PAUL A. LEVINE, M D Case Report Editor
Laryngeal involvement in scleromyxedema: A case report MICHAEL F. RAPP, MD, MANINDER GURAM, MD, HORST R. KONRAD, MD, NAT MODY, MD, and ROBERT TRAPP, MD, Kearney, Nebraska, Columbia, South Carolina, and Springfield, Illinois
scleromyxedema is a distinct, rare entity, designated as a primary cutaneous mucinosis in the absence of endocrine dysfunction. The origin of this disorder is unknown. It is characterized by generalized papules and plaques that cause extensive thickening and hardening of the skin. Histologic changes in the dermis include proliferation of fibroblasts and excessive deposition of hyaluronic acid. In many cases there is a serum monoclonal paraprotein. Although some patients have no visceral complications, it is often a systemic disease, Involvement of a variety of internal organs has been identified.'.2 We report this as the first documented case of laryngeal involvement in scleromyxedema. CASE REPORT
A 28-year-old man was admitted to the hospital because of fever, sore throat, cough, and dysphagia. For the previous 3 years his skin had become thick and hard. The skin involvement was predominantly of the face, neck, arms, hands, chest, and back. For the last year, he had pain in his fingers and ulcerations over his knuckles. For the last 3 weeks, he reported experiencing sore throat, hoarseness, and difficulty swallowing; in the last week, liquids regurgitated through his nose and cough and fever up to 40" C developed. The patient had lost 20 pounds over the last year. He denied
From the Department of Internal Medicine (Dr. Guram), the University of South Carolina, and the Departments of Otolaryngology (Dr. Konrad), Pathology (Dr. Mody), and Internal Medicine (Dr. Trapp), Southern Illinois University, Springfield. Dr. Rapp is in private practice in Kearney, Nebraska. Presented at the Annual Meeting of the American Academy of Otolaryngology-Head and Neck Surgery, New Orleans, La., Sept. 24-28, 1989. Received for publication Sept. 25, 1989; revision received Oct. 10, 1990; accepted Oct. 23, 1990. Reprint requests: Michael F. Rapp, MD, 1919 West 36th St., Kearney, NE 68847. 23/4126265
chest pain, but had experienced shortness of breath. He denied any muscle weakness, peripheral numbness or tingling, changes in vision, or headaches. He did not smoke and denied use of alcohol or recreational drugs. Family history was noncontributory. Until the disease began, he was employed as a minor league baseball player. His vital signs were normal, with the exception of an elevated temperature to 38.6" C. On examination, the skin was thick and "bound down" over the face-especially the forehead, ears and mouth. The skin of the neck, chest, arms, back, and abdomen were also involved and, to a lesser extent, the skin of the legs and feet (Fig. 1). Otolaryngologic examination demonstrated extensive hard papules ranging from 3 to 6 mm in diameter on his face. He was able to open his mouth a maximum of only 4 cm. The tongue and oral mucosa had normal appearance and movement. Indirect and direct examination showed the left half of the soft palate to be thick, with impeded movement, and the uvula was deviated to the right (Fig. 2). There was marked velopalatine insufficiency. The nasopharynx was normal. The left half of the hypopharynx was scarred. The larynx was rotated to the right and the epiglottis was thickened and scarred on the left, whereas the right half appeared normal (Fig. 3 ) . There was decreased mobility of the epiglottis. The right aryepiglottic fold and vocal cord were normal with good mobility. The left aryepiglottic fold and vocal cord were thick and scarred and, prior to videotaping, appeared paralyzed. There was marked pooling of secretions in the area of the piriform sinuses. Videotaping was performed using a Hopkins rod telescope. This revealed extremely impaired motion of the left vocal cord and palate. The chest expansion was decreased with ronchi in the left posterior and lateral base, and bibasilar fine crackles. The heart, abdominal, and rectal examinations were normal. Examination of the extremities showed sclerodactyly, with flexion contractures of the fingers. There were several small, wellhealed scars over the knuckles and the fingers. Both elbows had 15-degree flexion contractures. The range of motion of the wrists was minimally restricted bilaterally. The neurologic examination was normal. The white cell count was 13,600 per cubic millimeter,
