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Hypophosphatemic vitamin D-resistant rickets and multiple spindle and epithelioid nevi associated with linear nevus sebaceus syndrome
Journal of the American Academy of Dermatology Volume 29, Number I
9. 10. 11. 12. 13.
province of Trento (Italy). Am J Dermatopathol 1984; 6(suppl 1):283-8. Doherty VR, MacKie RM. Experience of a public education program on early detection of cutaneous malignant melanoma. Br Med J 1988;297:388-91. Fixler Zc. Melanoma/skin cancer screening program in a private office setting [Letter]' .T AM ACAD DERMATOL 1985;16:634-5. Arundell FD. Campaigns for the detectionand prevention of melanoma and skin cancers [Editorial]. J AM ACAD DERMATOL 1987;16:406-7. Koh HK, Caruso A, Gage I, et ai. Evaluation of melanoma/skin cancer screening in Massachusetts. Cancer 1990;65:375-9. BologniaJL, BerwickM, Fine.TA. Completefollow-up and evaluationof a skin cancer screeningin Connecticut.J AM ACAD DERMATOL 1990;23:1098-106.
Brief communications 109 14. Pehamberger H, Binder M, Honigsmann H, et al. Sonne ohne Reue: Ergebnisse der Aufklarungskampagne "Malignes Melanom", In: Waclawiczek HW, Gebhart W, Manfreda D, et ai. eds, Das maligne Melanom-oleizeiliger Stand in Diagnoseund Therapie, Berlin: Springer-Verlag, 1991: 15-20. 15. SAS InstituteInc. SAS Users Guide: Basic Version. 5th ed. Cary, NC: SAS Institute, 1985. 16. Binder M, PehambergerH, Steiner A, et al. Das maligne Melanom in Osterreich: Analyse des Patientenkollektivs der Ll.Iniversitats-Hautklinik Wien. 1963-1988. In: Orfanos CE, Garbe C, eds. Das maligne Melanom der Haut. Munich: W. Zuckschwert, 1990:25-31. 17. Clark WH, Elder DE, DuPont G, et al. Model predicting survivalin stage I melanoma based on tumor progression. J Nat Cancer Inst 1989;81:1893-904.
Hypophosphatemic vitamin D-resistant rickets and multiple spindle and epithelioid nevi associated with linear nevus sebaceus syndrome John R. Goldblum, MD, and John T. Headington, MD Ann Arbor, Michigan The complex of mental retardation and seizures associated with sebaceous nevi was described in 1962 by Feurstein and Mims.' Approximately 40% of sebaceous nevi, particularly those present in adolescence and adulthood, are ultimately associated with epithelial neoplasms.? However, there have been no reports of an association of spindle and epithelioid nevi (Spitz nevus) and nevus sebaceus. Although various skeletal anomalies have been described in the linear nevus sebaceus syndrome,' there have only been six previously documented cases of patients with nevus sebaceus and rickets/ osteomalacia, or more specifically, hypophosphatemic vitamin D-resistant rickets.v" We describe a patient with diffuse cutaneous involvement by nevus sebaceus associated with multiple spindle and epithelioid nevi and vitamin D-resistant rickets/osteomalacia.
From the Department of Pathology, University of Michigan Medical Center and Hospitals. Reprint requests: John R. Goldblum, MD, Department of Pathology, University of Michigan Hospitals, 1500 E. Medical Center Dr., Ann Arbor, MI 48105-0054. JAM ACAD DERMATOL
1993;29:109-11.
Copyright © 1993 by the American Academy of Dermatology, Inc. 0190-9622/93 $1.00 + .10 16/54/45163
CASE REPORT A 35-year-old man had an extensive, yellow-tan verrucous lesion shortly after birth on the righ t side of the scalp, face, external ear, and neck. Numerous pigmented lesions were also noted on the right side of the face and back, as well as three pink to tan papules, all of which were 6 mm or less, on the extremities and trunk. Biopsy specimens of the scalp lesion revealed nevus sebaceus. The pigmented lesions were both compound and intradermal nevi. The pink-tan papules had the diagnostic features of spindle and epithelioid nevi. When he was 15 months of age, thoracolumbar kyphoscoliosis, a right hip bone cyst, equinovarus of the right foot, and a right coxa valga subluxation were noticed. Radiographs of the lower extremities were interpreted as diagnostic ofrickets, and the patient was treated with oral vitamin D. Evaluation 2 years later revealed significant improvement in the rachitic changes. Recently, numerous verrucous lesions of the right pinna were noted. Biopsy specimens revealed basal cell carcinoma. Because of the extent of involvement, a right auricle amputation was done (Fig. l ). The resected auricle revealed diffuse papillomatous hyperplasia of the epidermis, with numerous small sessile and papillary projections from the epidermal surface characterized by lobules of well-differentiated sebaceous epithelium. Numerous normal-appearing apocrine glands were present immediately beneath the hyperplastic sebaceous epithelium (Fig. 2).
