Volume 13Number 5, Part INovember, 1985
history of intestinal disorders.' Patients experiencingabdominal pain, rectal bleeding, or severe diarrhea areadvised to discontinue therapy promptly.
Our group has now treated over one hundred patientswith oral isotretinoin and we have observed no gastricadverse reactions. Asked whether a history of inflammatory bowel disease should be considered a contraindication to the use of isotretinoin, a gastroenterologyconsultant writing in the Journal of the American Medical Association stated that neither he nor his colleagueshave observed one case in which ulcerative colitis orCrohn's disease has occurred following the use of thismedication.' I recently treated a patient afflicted withcystic acne and ulcerative proctitis with oral isotretinoin. No deleterious effect upon the gastrointestinaltract was noted.
Case report. A 19-year-old man presented with cysticacne involving his face and neck. In 1980 he had developedabdominal pain, weight loss, and constipation associated withpassage of blood and mucus. Sigmoidoscopy revealed edemaand friable tissue and rectal biopsy showed evidence of mucosal ulceration and crypt abscesses, consistent with a diagnosis of ulcerative colitis. He was placed on sulfasalazine,2 gm/day, with intermittent flare-ups requiring short coursesof oral prednisone. Because of gastric intolerance to tetracycline and erythromycin, he was placed on ampicillin, 1gmtday, in an attempt to control his severe cystic acne. Thecondition improved over the next 6 months but then flared,and in August 1983 he was placed on 80 rug/day of oralisotretinoin. Two weeks later a marked flare of the acne occurred. The isotretinoin dosage was decreased to 40 mg/day,ampicillin was again added, and the lesions were injectedwith triamcinolone. Within 2 weeks his condition had stabilized and the dosage of isotretinoin was increased to 80 rng/day. He remained on this dosage for the next 14 weeks.
During the entire course of isotretinoin he experienced nogastric or rectal abnormalities. Indeed, after the third monthhis dosage of sulfasalazine was cut in half. All laboratoryvalues, includingserum triglycerides, remained within normalrange.
As of January 1985 no new cystic lesions had been observed. Further, the patient had not experienced any cxacerbation of the colitis and had been off sulfasalazine for over6 months.
Comment. The use of oral isotretinoin does not appear linked to the onset of ulcerative colitis or Crohn'sdisease. Similarly, in patients with inflammatory boweldisease, isotretinoin therapy may not lead to exacerbation and would be indicated in the treatment of suchpersons also afflicted with cystic acne.
Stephen M. Schleicher, M.D.Ste. 2, 8945 Ridge Ave.Philadelphia, PA 19128
Correspondence 835
REFERENCES
I. Physicians' Desk Reference. Oradell, NI, 1985, MedicalEconomics Co., pp. 1665-1667.
2. Korelitz BI: Systemic 13-cis-retinoic acid therapy and exacerbation of colitis. JAMA 252:2463, 1984.
Gnathostomiasis (nodular migratoryeosinophilic panniculitis)
To the Editor:In 1979, gnathostomiasis (nodular migratory eosin
ophilic panniculitis) was detected for the first time inGuayaquil (Ecuador, South America). I Its existencewas confirmed in 1981 by the Department of Dermatology, Venereology and Allergy of the Institute Ecuatoriano de Seguridad Social of Guayaquil, Ecuador,when the third parasite stage in humans (Fig. 1) wasdiscovered for the first time in South America.v'
In 1985 we found the Gnathostoma parasite, in itsadult stage, in the stomachs of its definitive hosts, dogsand cats (Fig. 2). This was also reported for the first
Fig. 1. Third stage of the parasite found inhuman tissue.
-------,-,----------;...",..,.;...;."..,.,~....,
Fig. 2. Parasite in its adult form found in the stomachof a cat (definitive host).
836 Correspondence
Fig. 3. Clinical picture showing a peculiar erythematousplaque with an erysipeloid appearance.
Fig. 4. Histologic picture showing massive infiltrate ofeosinophils between fat cells and the septae.
time in America, establishing and confirming the presence of this disease in our country, Ecuador. The occurrence of this disease was known prior to this timeonly in Southeast Asia, in countries such as Thailand,Singapore, Indonesia, Taiwan, and Japan.
This illness is transmitted by the ingestion of raw orpartially cooked food, mainly fresh water fish, becausethe parasite does not live in salt water fish." In Ecuadorthere is a habit of eating a typical food called cebiche,which consists of small pieces of raw fish, preparedonly with lemon juice.
This disease manifests itself clinically as erythematous plaques of variable sizes that are slightly painfulon palpation and resemble panniculitis plaques or erysipelas located in cellular subcutaneous tissue (Fig. 3).The parasite has a tendency to migrate, evolving inflares that last 2 or 3 weeks, accompanied by tissueeosinophilia. The larva can localize in any part of thehuman and symptomatology depends on the organthrough which it migrates. Due to the symptoms andsigns in the skin, it has been called nodular migratoryeosinophilic panniculitis.
Journal of theAmerican Academy of
Dermatology
This illness, to proceed through its evolutionary lifecycle, needs a definitive host like dogs, cats, or tigers,an intermediate second host, a copepod of the genusCyclops, and a third host that makes the third stagelarva, such as fish, batrachians, and birds."
The human being is an abnormal host who gets thedisease from eating raw or poorly cooked food. Theillness can stay in the human organism in its third stagelarva for years. When the disease is detected, the diagnosis is easy and is confirmed by the pathologic features which are pathognomonic because there is a massive infiltrate of eosinophils between the fat cells (Fig.4) and by the peripheral eosinophilia.
The best way to avoid gnathostomiasis is prophylactic by not eating raw or poorly cooked food, especially fresh water fish. The best method of treatment issurgery, with extirpation of the larva from the lesion.Unfortunately, this is not always possible because ofthe migratory character of the illness. We have triedtreatment with praziquantel with good results. At present, there is an epidemic of this disease in Guayaquil,Ecuador, with around 200 registered cases.
In Mexico, gnathostomiasis has been reported in itsthird stage larva, but they have not found Gnathostomaspinigerum in its adult stage. The reported cases in theUnited States are not originally from this country; theyhave been found in other places.
Wenceslao Ollague, M.D.Department of Dermatology
University of Guayaquil, Post-Graduate School,and Department of Dermatology, Venereology and
Allergy of the I.E.S.S.Guayaquil-Ecuador, South America
REFERENCES1. Ollague W, Ollague J, Guevara de Veliz A, Peiiaherrera
S: Paniculitis Nodular Migratoria Eosinofflica (Gnathostomiasis Humana en Ecuador). Med Cutan lber Lat Am10:73-78, 1982.
2. Ollague W, Ollague J, Guevara de Veliz A, PeiiaherreraS: Gnathostomiase Humaine premiere mise en ecidencedu parasite en America du Sud. Ann Dermatol Venereal110:311-315, 1983.
3. Ollague W, Oilague J, Guevara de Veliz A, PeiiaherreraS: Humangnathostomiasis in Ecuador (nodularmigratoryeosinophilic panniculitis). lnt J Dermatol 23:647-651,1984.
4. Miyazaki 1; On the genus Gnathostoma and human gnathostomiasis withspecial referenceto Japan. Exp Parasitol9:338-370, 1960.
5. Daengsvang S, Thienprasitthi P, Chomcherngpat P: Further investigations on natural and experimental hosts oflarvae of Gnathostoma spinigeruminThailand. AmJ TropMed Hyg 15:727-729, 1966.