Embed Size (px)
Citation preview
El mixedema pretibial se puede ver en la enfermedad de Graves o en hipotiroidismo
Es infiltrativo simeacutetrico en la parte anterior de la tibia y dorso del pieacute con noacutedulos eritematosos rosados o color carne a violaacuteceos con edema difuso que puede terminar en elefantiasis
Si hay enf de Graves se ve oftalmopatiacutea
La mitad de los mixedemas ocurren cuando ya son eutiroideos con el tratamiento
La tiroiditis de Hashimoto da algo similar mixedematoso acral
En la cara hay nariz amplia labios gruesos lengua grande secresiones pegajosas sobre los paacuterpados y goteo de laacutegrimas
Siempre es depoacutesito de aacutecido hialuroacutenico y condroitiacuten sulfato en dermis
Se sugiere que las hormonas del tiroides afectan la siacutentesis y el catabolismo de mucopolisacaacuteridos y colaacutegeno en los fibroblastos en la oacuterbita y regioacuten pretibial
Tto difiacutecilhellip esteroides siteacutemicos o intralesionales sirven a veces
IgG intravenosa se ha informadohellip alguna mejoriacutea
Oral pentoxifylline and topical clobetasol propionate ointment in the treatment of pretibial myxoedema with concomitant improvement of Graves ophthalmopathyJ Eur Acad Dermatol Venereol 2007 Nov21(10)1441-3
Plaque form of pretibial myxedema in hypothyroidism
Dharmalingam M Seema G Khaitan B Karak A Ammini AC Plaque
form of pretibial myxedema in hypothyroidism Indian J Dermatol
Venereol Leprol 200167330-
Pretibial myxedema (PTM) is an infiltrative dermopathy It is a very rare
clinical finding and when present it is usually seen in 5-10 of Graves
thyrotoxicosis[1][2] However it has also been described in autoimmune
thyroid disease like Hashimotos thyroiditis and idiopathic hypothyroidism
[3] The diffuse non pitting variety is more commonly described The other
forms of plaque nodule and tubular are rare We present an uncommon
form of PTM the plaque form in a hypothyroid individual
A 27 - year - old man presenting with plaque lesions on the dorsum of the
leg and foot for the past 3 years was seen in our OPD Patient was
apparently normal three years back when he developed raised lesions on
the leg and foot A year ago he resorted to indigenous medicine both
systemic and local following which there was worsening of the lesions
with increasing size and serous discharge On further questioning he
admitted having cold intolerance lethargy and weight gain for the past one
year which worsened over the past two months There was no family
history of thyroid dysfunction or enlargement
His height was 165 cms with a body weight of 1005 kg and body mass
index (BMI) of 3673 The other physical examination was not contributory
except that the deep tendon reflexes were delayed The thyroid was not
enlarged Dermatological examination revealed well defined indurated
plaques measuring 8 x 6 cms having sloping margins mildly erythematous
with hyperpigmentation in the center lobulated surface with loss of hair on
anterior aspect of left leg Similar lesions measuring 2 x 3 cms and 2 x 2
cms were present on the right leg
Patient was biochemically evaluated the ft3 was 10 pgml (Normal - 1
4-44) and fT4 was o2ng dl (Normal - 08-20) with the TSH of 950 ulU
ml (Normal 02-5) The thyroid antibodies were positive thyroid
microsomal antibody (TMA) positive 11600 titre (N-Negative in this
dilution) and anti thyroglobulin antibody (TGA) positive 1 640 titre (N-
Negative in this dilution) The ultrasound of the thyroid showed a normal
right lobe with a small left lobe The CT of the orbit did not reveal any
enlargement infiltration of the ocular muscles Ultrasonogram of the skin
lesions showed the dermis and the epidermis to be thickened
Histopathology of the skin lesion showed a dermal mucin accumulation
which was compatible with pretibial myxedema
Discussion
Pretibial myxedema is a poorly understood autoimmune process usually
occurring with Graves thyrotoxicosis[1] Salvi et al have studied 76
patients with pretibial myxedema and found it to be present 7631 in
Graves 171 in Hashimotos thyroiditis and 65 in idiopathic
hypothyroidism[4] It was 64 of the times associated with
ophthalmopathy[3]
Epidemiological studies have shown that 4 of the patients with clinically
evident opthalmopathy have demopathy In the above patient the pretibial
lesions were present in a nongoitorous form of autoimmune thyroiditis
There was no associated orbiteropathy The lesions are more common in
the female in the sixth decade The msot common form of presentation is
the diffuse non pitting edema form It can appear as a raised plaque lesion
sharply circumscribed tubular or nodular lesion Very rarely they are
elephantiastic polypoid or fungating[5] The common sites include the
pretibial region and the dorsum of the foot The lesions present in the
patient were of the plaque variety which is an uncommon manifestation
In the study by Salvi et al[4] it was histopathologically confirmed in all the
patients though clinically suspected only in 28 The histopathologic
finding of mucin accumulation confirmed the diagnosis of pretibial
myxedema Ultrasound examination of the lesions showed a dermal
thickening[4] which was also confirmed in this patient
Pretibial myxedema presenting as a diffuse plaque form in a hypothyroid
young male is very uncommon
---------------------------------------------------------------------------------------
Successful combined pentoxifylline and intralesional triamcinolone acetonide treatment of severe pretibial myxedema Burhan Engin1 Munise Guumlmuumlşel1 Mustafa Oumlzdemir1 Mehtap Ccedilakir2
Dermatology Online Journal 13 (2) 16
1 Selccediluk University Meram Medical Faculty Department of Dermatology burhanengin2000yahoocom2 Selccediluk University Meram Medical Faculty Department of Internal Medicine
Pretibial myxedema (PTM) is an infrequent manifestation of autoimmune thyroiditis especially can be present in Graves disease [1] Massive intradermal deposition of mucin (acid mucopolysaccharide) produces the nodules or plaques on the lower legs [2] Various treatment modalities have been used for pretibial myxedema We herein demonstrated a patient who has been used pentoxifylline intralesional corticosteroid injection with a good clinical response
Clinical synopsis
Figure 1 Figure 2
Figures 1 and 2 Thickened plaques extending around left lower leg
In 2002 a 32-year-old man presented with a 7-month history of non-tender erythematous non-pruritic nodules symmetrically localized on his shins He had a diagnosis of Graves disease He was treated surgically with a subtotal thyroidectomy Thyroxine therapy was commenced for subsequent hypothyroidism The lesions grew slowly in size and new lesions developed near the original nodules approximately in 15 years On admission the patient demonstrated erythematous indurated nodules and plaques with no ulcers on the lateral and anterior aspects of the shin (Figs 1
and 2) The lesions were neither warm nor tender to the touch Bilateral exophthalmous was noted He had bilateral clubbing and melanonychia striate at right and left hand fingernails Blood cell counts biochemistry chest radiography and thyroid function tests were normal
Clobetasol propionate occlusions for 2-3 hours a day and elastic bandage at nights were applied regularly Pentoxifylline 400 mg three times a day was started A total dose of 10 ml of intralesional triamcinolone acetonide (5 mgml) was injected monthly After 3 months his lesions receded and only a few slight indurated plaques remained (Fig 2)
Discussion
