EVALUATION OF PUVASOL AND PUVASOL WITH TOPICAL BETAMETHASONE DIPROPIONATE PLUS SALICYLIC ACID LOTION IN THE TREATMENT OF SCALP PSORIASIS

The efficacy and safety of betamethsone dipropionate 0.05% with salicylic acid 2% scalp lotion was evaluated in 60 patients with moderate to severe scalp psoriasis. Out of 120 patients with scalp psoriasis 60 patients received PUVASOL alone and 60 patients received PUVASOL alongwith lotion 0.05% betamethasone dipropionate with 2% salicylic acid scalp application for 3 weeks. The erythema, induration, scales and pruritus steadily improved in patients throughout the 3 weeks treatment course with betamethasone dipropionate with salicylic acid scalp application. At the end of therapy 84.3% of those patients receiving PUVASOL and betamethasone dipropionate-salicylic acid combination had 75% improvement of their scalp psoriasis versus 34.9% of those patients using PUVASOL alone. Complete clearing of the scalp was seen in 35% patients receiving therapy with topical betamethasone-salicylic acid and 11.6% with PUVASOL alone. Local side effects were primarily burning and stinging in 5 (83%) cases treated with topical betamethasone salicylic acid scalp application and 1 (1.6%) receiving PUVASOL alone. Combined therapy with PUVASOL and topical betamethasone dispropionate 0.05% with salicyclic acid 2% application appears to be safe and an effective treatment for scalp psoriasis.KEY WORDS: Betamethasone dipropionate, PUVASOL, Photochemotherapy, Scalp psoriasis     

Biochemical characterization of primary hyperparathyroidism with and without kidney stones

The exact metabolic-physiological background for kidney stone formation in primary hyperparathyroidism (PHPT) is unclear. To obtain clarification, this retrospective data analysis was conducted in 131 patients with PHPT who had undergone a detailed ambulatory evaluation on a random diet since 1980. The baseline biochemical presentation of 78 patients with PHPT with stones was compared with that of 53 patients without stones. Compared to those without stones, the stone-forming patients had a more marked hypercalciuria (343 ± 148 vs. 273 ± 148 mg/day, P < 0.01). Urinary saturation of calcium oxalate and brushite was significantly higher in stone-formers. Serum PTH and fasting urinary calcium were similar between the two groups, but serum phosphorus was significantly lower in stone-formers. Serum calcitriol (available in some patients) showed a slightly higher mean value in stone-formers but the difference was not significant. The increment in urinary calcium after oral load of 1-g calcium was twofold higher among stone-formers. Radial shaft and L2–L4 bone mineral densities resided within the normal ranges. Stone-formers with PHPT display exaggerated urinary calcium excretion due to intestinal hyperabsorption of calcium, contributing to a greater enhancement of the saturation of stone-forming calcium salts.     

Long-term combined treatment with thiazide and potassium citrate in nephrolithiasis does not lead to hypokalemia or hypochloremic metabolic alkalosis

BACKGROUND: Potassium citrate is commonly used in combination with a thiazide diuretic in the medical management of recurrent hypercalciuric nephrolithiasis. However, concerns have been raised that administration of this nonchloride potassium alkali with a kaliuretic and natriuretic agent such as thiazide may not be efficacious in correcting or preventing hypokalemia, and may produce hypochloremic metabolic alkalosis. This retrospective analysis was conducted to determine if these two potential complications are encountered in patients on long-term potassium citrate and thiazide therapy. METHODS: Data were collected on 95 patients who had been on combination therapy for at least 4 months from the stone clinics of the University of Texas Southwestern Medical Center, Duke University Medical Center, and Ochsner Clinic. RESULTS: Mean serum potassium concentration remained within normal limits without a significant decrease during combined therapy. Serum chloride was significantly lower from pretreatment but by only 1 mEq/L and remained within normal limits throughout treatment. There was a small increase in serum bicarbonate concentration compared to the baseline level of less than 1 mEq/L at 8 to 12 and 18 to 24 months, but not at other treatment periods. CONCLUSION: Co-administration of potassium citrate did not induce hypokalemia or hypochloremic metabolic alkalosis in our thiazide-treated patient population.     

Photochemical inactivation of cell-associated human immunodeficiency virus in platelet concentrates

Photochemical decontamination (PCD) of platelet concentrates, with adequate preservation of platelet function, has been shown using 8- methoxypsoralen (8-MOP) and long wavelength UV light (UVA). To further evaluate this technique, models for the inactivation of pathogenic human cell-associated viruses and integrated proviral sequences are required. We have assessed the ability of the PCD technique to inactivate cell-associated human immunodeficiency virus 1 (HIV-1) in platelet concentrates. We correlated PCD inhibition of HIV-1 infectivity with 8-MOP-DNA adduct formation in contaminating nucleated cells, and measured the inhibition of polymerase chain reaction (PCR)- mediated amplification of cellular DNA sequences as a surrogate for inactivation of integrated proviral nucleic acid sequences. After PCD treatment (8-MOP 300 micrograms/mL, UVA 17 mW/cm2) for 60 minutes, 0.5 x 10(6) plaque-forming units (PFU)/mL of cell-associated HIV-1 were inactivated and no virus was detectable by infectivity assay. After 60 minutes of PCD, 15 8-MOP-DNA adducts per 1,000 bp were formed, while in the absence of UVA, no adducts were formed. PCR-mediated amplification of a 242-bp cellular DNA sequence (HLA-DQ-alpha) was inhibited when greater than eight psoralen-DNA adducts per 1,000 bp were present. These studies indicate that high titers of cell-associated HIV-1 in platelet concentrates were inactivated by PCD, and the numbers of 8-MOP- DNA adducts in nucleated cells were sufficient to inhibit amplification of DNA segments that encode for as few as 80 amino acids. Based on the frequency of 8-MOP-DNA adducts, for the 10-kb HIV-1 genome, the probability of an integrated genome without at least one 8-MOP adduct after 60 minutes of PCD was 10(-33).