Letters will be published as space permits and at the discretion of the editor. They should be typewritten double-spaced, with five or fewer references, should not exceed 500 words in length, and will be subject to editing. Letters are not acknowledged. For other details, see "Instructions for Authors."

Spironolactone-Induced Lichen Planus

To the Editor.\p=m-\Drugeruptions with the histological features of lichen planus have been attributed to a number of drugs.1,2

Recently, antihypertensive agents

uance

of

spironolactone

treatment

yielded

discontinuing spironolactone treatment, residual ery¬ thema and peripheral hyperpigmentation of the palmar lesions were present (Fig 2). She is currently normotensive and is only taking daily dignoxin. lesions. Three months after

cillamine: A case report with some biochemical observations. Dermatologica 150:372-374, 1975. 5. Saurat JH, Gluckman E, Bussel A, et al: Lichen planus-like eruption after bone marrow transplantation. Br J Dermatol 92:675-681, 1975.

Report of a Case.\p=m-\A 62-year-old woman had a three-month history of multiple, partially eroded nodose plaques with elevated borders and central fissures involving both palms, the fingers, and, to a lesser extent, both pretibial areas of the lower leg and upper back (Fig 1). A biopsy specimen of an initial palmar cutaneous lesion at its inception showed findings characteristic of lichen planus.

Anticonvulsant Effects of Local Anesthetics

2. Resolving palmar lichen-planuseruption with central erythema and peripheral hyperpigmentation.

Fig. like

Edited

by John D. Archer, MD, Senior Editor.

Detroit

study was supported in part by the Detroit Genera! Hospital Research Corporation. Amir H. Mehregan, MD, interpreted the histopathological sections. 1. Arndt KA: Lichen planus, in Fitzpatrick TB, Arndt KA, Clark WH, et al: Dermatology in General Medicine. New York, McGraw-Hill Book Co Inc, 1971, p 733. 2. Bruinsma W: A Guide to Drug Eruptions, Amsterdam, Excerpta Medica, 1973, p 63. 3. Almeyda J, Levantine A: Drug reactions. Br. J This

Dermatol 85:604, 1971. 4. Van de Staak WJBM, Cotton DWK, JonchheerVenneste MMH, et al: Lichenoid eruption following peni-

pertensive-diuretic spironolactone.

Medications included digoxin, propranolol hydrochloride, diazepam, spironolactone, and iron tablets. A drug was suspected as a cause of the lichen-planuslike eruption. Therapy with the iron tablets, diazepam, and propranolol was discontinued, each one week at a time. Digoxin and spironolactone therapy was maintained because of mild elevation of blood pressure. Periodic evaluation on a weekly basis for three months showed flares of the lichen-planus-like eruption every other week. Spironolactone was the only drug that she was taking on an everyother-week schedule. Prompt discontin-

Thomas F. Downham III, MD Detroit General Hospital Wayne State University School of Medicine

great flattening and resolution of the

such as methyldopa have been implicated.3 We report a cutaneous eruption with clinical and histopathological features of lichen planus that we consider to be caused by the antihy-

Fig f.—Typical lichen-planus-like eruption of palm.

activities of the skin, thereby causing the cutaneous eruption/ Other drugs or immune imbalances5 (eg, graft vs host reaction) may induce a chronic immune (hypersensitivity) reaction involving the basal cell layer of the epidermis leading to disturbances in epidermal cell growth and resulting in a lichen-planus-like pattern.



