Well, I went to the rheumatologist/dermatologist in Philly again today and I got the results of my skin biopsy back. Just in case you don't read the ENTIRE POST TODAY AS IT IS QUITE LENGTHY, the next step that the doctor has scheduled is for me to take part in their next conference in 2 weeks. I will basically be the discussion piece where doctors from all over attend, they will ask me questions, look at my rash, discuss my history, with the hope that with all of their medical brains and research being in one arena, someone will be able to diagnose this 6 year mystery.
I am going to share in detail what she said to me BUT JUST KNOW THAT IN SPITE OF THE COULD BE'S OR NOT, I STILL TRUST GOD!
So the biopsy report says the following verbatim,
"DIAGNOSIS Leg, left: SUPERFICIAL AND DEEP LYMPHOCYTIC INFILTRATE, SEE NOTE...
Microscopic Description:
Leg, left - Multiple initial and deeper levels have been cut and examined on this punch biopsy specimen. The epidermis shows basal layer pigmentation and focal areas of parakeratosis. In the dermis, there is a superficial and deep perivascular inflammatory infiltrate composed predominately of lymphocytes. Rare eosinophils are noted. The dermis demonstrates slightly increased mucin deposition, which is highlighted with colloidal iron staining. A PAS stain is performed, does not demonstrate fungal organisms, and does not show thickening of the basement membrane. Overall, the histologic findings are those of a superficial and deep perivascular lymphocytic infiltrate, which are features suggestive of a gyrate erythema. Erythema chronica migrans and tumid lupus erythematosus are also considered in the histologic differential diagnosis. Clinical correlation is recommended. This case has been reviewed at the Dermatopathology Consensus Conference.
SPECIMEN
Leg, left (Skin) : Punch
Clinical Diagnosis: ANNULAR ERYTHEMA
Clinical Description: Pt with probable sjrogens and annula erythema
Gross Description: Received in a formalin-containing bottle is a cylindrical piece of skin and adipose
tissue measuring 0.3 by 0.3 by 0.3 cm. The specimen is bisected and submitted
entirely in a single cassette. Due to shrinkage, measurements may be different than
those at time of procedure.
So what does this all mean? According to the doctor, it could be "tumid lupus erythematosus", which is a form of Lupus. My rashes aren't typical of a Lupus rash, but the arthritis and joint pain that I experience in conjunction with these rashes could support this diagnosis. Consequently, the description of this diagnosis has EXACT wording that was noted in my biopsy results. I am attaching information about this diagnosis from the following website, http://www.ncbi.nlm.nih.gov/pubmed/11926344 below.
Tumid lupus erythematosus.
Source
Department of Dermato ogy, Baylor College of Medicine, Houston, Texas 77030, USA.
Abstract
Tumid lupus erythematosus (TLE) is a variant of cutaneous lupus erythematosus. Most patients who present with these skin lesions are young women. The condition clinically resembles polymorphous light eruption, systemic lupus erythematosus (SLE), reticulated erythematous mucinosis, or gyrate erythema. Histopathologically, the lesions resemble classic lupus erythematosus because of their superficial and deep lymphohistiocytic inflammatory infiltrates and dermal mucin. However, unlike classic lupus erythematosus, there is little or no epidermal or dermo-epidermal involvement. Antinuclear antibody test results are usually negative. We describe 4 cases of TLE and discuss the differential diagnosis.
She also said that it could be "Erythema Chronica Migrans", which according to the following website http://dermis.multimedica.de/dermisroot/en/14922/diagnose.htm is described as the following, which I've pasted below...coincidentally ALL of my bloodword for Lyme disease has ALWAYS come back NEGATIVE. So the doctor has ruled this out but my rashes have typically taken on the form of a Lyme rash, and I've had similar symptoms to that of Lyme disease.
Erythema Chronicum Migrans
definition
A deep type of gyrate erythema that follows a bite by an ixodid tick; it is a stage-1 manifestation of LYME DISEASE. The site of the bite is characterized by a red papule that expands peripherally as a nonscaling, palpable band that clears centrally. This condition is often associated with systemic symptoms such as chills, fever, headache, malaise, nausea, vomiting, fatigue, backache, and stiff neck.
synonyms
Erythema Chronicum Migrans
UMLS
ECM - Erythema chronic migrans, ECM - Erythema chronicum migrans, Erythema chronica migrans, Erythema Chronicum Migrans, Erythema, chronicum migrans, Erythema, migrans, chronicum
images
9 images found for this diagnose
Gyrate Erythema is also associated with Lyme Disease and has the following information according to the following website http://www.ncbi.nlm.nih.gov/pubmed/3912086
Gyrate erythema.
