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NEUTROPENIA AND BETA-CAROTENE

SIR,-I read with interest the letter by Dr Shoenfeld et al. onneutropenia associated with hypercarotenaemia (May 29, p. 1245).This additional case-report illustrates the danger of consuminglarge amounts of vegetables or their products.However, administration of pure (crystalline) beta-carotene will

not cause leucopenia. In fact, according to Neiman and Klein-Obbink, Henschen reported that crystalline carotene did notproduce this toxic effect. The leucopenia was judged to be due toother constituents of carrots. In our studies of the treatment of the

photosensitivity associated with erythropoietic protoporphyria, wehave confirmed that high doses of pure beta-carotene do not causeleucopenia.2,3 Also, no such toxic effect has been reported in themore than thirty reports of the use of carotenoids in the treatment ofphotosensitivity in protoporphyria and other skin diseases. Theintake of large amounts of carotene will not lead to large amounts ofvitamin A in serum or to the symptoms of vitamin A toxicity. 1-4

_

If carotenoids are ever used prophylactically either for their ownantitumour effects or as sources of vitamin A or its derivatives,patients should be warned about the toxic effects of eating largeamounts of vegetables and urged to use pure pigments, despitetheir possibly higher cost. Preparations of pure beta-carotene arealready on the market in the United States and in Europe for thetreatment of photosensitivity.Channing Laboratory,Harvard Medical School,Boston, Massachusetts, 02115, U.S.A. MICHELINE M. MATHEWS-ROTH

SHARED CAPGRAS SYNDROME AND NIFEDIPINE

SIR,-The Capgras syndrome, in which a loved one is believed tobe an imposter, has been reported in less than a hundred cases sincefirst described in 1923. At first thought to be restricted to functionalpsychoses, the syndrome was later associated with gross brainlesions, organic mental syndromes, and endocrine disorders such ashypothyroidism and pseudohypoparath 72 roidism. 8-1 Recently ithas been observed in a few geriatric cases, but drug toxicity has notbeen implicated. We have observed an elderly couple with

complementary Capgras delusions, one with nifedipine therapy andthe other with multi-infarct dementia.A 79-year-old was evaluated at the geriatric clinic for progressive

forgetfulness for 4 years. She was disoriented for time, place, andsituation, often forgot what was just said, and was unable to retainthree words even for a few moments. Neurological testing revealedno localising signs, and the physical examination was otherwiseunremarkable. Psychological tests demonstrated deficits in

memory, word finding, and naming tasks consistent with moderatedementia. Laboratory tests, including thyroid and vitamin B 12studies, revealed no abnormalities. Computerised tomographyshowed a 1 cm radiolucency in the area of the right globus pallidus,dilated ventricles, and prominent cortical sulci. Multi-infarctdementia was diagnosed and she was followed up supportively.Subsequently, she began insisting that her spouse of 48 years wasnot her legitimate husband and that they were living immorally.

1. Nieman C, Klein-Obbink HJ. Biochemistry and pathology of hypervitaminosis A.Vitam Horm 1954; 12: 69-99.

2. Mathews-Roth MM, Pathak MA, Fitzpatrick TB, Harber LC, Kass EH. Betacaroteneas an oral protective agent in erythropoietic protoporphyria. JAMA 1974; 228:1004-08.

3. Mathews-Roth MM, Pathak MA, Fitzpatrick TB, Harber LC, Kass EH. Betacarotenetherapy for erythropoietic protoporphyria and other photosensitivity diseases. ArchDermatol 1977; 113: 1229-32.

4. Goodman AS, Gilman AG. Pharmacological basis of therapeutics, 4th ed. New York:Macmillan, 1980.

5. Mathews-Roth MM. Anti-tumor activity of beta-carotene, canthaxanthin and

phytoene. Oncology 1982; 39: 33-37.6. Capgras J, Reboul-Lachaux J. Illusion des soises dans un delire systematisé chronique.

Bull Soc Clin Méd 1923.7. Enoch MD. The Capgras syndrome. Acta Psychiatr Scand 1963; 39: 437-62.8. Weston MJ, Whitlock FA. Capgras syndrome following head injury. Br J Psychiatr

1971; 119: 25-31.9. MacCallum WAG. Capgras symptoms with an organic basis. Br J Psychiatr 1973; 123:

639-42.

