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To the Editor.— Byrd et al 1 presented a good description of what Birt and Davis 2 and we 3,4 call hereditary polymorphic light eruption (HPLE) of the American Indian. By not making this distinction, the authors overlooked some interesting aspects of a disorder that is unique for Native Americans of North, Central, and South America. 4 The large group of Finnish patients described by Jansen 5 exhibited such characteristic HPLE symptoms as autosomal dominant transmission, seasonal springtime onset, and a high incidence of cheilitis. 6 The frequent occurrence of cheilitis, often as the only presenting symptom of HPLE, has been reported in Canada, 7 the United States, 4 and Honduras. 8 Jansen did not cite cheilitis as the initial symptom in any of his patients, but its appearance in 47 (46%) of 103 persons leads one to wonder about a remote ancestral association with the American Indian. Although the

To the Editor.— In the AprilArchives(1980;116:433-444), Trau et al stated their case was the 12th case report of a patient with multiple clear cell acanthomas. Their case was the 11th. In their Table of the summary of previously reported cases, cases 4 and 5 are the same patient. The age in case 4 is not 59 years, as they reported, but 63 years, and he had his skin nodules four years, not five months. This patient was seen and his case was reported by myself and Dr Thorne 1 at the University of Minnesota Hospitals. One year later, he was seen at the Mayo Clinic and described by Landry and Winkelmann. 2 Dr Trau and co-workers could not have been aware of this information.

In Reply.— Greene et al presented a historic account of observations of hereditary cutaneous malignant melanoma (CMM) that has led to the simultaneous elucidation of a unique subset by Lynch and colleagues, 1,2 designated by them as the FAMMM syndrome , and by Greene and associates, who refer to it as DNS but have also called it the B-K mole syndrome and the large atypical nevus syndrome (LANS) . With respect to the contributions of other early investigators, our reports are replete with their efforts. Our concern with Rahbari and Mehregan's 3 study in our recent communication 4 is that they assigned sole credit for the delineation of the subset to only one group (Greene and associates), and thus did not mention the serious concern for the presence of other types of primary cancers in the FAMMM syndrome. More importantly, they used unsubstantiated historic genetic data to support the concept of their report of five cases of sporadic FAMMM syndrome. The statement of Frichot et al, 1 quoted by Greene et al, and interpreted as our admission of prior discovery by them, was taken out of context. In our yearly follow-up of patients with cancer at the Institute for Familial Cancer Management and Control at Creighton University, Omaha, we recognized, in the mid-70s, the existence of the FAMMM syndrome in the CMM pedigree reported by Lynch and Krush5 in 1968, before Dr Clark's oral presentation at the American Academy meeting in December 1976.

• T cells and T-cell subsets were determined in the peripheral blood of 12 patients with Behcet's syndrome and 30 normal healthy control subjects. When compared with the control group, the mean percentage of T cells for the group with Behcet's syndrome was significantly decreased (73% v 61%). The mean percentage of Tμ (helper) cells for the group with Behcet's syndrome (26%) was also significantly decreased from the mean value of the control group (42%). There was a concomitant significant increase of Tλ (suppressor) cells of the group with Behcet's syndrome (19%) over the mean value of the control group (10%). These results clearly indicated that there were alterations of T cells and T-cell subsets in this disease. ( Arch Dermatol 1983;119:307-310)

To the Editor.— In 1971 Wells described an unusual cutaneous eruption resembling acute cellulitis. Grossly it appears as single or multiple erythematous, edematous plaques and histologically demonstrates an intense eosinophilic infiltrate with an edematous dermis, which later is infiltrated by histiocytes. Many patients demonstrate a peripheral blood eosinophilia, and several authors have reported more striking hematologic alterations. Report of a Case.— A 36-year-old woman was seen in February 1981 for a cutaneous eruption that had been present since late 1980. The eruption was characterized by arcuate, raised, erythematous lesions on both wrists and thighs. Prior to admission, the patient had received erythromycin and prednisone. Cutaneous biopsy at that time revealed a nonspecific perivascular infiltrate composed of an admixture of lymphocytes with a substantial, but smaller, number of eosinophils. Scattered, small eosinophilic granules were present in an edematous dermis, with focal fragmentation of the collagen fibers. Laboratory studies indicated a hemoglobin