Laboratory studies showed an ESR of 58 mm/hr. Differential WBC count showed 6% eosinophils. Antinuclear factor and lupus erythematosus cell phenomena were normal. Periodic use of aluminum subacetate soaks, topical fluorinated steroid cream, and antibiotics for secondary infection were the main treatment. Comment.— Lichen-planus-like drug eruptions produce skin changes that persist over long periods of time." However, on withdrawal of therapy with the inciting drug, the majority of cutaneous drug eruptions showed

resolution—a useful clinical criterion help diagnose drug eruptions. This case showed evidence of resolution of the drug eruption on immediate with¬ drawal of spironolactone therapy. Only residual central erythema and to

peripheral

To the Editor.\p=m-\The communication concerned with the "Toxic Effects of Local Anesthetics" by Rudolph H. de Jong, MD (239:1166, 1978), briefly reviews some of the CNS effects of these agents and suggests that convulsions may be one consequence of increased levels made available to the brain. It should be noted, however, that in lower dose these same local anesthetics, rather than being proconvulsants or decreasing seizure

threshold,

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anticonvulsants1;

Walter B. Essman, MD. PhD Queens Hospital Center Affiliation Long Island Jewish-Hillside Medical Center

hyperpigmentation re¬ the palmar cutaneous

mained in lesions. Some lichen-planus-like drug erup¬ tions may represent a direct toxic effect of the drug on the enzymatic

serve as

this effect has been observed in the use of intravenous lidocaine in controlling status epilepticus in man, attenuating electrically-induced seizures in man,2 and blocking auditory convulsions in animals.3 Certainly there is a considerable overlap between the therapeutic range of such a local anesthetic as lidocaine in the treatment of ventricular arrhythmias and ventricular tachycardia and the clinical efficacy, within the same dose range, of this agent as an anticonvulsant.

Jamaica, NY

CG, Bohm E: Local Anaesthetics as Anticonvulsants. Stockholm, Almqvist & Wiksell, 1965, pp 71\x=req-\ 1. Bernhard

90.

2. Ottosson JO: Effect of lidocaine

on

the seizure

seaweed. Lack of this vitamin interferes with basic biochemical processes in normal tissue, thereby

in electroconvulsive therapy. Acta Psychiatr Scand 35:7, 1960. 3. Essman WB: Anticonvulsive properties of xylocaine in mice susceptible to audiogenic seizures. Arch Int Pharmacodyn Ther 164:376-386, 1966.

discharge

harming cancer patients.2 4. Increased ingestion of fruits and vegetables. Such a diet is high in bulk and low in calories, just opposite to the needs of cancer patients.2 In addi¬ tion, it is low in needed animal protein, thereby harming cancer patients.2 Furthermore, fruits and vegetables contain varying quanti¬ ties of the enzyme 0-glucosidase, which releases cyanide from laetrile,' thereby making cyanide poisoning

Aeromonas hydrophilia

Septicemia in a Previously Healthy Man the

To

Editor.\p=m-\Ramsay

al

et

(239:128, 1978) recently reported

a

of Aeromonas

hydrophilia sepsis in a patient undergoing hemodialysis therapy. We report a case of A hydrophilia septicemia seen at Walter Reed Army Medical Center. case

Report of Case.\p=m-\A79-year-old man with a history of heart disease, but otherwise in good health, was seen in the emergency room for two episodes of dull epigastric pain associated with nausea during a 24-hour period. The patient was admitted for possible myocardial infarction. Cardiac enzyme levels and ECGs showed no evidence of myocardial infarction, but on the second hospital day the patient had a temperature of 39 \s=deg\C.Four blood cultures grew A hydrophilia. The strain was sensitive to gentamicin, amikacin, and tobramycin and resistant to ampicillin, cephalothin, and carbenicillin. Stool culture subsequently grew A hydrophilia. He received a ten-day course of gentamicin sulfate, with resolution of epigastric pain and fever.

almost certain.

a

Comment.\p=m-\Aeromonashydrophilia

is a Gram-negative anaerobic rod found in natural water sources and as an occasional inhabitant of the nor¬ mal gastrointestinal tract. It is a rare cause of septicemia and usually is seen only in immunorepressed or debilitated patients.' Our patient rep¬ resents a case of A hydrophilia sepsis in an otherwise immunologically in¬ tact host. Frederic D'Alauro Richard Ansinelli, MD Walter Reed Army Medical Center

Georgetown University School of Medicine

Washington, DC 1.