110 Brief communications
Journal of the American Academy of Dermatology July 1993
Fig. 2. Nevus sebaceus of the pinna. Epidermis is irregular, with verrucous superficial configuration. Numerous papillary projections composed of lobules of well-differentiated sebaceous epithelium are present. Normal apocrine glands are located beneath these lobules.
Fig. 1. External surface of the pinn a, including the concha and the lobule, contain hyperkeratotic papillary projections. Small basaloid follicular proliferations, which in some areas were large enough to constitute basaloid hamartomas, were present. In several areas, sebaceous epithelium was more cellular and in a lobular pattern, forming sebaceous hamartomas. The reticular dermis was extensively altered by the presence of small apocrine hidrocystomas, ectatic apocrine secretory epithelium, and intradermal nevi.
DISCUSSION Linear nevus sebaceus syndrome is characterized by the triad of nevus sebaceus, mental retardation, and seizures. However, other organ systems may be involved. In particular, several bony anomalies have been associated, including bone cysts, kyphoscoliosis, and, rarely, hypophosphatemic vitamin D-resistant rickets, all of which were present in this patient To date, only six cases of vitamin D-resistant rickets associated with the linear nevus sebaceus syndrome have been reported. Hypophosphatemic vitamin D-resistant rickets has been reported in association with various other tumors, including mesenchymal and ossifying tumors,9-l2 and this phenomenon has been termed tumor-induced osteomalacia. In these reports, the
tumor-induced rickets/osteomalacia was characterized by remission of unexplained rickets/ osteomalacia after resection of the coexisting tumor, with clinical, radiographic, and biochemical amelioration of the bony abnormalities. Aschinberg et a1. 4 reported the case of a patient with nevus sebaceus and cutaneous fibroangiomas in whom resection of the cutaneous lesions resulted in reversal of the bony abnormalities. However, a homogenate of the fibroangiomas (and not the sebaceous nevus) induced phosphaturia when injected into a puppy. In this patient, it is unclear which factors may have resulted in the improvement in the patient's rickets. At the time of diagnosis, the patient was treated with oral vitamin D; after 2 years of therapy, there was evidence of improvement. However, during this interval the patient also had numerous excisions of his sebaceous nevi. An unusual feature in this patient is the multiple spindle and epithelioid nevi. Melanocytic nevi were noted in several of the previously reported patients with linear nevus sebaceus associated with vitamin D-resistant rickets. However, to our knowledge, there have been few reports of multiple spindle and epithelioid nevi,13, 14 but none in association with the linear nevus sebaceus syndrome, or with perturbations of calcium or phosphorus metabolism. REFERENCES
I. Feurstein R, Mims LC. Linear nevus sebaceus with convulsions and mental retardation. Am J Dis Child 1962; 104:675-9.
Journal of the American Academy of Dermatology Volume 29, Number I
2. Domingo J, Helwig EB. Malignant neoplasms associated with nevus sebaceusof Jadassohn. J AM ACAD DERMATOL 1979;1:545-56. 3. Solomon LM, Esterly NB. Epidermal and other congenital organoid nevi. Curr Probl Pediatr 1975;6:01-06. 4. Aschinberg LC, Solomon LM, Zeis PM, et al. Vitamin D-res istant rickets associated with epidermal nevus syndrome: demonstration of a phosphatur ic substance in the dermal lesions. J Pediatr 1977;91 :56-60. 5. Moorjani R, Shaw DO. Feurstein and Mims syndrome with resistant rickets. Pediatr Radiol 1976;5:120-2. 6. Carey DE, Drezner MK , Hamdan JA, et al. Hypophosphatemic rickets/osteomalacia in linear sebaceus nevus syndrome: a variant of tumor-induced osteomalacia. J Pediatr 1986;109:994-1000. 7. Skovby F, Svejgaard E, Moller J. Hypophosphatemic rickets in linear sebaceus nevus sequence. J Pediatr 1987; 111:855-7. 8. Sugarman GI, Reed WB. Two unusual neurocutaneous
Brief comm unications 111
9.