THE USE of accurate information in cancer genetics can aid the physician immeasurably in cancer-control efforts. The National Institutes of Health (NIH) consensus report dealing with precursors to malignant melanoma 1 failed to address certain evidence available about the genetics, tumor spectrum, and clinical facets of the natural history of the familial atypical multiple mole melanoma (FAMMM) syndrome. This term is synonymous with the hereditary dysplastic nevus syndrome (DNS) but is older and descriptive of all factors (clinical, genetic, and histological), while DNS is only a histological term. In addition, nevi may be absent, as will be discussed later, but the syndrome with its malignant potential can still be present. Thus, DNS is genetically inappropriate, as it does not describe the clinical spectrum of the FAMMM syndrome. 2 The report implied that the large atypical mole is distinctive of the FAMMM syndrome and is the sole cutaneous marker for this

• Sebaceous neoplasia have been observed in members of four families exhibiting the cancer family syndrome (CFS). This disorder is characterized by adenocarcinomas, particularly involving the (proximal) colon, endometrium, and ovary; an excess of multiple primary cancer; early age of cancer onset; and autosomal dominant pattern of inheritance. Multiple adenomatous polyps are lacking in this disorder. In four patients from three of these cancer-prone kindreds, cutaneous lesions were accompanied by multiple visceral adenocarcinomas, fulfilling the criteria for Torre's syndrome, a disease that heretofore has not shown notable familial clustering characteristic of the CFS. Therefore, the coexistence of rare sebaceous neoplasia and visceral cancer in CFS supports the notion that some cases of Torre's syndrome may in fact represent the more full phenotypic expression of the gene responsible for the CFS. (Arch Intern Med1981;141:607-611)

Hereditary polymorphic light eruption (HPLE) occurs in Indians of North and South America. Affected persons are sensitive to long ultraviolet radiation and therefore receive no substantial benefit from conventional sunscreens. We have treated 46 patients with HPLE at the Red Lake Reservation, Minn, with topically administered dihydroxyacetone and lawsone, orally given beta carotene, or both. Oral beta carotene afforded adequate photoprotection to 33 patients, and four additional patients were protected with the combined use of oral and topical agents. Epidemiologic studies support our proposals that HPLE is a causative factor in streptococcal pyoderma in the American Indian and may be associated with epidemics of streptococcal glomerulonephritis. (JAMA244:1456-1459, 1980)

To the Editor.— In the treatment of any disorder, the simultaneous use of two different therapies usually does little more than either individually. It is only occasionally that the effect of two different modes of treatment are additive. Yet, such an occurrence may be available in erythropoietic protoporphyria (EPP). Just recently, Mathews-Roth et al (228:1004, 1974) reported sevenfold (median) photoprotection in sunlight in EPP patients using orally administered β-carotene. In 1970 ( Br Med J 1:730, 1970), a 15-fold (median) increase in sunlight protection was reported in seven EPP patients using a topically administered dihydroxyacetone and lawsone preparation. Since then, we have treated six additional EPP patients with a stable preparation of dihydroxyacetone and lawsone (Duoshield). The Table summarizes the results. Since β-carotene is taken orally and the dihydroxyacetone and lawsonepreparation is used topically, the total photoprotective effect should be additive. Thus, we can approximately double the time these patients

In Reply.— Dr Jacoby states that our "rebuttal" lacked comprehension of the conference objectives. We participated in the conference, have published our data on the FAMMM syndrome widely, 1,2 and followed actively all of the research and issues discussed at the conference. We did not object to the theme of the conference; rather, we disagreed strongly with the conclusions. We must reject Dr Jacoby's statement that our rebuttal was misleading and that it was not in accord with the intent of the conference. Furthermore, Dr Jacoby's statement indicates that he did not comprehend the issues and the conclusions of the conference, which he was coordinating as acting director of the Office of Medical Applications of Research, NIH. We are deeply concerned about Dr Jacoby's confrontational letter, which is very defensive in character and implies a sacrosanct nature in the published conclusions of the expert panelists. Are we to believe that