Pretibial myxedema can be present in either Graves disease or hypothyroidism Our patient whose lesions started on his shins and went on his pretibial area has Graves disease [3] Pretibial myxedema is an infiltrative dermopathy that most frequently appears symmetrically on the anterior tibia and dorsum of the feet The usual presentation is that of bilateral asymmetric raised firm plaque or nodules of a pink to purple-brown hue Hyperhidrosis and hypertrichosis may overlie the affected areas in rare cases Rarely the lesions may be painful or pruritic Our patient had erythematous not itching firm plaques and nodules There was no maceration and hypertrichosis but the appearance of his legs were as peau dorange and there was no pitting edema Ophthalmopathy always accompanies cutaneous findings usually appears first and dermopathy much later Thyroid acropachy is a triad consisting of digital clubbing soft tissue swelling of hands and feet and periosteal new bone formation [3 4] Our patients ophthalmic changes occurred before dermopathy and he had clubbing of his fingernails
The mechanism that causes myxedema is unclear although animal model studies suggest that thyroid hormones affect the synthesis and catabolism of mucopolysaccharides and collagen by dermal fibroblasts The fibroblast in the orbital area and pretibial dermis share antigenic sites that underlie the autoimmune process
Figure 3
Figure 3 Lesions had receded and only a few slight indurated plaques remained
that causes Graves disease Thereby cross reaction contributes to the development of myxedema occurring long after euthyroid status is achieved through treatment [3] Whatever the cause of the increased glycosaminoglycan (GAG) production accumulation of GAG leads to the characteristic skin lesions associated with thyroid dermopathy The hyaluronic acid expands the dermal tissue and causes fluid to accumulate It may also cause compression or occlusion of small local lymphatic and thereby increase the dermal edema [1]
Treatment starts with avoiding the risk factors as avoiding tobacco and reducing weight then normalization of thyroid functions [4] High potency topical corticosteroids with occlusion or not or intralesional corticosteroids are the best approach but the cure rate is low In a prospective study nine patients with pretibial myxedema were treated with intralesional injections of triamcinolone acetonide Complete resolution was obtained in seven of the nine patients For most patients the monthly injection of 8 ml or less of a solution containing 5 mgml of triamcinolone proved to be the most effective dosage schedule [5] We used 10 ml (5 mgml) of triamcinolone acetonide monthly Clobetasol propionate occlusion over the legs for 2-3 hours a day was applied and detected no side effects Because of fluid accumulation the use of compressive bandages provides additional benefit as in our patient used elastic bandage at night [4]
Pentoxifylline an analogue of the methylxanthine theobromine inhibits the proliferation of fibroblasts derived from normal human skin and from skin of patients with some fibrotic disorders In subconfluent fibroblast cultures pentoxifylline treatment caused a dose-dependent inhibition of serum-driven fibroblast proliferation and glycosaminoglycan synthesis [6] Its usage widely accepted in pretibial myxedema however the efficacy of the drug and the results of the follow-up were not stated clearly in the literature After 3 months of combined pentoxifylline and intralesional triamcinolone acetonide our patients lesions have receded and another 3 months follow-up period they have not recurred
Treatment of PTM is often difficult We suggest that the easiest and effective treatment of PTM may be achieved by combined pentoxifylline and intralesional triamcinolone acetonide
References
1 Schwartz KM Fatourechi V Ahmed DDF Pond GR Dermopathy of Graves disease (Pretibial Myxedema) Long term outcome J Clin Endocrinol Metab 2002 Feb87(2)438-46 PubMed
2 Truhan AP Pretibial myxedema Am Fam Physician 1985 May31(5)135-8 PubMed
3 Chung-Leddon J Pretibial Myxedema Dermatol Online J 2001 Feb7(1)18 PubMed
4 Fatourechi V Pretibial myxedema pathophysiology and treatment options Am J Clin Dermatol 20056(5)295-309 Review PubMed
5 Lang PG Sisson JC Lynch PJ Intralesional triamsinolone therapy for pretibial myxedema Arch Dermatol 1975 Feb111(2)197-202 PubMed
6 Chang CC Chang TC Kao SC Kuo YF Chien LF Pentoxyfilline inhibits the proliferation and glycosaminoglycan synthesis of cultured fibroblasts derived from patients with Graves ophthalmopaty and pretibial myxedema Acta Endocrinol (Copenh) 1993 Oct129(4)322-7 PubMed
--------------------------------------------------------------------------------------
Postepy Hig Med Dosw (Online) 200660184-91
[The metabolism of glycosaminoglycans in the course of Graves disease][Article in Polish]
Winsz-Szczotka K Komosińska-Vassev K Olczyk K
Zakład Chemii Klinicznej i Diagnostyki Laboratoryjnej Slaskiej Akademii Medycznej Sosnowiec winszslamkatowicepl
Glycosaminoglycans (GAGs) which include chondroitin sulfate (CS) dermatan sulfates (DS) heparan sulfate (HS) heparin (H) keratan sulfate (KS) and hyaluronic acid (HA) are a group of linear polyanionic heteropolysaccharides The GAGs chains except for those of hyaluronic acid are covalently attached to core proteins forming proteoglycans (PGs) PGsGAGs are present at the cellular level as elements of the cell membrane and intracellular granules They are also components of the ground substance of the extracellular matrix These macromolecules are involved in cell adhesion migration and proliferation Alterations in GAGs metabolism may influence the pathogenesis of many disorders including Graves disease Graves disease is an autoimmune thyroid pathology characterized by hyperthyroidism thyroid hyperplasia as well as ophthalmopathy andor pretibial myxedema The pathogenesis of these extrathyroidal manifestations involves fibroblast activation and increased glycosaminoglycan synthesis and accumulation Disturbances in GAGs metabolism in tissue are associated with qualitative and quantitative GAGs
alterations in Graves patients serum and urine Although the mechanisms leading to the development of orbital andor skin complications in the course of Graves disease have not been fully elucidated it is postulated that they depend on both immunological disturbances and the hyperthyroid state SUMMARY The alterations in GAGs metabolism connected with Graves disease could lead to systemic changes in the proprieties of the extracellular matrix
clinical finding and when present it is usually seen in 5-10 of Graves
thyrotoxicosis[1][2] However it has also been described in autoimmune
thyroid disease like Hashimotos thyroiditis and idiopathic hypothyroidism
[3] The diffuse non pitting variety is more commonly described The other
forms of plaque nodule and tubular are rare We present an uncommon
form of PTM the plaque form in a hypothyroid individual
A 27 - year - old man presenting with plaque lesions on the dorsum of the
leg and foot for the past 3 years was seen in our OPD Patient was
apparently normal three years back when he developed raised lesions on
the leg and foot A year ago he resorted to indigenous medicine both
systemic and local following which there was worsening of the lesions
with increasing size and serous discharge On further questioning he
admitted having cold intolerance lethargy and weight gain for the past one
year which worsened over the past two months There was no family
history of thyroid dysfunction or enlargement
His height was 165 cms with a body weight of 1005 kg and body mass
index (BMI) of 3673 The other physical examination was not contributory
except that the deep tendon reflexes were delayed The thyroid was not
enlarged Dermatological examination revealed well defined indurated