Abstract
The gyrate erythemas consist of a nonspecific group (often called erythema annulare centrifugum) for which the cause is usually unknown, and three specific types (erythema marginatum rheumaticum, erythema chronicum migrans [Lyme disease], and erythema gyratum repens). The first specific type, erythema marginatum rheumaticum, has become extremely rare with the decline of its associated disease, rheumatic fever. The second specific type, erythema chronicum migrans, is caused by a spirochete transmitted by the I. ricinus complex of ticks. The third specific type, erythema gyratum repens, is uncommon, morphologically distinctive, and an indicator of serious disease, usually internal malignancy, in almost every instance.
I also looked up Superficial and Deep Lymphocytic Infiltrate and this is what I've discovered. This is what I found when I looked up Superficial and Deep Perivascular Dermatitis from the following website http://www.expertconsultbook.com/expertconsult/ob/book.do?method=display&type=bookPage&decorator=none&eid=4-u1.0-B978-1-4160-4580-9..00002-2--sc0070&isbn=978-1-4160-4580-9.
Superficial and Deep Perivascular Dermatitis
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According to the following website http://dermatology.cdlib.org/127/unknowns/infiltrate/rai.html Lymphocytic Infiltrate has the following history and information.
Lymphocytic infiltrate of Jessner
Department of Skin and STD, KMC Manipal. vandanamht@yahoo.com |
Clinical synopsis
A 58-year-old man presented with asymptomatic erythematous nodules and plaques on the trunk of 9-months duration. Lesions were few at onset but gradually progressed to involve the entire back, upper extremities, and the ears. There was no history of photosensitivity, sensory or motor deficit, or neuritis. There was no history of spontaneous resolution of the lesions. Cutaneous examination revealed multiple erythematous deeply infiltrated nodules and plaques on the back and upper arms. Their surface was smooth and shiny with no evidence of scaling, follicular plugging or scarring. There was nodular infiltration of the ear lobes bilaterally. All routine biochemical and hematological investigations were within normal limits. Slit-skin smear for acid fast bacilli was negative. Biopsy from a plaque revealed normal epidermis with well demarcated dense perivascular infiltrate and periadnexal infiltrate in the reticular dermis composed of mature lymphocytes.
Discussion
Benign lymphocytic infiltration of skin (LIS) was first described by Jessner and Kanof in 1953 [1]. Clinically it presents with asymptomatic reddish brown nodules and plaques that may show a central clearing producing a circinate arrangement. The lesions occur most commonly on the face, although the neck and back may be involved [2]. There is a marked male preponderance with the M : F ratio of 3 : 1; however, in female patients lesions tend to occur at a younger age than males. The lesions follow an indolent course lasting for weeks or months before resolving and in many cases subsequently recurring. It has been also reported in children [3]. Little is known about the pathogenesis of LIS except that it is characterized as a T-cell disorder [4]. Patients with LIS report their onset during the summer, and this, along with classic distribution over the sun-exposed areas, led to the hypothesis that LIS is a photosensitive disorder and that intense UV light can provoke LIS [5].
Histologically a moderately dense superficial and deep perivascular lymphocytic infiltrate is seen often with mucin between collagen bundles in the reticular dermis. Epidermal changes are lacking and the lymphoid cells are shown to be T lymphocytes by enzyme, histochemical, and immunohistochemical studies [6].
Discoid lupus erythematosus (DLE), polymorphous light eruption (PLE), and lymphoma have to be considered in the differential diagnosis. Of these, DLE may be particularly difficult to differentiate from LIS. In fact, some authors believe that Jessner lymphocytic infiltrate represents a non-scarring from of DLE based on a similar histological picture, occasional photosensitivity, and response to antimalarial agents. For our patient, clinically there was no scarring or atrophy, and histologically hyperkeratosis and follicular plugging were absent, for that reason DLE was excluded. Based on the differences between the numbers of OKT 6+ Langerhans cells, HLA DR T cells, Leu 8 cells, and NK cells, monoclonal antibody studies may be of additional help in making a diagnosis. Similarly, testing the basement membrane for direct immunofluorescence would be helpful. These were not done in our patient because of financial constraints.
Differentiating LIS from PLE is often a more difficult problem. Both can share the same clinical and histological features, although early lesions of PLE usually show papillary dermal edema that is not seen in LIS. The patients history is important in the differentiation, however it may be complicated further by the fact that LIS can also be exaggerated after sun exposure. In such cases, presence of active lesions on covered skin areas along with provocative phototesting are useful clues to help make a diagnosis.
Transition of LIS into malignant lymphoma has been reported. Using monoclonal antibodies to differentiate between LIS and lymphoma is possible [7].
Topical and intralesional steroids are used often as first line treatment and can be helpful. A range of systemic preparations have been tried particularly antimalarials, thalidomide [8], and etretinate [9]. Our patient was treated with dapsone (100mg daily) with complete subsidence of lesions at the end of 2 weeks.