362 Downloaded from oto.sagepub.com at Purdue University on June 6, 2016
Volume 104 Number 3 March 1991
Case Reports 363
with 72%' neutrophils. 18% bands. 17% lymphocytes. 5 % monocytes. and 3% eosinophils. The hemoglobin was 13.6 gniidl, with a hcmatocrit of4l. Serum protein elcctrophorcsis showed an IgG-lambda minor monoclonal spike. with slight elevation of alpha-? and gamma globulins. Urinalysis, serum chemistries. aldolasc, rheumatoid factor. antinuclcar antibodies, anti-smooth muscle antibodies, complement levels. cryoglobulins. thyroid profile. and thyroid-stimulating hormone (TSH) were all within normal limits. The chcst x-ray film revealed a left posterior pulmonary infiltrate. Radiographs of both hands showed contracture dcforniities of the proximal and distal interphalangcal joints of the second through fifth digits bilaterally. Early pencil-like deformities were noted in the left distal phalanx of the fifth digit. and soft tissue atrophy was seen over the distal ends of the digits. Video-esophagram showcd that the patient had difficulty initiating deglutition. Movement of the pharynx and hypopharynx were decreased. No food bolus was fornied within the mouth. The epiglottis did not move posteriorly. nor did the larynx elevate properly, resulting in intermittent aspiration. There was slight hypertrophy of the cricopharyngcus muscle. Esophageal manometric studies showed decreased frcquency and amplitude of peristalsis. and decreased upper and lower sphincter pressures. The upper esophageal sphincter relaxed normally. but no post-relaxation contraction was noted. Magnetic resonance imaging ofthe brain and the throat showed no abnorniality. Light microscopy of the skin biopsy was conbistent with the diagnosis of scleromyxedenia. Colloidal iron stain was positive for acid mucopolysaccharidcs. restricted to the upper portion of the dermis. The acid mucopolysacchuridcs were prcsent between collagen bundlcs. DISCUSSION Scleromyxedema-also known as generalized lichen a distinct. rare entity designated myxedematosus-is under primary cutaneous mucinoses in the absence of endocrine dysfunction. ' There has been an increasing number of reports in the literature, with approximately 125 cases identified to date. Scleromyxedema is characterized by generalized lichenoid papules and plaques, which cause extensive thickening of the skin of the face, neck. arms, hands, upper back, and chest, and (to a lesser extent) the abdominal wall and lower extremities. Decreased oral aperture, pharyngeal and esophageal dysfunction, acrosclerosis (stiffness and tightness of the skin of the fingers), flexion contractures, and increased atherosclerotic disease are common.' The association of other disease states. including bilateral superficial corneal opacities caused by protein deposition, multiple myeloma, Waldenstrom's niacroglobulineniia. nonHodgkin's lymphoma, esophageal aperistalsis. in-
Fig. 1. Patient as he presented. Note flexion controctures of elbows and fingers.
Hamrnatory myopathy, erosive arthritis, median neuropathy. and sicca complex, have been reported.'." The most common cause of death as a result of this disorder is aspiration pneumonia. although neurovascular disorders and niyocardial infarctions also occur at young ages.'." The cause of scleromyxedenia is unknown. It has no obvious association with infections, drugs, o r familial or environmental factors. Although there are certain similarities in the clinical presentation and histologic features with the cutaneous features of the thyroid-
Downloaded from oto.sagepub.com at Purdue University on June 6, 2016
OtolaryngologyHead and Neck Surgery
364 Case Reports
Fig. 2. Appearance of the soft palate. Note the asymmetry caused by thickening of the lel? pharyngeal tissue, resulting in decreased mobility Lettand rightare indicated by I and R.