To the Editor.— Housholder and Zeligman 1 recently described two patients with Torre's syndrome (TS) whose relatives also had visceral malignant neoplasms. Long survival was also noteworthy despite the occurrence of extensive visceral cancer. Their review of the literature disclosed several reports bearing on the occurrence of visceral malignant neoplasms in relatives of patients with TS. We have recently completed a study in which we clearly identify TS as the cutaneous phenotypic expression of the cancer family syndrome (CFS). The CFS is characterized by the following: (1) an early onset of colorectal cancer (preponderantly of the proximal colonic segment) in the absence of polyposis coli, (2) an association with other adenocarcinomas, particularly of the endometrium and ovary, (3) an excessive number of multiple primary cancers, (4) an occasional extraordinary tolerance of cancer, 2 and (5) more recently, our observation of an association with sebaceous neoplasia in a fraction of relatives

To the Editor.— Binford et al (1982; 247:2283-2292) discussed the state of the art in leprosy. They noticed the failure of transfer factor as a therapeutic tool. Saha et al 1 confirmed the failure of transfer factor, but they also reported the successful treatment of patients with leprosy with repeated whole WBC transfusions and the clearing of pathological, clinical, and histological findings. Earlier in 1972, the same technique 2 was reported in the successful treatment of lepromatous and tuberculoid patients with weekly transfusions of WBCs from normal histocompatible donors. Just recently, Sanchez and colleagues (personal communication, 1982), at the University of Puerto Rico, have duplicated these findings. These results open new avenues for immunologic research in the therapy for leprosy. Is the patient's immune system being temporarily or permanently restored to normal function so that the patient can successfully clear his disease? This and many other questions can and should

To the Editor.— Miao et al 1 reported that protoporphyrin levels in erythrocytes of patients with erythropoietic protoporphyria (EPP) were higher in winter than in summer and were elevated during administration of oral beta carotene. In developing a possible explanation for the protective effect of the carotenoid, they cited Piomelli et al 2 in support of statements that protoporphyrin leaks from erythrocytes of patients with EPP, and protoporphyrin is rapidly cleared from the plasma in vivo. Since this is not the first time Piomelli et al were cited about in vivo events in EPP, 3 a correction is in order. Despite use of the term "in vivo" in the title of the report, the study was an in vitro one. In fact, Scholnick et al 4 published information concerning in vivo turnover of plasma protoporphyrin. They administered tritiated δ-aminolevulinic acid (ALA- 3 H) and glycine labeled with radioactive carbon (glycine

To the Editor.— In reading the minutes 1 of theSociety Transactionsin the August 1976 issue of theArchives, the reader is left suspended in one of the discussions on the immunotherapy of leprosy. The minutes alluded to some leprosy research by a "Korean physician" in an obscure manner that invites inquiry. In 1972, Lim et al 2 reported that repeated whole WBC transfusions given over approximately a three-month period substantially cleared patients with either lepromatous or tuberculoid leprosy. The clinical, bacteriologie, and histologie data all became normal soon after the end of the immunotherapy and remained normal. These results were recently confirmed in a communication 3 that also reiterates the previous failure of the use of transfer factor. 4

To the Editor.— A letter by Mathews-Roth et al, published in theArchives(1979;115:1391-1392), describes a phototesting procedure that is presented as an objective, reproducible means of testing therapeutic efficacy of oral beta carotene in patients with erythropoietic protoporphyria (EPP). We maintain that the authors have not verified that their technique is reproducible or that it measures therapeutic efficacy, as we understand the terms. Apparently, the authors based their claims on two facts: that patients with EPP who obtained increased sunlight tolerance during beta carotene treatment also had increased tolerance to a modified solar simulator and that patients without clinical improvement did not have increased tolerance to the artificial light source. The reader should recognize that this type of distinction is qualitative rather than quantitative. To clarify this point, a positive qualitative result simply indicates the patient has increased sunlight tolerance; it does not disclose the magnitude of the increase.