References1. Jessner M, Kanof NB. Lymphocytic infiltration of the skin. Arch Dermatol 1953;68:447-449.2. Blaylock WK. Lymphocytic infiltration of the skin (Jessner and Kanof), in Demies DJ, McGuire J (eds) : Clinical Dermatology. New York, Harper & Row Publishers Inc, 1984 ; pg 1-3. 3. CR Higgins, Wakeel RAP, Cerio R. Childhood Jessner's lymphocytic infiltrate of the skin. Br J Dermatol 1994 ; 131 : 99-101. 4. Willemze R, Dijkstra A, Meijer CJLM. Lymphocytic infiltration of the skin (Jessner) : a T cell lymphoproliferative disease. Br J Dermatol 1984 ; 110 : 523-9. 5. Weber F, Schmutt M, Fritsch P, Sipp N. Lymphocytic infiltration of the skin is photosensitive variant of lupus erythematous : evidence by phototesting. Br J Dermatol 2001 ; 144 : 292-296. 6. Viljaranta S, Ranki A, Karimenii A, Nieminen P, Johansson L. Distribution of natural killer cells and lymphocyte subclasses in Jessner's lymphocytic infiltration of the skin and in cutaneous lesions of discoid and systemic lupus erythematosus. Br J Dermatol 1987;116:831-838. 7. Lange Wantzin G, Petri J, Nielsen M, Thomsen K. Benign lymphocytomas ; clinical and histologic aspects. In : Goos M, Christophers E, eds. Lymphoproliferative diseases of the skin. Berlin, West Germany ; Springer - Verlag ; 1982 : 212-214. 8. Moulin G, Bonnet F, Barrut D, Franc MP. Traitement de la maladie de Jessner et Kanof par la thalidomide. Ann Dermatol Venreol 1983 ; 110 : 611-14. 9. Morgan J, Adames J. Satisfactory resolution of Jessner's lymphocytic infiltrate of the skin following treatment with etretinate. Br J Dermatol 1990;122 : 570.
© 2006 Dermatology Online Journal
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Last but certainly not least, I also looked up the following information from the website http://dermnetnz.mobify.me/reactions/annular-erythema.html, which gives information about chronic annular (ring-shaped) and erythematous (red) skin eruptions, which is what all of my past skin biopsies stated. I am pasting the information from this site as well.
Erythema annulare centrifugum
This covers a number of chronic annular (ring-shaped) and erythematous (red) skin eruptions. A large number of other descriptive terms have been used to classify these types of lesions, some of which include figurate erythema, annular erythema, erythema perstans, erythema gyratum perstans, erythema gyratum repens and erythema figuratum perstans.
 |  |  Erythema gyratum repens (due to gastric carcinoma) |
What are the signs and symptoms?
Eruptions may occur at any time throughout life, from infancy to old age. The eruption usually begins as small raised pink-red spot that slowly enlarges and forms a ring shape while the central area flattens and clears. There may be an inner rim of scale. The rings enlarge at a rate of about 2-5 mm/day until they reach a diameter of about 6-8 cm. Sometimes the lesions do not form complete rings but grow into irregular shapes. One or several lesions may be present.
Lesions most often appear on the thighs and legs, but may occur on the face, trunk and arms. They are usually without symptoms but in some patients may cause mild itching.
What causes erythema annulare centrifugum?
Often no specific cause for the eruptions is found. However, it has been noted that erythema annulare centrifugum is sometimes linked to underlying diseases and conditions. These include:
- Bacterial, fungal and viral infections such as tuberculosis, sinusitis, candidiasis or tinea
- Drugs including chloroquine and hydroxychloroquine, oestrogen, penicillin and amitriptyline
- Cancer (especially the type known as erythema gyratum perstans, in which there are concentric and whirling rings)
- Food, most often blue cheese or tomatoes
- Recurrent or chronic appendicitis
- Cholestatic liver disease (blocked bile system)
- Graves disease (overactive thyroid gland)
In these situations, erythema annulare centrifugum resolves once the underlying cause is treated or the offending drug is stopped.
What is the treatment of erythema annulare centrifugum?
Erythema annulare centrifugum usually clears up by itself. Eruptions may be last from anywhere between a few weeks to many years (the average duration is 11 months). Most cases require no treatment, however topical corticosteroids may be helpful in reducing redness, swelling and itchiness.
Related information
References:
Book: Textbook of Dermatology. Ed Rook A, Wilkinson DS, Ebling FJB, Champion RH, Burton JL. Fourth edition. Blackwell Scientific Publications.
On DermNet NZ:
Other websites:
- Erythema Annulare Centrifugum – from Medscape Reference
Books:
See the DermNet NZ bookstore
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If you have any concerns with your skin or its treatment, see a dermatologist for advice.
If you have any concerns with your skin or its treatment, see a dermatologist for advice.
So many "could be's". But, God is able in all things!!! Stay encouraged sis. Healing comes from above, down, inside, out :)
ReplyDeleteP.S. Had our chiropractic consultation the other day and oh what I am learning!!! We are definitely fearfully and WONDERFULLY made. We go back on Tuesday for our care plan and 1st spinal adjustments. Will keep u posted.
Hey sis, yes He is!
DeleteYes, please let me know how the chiropractor goes.