pituitary dysfunction, no thyroid dysfunction has been documented in patients with scleromyxedema. There have been unsuccessful attempts to associate this entity with plasma cell dyscrasia because many patients with this disorder have a serum monoclonal paraproteinemia. As in the patient reported, the paraprotein is usually an IgG, but IgM and IgA paraproteins also O C C U ~ . ~ . ~ Interestingly, -’’ it has been hypothesized that this paraprotein may stimulate fibroblast production of hyaluronic acid and be the cause of the debilitating thickening of skin and internal organs. ‘’.I3 However, the serum monoclonal paraprotein is not a consistent finding and should not be used as a criterion for diagnosis.’ In those patients without an elevated paraprotein, there may be other factors that also result in the disease, or the serum level of the immunoglobulins may fluctuate during the disease course. Further studies are necessary to understand the role of abnormal proteins in scleromyxedema. Histologically, there is deposition of niucin (hyaluronic acid) in the superficial dermis, with proliferation of large, stellate, elongated fibroblasts associated with
irregularly arranged bundles of collagen. The epidermis is normal. I.’.’ Treatment has included electron beam therapy, ACTH and cortisone, methotrexate, cyclophosphamide, melphalan, and chlorambucil, with a wide variation in reported result^.'^^^^^'^ The laryngeal abnormalities have not been documented before in this group of patients. Decreased mobility and the altered morphology of the epiglottis and vocal cord contributed to both hoarseness and aspiration. The unilateral appearance of pharyngeal and laryngeal involvement cannot be easily explained because this is a systemic disease and bilateral involvement would be expected. While cranial nerve involvement was initially suspected, videotaping of the patient showed the decreased mobility was caused by the thickening of the pharyngeal tissues. No biopsy was taken of the pharynx, although it would have been interesting to compare this to the dermal findings. We do not know if the defect was limited to the mucosa or included the underlying muscle. Aspiration and resulting pneumonia is a common
Downloaded from oto.sagepub.com at Purdue University on June 6, 2016
Volume 104 Number 3
Case Reports 365
March 1991
Fig. 3. Appearance of the larynx demonstrates demarkation of mucosal thickening and atrophy of left hemilarynx. Black arrowhead indicates epiglottis at the mucosal transition; white arrow indicates right orytenoid, which has normal appearance and mobility. The left arytenoid is also thickened with decreased mobility and does not show up well on the photograph.(In color, this figure gives a better appreciation of the mucosal changes].
cause of death in scleromyxedema. Information regarding the status of the palate, pharynx, and glottis is valuable in the management of these patients and should be documented by appropriate otolaryngologic consultation. We w i s h t o thank Ms. Bernie Hatcher a n d t h e S o u t h e r n Illinois University Biomedical C o m m u n i c a t i o n s Department for their assistance i n preparation of this manuscript and presentation of the poster. REFERENCES 1. Truhan AP, Roenigk HH. The cutaneous niucinoses. J Am Acad
Derm 1986; 14: I - 18. 2. Gabriel SE. Peny HO. Oleson GB, Bowles CA. Scleromyxedema: a sclerodema-like disorder with systcmic manifegation. Medicine 1988:67:58-65. 3. Fudman U,Golbus J, Ike RW. Scleroniyxedema with systemic involvement mimics rheumatic discases. Arthritis Rheum 1986; 29:913-7. 4. Farmer ER, Hambrick GW. Shulman LE. Papular mucinosis. Arch Dermatol 1982;118:9-13.
5. Howsden SM. Hemdon JH. Freeman RG. Lichen myxedematosus: B dermal infiltrative disorder responsive to cyclophosphamide therapy. Arch Dermatol 1975;l I I: 1325-30. 6. Lowe NJ. Dufton PA, Hunter RD, Vickers CF. Electron-beam treatment of scleroniyxedema. Br J Dermatol 1982;10649-54. 7. Matsuoka LY. Wortsman J, Carlisle KS, Kupchella CK, Deitrich JG. The acquired cutaneous mucinoses. Arch Intern Med 1984;IU:1974-80. 8 . Pusateri TJ. Margo CE, Groden LR. Corneal manifestations of scleroniyxedema. Ophthalmology 1987:94:510-3. 9. Fowlkcs RW, Blaycock WK, Mullinax F. Immunologic studies in lichen myxedematosus. Arch Dermatol 1967;95:370-4. 10. Danby FW. Danby CW. Pruzansky W. Papular mucinosis with IgG(k) M component. Can Med Assoc J 1976;114:920-2. I I . Kitamura W. Matsuoka Y. Miyagawa S. Sakamoto K. Immunochemical analysis of the monoclonal paraprotein in scleromyxedema. J Invest Dermatol 1978;70:305-8. 12. Harper RA, Rispler J. Lichen myxedematosus serum stimulates human skin fibroblast proliferation. Science 1978:199545-7. 13. Yaron M, Yaron I. Yust 1. Brenner S. Lichen myxedematosus (scleromyxedenyt serum stimulates hyaluronic acid and prostaglandin E production by human libroblasts. J Rheumatol 1985;12:171-5. 14. Chandra JJ. Scleroniyxedema. Cutis 1979;24:549-52.