To the Editor.— Duray and Ernstoff 1 described 14 patients (probands) with acquired nonfamilial melanoma in which seven patients had histologically dysplastic nevi associated with primary cutaneous malignant melanoma. In defining their methodology, they made several statements that are crucial to understanding their conclusion. They stated that (1) "Our study was conducted primarily as a pathologic and medical chart review, with aid from the attending clinicians, and not as a detailed interview with multiple family members, yielding detailed pedigree studies"; (2) "We reviewed all histologic slides, pathologic reports, medical records (with the aid of the tumor registrar), and further information from the clinical attending physicians"; and (3) "All patients had no family histories for melanoma (back two generations) and thus were considered to have nonfamilial melanoma." The authors did not detail the depth of genetic verification of informative data on the pedigrees. It must be assumed that the information was

To the Editor.— Rahbari and Mehregan ( Arch Dermatol 1981;117:328-331) cited Reimer et al 1 and Clark et al 2 as reporting in 1978 the first example of the FAMMM syndrome. The first report of this syndrome, however, was made in 1968 by Lynch and Krush, 3 who described two remarkable cases that had together all three of the essential elements of the FAMMM syndrome: (1) multiple moles of varying sizes and shapes that were clinically suspected of being malignant and that histologically showed very active junctional activity; (2) multiple cutaneous malignant melanomas and inordinately long survival in one patient; and (3) pedigrees disclosing a possible association with primary cancers in other organs (pancreas, respiratory tract, breast, sarcoma, and cervix). These cases were again evaluated during the 1970s, as part of our ongoing study of cancer patients at our institute for Familial Cancer Management and Control, Omaha. In 1977, Frichot and

To the Editor.— Inoshita and Youngberg's 1 article had the following discrepancies that nullify their postulate dealing with a new syndrome (keratoacanthoma-visceral carcinoma syndrome) (1) the environmental exposure of the patient to uterine intracavitary radium implants (because of this the etiology of cervical carcinoma in this patient cannot be clearly assigned to any syndrome); (2) a lack of understanding of the heterogeneity of expression of the cancer family syndrome (CFS); and (3) inadequate genetic investigation of family members of the index patient. The extremely common carcinoma of the uterine cervix is linked etiologically to early coitus, multiple sexual partners, poor prenatal and postnatal care, and lower socioeconomic status, factors that were not considered. The etiology of the cancer in this patient was complicated by the environmental exposure of the patient to prior radiation therapy, which is an causative factor in cervical squamous cell carcinoma. Thus, this patient is not a case

To the Editor.— In the March 1977 issue of theArchives(113:345-352), Drs Rea and Levan reviewed the current concepts in the immunology of leprosy. They noted the work of Lim et al1 with respect to the treatment of leprosy patients with intravenous infusions of leukocytes from normal persons. Rea and Levan stated, "Lim et al reported improvement in lepromatous patients associated with the administration of deliberately mismatched leukocytes. To our knowledge, the confirmatory studies have not been reported." In the article by Lim et al,1 the patients who were treated were three lepromatous patients and one tuberculoid patient. The authors reported remission of the patients' leprosy as measured by the following three measures: clinical, histologic, and bacteriologic. Rea and Levan used the term "deliberately mismatched leukocytes" in referring to the whole WBC infusions. This may imply to the reader a major incompatibility with possibly ABO blood types. In the

