Treatment of periorbital wrinkles by repeated medium-depth chemical peels in dark-skinned individuals.

BACKGROUND: The periorbital region serves as a barometer of chronological and environmental age and, as such, persons often seek its cosmetic rejuvenation. OBJECTIVE: This study was conducted to determine the efficacy and safety of repeated, medium-depth chemical peels in the treatment of periorbital wrinkles in dark-skinned individuals. SUBJECTS AND METHODS: A total of 12 subjects (10 women and 2 men) with fine and/or medium-sized wrinkles were included in the study, the ages ranged from 30 to 55 years with a mean of 41.25. Focal, medium-depth peels of periorbital area including crow's foot wrinkles were performed using a combination of Jessner's solution followed by the application of 35% trichloroacetic acid (TCA). The study involved a four-session regimen. To be included in this study, the subject completed at least two peeling sessions, 1 month apart, and returned for follow-up according to the research schedule. RESULTS: Improvement occurred in 11 of 12 subjects. Marked improvement occurred in four subjects (33%), moderate improvement in three (25%), mild improvement in another three (25%), minimal improvement in one subject (8%), and no response in one subject (8%). There were seven patients with fine and five with medium periorbital wrinkles. For statistical analysis, the no and minimum response groups were categorized as nonresponders. The improvement that ranged between marked to mild occurred in 100% of subjects with fine wrinkles and 60% of subjects with medium wrinkles. Mild side effects appeared in four subjects (33%). CONCLUSION: It can be concluded that fine and/or medium periorbital wrinkling responds favorably to repeated, medium-depth chemical peels even in dark-skinned individuals with few mild side effects.

Oral zinc sulphate in the treatment of recalcitrant viral warts: randomized placebo-controlled clinical trial.

BACKGROUND: Viral warts are common dermatological diseases; although the rate of spontaneous recovery is high, it usually takes a long time, and some patients might not show this spontaneous healing. Zinc has an important effect on the immune system and it has been used as an immunomodulator to treat a variety of skin disorders. OBJECTIVE: To assess whether oral zinc was effective in treating viral warts of patients evaluated between May 1999 and April 2000. PATIENTS AND METHODS: This was a placebo-controlled clinical trial. Eighty patients with viral warts (common, plantar and plane) were all resistant to all forms of treatment. Each patient had > 15 warts. Forty patients were treated by oral zinc sulphate at a dose of 10 mg kg(-1) daily up to 600 mg day(-1) and followed-up for resolution of their warts and for any evidence of recurrence for 2-6 months. Another 40 patients were given a placebo oral treatment in the form of glucose, and followed-up for the same period. RESULTS: Only 23 patients of the first group (zinc treated) and 20 patients of the second group (placebo treated) completed the study. In all patients the serum level of zinc was low. In the zinc-treated group, the overall response was complete clearance of warts observed in 20 patients (86.9%) after 2 months of treatment. Fourteen patients (60.9%) showed complete disappearance of their warts after 1 month. Three patients (13.3%) failed to respond to the treatment after 2 months of therapy. The response to treatment was directly related to the increment in serum zinc level. No patient of the placebo-treated group showed any response. CONCLUSIONS: We conclude that zinc sulphate at a dose of 10 mg kg(-1) daily seems to be a highly efficacious therapeutic option for recalcitrant viral warts and proved to be safe with few adverse effects.

Subclinical human papillomavirus infection of the cervix.

OBJECTIVE: A prospective study to investigate a group of Iraqi woman with proved genital vulval warts, to seek evidence of human papillomavirus infection in apparently normal looking cervixes and to investigate the natural history of infection. METHODS: From December 1997 to August 1998, 20 women with vulval warts were enrolled along with 20 aged-matched control cases without warts. Their ages ranged between 19-48 years with a mean of 30.4 years, (+/- standard deviation = 2.3) for patients and 18-48 years with a mean of 29.7 (+/- standard deviation = 2.7) for the control group. General and gynecological examinations were carried out. Cervical swabs for associated genital infection, papilloma smears, speculoscopy and directed punch biopsies were carried out to detect subclinical human papillomavirus infections of the cervix and associated intraepithelial neoplasm. RESULTS: Cytology results showed that 11 (55%) of patients had evidence of cervical infection by human papillomavirus, 6 (30%) showed mild dysplastic changes, 3 (15%) showed moderate dysplastic changes, whilst 2 (10%) showed no dysplastic changes. Speculoscopy and acetowhitening was positive in 11 (55%) and collated histological results showed evidence of human papillomavirus infection in 9 patients (45%). As for the control group one case (5%) had evidence of human papillomavirus infection. CONCLUSION: Subclinical human papillomavirus infection is more common than was previously thought among Iraqi women. It may appear alone or in association with vulval or exophytic cervical warts, or both, and may be more common than the clinically obvious disease. Speculoscopy as an adjunctive method to colposcopy was found to be a simple and an easy to perform technique. Its combination with cytology gave relatively good results when it was used as a triage instrument, and may have a more promising performance in the future.