plaques measuring 8 x 6 cms having sloping margins mildly erythematous
with hyperpigmentation in the center lobulated surface with loss of hair on
anterior aspect of left leg Similar lesions measuring 2 x 3 cms and 2 x 2
cms were present on the right leg
Patient was biochemically evaluated the ft3 was 10 pgml (Normal - 1
4-44) and fT4 was o2ng dl (Normal - 08-20) with the TSH of 950 ulU
ml (Normal 02-5) The thyroid antibodies were positive thyroid
microsomal antibody (TMA) positive 11600 titre (N-Negative in this
dilution) and anti thyroglobulin antibody (TGA) positive 1 640 titre (N-
Negative in this dilution) The ultrasound of the thyroid showed a normal
right lobe with a small left lobe The CT of the orbit did not reveal any
enlargement infiltration of the ocular muscles Ultrasonogram of the skin
lesions showed the dermis and the epidermis to be thickened
Histopathology of the skin lesion showed a dermal mucin accumulation
which was compatible with pretibial myxedema
Discussion
Pretibial myxedema is a poorly understood autoimmune process usually
occurring with Graves thyrotoxicosis[1] Salvi et al have studied 76
patients with pretibial myxedema and found it to be present 7631 in
Graves 171 in Hashimotos thyroiditis and 65 in idiopathic
hypothyroidism[4] It was 64 of the times associated with
ophthalmopathy[3]
Epidemiological studies have shown that 4 of the patients with clinically
evident opthalmopathy have demopathy In the above patient the pretibial
lesions were present in a nongoitorous form of autoimmune thyroiditis
There was no associated orbiteropathy The lesions are more common in
the female in the sixth decade The msot common form of presentation is
the diffuse non pitting edema form It can appear as a raised plaque lesion
sharply circumscribed tubular or nodular lesion Very rarely they are
elephantiastic polypoid or fungating[5] The common sites include the
pretibial region and the dorsum of the foot The lesions present in the
patient were of the plaque variety which is an uncommon manifestation
In the study by Salvi et al[4] it was histopathologically confirmed in all the
patients though clinically suspected only in 28 The histopathologic
finding of mucin accumulation confirmed the diagnosis of pretibial
myxedema Ultrasound examination of the lesions showed a dermal
thickening[4] which was also confirmed in this patient
Pretibial myxedema presenting as a diffuse plaque form in a hypothyroid
young male is very uncommon
---------------------------------------------------------------------------------------
Successful combined pentoxifylline and intralesional triamcinolone acetonide treatment of severe pretibial myxedema Burhan Engin1 Munise Guumlmuumlşel1 Mustafa Oumlzdemir1 Mehtap Ccedilakir2
Dermatology Online Journal 13 (2) 16
1 Selccediluk University Meram Medical Faculty Department of Dermatology burhanengin2000yahoocom2 Selccediluk University Meram Medical Faculty Department of Internal Medicine
Pretibial myxedema (PTM) is an infrequent manifestation of autoimmune thyroiditis especially can be present in Graves disease [1] Massive intradermal deposition of mucin (acid mucopolysaccharide) produces the nodules or plaques on the lower legs [2] Various treatment modalities have been used for pretibial myxedema We herein demonstrated a patient who has been used pentoxifylline intralesional corticosteroid injection with a good clinical response
Clinical synopsis
Figure 1 Figure 2
Figures 1 and 2 Thickened plaques extending around left lower leg
In 2002 a 32-year-old man presented with a 7-month history of non-tender erythematous non-pruritic nodules symmetrically localized on his shins He had a diagnosis of Graves disease He was treated surgically with a subtotal thyroidectomy Thyroxine therapy was commenced for subsequent hypothyroidism The lesions grew slowly in size and new lesions developed near the original nodules approximately in 15 years On admission the patient demonstrated erythematous indurated nodules and plaques with no ulcers on the lateral and anterior aspects of the shin (Figs 1
and 2) The lesions were neither warm nor tender to the touch Bilateral exophthalmous was noted He had bilateral clubbing and melanonychia striate at right and left hand fingernails Blood cell counts biochemistry chest radiography and thyroid function tests were normal
Clobetasol propionate occlusions for 2-3 hours a day and elastic bandage at nights were applied regularly Pentoxifylline 400 mg three times a day was started A total dose of 10 ml of intralesional triamcinolone acetonide (5 mgml) was injected monthly After 3 months his lesions receded and only a few slight indurated plaques remained (Fig 2)
Discussion
Pretibial myxedema can be present in either Graves disease or hypothyroidism Our patient whose lesions started on his shins and went on his pretibial area has Graves disease [3] Pretibial myxedema is an infiltrative dermopathy that most frequently appears symmetrically on the anterior tibia and dorsum of the feet The usual presentation is that of bilateral asymmetric raised firm plaque or nodules of a pink to purple-brown hue Hyperhidrosis and hypertrichosis may overlie the affected areas in rare cases Rarely the lesions may be painful or pruritic Our patient had erythematous not itching firm plaques and nodules There was no maceration and hypertrichosis but the appearance of his legs were as peau dorange and there was no pitting edema Ophthalmopathy always accompanies cutaneous findings usually appears first and dermopathy much later Thyroid acropachy is a triad consisting of digital clubbing soft tissue swelling of hands and feet and periosteal new bone formation [3 4] Our patients ophthalmic changes occurred before dermopathy and he had clubbing of his fingernails
The mechanism that causes myxedema is unclear although animal model studies suggest that thyroid hormones affect the synthesis and catabolism of mucopolysaccharides and collagen by dermal fibroblasts The fibroblast in the orbital area and pretibial dermis share antigenic sites that underlie the autoimmune process
Figure 3
Figure 3 Lesions had receded and only a few slight indurated plaques remained
that causes Graves disease Thereby cross reaction contributes to the development of myxedema occurring long after euthyroid status is achieved through treatment [3] Whatever the cause of the increased glycosaminoglycan (GAG) production accumulation of GAG leads to the characteristic skin lesions associated with thyroid dermopathy The hyaluronic acid expands the dermal tissue and causes fluid to accumulate It may also cause compression or occlusion of small local lymphatic and thereby increase the dermal edema [1]
Treatment starts with avoiding the risk factors as avoiding tobacco and reducing weight then normalization of thyroid functions [4] High potency topical corticosteroids with occlusion or not or intralesional corticosteroids are the best approach but the cure rate is low In a prospective study nine patients with pretibial myxedema were treated with intralesional injections of triamcinolone acetonide Complete resolution was obtained in seven of the nine patients For most patients the monthly injection of 8 ml or less of a solution containing 5 mgml of triamcinolone proved to be the most effective dosage schedule [5] We used 10 ml (5 mgml) of triamcinolone acetonide monthly Clobetasol propionate occlusion over the legs for 2-3 hours a day was applied and detected no side effects Because of fluid accumulation the use of compressive bandages provides additional benefit as in our patient used elastic bandage at night [4]
