Reversible dilated cardiomyopathy associated with thyrotoxicosis.
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Biomedical subjects
Publications and source records attributed to S Bhandari.
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We report a case of disseminated histoplasmosis in a 60-year-old non-immunocompromised patient who presented to us with fever and hepatosplenomegaly. Sonographic & CT examination of the abdomen showed bilateral adrenal masses. Cytological examination of the aspirated material from the mass showed yeast forms of H. capsulatum.
Molecular defects affecting the transport of sodium, potassium and chloride in the nephron through the ROMK K+ channel, Na+/K+/2Cl- cotransporter, the Na+/Cl- cotransporter and chloride channel have been identified in patients with Bartter's and Gitelman's syndromes. Defects of the angiotensin II type I receptor and CFTR have also being described. These defects are simple (i.e., most are single amino acid substitutions) but affect key elements in tubular transport. The simplicity of the genetic defects may explain why the inheritance of these conditions remains unclear in most kindreds (i.e., not just recessive or dominant) and emphasises the crucial importance of the conformational structure of these channels. Application of this molecular information will allow the early genetic identification of patients with these syndromes and enable us to differentiate between the various disorders at a functional level. It may also identify a subgroup in which the heterozygous form may make patients potentially exquisitely sensitive to diuretics.
An open clinical trial was conducted in 30 patients of severe falciparum malaria with heavy parasitaemia (parasitized erythrocytes above 5%). Artemether (methyl ether of dihydroartemisinin-active principle isolated from Chinese plant Qinghaosu) was administered as 80 mg intramuscular injection twice on first day and then single dose of 80 mg intramuscular on 2nd to 5th day. The trial could be completed in 28 patients and two patients expired. In our observation falciparum malaria affected the young adults in their most productive period of life i.e. 25-44 yrs. All patients became afebrile by the 4th day with fever clearance time approximately 31.92 +/- 15.30 hr. Twenty-five patients (83.33%) became parasite free by 5th day with mean parasite clearance time approximately 47.04 +/- 19.95 hr. Deranged liver function and renal profile was observed in 63% and 50% patients respectively. Two patients, who died had very high degree of parasitaemia (50% and 16%) with cerebral malaria. One died due to multiorgan failure and other due to massive hematemesis and shock. The type of response achieved by artemether therapy was analysed as per WHO criteria suggested for chloroquine resistance. S response was observed in 25 patients (cure rate 83.33%). Two patients (6.66%) patients showed R II response, one patient (3.33%) showed R III response and R I response was not observed in any patient. No significant side effects were noted. This pilot study demonstrated that intramuscular artemether is a useful addition to antimalarial drugs in this era of multidrug resistant P. falciparum malaria showing high clinical potency with virtually no side effect.
This study assessed once-daily (OD), sustained-release (SR) diltiazem alone and in combination with ramipril in essential hypertension. Fifty patients with supine diastolic blood pressure (DBP) > or = 95-< or = 114 mm Hg were entered into the active treatment phase of the study after 2 weeks of placebo run-in. Sustained-release diltiazem 180 mg OD was administered for 2 weeks, then optimally titrated, at 2 week intervals, to SR diltiazem 240 mg OD and then SR diltiazem 180 mg + ramipril 2.5 mg OD to achieve supine DBP < or = 90 mm Hg. After 4 weeks of diltiazem monotherapy (SR diltiazem 180 mg or 240 mg OD) mean supine DBP was reduced from 102.84 +/- 3.81 mm Hg to 90.15 +/- 5.02 mm Hg (P < 0.01) and mean supine heart rate was reduced from 85.15 +/- 11.02 bpm to 77.62 +/- 11.45 bpm (p < 0.01). Diltiazem monotherapy reduced supine DBP to < or = 90 mm Hg in 35/45 (77.77%) patients. Combination therapy (SR diltiazem 180 mg + ramipril 2.5 mg OD), received by non-responders to diltiazem monotherapy, reduced supine DBP to < or = 90 mm Hg in 3/10 (30%) patients. Sinus bradycardia was observed in one patient. Sustained-release diltiazem alone and in combination with ramipril reduce blood pressure in a dose related manner and is well tolerated.