10.
II . 12.
13. 14.
disorders with facial cut aneous signs. Arch Neural 1969; 21:242-7. Prader A, Illig R, Uehlinger E, et al. Rachitis infolge knochentumors, Helv. Paedediatr Acta 1959;14:554-9. Olefsky J, Kempson R, Jones H , et aJ. "Tertiary" hyperparathyroidismand apparent "cure" of vitamin D-resistant rickets after removalof an ossifying mesenchyma l tumor of the pharynx. N Engl J Moo 1972;286:740-4. Pollack lA , Sch iUer A L, Crawford JD. Rickets and myopathy cured by removal of a nonossifying fibroma of bone. Pediatrics 1973;52:364-7. Dent C E, Friedman M. H ypophospha te mic osteomalacia with complete recovery. Br Med J 1964;1:1976-9. Weimer VM, Zuehlke RL. Multiple agminate spindleand epithelioid cell nevi in a n adul t. Arch Dermatol 1978; 114:1383-4. Capetanakis J. Juvenile melanoma disseminatum. Br J Dermatol 1975;92:207-11.
Acquired zinc deficiency in a breast-fed mature infant: A possible case of acquired maternal decreased zinc uptake by the mammary gland Ko-ichi Ando, MD,l! Yoshinori Goto, MD,a Yoshinari Matsumoto, MD,b and Masaru Ohashi, MD b Nagoya, Japan Acquired zinc deficiency in a healthy, term, breast-fed infant israre. 1-) It has been proposed that a deficiency of zincin breast milk is the cause. Previous authors suggested that the deficiency ofzincin breast milk is inherited rather than acquired. We report a caseof acquiredzincdeficiency in a healthy, term, breast-fed male infant, associated with a low zinc content in his mother's breast milk. His mother's serum zinc level was normal. The infant responded to oral zincsupplements and has continued to thrive after their withdrawal. The infant was the third child of healthy unrelated parents. Both of his older siblings also had been exclusively breast-fed and had shown nosymptoms ofzinc deficiency. This case suggests that zinc deficiency in mother's milk is not necessarily inherited, in contrast to earlier suggestions. From the Departments orDermatology, Nagoya FirstRedCross Hospital," and Nagoya Universi tySchool or M edicine," Reprinl requests: Ko-ichi A ndo, MD, Department or Dermatology, Nagoya First Red Cross Hospital, )-)5, Mi chishita-cho, N ak amura-ku, Nagoya 453 , Japan. .I AM ACAD DERMATOL 1993;29:111-2. C~pyright ® J 993 by theAmerican Academy or Dermatology, Inc. 0190-9622/93 $1.00 + .10 16/54/45164
CASE REPORT A Jap anese boy was born a t 39 weeks' gestation after an uncomplicated pregnancy. His birth weight was 2730 gm. He was the third child of unrelated parents. The infant fed well, solely from his mother's breast, and his initial growth was normal. Bo th his older sister and brother a lso had been term infants and were exclusively breastfed; they had never shown symptoms of zinc deficiency . A refractor y diaper rash began when the infant was 6 wee ks old; it spread gradually to involve the neck, ears, perioral regions, fingers, and feet. D iarrhea then developed. T opical thera py with various agents including corticosteroid ointmen t was prescribed , but there was no improvement. The infant was admi tted a t 9 weeks of age when his weight was 5130 gm. A n encrusted eczematous eruption around the orifices a nd on the extremities was present ( Fig. I). There was a sm all amount of terminal hair on t he scalp. The infant wa s irritable. Topical therapy with antifungal and a ntibacterial ointments and system ic intravenous a ntibiotic therapy slightly improved the eruption. The possibility of zinc deficiency was considered . The in fant 's serum zinc level was 11 JLgjdl (nor mal range 65 to 110 p.gjdI) . Z inc level in the mother's milk was 16 p.gjdl (80 to 260 pg/dl), whereas her serum zinc level was 81 j.tgjd l. The laboratory findings indicated that the infant's illness was caused by a zinc deficiency because of a low zinc content in his mother's
9. 10. 11. 12. 13.