Pentoxifylline an analogue of the methylxanthine theobromine inhibits the proliferation of fibroblasts derived from normal human skin and from skin of patients with some fibrotic disorders In subconfluent fibroblast cultures pentoxifylline treatment caused a dose-dependent inhibition of serum-driven fibroblast proliferation and glycosaminoglycan synthesis [6] Its usage widely accepted in pretibial myxedema however the efficacy of the drug and the results of the follow-up were not stated clearly in the literature After 3 months of combined pentoxifylline and intralesional triamcinolone acetonide our patients lesions have receded and another 3 months follow-up period they have not recurred
Treatment of PTM is often difficult We suggest that the easiest and effective treatment of PTM may be achieved by combined pentoxifylline and intralesional triamcinolone acetonide
References
1 Schwartz KM Fatourechi V Ahmed DDF Pond GR Dermopathy of Graves disease (Pretibial Myxedema) Long term outcome J Clin Endocrinol Metab 2002 Feb87(2)438-46 PubMed
2 Truhan AP Pretibial myxedema Am Fam Physician 1985 May31(5)135-8 PubMed
3 Chung-Leddon J Pretibial Myxedema Dermatol Online J 2001 Feb7(1)18 PubMed
4 Fatourechi V Pretibial myxedema pathophysiology and treatment options Am J Clin Dermatol 20056(5)295-309 Review PubMed
5 Lang PG Sisson JC Lynch PJ Intralesional triamsinolone therapy for pretibial myxedema Arch Dermatol 1975 Feb111(2)197-202 PubMed
6 Chang CC Chang TC Kao SC Kuo YF Chien LF Pentoxyfilline inhibits the proliferation and glycosaminoglycan synthesis of cultured fibroblasts derived from patients with Graves ophthalmopaty and pretibial myxedema Acta Endocrinol (Copenh) 1993 Oct129(4)322-7 PubMed
--------------------------------------------------------------------------------------
Postepy Hig Med Dosw (Online) 200660184-91
[The metabolism of glycosaminoglycans in the course of Graves disease][Article in Polish]
Winsz-Szczotka K Komosińska-Vassev K Olczyk K
Zakład Chemii Klinicznej i Diagnostyki Laboratoryjnej Slaskiej Akademii Medycznej Sosnowiec winszslamkatowicepl
Glycosaminoglycans (GAGs) which include chondroitin sulfate (CS) dermatan sulfates (DS) heparan sulfate (HS) heparin (H) keratan sulfate (KS) and hyaluronic acid (HA) are a group of linear polyanionic heteropolysaccharides The GAGs chains except for those of hyaluronic acid are covalently attached to core proteins forming proteoglycans (PGs) PGsGAGs are present at the cellular level as elements of the cell membrane and intracellular granules They are also components of the ground substance of the extracellular matrix These macromolecules are involved in cell adhesion migration and proliferation Alterations in GAGs metabolism may influence the pathogenesis of many disorders including Graves disease Graves disease is an autoimmune thyroid pathology characterized by hyperthyroidism thyroid hyperplasia as well as ophthalmopathy andor pretibial myxedema The pathogenesis of these extrathyroidal manifestations involves fibroblast activation and increased glycosaminoglycan synthesis and accumulation Disturbances in GAGs metabolism in tissue are associated with qualitative and quantitative GAGs
alterations in Graves patients serum and urine Although the mechanisms leading to the development of orbital andor skin complications in the course of Graves disease have not been fully elucidated it is postulated that they depend on both immunological disturbances and the hyperthyroid state SUMMARY The alterations in GAGs metabolism connected with Graves disease could lead to systemic changes in the proprieties of the extracellular matrix
right lobe with a small left lobe The CT of the orbit did not reveal any
enlargement infiltration of the ocular muscles Ultrasonogram of the skin
lesions showed the dermis and the epidermis to be thickened
Histopathology of the skin lesion showed a dermal mucin accumulation
which was compatible with pretibial myxedema
Discussion
Pretibial myxedema is a poorly understood autoimmune process usually
occurring with Graves thyrotoxicosis[1] Salvi et al have studied 76
patients with pretibial myxedema and found it to be present 7631 in
Graves 171 in Hashimotos thyroiditis and 65 in idiopathic
hypothyroidism[4] It was 64 of the times associated with
ophthalmopathy[3]
Epidemiological studies have shown that 4 of the patients with clinically
evident opthalmopathy have demopathy In the above patient the pretibial
lesions were present in a nongoitorous form of autoimmune thyroiditis
There was no associated orbiteropathy The lesions are more common in
the female in the sixth decade The msot common form of presentation is
the diffuse non pitting edema form It can appear as a raised plaque lesion
sharply circumscribed tubular or nodular lesion Very rarely they are
elephantiastic polypoid or fungating[5] The common sites include the
pretibial region and the dorsum of the foot The lesions present in the
patient were of the plaque variety which is an uncommon manifestation
In the study by Salvi et al[4] it was histopathologically confirmed in all the
patients though clinically suspected only in 28 The histopathologic
finding of mucin accumulation confirmed the diagnosis of pretibial
myxedema Ultrasound examination of the lesions showed a dermal
thickening[4] which was also confirmed in this patient
Pretibial myxedema presenting as a diffuse plaque form in a hypothyroid
young male is very uncommon
---------------------------------------------------------------------------------------
Successful combined pentoxifylline and intralesional triamcinolone acetonide treatment of severe pretibial myxedema Burhan Engin1 Munise Guumlmuumlşel1 Mustafa Oumlzdemir1 Mehtap Ccedilakir2
Dermatology Online Journal 13 (2) 16
1 Selccediluk University Meram Medical Faculty Department of Dermatology burhanengin2000yahoocom2 Selccediluk University Meram Medical Faculty Department of Internal Medicine
Pretibial myxedema (PTM) is an infrequent manifestation of autoimmune thyroiditis especially can be present in Graves disease [1] Massive intradermal deposition of mucin (acid mucopolysaccharide) produces the nodules or plaques on the lower legs [2] Various treatment modalities have been used for pretibial myxedema We herein demonstrated a patient who has been used pentoxifylline intralesional corticosteroid injection with a good clinical response
Clinical synopsis
Figure 1 Figure 2
Figures 1 and 2 Thickened plaques extending around left lower leg
In 2002 a 32-year-old man presented with a 7-month history of non-tender erythematous non-pruritic nodules symmetrically localized on his shins He had a diagnosis of Graves disease He was treated surgically with a subtotal thyroidectomy Thyroxine therapy was commenced for subsequent hypothyroidism The lesions grew slowly in size and new lesions developed near the original nodules approximately in 15 years On admission the patient demonstrated erythematous indurated nodules and plaques with no ulcers on the lateral and anterior aspects of the shin (Figs 1
and 2) The lesions were neither warm nor tender to the touch Bilateral exophthalmous was noted He had bilateral clubbing and melanonychia striate at right and left hand fingernails Blood cell counts biochemistry chest radiography and thyroid function tests were normal
Clobetasol propionate occlusions for 2-3 hours a day and elastic bandage at nights were applied regularly Pentoxifylline 400 mg three times a day was started A total dose of 10 ml of intralesional triamcinolone acetonide (5 mgml) was injected monthly After 3 months his lesions receded and only a few slight indurated plaques remained (Fig 2)
Discussion