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Laryngeal involvement in scleromyxedema: A case report MICHAEL F. RAPP, MD, MANINDER GURAM, MD, HORST R. KONRAD, MD, NAT MODY, MD, and ROBERT TRAPP, MD, Kearney, Nebraska, Columbia, South Carolina, and Springfield, Illinois
scleromyxedema is a distinct, rare entity, designated as a primary cutaneous mucinosis in the absence of endocrine dysfunction. The origin of this disorder is unknown. It is characterized by generalized papules and plaques that cause extensive thickening and hardening of the skin. Histologic changes in the dermis include proliferation of fibroblasts and excessive deposition of hyaluronic acid. In many cases there is a serum monoclonal paraprotein. Although some patients have no visceral complications, it is often a systemic disease, Involvement of a variety of internal organs has been identified.'.2 We report this as the first documented case of laryngeal involvement in scleromyxedema. CASE REPORT
A 28-year-old man was admitted to the hospital because of fever, sore throat, cough, and dysphagia. For the previous 3 years his skin had become thick and hard. The skin involvement was predominantly of the face, neck, arms, hands, chest, and back. For the last year, he had pain in his fingers and ulcerations over his knuckles. For the last 3 weeks, he reported experiencing sore throat, hoarseness, and difficulty swallowing; in the last week, liquids regurgitated through his nose and cough and fever up to 40" C developed. The patient had lost 20 pounds over the last year. He denied
From the Department of Internal Medicine (Dr. Guram), the University of South Carolina, and the Departments of Otolaryngology (Dr. Konrad), Pathology (Dr. Mody), and Internal Medicine (Dr. Trapp), Southern Illinois University, Springfield. Dr. Rapp is in private practice in Kearney, Nebraska. Presented at the Annual Meeting of the American Academy of Otolaryngology-Head and Neck Surgery, New Orleans, La., Sept. 24-28, 1989. Received for publication Sept. 25, 1989; revision received Oct. 10, 1990; accepted Oct. 23, 1990. Reprint requests: Michael F. Rapp, MD, 1919 West 36th St., Kearney, NE 68847. 23/4126265
chest pain, but had experienced shortness of breath. He denied any muscle weakness, peripheral numbness or tingling, changes in vision, or headaches. He did not smoke and denied use of alcohol or recreational drugs. Family history was noncontributory. Until the disease began, he was employed as a minor league baseball player. His vital signs were normal, with the exception of an elevated temperature to 38.6" C. On examination, the skin was thick and "bound down" over the face-especially the forehead, ears and mouth. The skin of the neck, chest, arms, back, and abdomen were also involved and, to a lesser extent, the skin of the legs and feet (Fig. 1). Otolaryngologic examination demonstrated extensive hard papules ranging from 3 to 6 mm in diameter on his face. He was able to open his mouth a maximum of only 4 cm. The tongue and oral mucosa had normal appearance and movement. Indirect and direct examination showed the left half of the soft palate to be thick, with impeded movement, and the uvula was deviated to the right (Fig. 2). There was marked velopalatine insufficiency. The nasopharynx was normal. The left half of the hypopharynx was scarred. The larynx was rotated to the right and the epiglottis was thickened and scarred on the left, whereas the right half appeared normal (Fig. 3 ) . There was decreased mobility of the epiglottis. The right aryepiglottic fold and vocal cord were normal with good mobility. The left aryepiglottic fold and vocal cord were thick and scarred and, prior to videotaping, appeared paralyzed. There was marked pooling of secretions in the area of the piriform sinuses. Videotaping was performed using a Hopkins rod telescope. This revealed extremely impaired motion of the left vocal cord and palate. The chest expansion was decreased with ronchi in the left posterior and lateral base, and bibasilar fine crackles. The heart, abdominal, and rectal examinations were normal. Examination of the extremities showed sclerodactyly, with flexion contractures of the fingers. There were several small, wellhealed scars over the knuckles and the fingers. Both elbows had 15-degree flexion contractures. The range of motion of the wrists was minimally restricted bilaterally. The neurologic examination was normal. The white cell count was 13,600 per cubic millimeter,
