My son was born with APLASIA CUTIS CONGENITA, and at one year of age why is it becoming red and scabby?

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For the first year of his life, the patch of hairless skin was the color of the rest of his skin, but at 1 year of age it is changing color to a pinkish-red. It is also feeling like a bump now. Why?
go to the Doctor. SOON!  (+ info)

Is anyone else naturally born with cutis anserina, better known as goose bumps on your skin? Is there a cure?

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I was born with goosebumps all along my arms and legs, and nothing online seemed to tell me why I'm born with them, it just said that goosebumps are a result of coldness/fright etc... Is anyone else born with goose bumps and is there a cure for them?
Well, I'm not so sure if I have what you have, but I think I might. I have a lot of teeny tiny bumps on my upper arms. Both me and my mom and my siblings and some relatives from my mom's side of the family have it. I remember that when I was little my mom would take us to the doctor because of it. I don't really remember what the doctor thought of the tiny bumps on our arms but I don't ever remember taking medication for it and my mom said that the doctor said that nothing was wrong. I personally don't mind the little bumps, so I don't know if there's a cure for them, sorry.  (+ info)

has anyone ever heard of a skin condition called aplasia cutis congenita?

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my son was born with a bald spot in the middle ofhis head and the doctors said thats what it is and they recommended plastic surgery but hes 3 and im afraid something bads going to happen? any advice?
Go for the surgery. Skin is a primary protection of the body. If bugs can penetrate it big problem. The secondary protection system comes to play (the immune system). Some of the bugs are can cause serious problem because they are not even supposed to end up in an area they are not supposed to. As with the head, it is more dangerous. I suggest that you go ahead with the plastic surgery. Decision is still yours. I am not coercing you in any way but advising.  (+ info)

what is the common name of the condition known by docters as cutis ansirin?

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a siries of books by r.l. stine
I think that you mean cutis anserina? Anyways, that's a series of horror books called "Goosebumps" by R.L. Stine. R.L.Stine's motto is "Reader beware--you're in for a scare!"  (+ info)

My son was born with a membranous aplasia cutis,?

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When he was born he had to be vaccumed out when he was born and the docters said it was from the vaccume, but it has a ring of hair around it. He just had his well child check yesterday and my grandma brought the thing in his head to the docters attention, and told us that it was membranous aplasia cutis, I now have to take my son to Portland on monday, and I do not know much about it, does anyone know anything about this?
Aplasia cutis congenita (ACC) is part of a heterogenous group of disorders first reported by Cordon in 1767 and is characterized by the absence of a portion of skin in a localized or widespread area at birth. It most commonly (70%) manifests as a solitary defect on the scalp, but sometimes it may occur as multiple lesions. The lesions are noninflammatory and well demarcated, and they range in size from 0.5-10 cm. ACC may be circular, oval, linear, or stellate in configuration. At birth, the lesions may have already healed with scarring or may remain superficially eroded to deeply ulcerated, occasionally involving the dura or the meninges.

Defects in the skin that form early in gestation may heal before delivery and appear as an atrophic, membranous, or parchmentlike scar with associated alopecia, whereas less mature defects present as ulcerations. Most lesions occur on the scalp vertex just lateral to the midline, but defects may also occur on the face, the trunk, or the limbs, sometimes symmetrically. The depth may involve only the epidermis and the upper dermis, resulting in minimal alopecic scarring, or the defect may extend to the deep dermis, the subcutaneous tissue, or rarely the periosteum, the skull, and the dura.

ACC is an uncommon anomaly of newborns. More than 500 cases have been reported since it was first described, but because of significant underreporting of this generally benign disorder, the precise frequency is unknown. One estimate of incidence is approximately 3 in 10,000 births.

Causes

No unifying theory can account for all lesions of ACC. Because this condition is the phenotypic result of more than one disease process, it is likely that more than one mechanism is involved. Mechanisms include genetic factors, teratogens (eg, methimazole, carbimazole, misoprostol, valproic acid), compromised vasculature to the skin, and trauma. Of particular note is the association of fetus papyraceous with bilaterally symmetric ACC.
The proximity of scalp ACC to the scalp hair whorl, which is thought to be the point of maximum tensile force during rapid brain growth, has led to the hypothesis that tension-induced disruption of the overlying skin occurs at 10-15 weeks of gestation when hair direction, patterning, and rapid brain growth occur.
Early rupture of the amniotic membranes, forming amniotic bands, has appeared to be the cause of ACC in several cases.
The bullous variant of ACC reveals a distinct histologic pattern identical to those in encephaloceles and meningoceles. This supports a hypothesis that this variant of aplasia cutis may represent the form fruste of a neural tube closure defect.  (+ info)

the eating disoder characterized by compusive overeating followed by self-induced vomiting and the use of laxa?