Squamous cell carcinoma complicating prurigo nodularis.

Squamous cell carcinoma complicating ulcerative prurigo nodularis is described in 2 patients who were having prurigo nodularis on dorsum of the feet for duration of many years. Biopsy specimens from the ulcerating nodules showed features of squamous cell carcinoma. This finding has not been previously reported. Squamous cell carcinoma should be considered in the evaluation of long standing ulcerative lesion of prurigo nodularis especially when not responding to conventional therapy.

The exogenous origin of trimethylamine in the mouse.

Although it is now generally regarded that the origin of urinary trimethylamine (TMA) is via the action of intestinal microflora on precursors such as choline, little direct evidence exists. The normal production of urinary TMA was shown to be absent in germ-free mice and greatly reduced in antibiotic-pretreated animals. Cohabitation of germ-free mice with conventional animals restored their ability to excrete TMA. This study invokes a fundamental role for the intestinal microflora in the provision of TMA from precursors within the food.

The fate of trimethylamine in the rat.

The metabolism and excretion of [14C]-trimethylamine has been investigated in seven strains of rat. Over 75% of the administered radioactivity was excreted via the urine within the first day, with up to 9% in the faeces. At this dose level (15 mg/kg body wt) N-oxidation was the major metabolic pathway encountered (45% excreted dose) whilst demethylation was only of minor importance (3%). The remaining compound was excreted unchanged. No significant differences were observed between the strains studied.

Variable metabolism of pinacidil: lack of correlation with the debrisoquine and trimethylamine C- and N-oxidative polymorphisms.

1. The urinary excretion of pinacidil and its N-oxide in man was found to vary over a five-fold range. 2. Studies in individuals with inherited deficiencies for C-hydroxylation (debrisoquine type) and trimethylamine N-oxidation showed that the N-oxidation of pinacidil did not co-segregate with these oxidative polymorphisms. 3. It is concluded that the variable N-oxidation of pinacidil is most likely to be due to variations in the activity of the P-450 isozymes rather than in the microsomal flavoprotein containing mixed-function amine oxidase of Ziegler which is considered to be responsible for the N-oxidation of trimethylamine.

Trimethylaminuria: the detection of carriers using a trimethylamine load test.

A method potentially of value for investigating putative heterozygotes or carriers of trimethylaminuria by using a single oral dose of trimethylamine (TMA) is described. For healthy volunteers under normal dietary condition and following oral challenge with 300 mg and 600 mg TMA-base, over 90% of the urinary TMA was excreted in the form of TMA (93.6 +/- 1.6%). However, at a dose level of 900 mg TMA-base, there was clear evidence of saturation of the N-oxidation reaction as urinary TMA excretion declined to 77.2% (range 74.8-78.9) of the total dose of TMA. By contrast, in pedigree studies based upon propositi with trimethylaminuria, several parents were identified who showed clear evidence of saturation of the N-oxidation of TMA at the 600 mg TMA-base dose level, but not at 300 mg TMA-base or under normal dietary condition. In these individuals, the proportion of urinary TMA as trimethylamine N-oxide (TMAO) declined to (77.3 +/- 1.7%). Accordingly we propose that the oral administration of 600 mg TMA-base and the analysis of the following 0-8-h urine collection may be useful for the investigation of possible carriers of trimethylaminuria.

Trimethylaminuria ('fish-odour syndrome'): a study of an affected family.