To the Editor.— A recent report 1 on ultraviolet light sources showed that the ultraviolet output of a solar simulator was similar to the natural spectrum of sunlight. For this reason, investigators are using this artificial light source to evaluate the effectiveness of sun-protective agents prior to sunlight performance tests. Implicit in this method is the assumption that the data obtained with such artificial light sources can be used to predict the results in sunlight tests. A recent study 2 with patients having erythropoietic protoporphyria (EPP) compared the ultraviolet protective qualities of orally administered β-carotene in tests using sunlightand a solar simulator. The authors reported that the results showed the qualitative protective effect of β-carotene with either light conditions, but they were concerned about "a lack of more quantitative correlation." We compared their data 2 obtained with sunlight and xenon-arc light in the 21 patients who had both tests by comparing the protective factors obtained with each light source (Table). The correlation coefficient for this comparison was

To the Editor.— The metabolic disorder characterized by elevated protoporphyrin in red blood cells (RBC) and feces was first described by Kosenow and Treibs1in 1953, but it was not clearly defined until the report by Magnus et al2in 1961. The latter authors named the disease erythropoietic protoporphyria (EPP) because of the obvious involvement of the erythrocytes and normoblasts. Recently, some investigators have concluded that the liver synthesizes most of the excess fecal protoporphyrin, and therefore the disease should be renamed erythrohepatic protoporphyria.3-5However, as noted by Tschudy et al,6a systematic classification of the porphyrias will not be possible until all the enzymic defects of these ailments are determined. Because the present level of knowledge is far below this goal, we suggest it would be premature to rename EPP, since EPP is a phrase that is well entrenched in the minds of students of

To the Editor.— In their reply to our communication in the August 1980Archives(116:863-864), Poh-Fitzpatrick and Mathews-Roth still insist that the studies of Piomelli et al 1 were partly in vivo. To resolve this semantic discordance, we will present our concept of an in vivo biochemical experiment. We visualize (at least) the following two broad types of study: (1) Collect specimens from a live animal, make the animal undergo stress, and collect specimens at recorded intervals. The specimens are then analyzed for a metabolite of interest to determine the effect of the experimental stress on turnover of the metabolite. (2) Administer radiotracers to a live animal, collect specimens, and monitor the rise and fall of radioactivity in a metabolite of interest. This type of experiment was conducted by Scholnick et al 2 and by Schwartz et al 3 to monitor protoporphyrin (PP) turnover in patients with erythropoietic protoporphyria (EPP).

To the Editor.— A hereditary form of polymorphous light eruption affects Indians from the central plains of Canada and the United States 1 to Central and South America. 2 Exposure to sunlight leads to pruritic macular, papular, and vesicular eruptions, sometimes with pyoderma and scarring. Symptoms appear in early spring in those in the northern hemisphere and persist until late fall. Patients are sensitive to long exposure to ultraviolet radiation (symptoms appear after exposure through window glass) and therefore receive no protection from commercial sunscreens. The clinical aspects and seasonal appearance of symptoms are reminiscent of erythropoietic protoporphyria (EPP), but neither we nor Birt and Davis 1 have detected elevated porphyrin levels in patients. Oral beta carotene is recommended for photoprotection of persons with EPP (Solatene package insert, Roche Laboratories, 1975). We reasoned that, since the disorder affecting American Indians resembles EPP, oral beta carotene may also protect these persons.

The protective effect of a sunscreen filter chemically induced in normal skin was tested by using direct sunlight exposure to assure effectiveness. The topical preparation was applied immediately after mixing. Washing with soap and water did not remove the protective filter. Greater protection resulted from repetitive use or increase of the applied quantity, or both. Separate application of either component of the mixture produced no significant protection in clinical trials and in vitro experiments.