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a. malnutrition.
b. cirrhosis.
c. anorexia nervosa
d. bulimia
d. bulimia

.  (+ info)

I would like to hear from anyone who has knowledge of the rare skin disorder, osteoma cutis. And treatments.?

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Osteoma cutis is little bits of calcium deposits under the skin (mine is where I had acne when I was younger.) I had dermabrasion many years ago, but the condition recurred because of the time it took for healing...it forms in scar tissue.
Osteoma Cutis
Last Updated: February 15, 2005 Rate this Article
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Synonyms and related keywords: bone in the skin, Albright hereditary osteodystrophy, Albright's hereditary osteodystrophy, miliary osteomas

AUTHOR INFORMATION Section 1 of 9
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Author: Kevaghn P Fair, DO, Consulting Staff, Department of Pathology, Dominion Pathology Laboratories

Kevaghn P Fair, DO, is a member of the following medical societies: American Osteopathic Association, American Society of Clinical Pathologists, American Society of Dermatopathology, and College of American Pathologists

Editor(s): James W Patterson, MD, Director of Dermatopathology, Professor of Pathology and Dermatology, Departments of Pathology and Dermatology, University of Virginia Medical Center; David F Butler, MD, Professor, Texas A&M University College of Medicine; Director, Division of Dermatology, Scott and White Clinic; Rosalie Elenitsas, MD, Associate Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System; Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University; and William D James, MD, Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System

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INTRODUCTION Section 2 of 9
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Background: Strictly defined, osteoma cutis refers to the presence of bone within the skin in the absence of a preexisting or associated lesion, as opposed to secondary types of cutaneous ossification that occur by metaplastic reaction to inflammatory, traumatic, and neoplastic processes.


Pathophysiology: Bone arises in skin and soft tissues through mesenchymal (membranous) ossification without cartilage precursors or models (enchondral ossification, as in the skeletal system).

The lesions of osteoma cutis differ from tumoral calcinosis in that they represent bone formation, and calcinosis refers to calcium salt deposits.

In addition to colonic polyposis, epidermal cysts of the face and the scalp, and multiple fibromas, osteomatosis in the form of intraosseous (not cutaneous) osteomas may develop within the membranous bones of the head in Gardner syndrome.


Frequency:


In the US: Although said to be rare, with no well-defined data on the incidence, a plethora of conditions and syndromes may be found in association with osteoma cutis, and the frequency of its occurrence varies accordingly. Primary lesions with no underlying cause are even more rare, but they account for approximately 20% of all cases.
Mortality/Morbidity: Osteoma cutis is not life threatening, although local discomfort and/or disfigurement may lead the patient to seek consultation.

Race: No race is predisposed to develop osteoma cutis.

Sex: Generally, no distinct sexual predominance exists. However, one cause of osteoma cutis, Albright hereditary osteodystrophy, occurs with a female-to-male ratio of 2:1.

Age: Osteoma cutis may occur at any age.



CLINICAL Section 3 of 9
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History:

Patients may report having hard areas in the skin.
A familial occurrence of Albright hereditary osteodystrophy may be present.
Physical:

The presentations of osteoma cutis can be highly variable, with clinical entities that are defined by the number, the form, and the location of the lesions.
Osteomas may present as single or multiple, extremely hard nodules, plaques, or miliary tumors.
The face, the extremities, the scalp, the digits, and the subungual regions are the most commonly affected sites.
Causes: Osteoma cutis is a feature in several groups of patients.

Albright hereditary osteodystrophy, which includes most patients with pseudohypoparathyroidism and pseudopseudohypoparathyroidism, is due to an autosomal dominant defect in the alpha subunit of intracellular guanyl nucleotide-binding protein (G protein).
The characteristic phenotype includes short stature, a round face, defective teeth, mental retardation, brachydactyly, and osteomas of the soft tissue and the skin.
Tetany is often the presenting sign of pseudohypoparathyroidism, formerly called Albright hereditary osteodystrophy. In addition to skeletal system abnormalities, lesions of osteoma cutis are frequently observed.
Single, small osteomas, arising later in life, sometimes with transepidermal elimination of bony fragments may be a cause.
Multiple, miliary osteomas of the face, following acne, neurotic excoriation, or dermabrasion is a possible cause.
Congenital plaquelike osteomatosis or limited dermal ossification is generally present from birth; the skin of the scalp or the extremities is often affected.
Fibrodysplasia ossificans heteroplasia and fibrodysplasia ossificans progressiva are possible causes.
Miscellaneous rare disorders with or without cartilaginous elements include osteomas of the distal extremities and multiple osteomas of childhood unrelated to Albright hereditary osteodystrophy.
DIFFERENTIALS Section 4 of 9
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Calcinosis Cutis



Other Problems to be Considered:

