occult.

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Context: Aortic stiffness is increased in Marfan syndrome contributing to aortic dilatation and rupture, the major cause of premature death in this population. Angiotensin-converting enzyme inhibitors have been shown to reduce arterial stiffness.

Objective: To determine whether perindopril therapy reduces aortic stiffness and attenuates aortic dilatation in patients with Marfan syndrome.

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Out of hospital cardiac arrest is generally managed by cardiopulmonary resuscitation (CPR) and defibrillation. The precordial thump can also be used in the initial management of witnessed cardiac arrest whilst awaiting direct current cardioversion. However, complications are associated with a precordial thump.

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Pulmonary hypertension secondary to residual Potts shunt is not an uncommon phenomenon. A 59-year-old male with a history of tetralogy of Fallot was noted, on a full heart study, to have persistent pulmonary hypertension, normal left ventricular function, severe aortic regurgitation, and a residual Potts shunt. A previous surgical attempt at closure of the shunt during definitive repair was unsuccessful.

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Background: Treatment of advanced systolic heart failure (HF) with the aldosterone antagonist spironolactone on the background of angiotensin converting enzyme inhibition (ACEI) is well established. However, the only large prospective trial to investigate this therapy (RALES) predated the routine use of beta-blockade in HF. The widespread practice of combining ACEI, beta-blockers and spironolactone in HF management has led to serious concerns regarding hyperkalemia.

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Introduction: Although morbidity and mortality associated with chest pain are related to time to intervention, many patients have delayed ED presentations. We aimed to assess the extent of and reasons for prehospital delay, and identify patient subgroups more at risk of delayed presentation.

Methods: This was an analytical, cross-sectional survey of patients with undifferentiated, potentially ischaemic chest pain, at a tertiary referral ED.

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Objective: This study reviewed the ED management of new onset atrial fibrillation (AF) in previously well patients aged less than 60 years.

Methods: We undertook a retrospective review of ED patients from 1998 to 2002 inclusive. The main outcome measures were approaches to rate or rhythm control and anticoagulation, the use of echocardiography, the value of diagnostic testing and the frequency of hospital admission.

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There is growing evidence that essential hypertension is commonly neurogenic and is initiated and sustained by sympathetic nervous system overactivity. Potential mechanisms include increased central sympathetic outflow, altered norepinephrine (NE) neuronal reuptake, diminished arterial baroreflex dampening of sympathetic nerve traffic, and sympathetic neuromodulation by angiotensin II. To address this issue, we used microneurography and radiotracer dilution methodology to measure regional sympathetic activity in 22 hypertensive patients and 11 normotensive control subjects.

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Results from animal experimentation suggest a 2-way interaction between leptin and the sympathetic nervous system, with leptin causing sympathetic activation and conversely, with the sympathetic system exercising regulatory feedback inhibition over leptin release. We have now tested this hypothesis in humans. In the absence of results from leptin infusions, to test for sympathetic stimulation of leptin release, we sought a quantitative naturalistic linkage of sympathetic activity with leptin plasma concentration across a broad range of leptin values in men of widely differing adiposity.

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This study examined the effects of low doses of intravenous clonidine on regional and global sympathetic nervous system activity in heart failure. In heart failure, adrenoceptor-blocking treatments have a limited sphere of activity. Centrally acting sympatholytic therapies should be further investigated, with a specific emphasis on targeting cardiac and renal sympathetic overactivity.

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Background: Although it is established that heightened sympathetic drive exists in congestive heart failure (CHF), the reflex processes by which this may occur and the sites in the central nervous system that may be responsible for mediating this process are not yet fully elucidated.

Methods And Results: Eight patients with moderate to severe CHF and 8 healthy control subjects underwent simultaneous arterial and bilateral internal jugular venous blood sampling and cerebral venous blood pool scanning for anatomical determination of the origin of internal jugular venous blood flow. We estimated sympathetic nervous activity by measuring total body norepinephrine (NE) spillover using radiotracer methodology and determined brain NE turnover by measuring the internal jugular overflow of NE and its lipophilic metabolites, 3-methoxy-4-hydroxyphenylglycol and 3,4-dihydroxyphenylglycol.

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