Pretibial myxedema can be present in either Graves disease or hypothyroidism Our patient whose lesions started on his shins and went on his pretibial area has Graves disease [3] Pretibial myxedema is an infiltrative dermopathy that most frequently appears symmetrically on the anterior tibia and dorsum of the feet The usual presentation is that of bilateral asymmetric raised firm plaque or nodules of a pink to purple-brown hue Hyperhidrosis and hypertrichosis may overlie the affected areas in rare cases Rarely the lesions may be painful or pruritic Our patient had erythematous not itching firm plaques and nodules There was no maceration and hypertrichosis but the appearance of his legs were as peau dorange and there was no pitting edema Ophthalmopathy always accompanies cutaneous findings usually appears first and dermopathy much later Thyroid acropachy is a triad consisting of digital clubbing soft tissue swelling of hands and feet and periosteal new bone formation [3 4] Our patients ophthalmic changes occurred before dermopathy and he had clubbing of his fingernails
The mechanism that causes myxedema is unclear although animal model studies suggest that thyroid hormones affect the synthesis and catabolism of mucopolysaccharides and collagen by dermal fibroblasts The fibroblast in the orbital area and pretibial dermis share antigenic sites that underlie the autoimmune process
Figure 3
Figure 3 Lesions had receded and only a few slight indurated plaques remained
that causes Graves disease Thereby cross reaction contributes to the development of myxedema occurring long after euthyroid status is achieved through treatment [3] Whatever the cause of the increased glycosaminoglycan (GAG) production accumulation of GAG leads to the characteristic skin lesions associated with thyroid dermopathy The hyaluronic acid expands the dermal tissue and causes fluid to accumulate It may also cause compression or occlusion of small local lymphatic and thereby increase the dermal edema [1]
Treatment starts with avoiding the risk factors as avoiding tobacco and reducing weight then normalization of thyroid functions [4] High potency topical corticosteroids with occlusion or not or intralesional corticosteroids are the best approach but the cure rate is low In a prospective study nine patients with pretibial myxedema were treated with intralesional injections of triamcinolone acetonide Complete resolution was obtained in seven of the nine patients For most patients the monthly injection of 8 ml or less of a solution containing 5 mgml of triamcinolone proved to be the most effective dosage schedule [5] We used 10 ml (5 mgml) of triamcinolone acetonide monthly Clobetasol propionate occlusion over the legs for 2-3 hours a day was applied and detected no side effects Because of fluid accumulation the use of compressive bandages provides additional benefit as in our patient used elastic bandage at night [4]
Pentoxifylline an analogue of the methylxanthine theobromine inhibits the proliferation of fibroblasts derived from normal human skin and from skin of patients with some fibrotic disorders In subconfluent fibroblast cultures pentoxifylline treatment caused a dose-dependent inhibition of serum-driven fibroblast proliferation and glycosaminoglycan synthesis [6] Its usage widely accepted in pretibial myxedema however the efficacy of the drug and the results of the follow-up were not stated clearly in the literature After 3 months of combined pentoxifylline and intralesional triamcinolone acetonide our patients lesions have receded and another 3 months follow-up period they have not recurred
Treatment of PTM is often difficult We suggest that the easiest and effective treatment of PTM may be achieved by combined pentoxifylline and intralesional triamcinolone acetonide
References
1 Schwartz KM Fatourechi V Ahmed DDF Pond GR Dermopathy of Graves disease (Pretibial Myxedema) Long term outcome J Clin Endocrinol Metab 2002 Feb87(2)438-46 PubMed
2 Truhan AP Pretibial myxedema Am Fam Physician 1985 May31(5)135-8 PubMed
3 Chung-Leddon J Pretibial Myxedema Dermatol Online J 2001 Feb7(1)18 PubMed
4 Fatourechi V Pretibial myxedema pathophysiology and treatment options Am J Clin Dermatol 20056(5)295-309 Review PubMed
5 Lang PG Sisson JC Lynch PJ Intralesional triamsinolone therapy for pretibial myxedema Arch Dermatol 1975 Feb111(2)197-202 PubMed
6 Chang CC Chang TC Kao SC Kuo YF Chien LF Pentoxyfilline inhibits the proliferation and glycosaminoglycan synthesis of cultured fibroblasts derived from patients with Graves ophthalmopaty and pretibial myxedema Acta Endocrinol (Copenh) 1993 Oct129(4)322-7 PubMed
--------------------------------------------------------------------------------------
Postepy Hig Med Dosw (Online) 200660184-91
[The metabolism of glycosaminoglycans in the course of Graves disease][Article in Polish]
Winsz-Szczotka K Komosińska-Vassev K Olczyk K
Zakład Chemii Klinicznej i Diagnostyki Laboratoryjnej Slaskiej Akademii Medycznej Sosnowiec winszslamkatowicepl
Glycosaminoglycans (GAGs) which include chondroitin sulfate (CS) dermatan sulfates (DS) heparan sulfate (HS) heparin (H) keratan sulfate (KS) and hyaluronic acid (HA) are a group of linear polyanionic heteropolysaccharides The GAGs chains except for those of hyaluronic acid are covalently attached to core proteins forming proteoglycans (PGs) PGsGAGs are present at the cellular level as elements of the cell membrane and intracellular granules They are also components of the ground substance of the extracellular matrix These macromolecules are involved in cell adhesion migration and proliferation Alterations in GAGs metabolism may influence the pathogenesis of many disorders including Graves disease Graves disease is an autoimmune thyroid pathology characterized by hyperthyroidism thyroid hyperplasia as well as ophthalmopathy andor pretibial myxedema The pathogenesis of these extrathyroidal manifestations involves fibroblast activation and increased glycosaminoglycan synthesis and accumulation Disturbances in GAGs metabolism in tissue are associated with qualitative and quantitative GAGs
alterations in Graves patients serum and urine Although the mechanisms leading to the development of orbital andor skin complications in the course of Graves disease have not been fully elucidated it is postulated that they depend on both immunological disturbances and the hyperthyroid state SUMMARY The alterations in GAGs metabolism connected with Graves disease could lead to systemic changes in the proprieties of the extracellular matrix
Pretibial myxedema presenting as a diffuse plaque form in a hypothyroid
young male is very uncommon
---------------------------------------------------------------------------------------
Successful combined pentoxifylline and intralesional triamcinolone acetonide treatment of severe pretibial myxedema Burhan Engin1 Munise Guumlmuumlşel1 Mustafa Oumlzdemir1 Mehtap Ccedilakir2
Dermatology Online Journal 13 (2) 16
1 Selccediluk University Meram Medical Faculty Department of Dermatology burhanengin2000yahoocom2 Selccediluk University Meram Medical Faculty Department of Internal Medicine
Pretibial myxedema (PTM) is an infrequent manifestation of autoimmune thyroiditis especially can be present in Graves disease [1] Massive intradermal deposition of mucin (acid mucopolysaccharide) produces the nodules or plaques on the lower legs [2] Various treatment modalities have been used for pretibial myxedema We herein demonstrated a patient who has been used pentoxifylline intralesional corticosteroid injection with a good clinical response
Clinical synopsis
Figure 1 Figure 2
Figures 1 and 2 Thickened plaques extending around left lower leg