OBJECTIVES: We investigated the role of three-dimensional echocardiography in assessing mitral valve anatomy in greater detail in patients immediately before and after balloon mitral valvuloplasty (BMV). BACKGROUND: Three-dimensional echocardiography is a recently developed, evolving imaging technique that allows visualization of intracardiac structures from any perspective. METHODS: We studied 19 patients undergoing BMV using transesophageal echocardiography (TEE) (Chicago, Illinois) to image the mitral valve. The TEE was interfaced to a TomTec three-dimensional workstation that allows electrocardiographic and respiratory cycle gated image acquisition. The acquired images are digitized, and after postprocessing a three-dimensional image is reconstructed. The mitral valve was viewed "en-face" as if looking up from the left ventricle. RESULTS: The mean mitral valve area (by pressure half-time from the Doppler of the two-dimensional echocardiogram) increased after BMV from 0.86+/-0.06 cm2 to 2.07+/-0.10 cm2, p < 0.0001. This was similar to the mitral valve areas obtained by planimetry from the three-dimensional images. The three-dimensional reconstructions showed a complete commissural split in 10 patients and partial splitting in 9 patients. In three of the eight patients who had an increase in the amount of mitral regurgitation secondary to BMV, the three-dimensional reconstructions were able to detect tears within the valve leaflet. One leaflet tear actually extended up to the mitral valve annulus and was associated with the only case of severe mitral regurgitation. CONCLUSIONS: The three-dimensional echocardiographic reconstruction enabled visualization of the mitral valve so that commissural splitting and leaflet tears not seen on the two-dimensional echocardiogram became visible.
INTRODUCTION: Iron replacement therapy reduces the demand for erythropoietin (EPO) in some dialysis patients. It has been postulated that iron supply to the bone marrow is a rate-limiting step in the process of erythropoiesis under erythropoietin stimulation. METHODS: We evaluated the economic benefit of intravenous iron therapy for this purpose in a prospective, non-blinded study of 22 haemodialysis patients, 16 male, six female, mean age 62 years (range 24-80 years). All patients had a serum ferritin (SF) of < or = 60 microg/L, despite oral iron therapy. Patients with high aluminium and/or parathyroid hormone (PTH) levels, underlying bleeding/haematological disorders or active inflammatory diseases were excluded. Patients were established on subcutaneous EPO and given intravenous iron over seven consecutive dialysis sessions (total dose 1050 mg) and supplemental monthly doses with regular monitoring for 4 months. RESULTS: The median EPO dose was 4000 units/week (mean 6050 units/week) pre-treatment and 2000 units/week (mean 3700 units) at 6 weeks post intravenous iron therapy (P=0.03). No serious adverse events occurred in the 154 treatment sessions of intravenous iron. Mean haemoglobin (Hb) level remained constant at 6 and 12 weeks (P=0.087). Serum ferritin levels (P< 0.0001) rose significantly, while a reduction in transferrin saturation (TS) became significant at the end of the study (P=0.0047). The use of intravenous iron allowed a substantial monthly cost saving per patient in our unit. CONCLUSION: Intravenous iron therapy is a safe and cost-effective method for maintaining or improving Hb levels with a more effective utilization of EPO in patients with low SF levels despite oral iron therapy.
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We studied positivity for anti-cardiolipin antibody, intraglomerular capillary thrombi on renal biopsy, and the progression of renal disease in 51 patients (10 male and 41 female), mean age 37 years (range 17-65 years), with a diagnosis of systemic lupus erythematosis and clinically evident nephritis confirmed by renal biopsy. Serum creatinine, serum indicators of disease activity and biopsies were analysed in subgroups according to thrombi and anticardiolipin status. End-points were death or chronic dialysis requirement and survival. Degree of sclerosis, crescent formation and necrosed glomeruli were all greater in those specimens positive for thrombi and in those specimens of patients who were serum ACA-positive, suggesting a relationship to disease activity/severity at presentation. The increase in serum anti-DNA antibodies and ANA and the reduction in C3 and C4 were significant in ACA-positive patients, with a strong relationship to disease activity when compared with changes in the ACA-negative patients (p < 0.05 in all cases). There was no significant difference when patients were separated according to the presence or absence of thrombi. Renal function at presentation was worse in patients with intracapillary thrombi and ACA positivity (p = 0.085 and p = 0.042, respectively). All patients progressed, but only those with intracapillary thrombi or anti-cardiolipin antibody positivity had a significant deterioration in renal function. Twenty-one thrombotic episodes occurred in 14 patients, of whom 13 were ACA-positive. Anticardiolipin antibody is a strong predictor of the presence of intraglomerular thrombi in SLE patients with renal involvement. The presence of thrombi and/or anticardiolipin antibodies indicate a worse long-term renal outcome. Anti-cardiolipin antibody positivity is a strong predictor of systemic vascular thrombotic complications.
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