10. Hayman MA, Abrams R. Capgras syndrome and cerebral dysfunction. Br J Psychiatr1977; 130: 68-71.

11. Christodoulou GN. The syndrome of Capgras. Br J Psychiatr 1977; 130: 556-64.12. Goldfarb AI, Weiner MB. The Capgras syndrome as an adaptational maneuver in old

age Am J Psychiatr 1977; 134: 1434-36.

This assertion (very upsetting to her husband) persisted despiteefforts to dissuade her.The husband, aged 82, then presented to the clinic, having

developed the idea that his wife left their home each day and wasreplaced for several hours by a younger woman, destitute andhomeless, thus needing his reassurance and support. This ideadeveloped after he had taken nifedipine 10 mg twice daily for oneweek for worsening angina. (He had taken propranolol, isosorbide,and nitroglycerine for angina for 4 years.) He was fully oriented butforgetful. Laboratory studies revealed a mild anaemia (haematocrit38%) but no evident cause for his mental state. Electroencepha-lography showed left temporal slowing and computerisedtomography revealed left temporal atrophy. Nifedipine was

stopped, the other medications were continued, and he was treatedwith haloperidol (1 mg nightly). The delusion cleared within 3weeks.The occurrence of two cases in one household casts doubt on the

supposed rarity of the Capgras syndrome. It has been associatedwith bilateral frontal or temporal lesions. 13 The left temporal lesionpredating the delusion was a predisposing factor in the husband.The onset of his delusion coincided with his wife’s renunciation ofhim and with nifedipine therapy. Since nifedipine has beenassociated with cerebral ischaemia,14 our case should further alertclinicians to its possible central nervous system toxicity.

Departments of PsychiatryMedicine, and Neurology,

New York University-BellevueHospital Medical Centers,

New York, N.Y. 10016, U.S.A.

GERALD S. FRANKLIN

JASON W. BROWNMICHAEL L. FREEDMAN

TREATMENT WITH HUMAN INSULIN INOUTPATIENT DIABETICS

SIR,-Semisynthetic human insulin is increasingly being used forthe treatment of diabetes, but most reports on the effect of humaninsulin come from investigations of non-diabetics or of diabeticinpatients. 1.3 We have followed up a group of diabetic outpatientstreated with semisynthetic human insulin for 3 months.Twenty-two diabetics were included in the study. All have been

followed up regularly in our diabetics clinic for at least 12 months,being treated with highly purified porcine insulin. The patientswere aged between 11 and 60 years, and diabetes duration variedbetween 1 5 and 39 years. None of them had advanced, long-termdiabetic complications.Human semisynthetic insulin purified to monocomponent

specification was supplied by Novo Industri, Copenhagen.After informed consent the patients were switched from porcine

to human insulin without change of the daily insulin dose. Thepatients were seen monthly in the diabetes clinic. Fasting blood

13. Alexander MP, Stuss DT, Benson DF. Capgras syndrome: a reduplicativephenomenon. Neurology 1979; 29: 334-39.

14. Nobile-Orazio E, Sterzi R. Cerebral ischaemia after nifedipine treatment. Br Med J1981; 283: 948.

1. Owens DR, Jones MK, Hayes TM, Heding LG, Alberti KGMM, Home PD, BurrinJM, Newcombe RG. Human insulin: Study of safety and efficacy in man. Br Med J1981; 282: 1264-66.

2. Owens DR, Hayes TM, Alberti KGMM, Jones MK, Heding LG, Home PD, BurrinJM. Comparative study of subcutaneous, intramuscular, and intravenousadministration of human insulin. Lancet 1981; ii: 118-22.

3. Sestoft L, Vølund AA, Hildebrandt P, Birch K. Clinical evaluation ofhuman insulin indiabetics: Absorption and blood glucose regulation. Diabetologia 1981, 21:

324(abstr).

HAEMOGLOBIN A, AND FASTING BLOOD GLUCOSE VALUES INPATIENTS ON PORCINE INSULIN AND AFTER THREE MONTHS ON

HUMAN INSULIN