In this survey, 103 consecutive patients with psoriasis were studied with respect to their (1) oral glucose tolerance tests, (2) family history of diabetes mellitus and/or psoriasis, and (3) urinalyses. Using conservative diagnostic criteria, 25% of these 103 psoriatic patients were found to have diabetes. The statistical possibility that this observation resulted from chance alone was less than 1 in 2,000 (P The family histories of these same 103 psoriatic patients revealed the frequent occurrence of diabetes and psoriasis in their relatives. The probability that these frequencies occurred in an independent manner is less than I in 50 (ie, between P>0.01 and

In 1967 a prospective study was undertaken to assess the alleged relationship between palmar keratoses and the presence of identifiable visceral malignancies. The study group consisted of 648 essentially asymptomatic adults who underwent comprehensive examinations for cancer with special attention to the presence of palmar keratoses. Palmar keratoses were present in 24.4% of the 648, including 28.4% of men and 19.9% of women. Each of the 648 was followed for three years subsequent to examination at the Cancer Detection Center. Of the 158 in the group with keratoses, 1.9% developed identifiable visceral cancers during 3+ years of follow-up study; for 490 without keratoses, 1.8% developed cancers. The findings of this study demonstrate that asymptomatic persons with palmar keratoses are neither more nor less likely to harbor identifiable cancers than those who do not have these skin lesions.

A case is described of atypical vascular lesions occurring successively on the face. The differential diagnostic possibilities are discussed in connection with its peculiar clinical course and unusual histology. The presence of large endothelial cells in histologic sections supports the idea that pyogenic granuloma may be primarily of a vascular origin rather than a reactive granuloma.

Multiple glomus tumors are uncommon. Sluiter and Postma,4in 1960, in an extensive review of the literature indicated that there were less than 2 dozen reported cases in contrast to the more than 350 cases of single glomangiomas. In view of their excellent paper, it is not our purpose in this brief communication to review the total subject of multiple glomus tumor. We wish only to(a) indicate the familial nature of this tumor,and(b) point out the microscopic difference between this lesion and the ordinary glomangioma. The number of case reports of familial occurrence of the multiple glomus tumor are few. In a complete review of the literature we were able to find only three. Touraine et al.1found multiple tumors in a father and daughter but did not attempt a complete family analysis. Kaufman and Clark2studied a family from which we have partially

Abnormal in vitro red cell photohemolysis can be used as a diagnostic aid for erythropoietic protoporphyria. Photohemolysis is regularly present in erythropoietic protoporphyria and is negligible in normal subjects, in patients with polymorphic light eruption, and in lead poisoning. A simple technique consists of irradiating a suspension of red cells diluted 1:500 in Ringer's solution by using a modified x-ray view box equipped with blacklight fluorescent tubes to serve as the irradiation apparatus. After three hours of exposure presence of photohemolysis is determined by direct visual or by photometric examination of the supernatant fluid. The technique does not involve a chemical or fluorometric analysis.

To the Editor.— A recent publication by Halprin et al 1 aided the understanding of epidermal glycogen metabolism. Space limitations preclude the rigorous discussion of rationale that this report deserves, but several points require clarification. Adenosine-3′, 5′-cyclic monophosphoric acid (cyclic AMP) and theophylline were mentioned in the "Material and Methods," section, but there is no further reference to their use. The source of a α-glucosidase was not reported; as we noted recently, 2 purified enzyme is available from Boehringer Mannheim Corp (No. 15043 EAAU). In our hands, there is no need to augment this preparation with α-amylase to obtain quantitative glycogen hydrolysis. The reference to Huijing 3 for glycogen assay details applies only to the glucosidase incubation step, since he detected glucose with glucose oxidase, and Halprin et al employed a fluorometric hexokinase-based assay. The comment that 0.2-mm keratome slices of normal and psoriatic skin contained about 85% epidermis is

To the Editor.— During the past decade, we have successfully used a sunscreen containing dihydroxyacetone/ naphthoquinone (lawsone) for patients with all types of cutaneous photosensitivity. 1 An advantage of this sunscreen is its capacity to induce a broad "ultraviolet shield" (290 to 405 nm) in the uppermost layer of the skin. In order to induce ultraviolet protection, the patient's skin must have an intact keratin layer. The amount of photoprotection achieved by a patient depends upon the following: (1) the chemical reactivity of the skin with the sunscreen; (2) the thickness of the keratin layer; (3) the number of applications of the sunscreen per day; (4) the degree of the patient's photosensitivity; and (5) the quanta of light per unit time received by the patient. Because of these variables, there is a wide spectrum of protective responses in our study 1 from less than one hour to more than eight