province of Trento (Italy). Am J Dermatopathol 1984; 6(suppl 1):283-8. Doherty VR, MacKie RM. Experience of a public education program on early detection of cutaneous malignant melanoma. Br Med J 1988;297:388-91. Fixler Zc. Melanoma/skin cancer screening program in a private office setting [Letter]' .T AM ACAD DERMATOL 1985;16:634-5. Arundell FD. Campaigns for the detectionand prevention of melanoma and skin cancers [Editorial]. J AM ACAD DERMATOL 1987;16:406-7. Koh HK, Caruso A, Gage I, et ai. Evaluation of melanoma/skin cancer screening in Massachusetts. Cancer 1990;65:375-9. BologniaJL, BerwickM, Fine.TA. Completefollow-up and evaluationof a skin cancer screeningin Connecticut.J AM ACAD DERMATOL 1990;23:1098-106.
Brief communications 109 14. Pehamberger H, Binder M, Honigsmann H, et al. Sonne ohne Reue: Ergebnisse der Aufklarungskampagne "Malignes Melanom", In: Waclawiczek HW, Gebhart W, Manfreda D, et ai. eds, Das maligne Melanom-oleizeiliger Stand in Diagnoseund Therapie, Berlin: Springer-Verlag, 1991: 15-20. 15. SAS InstituteInc. SAS Users Guide: Basic Version. 5th ed. Cary, NC: SAS Institute, 1985. 16. Binder M, PehambergerH, Steiner A, et al. Das maligne Melanom in Osterreich: Analyse des Patientenkollektivs der Ll.Iniversitats-Hautklinik Wien. 1963-1988. In: Orfanos CE, Garbe C, eds. Das maligne Melanom der Haut. Munich: W. Zuckschwert, 1990:25-31. 17. Clark WH, Elder DE, DuPont G, et al. Model predicting survivalin stage I melanoma based on tumor progression. J Nat Cancer Inst 1989;81:1893-904.
Hypophosphatemic vitamin D-resistant rickets and multiple spindle and epithelioid nevi associated with linear nevus sebaceus syndrome John R. Goldblum, MD, and John T. Headington, MD Ann Arbor, Michigan The complex of mental retardation and seizures associated with sebaceous nevi was described in 1962 by Feurstein and Mims.' Approximately 40% of sebaceous nevi, particularly those present in adolescence and adulthood, are ultimately associated with epithelial neoplasms.? However, there have been no reports of an association of spindle and epithelioid nevi (Spitz nevus) and nevus sebaceus. Although various skeletal anomalies have been described in the linear nevus sebaceus syndrome,' there have only been six previously documented cases of patients with nevus sebaceus and rickets/ osteomalacia, or more specifically, hypophosphatemic vitamin D-resistant rickets.v" We describe a patient with diffuse cutaneous involvement by nevus sebaceus associated with multiple spindle and epithelioid nevi and vitamin D-resistant rickets/osteomalacia.
From the Department of Pathology, University of Michigan Medical Center and Hospitals. Reprint requests: John R. Goldblum, MD, Department of Pathology, University of Michigan Hospitals, 1500 E. Medical Center Dr., Ann Arbor, MI 48105-0054. JAM ACAD DERMATOL
1993;29:109-11.
Copyright © 1993 by the American Academy of Dermatology, Inc. 0190-9622/93 $1.00 + .10 16/54/45163
CASE REPORT A 35-year-old man had an extensive, yellow-tan verrucous lesion shortly after birth on the righ t side of the scalp, face, external ear, and neck. Numerous pigmented lesions were also noted on the right side of the face and back, as well as three pink to tan papules, all of which were 6 mm or less, on the extremities and trunk. Biopsy specimens of the scalp lesion revealed nevus sebaceus. The pigmented lesions were both compound and intradermal nevi. The pink-tan papules had the diagnostic features of spindle and epithelioid nevi. When he was 15 months of age, thoracolumbar kyphoscoliosis, a right hip bone cyst, equinovarus of the right foot, and a right coxa valga subluxation were noticed. Radiographs of the lower extremities were interpreted as diagnostic ofrickets, and the patient was treated with oral vitamin D. Evaluation 2 years later revealed significant improvement in the rachitic changes. Recently, numerous verrucous lesions of the right pinna were noted. Biopsy specimens revealed basal cell carcinoma. Because of the extent of involvement, a right auricle amputation was done (Fig. l ). The resected auricle revealed diffuse papillomatous hyperplasia of the epidermis, with numerous small sessile and papillary projections from the epidermal surface characterized by lobules of well-differentiated sebaceous epithelium. Numerous normal-appearing apocrine glands were present immediately beneath the hyperplastic sebaceous epithelium (Fig. 2).
