114 Correspondence

Journal of the American Academy of

Dermatology

As a result its individual filaments contact the tooth surface and scrape off the organized microbial colonies. At present, most periodontists in the United States seem to recommend the use of unwaxed dental floss. Ag- gressive use of dental floss, waxed or unwaxed, can insult the gingiva and cause bleeding, ulceration, gin- gival cleft, and recession?

In 1979, Goldman g described the presence of uni- lateral angular cheilitis in two patients and attributed it to the use of unwaxed dental floss for dental hygiene. Rubbing of the dental floss against the oral commis- sures, especiaily when the mouth was wide open, was believed to be the probable cause for the development of angular cheilitis. Goldman suggested that patients who need dental floss for dental hygiene should use waxed dental floss and should not open their mouths too widely.

In our patients the lesions of angular cheilitis first appeared several weeks after the initiation of dental flossing. No other predisposing factors of angular chei- litis could be determined. The development of angular cheilitis was unrelated to the type of dental floss, waxed or unwaxed, that had been in use. We presume that the probable cause of angular cheilitis was the combined effect of the maceration resulting from excessive mouth rinsing and the traumatizing use of dental floss.

Overhydration of the skin produces swelling of the stratum corneum. Desiccation, caused by dry and windy climate, produces shrinkage of the epidermal ceils. The alternating swelling and shrinkage result in cellular damage, which predisposes the epidermis to mechanical trauma with resultant fissuring and secondary infec- tions? Nonaggressive use of dental floss and reduced amount of mouth rinsing were the two principles in the instructions for the first group and resulted in complete disappearance of further episodes of angular cheilitis. This circumstantial evidence, together with the fact that

bo th principles mentioned had been observed in the second group who lacked angular cheititis, strongly support our hypothesis.

Our cases presented herein draw attention to a der- matologic complication of dental flossing. Dental floss must be included in the differential diagnosis of the causes of angular cheilitis.

Michael Kahana, M.D., Ran Yahalom, D.M.D., * and Miriam Schewach-Millet, M.D.

The Chaim Sheba Medical Center Tel-Hashomer and SackIer School of Medicine

Tel-Aviv University, Israel

*Israeli Air-Force, IDF.

REFERENCES 1. Chemosky ME: Dental conditions of diagnostic aid in

macocutaneous medicine. Arch Dermatol 84:115-122, 1961.

2. Domonkos AN, Arnold HL, Odom RB: Diseases of the skin. Philadelphia, 1982, W. B. Saunders Co., p. 305.

3. Goldman HM, Cohen DW: Periodontal therapy. St. Lous, 1980, The C. V. Mosby Co., pp. 502-504.

4. Goldman L: Dental floss as a factor in the development of perl~che. Arch Dermatol 115:108, 1979.

5. Chernosky ME: Dry skin and its consequences. J Am Med Worn Assoc 27:133-142, 145, 1972.

Atopic eczema unresponsive to evening primrose oil (linoleic and ~/-linolenic acids)

To the Editor: In a controlled study recently published on the oral treatment of atopic eczema with evening primrose oil (J AM ACAD DERMATOL 13:959-965, 1985), Balnford et al were unable to show any favorable effect. I want to attest to their conclusion by briefly reporting a preliminary pilot study performed during the period March 1983 to January 1984. The series comprised eight adult patients, six women and two men aged 18 to 39 years (mean, 28 years) with a long history of severe atopic eczema. The capsules used were iden- tical to those used by Bamford et al (each containing 500 mg of oil (9% ~/-linolenic acid and 72% linolcic acid with small amounts of palmitic, oleic, and stearic acids) and were supplied by Efamol Ltd., London. The dosage was four capsules twice daily with a total of 800 in five patients, 600 in two, and 500 in one. The shortest period of treatment was thus more than 2 months and in most cases well over 3 months. The patients were asked to assess itching, dryness of the skin, and general impression of their condition on an analog scale from 0-10 at the start of the trial and at monthly attendances at the clinic, when they were also examined clinically (Table I). As ~/-linolenic acid could theoretically influence the state of the prostaglandin and immunologic systems, ~'2 the response to topical appli- cation of nicotinate (Trafuril) and the serum concentra- tion of IgE were determined at the start and end of the trial, as was also the total eosinophil count. All patients were very eager to take part in the trial after being informed of the theory of action of the preparation, and this was reckoned to exert a considerable placebo effect; their subjective assessments very likely reflect such an effect. On the other hand, none of the patients felt the eczema had improved at the end of the trial.