CUTANEOUS manifestations of the carcinoid syndrome commonly include transient flushing of the face and upper trunk, patchy cyanosis, and telangiectasia. 1 There have been occasional reports of severe pruritus, "orange blotches," 2 pellagra-like dermatitis, 3 acropachyderma, pachyperiostitis, 4 and sclerodermatous changes. 5 The occurrence of cutaneous metastatic nodules is infrequent. 4,6-9 After recent observation of a patient with the carcinoid syndrome with nodular cutaneous metastases as well as two unusual necrotic areas involving the skin, we reviewed the literature and were unable to find a report concerned with the latter lesions. Case Report A 62-year-old white man was first admitted to the University of Minnesota Hospitals in March 1967 with a diagnosis of carcinoid syndrome which had been confirmed elsewhere by abdominal exploration. Because of hepatic metastasis in the right lobe of the liver, it was removed in April 1965. A metastatic lesion in the mediastinum was removed in

In a survey at the University of Minnesota Hospitals, we have not confirmed the conclusions from the similar study done by Dobson and associates at the University of Oregon regarding an association of internal cancer and palmar keratoses. Palmar keratoses were found in approximately similar frequency in our normal subjects and our patients with internal malignancy. We believe that the presence of palmar keratoses is not by itself an indication of need for a systemic search for malignancy.

To the Editor.— The current interest in therapeutic vitamin supplementation has produced a confused picture with respect to porphyria. As noted by Mustajoki inThe Journal(221:714, 1972), the results of vitamin E therapy are contradictory. Thus, his group observed no clinical improvement in four patients with acute intermittent porphyria and one with variegate porphyria; whereas Nair et al 1 reported the successful use of vitamin E in porphyria. Ludwig 2 detected low tocopherol levels in persons with erythropoietic protoporphyria (EPP) and observed that the vitamin inhibited the in vitro photohemolysis of their red cells. This disease (EPP) is a good model for evaluating therapeutic agents, because it provides a sensitive in vivo criterion of efficacy (prevention of sunlight photosensitivity) as well as an in vitro standard (inhibition of erythrocyte photohemolysis). Provitamin A (β-carotene) has been employed successfully in EPP patients by Mathews-Roth et al. 3 Although the rationale for

To the Editor.— In the article "Histogenesis of Skin Appendage Tumors," 1 the authors state "By histochemical criteria, cylindroma did not show definite differentiation either in apocrine or eccrine direction." Histochemical data, published previously, are not in agreement with their statement. 2-5 The interpretation of the periodic-acid Schiff (PAS) stain was expanded to evince that with a yellow counter stain (picric acid), there were two basic colors observed in mammalian tissue sections after diastase digestion. The two diastase resistant (D) colors were magenta (M) and red (R). If the next tissue section was stained with alcian blue (AB), the magenta substance was AB positive ( + ) and the red substance was AB negative ( - ). If alcian blue was used as a counter stain or if the PAS was used alone, the two colors were not discernible. The results of the PAS picric reaction under controlled conditions 2,4 indicated acidic carbohydrates or carbohydrate protein

Photoparesthesia may be the only clinical finding in patients with erythropoietic protoporphyria. An erroneous diagnosis of psychogenic pruritus, as in our patient, is corrected by the finding of elevated erythrocyte protoporphyrin levels as well as by an increase in the ratio of fecal protoporphyrin:coproporphyrin. The possible application of similar chemical findings to the diagnosis of the heterozygous carrier state is noted.

The immunoelectrophoretic patterns (IEP) of serum proteins of leprosy patients were studied. The β 2M immunoglobulins were elevated in the sera of patients having the lepromatous type of leprosy but were not elevated in the sera of patients having the tuberculoid type of leprosy. These serum globulin changes may prove to be useful in differentiating these two types of leprosy.