110 Brief communications
Journal of the American Academy of Dermatology July 1993
Fig. 2. Nevus sebaceus of the pinna. Epidermis is irregular, with verrucous superficial configuration. Numerous papillary projections composed of lobules of well-differentiated sebaceous epithelium are present. Normal apocrine glands are located beneath these lobules.
Fig. 1. External surface of the pinn a, including the concha and the lobule, contain hyperkeratotic papillary projections. Small basaloid follicular proliferations, which in some areas were large enough to constitute basaloid hamartomas, were present. In several areas, sebaceous epithelium was more cellular and in a lobular pattern, forming sebaceous hamartomas. The reticular dermis was extensively altered by the presence of small apocrine hidrocystomas, ectatic apocrine secretory epithelium, and intradermal nevi.
DISCUSSION Linear nevus sebaceus syndrome is characterized by the triad of nevus sebaceus, mental retardation, and seizures. However, other organ systems may be involved. In particular, several bony anomalies have been associated, including bone cysts, kyphoscoliosis, and, rarely, hypophosphatemic vitamin D-resistant rickets, all of which were present in this patient To date, only six cases of vitamin D-resistant rickets associated with the linear nevus sebaceus syndrome have been reported. Hypophosphatemic vitamin D-resistant rickets has been reported in association with various other tumors, including mesenchymal and ossifying tumors,9-l2 and this phenomenon has been termed tumor-induced osteomalacia. In these reports, the
tumor-induced rickets/osteomalacia was characterized by remission of unexplained rickets/ osteomalacia after resection of the coexisting tumor, with clinical, radiographic, and biochemical amelioration of the bony abnormalities. Aschinberg et a1. 4 reported the case of a patient with nevus sebaceus and cutaneous fibroangiomas in whom resection of the cutaneous lesions resulted in reversal of the bony abnormalities. However, a homogenate of the fibroangiomas (and not the sebaceous nevus) induced phosphaturia when injected into a puppy. In this patient, it is unclear which factors may have resulted in the improvement in the patient's rickets. At the time of diagnosis, the patient was treated with oral vitamin D; after 2 years of therapy, there was evidence of improvement. However, during this interval the patient also had numerous excisions of his sebaceous nevi. An unusual feature in this patient is the multiple spindle and epithelioid nevi. Melanocytic nevi were noted in several of the previously reported patients with linear nevus sebaceus associated with vitamin D-resistant rickets. However, to our knowledge, there have been few reports of multiple spindle and epithelioid nevi,13, 14 but none in association with the linear nevus sebaceus syndrome, or with perturbations of calcium or phosphorus metabolism. REFERENCES
I. Feurstein R, Mims LC. Linear nevus sebaceus with convulsions and mental retardation. Am J Dis Child 1962; 104:675-9.
Journal of the American Academy of Dermatology Volume 29, Number I
2. Domingo J, Helwig EB. Malignant neoplasms associated with nevus sebaceusof Jadassohn. J AM ACAD DERMATOL 1979;1:545-56. 3. Solomon LM, Esterly NB. Epidermal and other congenital organoid nevi. Curr Probl Pediatr 1975;6:01-06. 4. Aschinberg LC, Solomon LM, Zeis PM, et al. Vitamin D-res istant rickets associated with epidermal nevus syndrome: demonstration of a phosphatur ic substance in the dermal lesions. J Pediatr 1977;91 :56-60. 5. Moorjani R, Shaw DO. Feurstein and Mims syndrome with resistant rickets. Pediatr Radiol 1976;5:120-2. 6. Carey DE, Drezner MK , Hamdan JA, et al. Hypophosphatemic rickets/osteomalacia in linear sebaceus nevus syndrome: a variant of tumor-induced osteomalacia. J Pediatr 1986;109:994-1000. 7. Skovby F, Svejgaard E, Moller J. Hypophosphatemic rickets in linear sebaceus nevus sequence. J Pediatr 1987; 111:855-7. 8. Sugarman GI, Reed WB. Two unusual neurocutaneous
Brief comm unications 111
9.