Objectively, no convincing improvement took place during the trial, but there were, of course, fluctuations. Only one patient showed a change in response to Tra-

Volume 15 Number i July, 1986

Correspondence 115

Table I , Analog scale assessment by patient during trim

Start l End

General condition 6.4 4.5 Itching 6.0 4.5 Dryness of skin 6.4 4.0

furil from vasoconstriction to vasodilatation. The mean IgE concentration rose from 2,848 kU/liter to 3,115 kU/liter, with standard deviations of nearly 3,500. Eo- sinophil count increased in three patients and decreased in four, the mean values being 635 × 106/liter at the start and 523 × 106/liter at the end, with standard de- viations similar to the means.

Thus, evening primrose oil had no convincing effects in this small series; there was no effect on the immu- nologic system as mirrored b y the IgE concentration, and there was no change in prostaglandins as expressed by the response to Trafuril.

Marcus Skogh, M.D. University Hospital, S-581 85 Linkdping Sweden

REFERENCES 1. Manku MS, Horrobin DF, Morse N, et al: Reduced levels

of prostaglandin precursors in the blood of atopic patients. Prostaglandins Leukotrienes Med 9:615-628, 1982.

2. Chouaib S, Chatenoud L, Klatzmann D, et al: The mech- anism of inhibition of human IL2 production. 1I. PGE2 induction of suppressor T lymphocytes. J Immunol 132:1851-1857, 1984.

Reply

To the Editor: Because my study dealt with cases with less extensive atopic eczema (at the beginning of the study, 11% of our patients and 50% of Wnght's patients had 50% of skin involved), I am glad to see my results are similar to Dr. Skogh's results in his pilot study (using a lower, 4 gin/day, dose of evening primrose oil) in patients with severe atopic eczema.

Joel T. Bamford, M.D. 2418 East Fifth St., Duluth, MN 55812

Pemphigus vulgaris in sisters

To the Editor: The familial occurrence of pemphigus was first noted by Morris in 1917. ~ Subsequently a few other similar cases have been reported. 2~° We report the development of pemphigus vulgaris in a 56-year-

old white woman 12 years after its onset in her older sister. Human lymphocyte antigen (HLA) types of these patients are compared with those of other patients with nonfamilial pemphigus. To our knowledge, HLA typing has not been reported previously in familial pemphigus.

Case reports. Reports of cases 1 and 2 follow. Case 1. A 56-year-old white woman of Italian descent was

first seen in November 1977 complaining of sores in her mouth and on her chest, back, nose, and face thathad been present for about 2 months. Cutaneous and mucosal exami- nations demonstrated denuded areas on the external aspects of the ears, right temporal region of the face, tip of the nose, chest, back, and oral mucosa. The remainder of the physical examination was unremarkable. Histologic examination of a biopsy specimen from a chest lesion revealed a suprabasilar, acantholytic cleft within the epidermis. Direct immunofluo- rescence showed intercellular straining of the epidermis with IgG. Indirect immunofluoreseence was negative.

Her pemphigus was initially treated with prednisone, 140 mg daily, and intramuscular gold sodium thiomalate, 50 mg weekly. The patient developed steroid psychosis, at which time the steroid dosage was quickly tapered and treatment with azathioprine, 50 mg daily was started. After she had received a total of 685 nag of gold sodium thiomalate, the gold injections were discontinued and she was treated with azathioprine, 100 mg daily. Her pemphigus has been under control since that time with intermittent courses of low-dose prednisone and azathioprine.

Case 2. A 56-year-old white woman (sister of Patient 1) was seen in 1965 with a severe blistering eruption. Biopsy for routine histology showed a suprabasilar, acantholytic cleft in the epidermis and she was diagnosed as having pemphigus vulgaris. The patient was treated with intravenous adreno- corticotropic hormone (ACTH), initially with 80 units daily and then the dosage was increased to 160 units intramuscularly daily following an exacerbation of the disease. She was treated with low doses of ACTH and then prednisone was given for several years. The pemphigus flared in May 1975. Direct immunofluoreseence studies were negative. Indirect immu- nofluoreseence showed the presence of pemphigus antibodies at a titer of 1:80 in monkey esophagus. Her pemphigus has been under control since that time with intermittent courses of prednisone. The family history is otherwise negative for pemphigus or other autoimmune disorders.

HLA typing. Patient 1 was HLA type A2, Bw35, Bw51, and DRw4. Patient 2 was HLA type A2, Bw2, Bw51, and DRw4.

Comment. There have been fourteen cases of the familial occurrence of pemphigus reported in the En- glish literature. H0 To our knowledge, none of these patients has been studied for HLA type. Both of our patients were studied and found to be positive for A2, Bw51, and DRw4. The association of certain HLA