362 Downloaded from oto.sagepub.com at Purdue University on June 6, 2016
Volume 104 Number 3 March 1991
Case Reports 363
with 72%' neutrophils. 18% bands. 17% lymphocytes. 5 % monocytes. and 3% eosinophils. The hemoglobin was 13.6 gniidl, with a hcmatocrit of4l. Serum protein elcctrophorcsis showed an IgG-lambda minor monoclonal spike. with slight elevation of alpha-? and gamma globulins. Urinalysis, serum chemistries. aldolasc, rheumatoid factor. antinuclcar antibodies, anti-smooth muscle antibodies, complement levels. cryoglobulins. thyroid profile. and thyroid-stimulating hormone (TSH) were all within normal limits. The chcst x-ray film revealed a left posterior pulmonary infiltrate. Radiographs of both hands showed contracture dcforniities of the proximal and distal interphalangcal joints of the second through fifth digits bilaterally. Early pencil-like deformities were noted in the left distal phalanx of the fifth digit. and soft tissue atrophy was seen over the distal ends of the digits. Video-esophagram showcd that the patient had difficulty initiating deglutition. Movement of the pharynx and hypopharynx were decreased. No food bolus was fornied within the mouth. The epiglottis did not move posteriorly. nor did the larynx elevate properly, resulting in intermittent aspiration. There was slight hypertrophy of the cricopharyngcus muscle. Esophageal manometric studies showed decreased frcquency and amplitude of peristalsis. and decreased upper and lower sphincter pressures. The upper esophageal sphincter relaxed normally. but no post-relaxation contraction was noted. Magnetic resonance imaging ofthe brain and the throat showed no abnorniality. Light microscopy of the skin biopsy was conbistent with the diagnosis of scleromyxedenia. Colloidal iron stain was positive for acid mucopolysaccharidcs. restricted to the upper portion of the dermis. The acid mucopolysacchuridcs were prcsent between collagen bundlcs. DISCUSSION Scleromyxedema-also known as generalized lichen a distinct. rare entity designated myxedematosus-is under primary cutaneous mucinoses in the absence of endocrine dysfunction. ' There has been an increasing number of reports in the literature, with approximately 125 cases identified to date. Scleromyxedema is characterized by generalized lichenoid papules and plaques, which cause extensive thickening of the skin of the face, neck. arms, hands, upper back, and chest, and (to a lesser extent) the abdominal wall and lower extremities. Decreased oral aperture, pharyngeal and esophageal dysfunction, acrosclerosis (stiffness and tightness of the skin of the fingers), flexion contractures, and increased atherosclerotic disease are common.' The association of other disease states. including bilateral superficial corneal opacities caused by protein deposition, multiple myeloma, Waldenstrom's niacroglobulineniia. nonHodgkin's lymphoma, esophageal aperistalsis. in-
Fig. 1. Patient as he presented. Note flexion controctures of elbows and fingers.
Hamrnatory myopathy, erosive arthritis, median neuropathy. and sicca complex, have been reported.'." The most common cause of death as a result of this disorder is aspiration pneumonia. although neurovascular disorders and niyocardial infarctions also occur at young ages.'." The cause of scleromyxedenia is unknown. It has no obvious association with infections, drugs, o r familial or environmental factors. Although there are certain similarities in the clinical presentation and histologic features with the cutaneous features of the thyroid-
Downloaded from oto.sagepub.com at Purdue University on June 6, 2016
OtolaryngologyHead and Neck Surgery
364 Case Reports
Fig. 2. Appearance of the soft palate. Note the asymmetry caused by thickening of the lel? pharyngeal tissue, resulting in decreased mobility Lettand rightare indicated by I and R.