In 2002 a 32-year-old man presented with a 7-month history of non-tender erythematous non-pruritic nodules symmetrically localized on his shins He had a diagnosis of Graves disease He was treated surgically with a subtotal thyroidectomy Thyroxine therapy was commenced for subsequent hypothyroidism The lesions grew slowly in size and new lesions developed near the original nodules approximately in 15 years On admission the patient demonstrated erythematous indurated nodules and plaques with no ulcers on the lateral and anterior aspects of the shin (Figs 1
and 2) The lesions were neither warm nor tender to the touch Bilateral exophthalmous was noted He had bilateral clubbing and melanonychia striate at right and left hand fingernails Blood cell counts biochemistry chest radiography and thyroid function tests were normal
Clobetasol propionate occlusions for 2-3 hours a day and elastic bandage at nights were applied regularly Pentoxifylline 400 mg three times a day was started A total dose of 10 ml of intralesional triamcinolone acetonide (5 mgml) was injected monthly After 3 months his lesions receded and only a few slight indurated plaques remained (Fig 2)
Discussion
Pretibial myxedema can be present in either Graves disease or hypothyroidism Our patient whose lesions started on his shins and went on his pretibial area has Graves disease [3] Pretibial myxedema is an infiltrative dermopathy that most frequently appears symmetrically on the anterior tibia and dorsum of the feet The usual presentation is that of bilateral asymmetric raised firm plaque or nodules of a pink to purple-brown hue Hyperhidrosis and hypertrichosis may overlie the affected areas in rare cases Rarely the lesions may be painful or pruritic Our patient had erythematous not itching firm plaques and nodules There was no maceration and hypertrichosis but the appearance of his legs were as peau dorange and there was no pitting edema Ophthalmopathy always accompanies cutaneous findings usually appears first and dermopathy much later Thyroid acropachy is a triad consisting of digital clubbing soft tissue swelling of hands and feet and periosteal new bone formation [3 4] Our patients ophthalmic changes occurred before dermopathy and he had clubbing of his fingernails
The mechanism that causes myxedema is unclear although animal model studies suggest that thyroid hormones affect the synthesis and catabolism of mucopolysaccharides and collagen by dermal fibroblasts The fibroblast in the orbital area and pretibial dermis share antigenic sites that underlie the autoimmune process
Figure 3
Figure 3 Lesions had receded and only a few slight indurated plaques remained
that causes Graves disease Thereby cross reaction contributes to the development of myxedema occurring long after euthyroid status is achieved through treatment [3] Whatever the cause of the increased glycosaminoglycan (GAG) production accumulation of GAG leads to the characteristic skin lesions associated with thyroid dermopathy The hyaluronic acid expands the dermal tissue and causes fluid to accumulate It may also cause compression or occlusion of small local lymphatic and thereby increase the dermal edema [1]
Treatment starts with avoiding the risk factors as avoiding tobacco and reducing weight then normalization of thyroid functions [4] High potency topical corticosteroids with occlusion or not or intralesional corticosteroids are the best approach but the cure rate is low In a prospective study nine patients with pretibial myxedema were treated with intralesional injections of triamcinolone acetonide Complete resolution was obtained in seven of the nine patients For most patients the monthly injection of 8 ml or less of a solution containing 5 mgml of triamcinolone proved to be the most effective dosage schedule [5] We used 10 ml (5 mgml) of triamcinolone acetonide monthly Clobetasol propionate occlusion over the legs for 2-3 hours a day was applied and detected no side effects Because of fluid accumulation the use of compressive bandages provides additional benefit as in our patient used elastic bandage at night [4]
Pentoxifylline an analogue of the methylxanthine theobromine inhibits the proliferation of fibroblasts derived from normal human skin and from skin of patients with some fibrotic disorders In subconfluent fibroblast cultures pentoxifylline treatment caused a dose-dependent inhibition of serum-driven fibroblast proliferation and glycosaminoglycan synthesis [6] Its usage widely accepted in pretibial myxedema however the efficacy of the drug and the results of the follow-up were not stated clearly in the literature After 3 months of combined pentoxifylline and intralesional triamcinolone acetonide our patients lesions have receded and another 3 months follow-up period they have not recurred
Treatment of PTM is often difficult We suggest that the easiest and effective treatment of PTM may be achieved by combined pentoxifylline and intralesional triamcinolone acetonide
References
1 Schwartz KM Fatourechi V Ahmed DDF Pond GR Dermopathy of Graves disease (Pretibial Myxedema) Long term outcome J Clin Endocrinol Metab 2002 Feb87(2)438-46 PubMed
2 Truhan AP Pretibial myxedema Am Fam Physician 1985 May31(5)135-8 PubMed
3 Chung-Leddon J Pretibial Myxedema Dermatol Online J 2001 Feb7(1)18 PubMed
4 Fatourechi V Pretibial myxedema pathophysiology and treatment options Am J Clin Dermatol 20056(5)295-309 Review PubMed
5 Lang PG Sisson JC Lynch PJ Intralesional triamsinolone therapy for pretibial myxedema Arch Dermatol 1975 Feb111(2)197-202 PubMed
6 Chang CC Chang TC Kao SC Kuo YF Chien LF Pentoxyfilline inhibits the proliferation and glycosaminoglycan synthesis of cultured fibroblasts derived from patients with Graves ophthalmopaty and pretibial myxedema Acta Endocrinol (Copenh) 1993 Oct129(4)322-7 PubMed
--------------------------------------------------------------------------------------
Postepy Hig Med Dosw (Online) 200660184-91
[The metabolism of glycosaminoglycans in the course of Graves disease][Article in Polish]
Winsz-Szczotka K Komosińska-Vassev K Olczyk K
Zakład Chemii Klinicznej i Diagnostyki Laboratoryjnej Slaskiej Akademii Medycznej Sosnowiec winszslamkatowicepl
Glycosaminoglycans (GAGs) which include chondroitin sulfate (CS) dermatan sulfates (DS) heparan sulfate (HS) heparin (H) keratan sulfate (KS) and hyaluronic acid (HA) are a group of linear polyanionic heteropolysaccharides The GAGs chains except for those of hyaluronic acid are covalently attached to core proteins forming proteoglycans (PGs) PGsGAGs are present at the cellular level as elements of the cell membrane and intracellular granules They are also components of the ground substance of the extracellular matrix These macromolecules are involved in cell adhesion migration and proliferation Alterations in GAGs metabolism may influence the pathogenesis of many disorders including Graves disease Graves disease is an autoimmune thyroid pathology characterized by hyperthyroidism thyroid hyperplasia as well as ophthalmopathy andor pretibial myxedema The pathogenesis of these extrathyroidal manifestations involves fibroblast activation and increased glycosaminoglycan synthesis and accumulation Disturbances in GAGs metabolism in tissue are associated with qualitative and quantitative GAGs
alterations in Graves patients serum and urine Although the mechanisms leading to the development of orbital andor skin complications in the course of Graves disease have not been fully elucidated it is postulated that they depend on both immunological disturbances and the hyperthyroid state SUMMARY The alterations in GAGs metabolism connected with Graves disease could lead to systemic changes in the proprieties of the extracellular matrix