Cartilaginous tumors of the skin
Foreign body
Gouty tophus
Myositis ossificans
Secondary (heterotopic) ossification

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WORKUP Section 5 of 9
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Lab Studies:


Serum calcium and parathyroid hormone (PTH) levels help to define Albright hereditary osteodystrophy.
Imaging Studies:


Plain radiographs demonstrate lesions but are not necessary for diagnosis.
Procedures:


Excisional biopsy for diagnosis, relief of discomfort, or cosmesis may be performed.
Histologic Findings: Small spicules to large masses of mature bone are found in the dermis or extend into the subcutaneous tissue. Spicules of bone may enclose areas of mature fat, recapitulating a medullary cavity, but hematopoietic elements are seldom observed (see Image 3).
TREATMENT Section 6 of 9
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Medical Care:

Removal by excision or laser resurfacing to unroof overlying skin may be performed. Treatment with the Er:YAG laser may result in less hypopigmentation and scarring than with the carbon dioxide laser.
Other reported treatments with unproven efficacy include the following:
Topical application of tretinoin to provoke transepidermal elimination
Etidronate disodium taken orally
Consultations: When several lesions are noted, especially in pediatric patients, evaluation for associated syndromes may be warranted. FOLLOW-UP Section 7 of 9
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Prognosis:


Osteosarcoma or other malignancies have not been reported to arise within osteoma cutis.
PICTURES Section 8 of 9
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Caption: Picture 1. Solitary nodule on the frontal part of the scalp.
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Caption: Picture 2. Miliary cutaneous osteomata. Multiple, small, bluish, stony-hard nodules in an acneiform distribution along the cheeks.
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Caption: Picture 3. A microscopic view of osteoma cutis shows well-formed mature trabecular bone just beneath the epidermis. Note the absence of hematopoietic elements in the medullary spaces.
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BIBLIOGRAPHY Section 9 of 9
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Altman JF, Nehal KS, Busam KJ, Halpern AC: Treatment of primary miliary osteoma cutis with incision, curettage, and primary closure. J Am Acad Dermatol 2001 Jan; 44(1): 96-9[Medline].
Burgdorf W, Nasemann T: Cutaneous osteomas: a clinical and histopathologic review. Arch Dermatol Res 1977 Dec 12; 260(2): 121-35[Medline].
Cohen AD, Chetov T, Cagnano E, et al: Treatment of multiple miliary osteoma cutis of the face with local application of tretinoin (all-trans-retinoic acid): a case report and review of the literature. J Dermatolog Treat 2001 Sep; 12(3): 171-3[Medline].
Ragsdale BD: Lever's Histopathology of the Skin. Philadelphia, Pa: Lippincott-Raven; 1997: 965-7.
Roth SI, Stowell RE, Helwig EB: Cutaneous ossification. Report of 120 cases and review of the literature. Arch Pathol 1963; 76(1): 44-54[Medline].
Watsky KL: In: Arndt KA, ed. Cutaneous Medicine and Surgery. Philadelphia, Pa: WB Saunders; 1996: 1828-31.
Weedon D, ed: Skin Pathology. 2nd ed. New York, NY: Churchill Livingstone; 2002: 355-7.  (+ info)

Cutis Anserina aka goosebumps?

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Is there any drugs that specifically cause Cutis Anserina, and is it harmful.

Please do not replay with Meth, Cocaine, or any illegal drugs I am speaking mostly medical. I thought Epinephrine injections do cause it, but I do not know if this is true...
Goose bumps are created when tiny muscles at the base of each hair, contract and pull the hair erect. It's a response to cold, mental/psychological influences such as fear or excitement or to an "adrenalin" flow. They're not harmful. What would be harmful is taking epinephrine injections for something that is not a medical condition and without the supervision & advise of a medical professional. If you've had an Epinephrine injection it is highly likely it may cause goosebumps, due to the adrenaline rush. It's not listed as a side effect, but as one article put it - it's best to consult your doctor, because sometimes not all side effects will be listed. Opiate withdrawal can also cause this condition. For example, a long time user of codeine for pain management and then stops medication. This may not answer all of your questions, but I hope it helps. Below are some informative links on Cutis Anserina and Epinephrine.  (+ info)

can anyone tell me about aplasia cutis?

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my baby was born with aplasia cutis and i am searching for a cure can u help??
  (+ info)

Ridges on Scalp (cutis verticis gyrata)?

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After years of trying to figure out whats going on with my head and the lines (ridges) causing my hair to look thinner,, I came across (cutis verticis gyrata) . This seems to be the answer to my scalp mystery. Are there and treatments for this,, or are there surgeries to correct it???Is a Dermatologist the specialized doctor to get a proper opinion for syndrome. I am quite sure that it is CVG
Rogaine for men  (+ info)

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