Pattern of hospital admission and outcome in Parkinson’s disease: A study from Punjab, India

Background: The hospitalization rates of patients with Parkinson’s disease (PD) are 1.45 times higher than for age matched controls. We studied the causes for admission, hospital course and outcomes in PD population so that preventive measures could be developed. Methods: We prospectively studied patients with the diagnosis of PD admitted to a tertiary care hospital in Ludhiana, India from January, 2012 to December, 2014. Etiology for hospitalization was determined and the patients were divided into two groups, admission due to causes related to PD or not associated with PD. The PD related admissions were further categorized into Group I: directly disease related causes and Group II: indirectly disease related causes. The primary outcome was mortality. The secondary outcome measures were duration of hospitalization, requirement for ICU, need for mechanical ventilation and complications. Results: There were 146 patients of PD out of 25,326 hospital admissions. Forty two patients (28.7%) had direct cause, 73(50%) had indirect cause and 31(21.2%) were non-PD related admissions. The mean age was 68.5+9.9 years, 97males (66.7%). There were 16(10.9%) deaths. The commonest cause of admission was infections and encephalopathy. The indirect PD related admission had significantly higher age (p= 0.0014), increased risk of ICU admission (p=0.011), need for mechanical ventilation (p < 0.005) and longer duration of hospital stay (p=0.0001) as compared to group I. Also there was a six fold increased risk of death in this group (p 0.034). Conclusion: As disease progresses, the indirect reasons for admission becomes more troublesome than the initial motor complaints.

Acute renal failure complicating rifampicin therapy.

BACKGROUND : Since 1971, 55 case-reports of rifampicin-induced acute renal failure (ARF) have been published. Covic et al described 60 consecutive cases of rifampicin-induced ARF during a period of eight years (1987-1995) from Iasi Dialysis Centre, Romania. The systenic data on this condition are not available, in view of the anecdotal nature of the observation from our country. OBJECTIVE: The aims of study were to analyze clinical features, course and outcome of ARF complicating rifampicin therapy at our centre. METHODS: We retrospectively studied prevalence, clinical presentations and renal histology and outcome of 11 cases (eight males, three females, aged 42-72 years) who were referred to Nephrology Unit of University Hospital, Varanasi for acute renal failure following retreatment with rifampicin between period of 1994-1999. RESULTS: The gastrointestinal symptoms (abdominal pain, nausea and vomiting) and 'flu like' (fever, weakness and body ache) syndrome were the most frequent presenting features. The clinical signs of intravascular hemolysis were observed in four cases. The commonest laboratory findings included: Anaemia (7), leukocytosis (5), thrombocytopenia (3) and toxic hepatitis in (2) patients. Toxic hepatitis, hemolysis and ARF was seen in one patient in combination. The typical clinical features of allergic interstitial nephritis and acute tubular necrosis were seen in six and two patients respectively. Renal biopsy in three cases revealed; crescentic GN (1) and ATN in (2) patients. Acute renal failure complicating rifampicin accounted for 1.8% (11/607) of all ARF cases hospitalized in our centre during the study period. Renal function returned to normal in nine cases and one patient died on account of hepatic failure (toxic hepatitis). The patients with crescentic GN remained anuric and became dialysis dependent. Thus, clinical course of rifampicin induced ARF was favourable; with only one mortality, compared to a 18% mortality rate among all ARF patients. CONCLUSION: Acute renal failure complicating rifampicin therapy is not an uncommon condition, and typically occurs after reintroduction of rifampicin. The renal prognosis is usually favourable. Intermittent or interrupted therapy appears to be a significant risk factor for the development of acute renal failure.

Isolation, purification, immobilization of oxalate oxidase and its clinical applications.

Oxalate oxidase known to catalyse the aerobic oxidation of oxalic acid into CO2 and H2O2, has been found in bacteria, fungi, mosses and some higher plants. So far, a membrane bound oxalate oxidase from Pseudomonas sp. OX-53 and a soluble oxalate oxidase from seedling plants of barley and grain sorghum has been purified to homogeneity by conventional purification methods. The enzyme has been immobilized onto insoluble support such as nylon tubing, zirconia coated alkylamine glass, polyamide membrane, CO2 gas sensing electrode, H2O2 sensor probe and polyanionic electrolyte such as ethylaminemaleic anhydride (EMA). Compared to free enzyme the immobilized enzyme showed an increase in optimum pH, decrease in Vmax and time for maximum activity, higher resistance to inhibition by NaCl but no change in Km value. The immobilized enzyme has been used in both continuous flow system and discrete assays and in enzyme electrode for determination of oxalate in urine, blood and food stuff, which is essentially required for the diagnosis and treatment of hyperoxaluria and calcium oxalate urinary stones. The degradation of endogenous oxalate in rat by immobilized oxalate oxidase has opened a new vistas in enzyme therapy of hyperoxaluria.