Bulger RJ, Sherris JC: The clinical significance of hydrophilia. Arch Intern Med 118:562-564,

Aeromonas 1966.

See also JAMA 239:171,2, 1978.—Eu.

Dysphagia From Thoracic Ankylotic Spur

mins. About three months previously he noted that one of his large vitamin capsules became lodged in his esophagus; it took a long time for the capsule to pass into his stomach. The vitamin became progressively harder to swallow. A barium swallow showed impingement of the esophagus between a huge ankylotic spur at D8-9 and the right atrium of the heart (Figure). The patient also has ankylosis in the cervical spine and matches the HLAB27 histocompatibility antigen. The patient does not wish osteophytectomy. Michael R. Rask, MD Sahara Ranch Medical Center Las Vegas

Nutritionally Unsound 'Nutritional and Metabolic Antineoplastic Diet' of The

Laetrile

Proponents

To the Editor.\p=m-\InLaetrile Case Histories, Richardson and Griffin' delineate the "nutritional and metabolic antineoplastic diet" of laetrile proponents. The diet calls for the

following:

1. No meat, fish, or fowl. These are the major sources of absorbable iron in the American diet. Their lack results in a much higher frequency of iron deficiency and iron deficiency

anemia, thereby harming

To the Editor.\p=m-\Ihave seen a patient with dysphagia from an ankylotic thoracic spur. The esophagus was impinged between the spur and the heart.

Report of a Case.\p=m-\An 80-year-old

Barium swallow done April 3, 1978. Huge ankylotic spur at D8-9 causing impingement of esophagus (E) between spur and right atrium (RA) of patient's heart.

man

has been careful about his health all his life and had been known to have ankylosing spondylitis since he was much younger. He exercises daily and takes vita-

cancer

patients.2 2. No dairy products. These are the

main sources of calcium in the American diet. Lack of adequate calcium damages bone maintenance, thereby

harming cancer patients.2 3. No animal protein. Animal

pro-

tein is the exclusive source of vitamin B12 in the American diet, with the exception of vitamin B12-fortified foods and microorganisms such as

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5. Megadoses of vitamin C (ascor¬ bic acid). In studies being prepared for publication with Dr R. C. Backer, we found that megadoses of vitamin C release cyanide from laetrile. This increases the probability that the patient will suffer not only from chronic cyanide poisoning, with pro¬

gressive fatigue, weakness, nerve damage, blindness, and deafness, but also acute bouts of cyanide hypoten¬ sion, nausea, vomiting, abdominal cramps, rash, fever, diarrhea, head¬ aches, vertigo, dyspnea, paralysis, unconsciousness, convulsions, and death.' Other possible undesirable effects of megadoses of vitamin C are

delineated elsewhere.4 6. Megadoses of vitamin E. Possi¬ ble undesirable effects of megadoses of vitamin E are delineated else¬ where/ 7. Oral pancreatic enzymes. These have no value except in pancreatic disease.2 Since they are proteins, they are destroyed in the intestine, and thereby not only waste money, but also are a possible source of undesir¬ able side effects for cancer patients.2 8. Pangamic acid ("vitamin B15"). Proponents have trade named this substance as a vitamin, but the Food and Drug Administration is not aware of any accepted scientific evidence that this substance has nutritional properties, states it "is not generally recognized by scientific experts as safe for human consump¬ tion," and considers it illegal to be sold as a dietary supplement (FDA Talk Paper, March 31, 1978). 9. Laetrile. This chemical was iso¬ lated in 1835 as amygdalin. It is a cyanogenetic glycoside, which the FDA states has no known value in human nutrition.' It has been pro¬ posed as a cancer remedy since 1845, but was never found to be of any value against cancer.' In the time of the pharoahs, it was used as an extract for official executions. Pro¬ ponents trade named amygdalin as

Anticonvulsant effects of local anesthetics.

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