and 2) The lesions were neither warm nor tender to the touch Bilateral exophthalmous was noted He had bilateral clubbing and melanonychia striate at right and left hand fingernails Blood cell counts biochemistry chest radiography and thyroid function tests were normal
Clobetasol propionate occlusions for 2-3 hours a day and elastic bandage at nights were applied regularly Pentoxifylline 400 mg three times a day was started A total dose of 10 ml of intralesional triamcinolone acetonide (5 mgml) was injected monthly After 3 months his lesions receded and only a few slight indurated plaques remained (Fig 2)
Discussion
Pretibial myxedema can be present in either Graves disease or hypothyroidism Our patient whose lesions started on his shins and went on his pretibial area has Graves disease [3] Pretibial myxedema is an infiltrative dermopathy that most frequently appears symmetrically on the anterior tibia and dorsum of the feet The usual presentation is that of bilateral asymmetric raised firm plaque or nodules of a pink to purple-brown hue Hyperhidrosis and hypertrichosis may overlie the affected areas in rare cases Rarely the lesions may be painful or pruritic Our patient had erythematous not itching firm plaques and nodules There was no maceration and hypertrichosis but the appearance of his legs were as peau dorange and there was no pitting edema Ophthalmopathy always accompanies cutaneous findings usually appears first and dermopathy much later Thyroid acropachy is a triad consisting of digital clubbing soft tissue swelling of hands and feet and periosteal new bone formation [3 4] Our patients ophthalmic changes occurred before dermopathy and he had clubbing of his fingernails
The mechanism that causes myxedema is unclear although animal model studies suggest that thyroid hormones affect the synthesis and catabolism of mucopolysaccharides and collagen by dermal fibroblasts The fibroblast in the orbital area and pretibial dermis share antigenic sites that underlie the autoimmune process
Figure 3
Figure 3 Lesions had receded and only a few slight indurated plaques remained
that causes Graves disease Thereby cross reaction contributes to the development of myxedema occurring long after euthyroid status is achieved through treatment [3] Whatever the cause of the increased glycosaminoglycan (GAG) production accumulation of GAG leads to the characteristic skin lesions associated with thyroid dermopathy The hyaluronic acid expands the dermal tissue and causes fluid to accumulate It may also cause compression or occlusion of small local lymphatic and thereby increase the dermal edema [1]
Treatment starts with avoiding the risk factors as avoiding tobacco and reducing weight then normalization of thyroid functions [4] High potency topical corticosteroids with occlusion or not or intralesional corticosteroids are the best approach but the cure rate is low In a prospective study nine patients with pretibial myxedema were treated with intralesional injections of triamcinolone acetonide Complete resolution was obtained in seven of the nine patients For most patients the monthly injection of 8 ml or less of a solution containing 5 mgml of triamcinolone proved to be the most effective dosage schedule [5] We used 10 ml (5 mgml) of triamcinolone acetonide monthly Clobetasol propionate occlusion over the legs for 2-3 hours a day was applied and detected no side effects Because of fluid accumulation the use of compressive bandages provides additional benefit as in our patient used elastic bandage at night [4]
Pentoxifylline an analogue of the methylxanthine theobromine inhibits the proliferation of fibroblasts derived from normal human skin and from skin of patients with some fibrotic disorders In subconfluent fibroblast cultures pentoxifylline treatment caused a dose-dependent inhibition of serum-driven fibroblast proliferation and glycosaminoglycan synthesis [6] Its usage widely accepted in pretibial myxedema however the efficacy of the drug and the results of the follow-up were not stated clearly in the literature After 3 months of combined pentoxifylline and intralesional triamcinolone acetonide our patients lesions have receded and another 3 months follow-up period they have not recurred
Treatment of PTM is often difficult We suggest that the easiest and effective treatment of PTM may be achieved by combined pentoxifylline and intralesional triamcinolone acetonide
References
1 Schwartz KM Fatourechi V Ahmed DDF Pond GR Dermopathy of Graves disease (Pretibial Myxedema) Long term outcome J Clin Endocrinol Metab 2002 Feb87(2)438-46 PubMed
2 Truhan AP Pretibial myxedema Am Fam Physician 1985 May31(5)135-8 PubMed
3 Chung-Leddon J Pretibial Myxedema Dermatol Online J 2001 Feb7(1)18 PubMed
4 Fatourechi V Pretibial myxedema pathophysiology and treatment options Am J Clin Dermatol 20056(5)295-309 Review PubMed
5 Lang PG Sisson JC Lynch PJ Intralesional triamsinolone therapy for pretibial myxedema Arch Dermatol 1975 Feb111(2)197-202 PubMed
6 Chang CC Chang TC Kao SC Kuo YF Chien LF Pentoxyfilline inhibits the proliferation and glycosaminoglycan synthesis of cultured fibroblasts derived from patients with Graves ophthalmopaty and pretibial myxedema Acta Endocrinol (Copenh) 1993 Oct129(4)322-7 PubMed
--------------------------------------------------------------------------------------
Postepy Hig Med Dosw (Online) 200660184-91
[The metabolism of glycosaminoglycans in the course of Graves disease][Article in Polish]
Winsz-Szczotka K Komosińska-Vassev K Olczyk K
Zakład Chemii Klinicznej i Diagnostyki Laboratoryjnej Slaskiej Akademii Medycznej Sosnowiec winszslamkatowicepl
Glycosaminoglycans (GAGs) which include chondroitin sulfate (CS) dermatan sulfates (DS) heparan sulfate (HS) heparin (H) keratan sulfate (KS) and hyaluronic acid (HA) are a group of linear polyanionic heteropolysaccharides The GAGs chains except for those of hyaluronic acid are covalently attached to core proteins forming proteoglycans (PGs) PGsGAGs are present at the cellular level as elements of the cell membrane and intracellular granules They are also components of the ground substance of the extracellular matrix These macromolecules are involved in cell adhesion migration and proliferation Alterations in GAGs metabolism may influence the pathogenesis of many disorders including Graves disease Graves disease is an autoimmune thyroid pathology characterized by hyperthyroidism thyroid hyperplasia as well as ophthalmopathy andor pretibial myxedema The pathogenesis of these extrathyroidal manifestations involves fibroblast activation and increased glycosaminoglycan synthesis and accumulation Disturbances in GAGs metabolism in tissue are associated with qualitative and quantitative GAGs
alterations in Graves patients serum and urine Although the mechanisms leading to the development of orbital andor skin complications in the course of Graves disease have not been fully elucidated it is postulated that they depend on both immunological disturbances and the hyperthyroid state SUMMARY The alterations in GAGs metabolism connected with Graves disease could lead to systemic changes in the proprieties of the extracellular matrix
that causes Graves disease Thereby cross reaction contributes to the development of myxedema occurring long after euthyroid status is achieved through treatment [3] Whatever the cause of the increased glycosaminoglycan (GAG) production accumulation of GAG leads to the characteristic skin lesions associated with thyroid dermopathy The hyaluronic acid expands the dermal tissue and causes fluid to accumulate It may also cause compression or occlusion of small local lymphatic and thereby increase the dermal edema [1]