1. Beginning with a single propositus, who had been previously diagnosed at the age of 10 as suffering from trimethylaminuria (fish-odour syndrome), both her parents and two sisters were investigated biochemically with respect to their ability to N-oxidize trimethylamine (TMA), both when derived from the diet and when administered exogenously. 2. Both the propositus and a second sister were markedly deficient in their ability to N-oxidize TMA, both when derived from the diet and when given as such; furthermore, both siblings readily developed the symptoms of fish-odour syndrome as characterized by a strong objectionable breath and body odour shortly after the oral administration of TMA (300 mg). 3. At this dose level of TMA, neither of the parents nor the third sister showed any evidence of impaired N-oxidation ability nor did they experience any 'fish-odour' symptoms. 4. With an oral challenge of 600 mg of TMA, both the parents showed a clear impairment of N-oxidation capacity which was not seen in six healthy unrelated volunteers. Both parents experienced a fish-odour syndrome at this level of TMA challenge. 5. The family data support the hypothesis that trimethylaminuria is an inborn error in the ability to N-oxidize TMA which is inherited as an autosomal recessive trait. Furthermore, experience with this family suggests that an oral challenge dose with 600 mg of TMA may be used to identify carriers of the condition.

Disclosure of the metabolic retroversion of trimethylamine N-oxide in humans: a pharmacogenetic approach.

Trimethylamine N-oxide (TMAO), which is naturally occurring in dietary marine fish, is well absorbed and excreted apparently unchanged as judged by end-product analysis. Such observations may conceal the fact that the amine N-oxide has undergone a sequence of deoxygenation and oxygenation reactions only to revert to the parental form and be excreted as such--a process that we propose to call metabolic retroversion. To evaluate this phenomenon for TMAO we have investigated the fate of the orally administered substance in healthy volunteers and in four subjects previously phenotyped as having an inherited deficiency with respect to the metabolic N-oxidation of trimethylamine (TMA). Two of these subjects were typed as homozygous affected and the other two as "carriers." If substantial reduction of orally administered TMAO occurs during the course of its postulated retroverted metabolism, it was hypothesized that this would be revealed by the extensive urinary excretion of unoxidized TMA by the four affected subjects. After oral TMAO administration in the four healthy subjects, greater than 94% of the urinary TMA was in the form of TMAO and only less than 4% as the free base. However, after oral TMAO in the two homozygous-affected subjects, unoxidized TMA accounted for 35% and 51%, respectively, of the total urinary TMA, the balance being due to TMAO. For the carrier subjects, TMA accounted for 12% and 16% of the total urinary TMA after TMAO administration. It is thus clear that the urinary excretion of unoxidized TMA is increased greatly in affected subjects with an inherited deficiency of N-oxidation after the oral administration of TMAO.(ABSTRACT TRUNCATED AT 250 WORDS)

A genetic polymorphism of the N-oxidation of trimethylamine in humans.

Trimethylamine (TMA) and its N-oxide (TMAO) are normal components of human urine. They are present in the diet and also derived from the enterobacterial metabolism of precursors such as choline. Dietary TMA is almost entirely metabolized to and excreted as TMAO. However, the extent to which TMA undergoes N-oxidation appears to be polymorphic in a British white population study (n = 169). Two propositi were identified with relative TMA N-oxidation deficiency that was further confirmed by oral challenge with TMA (600 mg). The study of the families of the two propositi, as well as those of two identified subjects with trimethylaminuria, under both normal dietary conditions and after oral TMA challenge strongly indicates that the conditions of impaired N-oxidation is inherited as a recessive trait. It is proposed that the N-oxidation of TMA in humans is polymorphic and under single gene diallelic control in which individuals who are homozygous for the variant allele exhibit marked N-oxidation deficiency and trimethylaminuria.

The metabolism of 14C-labelled trimethylamine and its N-oxide in man.

The metabolism and elimination of 14C-labelled trimethylamine and its N-oxide (100 mg orally) were studied in three male volunteers. For both compounds the urine was the major route of elimination, with 95% of the administered 14C being voided in the first 24 h. No radioactivity was found in expired air. The majority (greater than 95%) of the urinary 14C from both compounds was excreted as trimethylamine N-oxide.

The relative importance of N-oxidation and N-demethylation in the metabolism of trimethylamine in man.

The metabolism of orally administered trimethylamine has been studied in 4 male volunteers at 2 dose levels. N-Oxidation was the major route of metabolism whilst N-demethylation was negligible and only significant at the higher dose level.