pituitary dysfunction, no thyroid dysfunction has been documented in patients with scleromyxedema. There have been unsuccessful attempts to associate this entity with plasma cell dyscrasia because many patients with this disorder have a serum monoclonal paraproteinemia. As in the patient reported, the paraprotein is usually an IgG, but IgM and IgA paraproteins also O C C U ~ . ~ . ~ Interestingly, -’’ it has been hypothesized that this paraprotein may stimulate fibroblast production of hyaluronic acid and be the cause of the debilitating thickening of skin and internal organs. ‘’.I3 However, the serum monoclonal paraprotein is not a consistent finding and should not be used as a criterion for diagnosis.’ In those patients without an elevated paraprotein, there may be other factors that also result in the disease, or the serum level of the immunoglobulins may fluctuate during the disease course. Further studies are necessary to understand the role of abnormal proteins in scleromyxedema. Histologically, there is deposition of niucin (hyaluronic acid) in the superficial dermis, with proliferation of large, stellate, elongated fibroblasts associated with
irregularly arranged bundles of collagen. The epidermis is normal. I.’.’ Treatment has included electron beam therapy, ACTH and cortisone, methotrexate, cyclophosphamide, melphalan, and chlorambucil, with a wide variation in reported result^.'^^^^^'^ The laryngeal abnormalities have not been documented before in this group of patients. Decreased mobility and the altered morphology of the epiglottis and vocal cord contributed to both hoarseness and aspiration. The unilateral appearance of pharyngeal and laryngeal involvement cannot be easily explained because this is a systemic disease and bilateral involvement would be expected. While cranial nerve involvement was initially suspected, videotaping of the patient showed the decreased mobility was caused by the thickening of the pharyngeal tissues. No biopsy was taken of the pharynx, although it would have been interesting to compare this to the dermal findings. We do not know if the defect was limited to the mucosa or included the underlying muscle. Aspiration and resulting pneumonia is a common
Downloaded from oto.sagepub.com at Purdue University on June 6, 2016
Volume 104 Number 3
Case Reports 365
March 1991
Fig. 3. Appearance of the larynx demonstrates demarkation of mucosal thickening and atrophy of left hemilarynx. Black arrowhead indicates epiglottis at the mucosal transition; white arrow indicates right orytenoid, which has normal appearance and mobility. The left arytenoid is also thickened with decreased mobility and does not show up well on the photograph.(In color, this figure gives a better appreciation of the mucosal changes].
cause of death in scleromyxedema. Information regarding the status of the palate, pharynx, and glottis is valuable in the management of these patients and should be documented by appropriate otolaryngologic consultation. We w i s h t o thank Ms. Bernie Hatcher a n d t h e S o u t h e r n Illinois University Biomedical C o m m u n i c a t i o n s Department for their assistance i n preparation of this manuscript and presentation of the poster. REFERENCES 1. Truhan AP, Roenigk HH. The cutaneous niucinoses. J Am Acad
Derm 1986; 14: I - 18. 2. Gabriel SE. Peny HO. Oleson GB, Bowles CA. Scleromyxedema: a sclerodema-like disorder with systcmic manifegation. Medicine 1988:67:58-65. 3. Fudman U,Golbus J, Ike RW. Scleroniyxedema with systemic involvement mimics rheumatic discases. Arthritis Rheum 1986; 29:913-7. 4. Farmer ER, Hambrick GW. Shulman LE. Papular mucinosis. Arch Dermatol 1982;118:9-13.
5. Howsden SM. Hemdon JH. Freeman RG. Lichen myxedematosus: B dermal infiltrative disorder responsive to cyclophosphamide therapy. Arch Dermatol 1975;l I I: 1325-30. 6. Lowe NJ. Dufton PA, Hunter RD, Vickers CF. Electron-beam treatment of scleroniyxedema. Br J Dermatol 1982;10649-54. 7. Matsuoka LY. Wortsman J, Carlisle KS, Kupchella CK, Deitrich JG. The acquired cutaneous mucinoses. Arch Intern Med 1984;IU:1974-80. 8 . Pusateri TJ. Margo CE, Groden LR. Corneal manifestations of scleroniyxedema. Ophthalmology 1987:94:510-3. 9. Fowlkcs RW, Blaycock WK, Mullinax F. Immunologic studies in lichen myxedematosus. Arch Dermatol 1967;95:370-4. 10. Danby FW. Danby CW. Pruzansky W. Papular mucinosis with IgG(k) M component. Can Med Assoc J 1976;114:920-2. I I . Kitamura W. Matsuoka Y. Miyagawa S. Sakamoto K. Immunochemical analysis of the monoclonal paraprotein in scleromyxedema. J Invest Dermatol 1978;70:305-8. 12. Harper RA, Rispler J. Lichen myxedematosus serum stimulates human skin fibroblast proliferation. Science 1978:199545-7. 13. Yaron M, Yaron I. Yust 1. Brenner S. Lichen myxedematosus (scleromyxedenyt serum stimulates hyaluronic acid and prostaglandin E production by human libroblasts. J Rheumatol 1985;12:171-5. 14. Chandra JJ. Scleroniyxedema. Cutis 1979;24:549-52.
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