Treatment starts with avoiding the risk factors as avoiding tobacco and reducing weight then normalization of thyroid functions [4] High potency topical corticosteroids with occlusion or not or intralesional corticosteroids are the best approach but the cure rate is low In a prospective study nine patients with pretibial myxedema were treated with intralesional injections of triamcinolone acetonide Complete resolution was obtained in seven of the nine patients For most patients the monthly injection of 8 ml or less of a solution containing 5 mgml of triamcinolone proved to be the most effective dosage schedule [5] We used 10 ml (5 mgml) of triamcinolone acetonide monthly Clobetasol propionate occlusion over the legs for 2-3 hours a day was applied and detected no side effects Because of fluid accumulation the use of compressive bandages provides additional benefit as in our patient used elastic bandage at night [4]
Pentoxifylline an analogue of the methylxanthine theobromine inhibits the proliferation of fibroblasts derived from normal human skin and from skin of patients with some fibrotic disorders In subconfluent fibroblast cultures pentoxifylline treatment caused a dose-dependent inhibition of serum-driven fibroblast proliferation and glycosaminoglycan synthesis [6] Its usage widely accepted in pretibial myxedema however the efficacy of the drug and the results of the follow-up were not stated clearly in the literature After 3 months of combined pentoxifylline and intralesional triamcinolone acetonide our patients lesions have receded and another 3 months follow-up period they have not recurred
Treatment of PTM is often difficult We suggest that the easiest and effective treatment of PTM may be achieved by combined pentoxifylline and intralesional triamcinolone acetonide
References
1 Schwartz KM Fatourechi V Ahmed DDF Pond GR Dermopathy of Graves disease (Pretibial Myxedema) Long term outcome J Clin Endocrinol Metab 2002 Feb87(2)438-46 PubMed
2 Truhan AP Pretibial myxedema Am Fam Physician 1985 May31(5)135-8 PubMed
3 Chung-Leddon J Pretibial Myxedema Dermatol Online J 2001 Feb7(1)18 PubMed
4 Fatourechi V Pretibial myxedema pathophysiology and treatment options Am J Clin Dermatol 20056(5)295-309 Review PubMed
5 Lang PG Sisson JC Lynch PJ Intralesional triamsinolone therapy for pretibial myxedema Arch Dermatol 1975 Feb111(2)197-202 PubMed
6 Chang CC Chang TC Kao SC Kuo YF Chien LF Pentoxyfilline inhibits the proliferation and glycosaminoglycan synthesis of cultured fibroblasts derived from patients with Graves ophthalmopaty and pretibial myxedema Acta Endocrinol (Copenh) 1993 Oct129(4)322-7 PubMed
--------------------------------------------------------------------------------------
Postepy Hig Med Dosw (Online) 200660184-91
[The metabolism of glycosaminoglycans in the course of Graves disease][Article in Polish]
Winsz-Szczotka K Komosińska-Vassev K Olczyk K
Zakład Chemii Klinicznej i Diagnostyki Laboratoryjnej Slaskiej Akademii Medycznej Sosnowiec winszslamkatowicepl
Glycosaminoglycans (GAGs) which include chondroitin sulfate (CS) dermatan sulfates (DS) heparan sulfate (HS) heparin (H) keratan sulfate (KS) and hyaluronic acid (HA) are a group of linear polyanionic heteropolysaccharides The GAGs chains except for those of hyaluronic acid are covalently attached to core proteins forming proteoglycans (PGs) PGsGAGs are present at the cellular level as elements of the cell membrane and intracellular granules They are also components of the ground substance of the extracellular matrix These macromolecules are involved in cell adhesion migration and proliferation Alterations in GAGs metabolism may influence the pathogenesis of many disorders including Graves disease Graves disease is an autoimmune thyroid pathology characterized by hyperthyroidism thyroid hyperplasia as well as ophthalmopathy andor pretibial myxedema The pathogenesis of these extrathyroidal manifestations involves fibroblast activation and increased glycosaminoglycan synthesis and accumulation Disturbances in GAGs metabolism in tissue are associated with qualitative and quantitative GAGs
alterations in Graves patients serum and urine Although the mechanisms leading to the development of orbital andor skin complications in the course of Graves disease have not been fully elucidated it is postulated that they depend on both immunological disturbances and the hyperthyroid state SUMMARY The alterations in GAGs metabolism connected with Graves disease could lead to systemic changes in the proprieties of the extracellular matrix
2 Truhan AP Pretibial myxedema Am Fam Physician 1985 May31(5)135-8 PubMed
3 Chung-Leddon J Pretibial Myxedema Dermatol Online J 2001 Feb7(1)18 PubMed
4 Fatourechi V Pretibial myxedema pathophysiology and treatment options Am J Clin Dermatol 20056(5)295-309 Review PubMed
5 Lang PG Sisson JC Lynch PJ Intralesional triamsinolone therapy for pretibial myxedema Arch Dermatol 1975 Feb111(2)197-202 PubMed
6 Chang CC Chang TC Kao SC Kuo YF Chien LF Pentoxyfilline inhibits the proliferation and glycosaminoglycan synthesis of cultured fibroblasts derived from patients with Graves ophthalmopaty and pretibial myxedema Acta Endocrinol (Copenh) 1993 Oct129(4)322-7 PubMed
--------------------------------------------------------------------------------------
Postepy Hig Med Dosw (Online) 200660184-91
[The metabolism of glycosaminoglycans in the course of Graves disease][Article in Polish]
Winsz-Szczotka K Komosińska-Vassev K Olczyk K
Zakład Chemii Klinicznej i Diagnostyki Laboratoryjnej Slaskiej Akademii Medycznej Sosnowiec winszslamkatowicepl
Glycosaminoglycans (GAGs) which include chondroitin sulfate (CS) dermatan sulfates (DS) heparan sulfate (HS) heparin (H) keratan sulfate (KS) and hyaluronic acid (HA) are a group of linear polyanionic heteropolysaccharides The GAGs chains except for those of hyaluronic acid are covalently attached to core proteins forming proteoglycans (PGs) PGsGAGs are present at the cellular level as elements of the cell membrane and intracellular granules They are also components of the ground substance of the extracellular matrix These macromolecules are involved in cell adhesion migration and proliferation Alterations in GAGs metabolism may influence the pathogenesis of many disorders including Graves disease Graves disease is an autoimmune thyroid pathology characterized by hyperthyroidism thyroid hyperplasia as well as ophthalmopathy andor pretibial myxedema The pathogenesis of these extrathyroidal manifestations involves fibroblast activation and increased glycosaminoglycan synthesis and accumulation Disturbances in GAGs metabolism in tissue are associated with qualitative and quantitative GAGs
alterations in Graves patients serum and urine Although the mechanisms leading to the development of orbital andor skin complications in the course of Graves disease have not been fully elucidated it is postulated that they depend on both immunological disturbances and the hyperthyroid state SUMMARY The alterations in GAGs metabolism connected with Graves disease could lead to systemic changes in the proprieties of the extracellular matrix
alterations in Graves patients serum and urine Although the mechanisms leading to the development of orbital andor skin complications in the course of Graves disease have not been fully elucidated it is postulated that they depend on both immunological disturbances and the hyperthyroid state SUMMARY The alterations in GAGs metabolism connected with Graves disease could lead to systemic changes in the proprieties of the extracellular matrix
