Migraine is a chronic, recurrent, disabling condition that affects millions of people in the US and worldwide. Proper acute care treatment for migraineurs is essential for a full return of function and productivity. Triptans are serotonin (5-HT)(1B/1D) receptor agonists that are generally effective, well tolerated and safe. Seven triptans are available worldwide, although not all are available in every country, with multiple routes of administration, giving doctors and patients a wide choice. Despite the similarities of the available triptans, pharmacological heterogeneity offers slightly different efficacy profiles. All triptans are superior to placebo in clinical trials, and some, such as rizatriptan 10 mg, eletriptan 40 mg, almotriptan 12.5 mg, and zolmitriptan 2.5 and 5 mg are very similar to each other and to the prototype triptan, sumatriptan 100 mg. These five are known as the fast-acting triptans. Increased dosing can offer increased efficacy but may confer a higher risk of adverse events, which are usually mild to moderate and transient in nature. This paper critically reviews efficacy, safety and tolerability for the different formulations of sumatriptan, zolmitriptan, rizatriptan, naratriptan, almotriptan, eletriptan and frovatriptan.

The heavy metal mercury elicits a genetically restricted, anti-nucleolar autoantibody response that targets fibrillarin, a 34-kDa protein component of many small nucleolar ribonucleoprotein particles. The mechanisms by which a toxin such as mercury elicits an autoantibody response that predominantly targets a single intracellular protein autoantigen remain uncertain, but may be prefaced by mercury gaining access to the intracellular environment. Mercury-induced cell death was associated with loss of fibrillarin antigenicity and modification of the molecular properties of fibrillarin as revealed by aberrant migration under nonreducing conditions in SDS-PAGE. Addition of mercury to isolated nuclei also resulted in aberrant migration of fibrillarin, but not other nuclear autoantigens. The sensitivity of the HgCl2-induced modification of fibrillarin to 2-ME, iodoacetamide, and hydrogen peroxide suggested interaction of mercury with the two cysteines in the fibrillarin sequence. This was confirmed by mutation of the cysteines to alanines, which abolished the aberrant migration of fibrillarin in the presence of HgCl2. The modification of the molecular structure of fibrillarin by mercury reduced immunoprecipitation by anti-fibrillarin autoantibodies, pointing to unmodified fibrillarin as the B cell Ag and implicating mercury-modified fibrillarin as the source of T cell antigenicity. These observations demonstrate for the first time that an environmental toxin can alter the physicochemical properties of an autoantigen and may help to explain the antigenic specificity of mercury-induced murine autoimmunity.

A sensitive fluorescence procedure for the determination of indapamide in plasma and whole blood was developed. The procedure requires preextraction of the biological sample followed by continuous-flow analysis. The assay is sensitive to indapamide levels of 25 ng/ml in plasma and blood. A linear response from 25 to 200 ng/ml is observed. The procedure also can be used to measure urinary levels of indapamide. The assay has been used to obtain whole blood and plasma level curves from subjects receiving 2.5 mg of indapamide.

Zinc deficiency dermatitis is a recognized complication of prolonged total parenteral nutrition (TPN) in adults and children. Ten cases of a characteristic dermatosis developing in premature infants with hypozincemia while on long-term TPN are described. The infants presented a defined group of premature neonates who were born between 25 and 28 weeks' gestation with birth weights of less than 1,200 gm and who had received continuous prolonged TPN. The characteristic skin changes appeared on an average of 91 days after birth, with prominent and early involvement of the neck fold crease. Lesions also occurred on the cheeks, buttocks, and genitalia, but spared the extremities. In seven of the ten cases, the skin changes and low serum zinc levels developed 1 to 5 days after an episode of bacterial sepsis or signs of physiologic stress.

Indapamide, an antihypertensive agent, is an aryl sulfonamide that inhibits carbonic anhydrase in vitro but not in vivo. An assay was developed for indapamide in drug-rodent food mixtures that utilizes this inhibitory effect. Indapamide was extracted from the mixtures with methanol, and an aqueous dilution of the extract was sampled by a continuous-flow system. In the system, the drug was extracted with butanol and then back-extracted into alkali. This solution was neutralized, buffered, and mixed with bovine erythrocyte carbonic anhydrase. The substrate, p-nitrophenyl acetate, was added, the solution was incubated, and the amount of p-nitrophenol formed was measured. The assay was sensitive to 20 micrograms of indapamide/g of food, and 20 unknown samples could be analyzed per hour on the continuous-flow system. It is possible that the method could be extended to the analysis of other toxicological test substances that inhibit carbonic anhydrase in vitro.