10.
II . 12.
13. 14.
disorders with facial cut aneous signs. Arch Neural 1969; 21:242-7. Prader A, Illig R, Uehlinger E, et al. Rachitis infolge knochentumors, Helv. Paedediatr Acta 1959;14:554-9. Olefsky J, Kempson R, Jones H , et aJ. "Tertiary" hyperparathyroidismand apparent "cure" of vitamin D-resistant rickets after removalof an ossifying mesenchyma l tumor of the pharynx. N Engl J Moo 1972;286:740-4. Pollack lA , Sch iUer A L, Crawford JD. Rickets and myopathy cured by removal of a nonossifying fibroma of bone. Pediatrics 1973;52:364-7. Dent C E, Friedman M. H ypophospha te mic osteomalacia with complete recovery. Br Med J 1964;1:1976-9. Weimer VM, Zuehlke RL. Multiple agminate spindleand epithelioid cell nevi in a n adul t. Arch Dermatol 1978; 114:1383-4. Capetanakis J. Juvenile melanoma disseminatum. Br J Dermatol 1975;92:207-11.
Acquired zinc deficiency in a breast-fed mature infant: A possible case of acquired maternal decreased zinc uptake by the mammary gland Ko-ichi Ando, MD,l! Yoshinori Goto, MD,a Yoshinari Matsumoto, MD,b and Masaru Ohashi, MD b Nagoya, Japan Acquired zinc deficiency in a healthy, term, breast-fed infant israre. 1-) It has been proposed that a deficiency of zincin breast milk is the cause. Previous authors suggested that the deficiency ofzincin breast milk is inherited rather than acquired. We report a caseof acquiredzincdeficiency in a healthy, term, breast-fed male infant, associated with a low zinc content in his mother's breast milk. His mother's serum zinc level was normal. The infant responded to oral zincsupplements and has continued to thrive after their withdrawal. The infant was the third child of healthy unrelated parents. Both of his older siblings also had been exclusively breast-fed and had shown nosymptoms ofzinc deficiency. This case suggests that zinc deficiency in mother's milk is not necessarily inherited, in contrast to earlier suggestions. From the Departments orDermatology, Nagoya FirstRedCross Hospital," and Nagoya Universi tySchool or M edicine," Reprinl requests: Ko-ichi A ndo, MD, Department or Dermatology, Nagoya First Red Cross Hospital, )-)5, Mi chishita-cho, N ak amura-ku, Nagoya 453 , Japan. .I AM ACAD DERMATOL 1993;29:111-2. C~pyright ® J 993 by theAmerican Academy or Dermatology, Inc. 0190-9622/93 $1.00 + .10 16/54/45164
CASE REPORT A Jap anese boy was born a t 39 weeks' gestation after an uncomplicated pregnancy. His birth weight was 2730 gm. He was the third child of unrelated parents. The infant fed well, solely from his mother's breast, and his initial growth was normal. Bo th his older sister and brother a lso had been term infants and were exclusively breastfed; they had never shown symptoms of zinc deficiency . A refractor y diaper rash began when the infant was 6 wee ks old; it spread gradually to involve the neck, ears, perioral regions, fingers, and feet. D iarrhea then developed. T opical thera py with various agents including corticosteroid ointmen t was prescribed , but there was no improvement. The infant was admi tted a t 9 weeks of age when his weight was 5130 gm. A n encrusted eczematous eruption around the orifices a nd on the extremities was present ( Fig. I). There was a sm all amount of terminal hair on t he scalp. The infant wa s irritable. Topical therapy with antifungal and a ntibacterial ointments and system ic intravenous a ntibiotic therapy slightly improved the eruption. The possibility of zinc deficiency was considered . The in fant 's serum zinc level was 11 JLgjdl (nor mal range 65 to 110 p.gjdI) . Z inc level in the mother's milk was 16 p.gjdl (80 to 260 pg/dl), whereas her serum zinc level was 81 j.tgjd l. The laboratory findings indicated that the infant's illness was caused by a zinc deficiency because of a low zinc content in his mother's