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AmazonSmile (smile.amazon.com) is a simple and automatic way for you to support the IPPF every time you shop, at no cost to you. When you shop at smile.amazon.com, you’ll find the exact same low prices, vast selection and convenient shopping experience as Amazon.com, with the added bonus that Amazon will donate a portion of the purchase price to the IPPF.  To shop at AmazonSmile simply go to smile.amazon.com from the web browser on your computer or mobile device. You may also want to add a bookmark to smile.amazon.com to make it even easier to return and start your shopping at AmazonSmile.

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It is suggested that some dermatological diseases due to their chronicity, impact on the body image, unlikelihood of complete recovery and frequent recurrences are one of the major predisposing factors towards depression. Therefore, we aimed to evaluate the rate and level of depression among pemphigus vulgaris and pemphigus foliaceus patients, two of the most common causes of hospitalization in dermatology units. This research was conducted on 55 patients with active pemphigus vulgaris and pemphigus foliaceus referring to pemphigus clinics or admitted

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as inpatients to the dermatology ward of Qaem and Imam Reza hospitals, Mashhad, Iran, from April 2008 to September 2009. The research tool was the Beck Depression Inventory. Collected data was analyzed by χ(2) -test Student’s t-test. Twenty-six (47.3%) patients were female and 29 (52.7%) were male. The mean age was 42.34 ± 18.98 years. The prevalence rate of clinical depression was 28% in pemphigus vulgaris and 20% in pemphigus foliaceus cases. Depression prevalence showed no significant difference between these two groups (P = 0.873). In conclusion, pemphigus patients are at risk for mild depression.

The Journal of dermatology

 

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Friday, April 25, 2014

3:00 pm Registration Opens
4:00 pm Welcome, Opening Remarks and Weekend Overview (Sahana Vyas and Will Zrnchik)
4:15 pm – 6:00 pm SESSION I – INTRODUCTION TO P/P
4:15 pm Pemphigus: Disease Classification & Clinical Features (Animesh Sinha)
4:45 pm The IPPF Registry and PV: What the Data Tells Us (Amit Shah)
5:00 pm Pemphigoid (Razzaque Ahmed)
5:30 pm Q&A (Ahmed, Sinha, Shah)
6:00 pm – 8:00 pm Welcome Reception sponsored by KabaFusion

Saturday, April 26, 2014

8:00 am Morning Beverage Service
8:00 am Registration Opens
8:30 am Opening Remarks (Sahana Vyas and Will Zrnchik)
8:35 am IPPF Awareness Campaign (Kate Frantz)
8:45 am Being a Citizen of the IPPF (Badri Rengarajan)
9:00 am – 10:30 am SESSION II – TREATMENT OPTIONS
9:00 am Treatment Options (Grant Anhalt)
9:30 am Personalized Treatment (Sergei Grando)
10:00 am Treatment Side Effects (Razzaque Ahmed)
10:30 pm Understanding IVIg (Mike Rigas)
10:50 am Break (coffee, tea, water, breads, etc)
11:00 am – 12:30 pm SESSION III – LIVING WITH P/P
11:00 am Building a Personal Support Network (Victoria Carlan)
11:20 am Awareness and You (Kate Frantz)
11:40 am Stress and Autoimmunity (Firdaus Dhabhar)
12:30 pm Afternoon Overview and Instructions (Sahana Vyas and Marc Yale)
12:30 pm Attendees on their own / Speaker Open Discussions
5:30 pm – 10:30 pm IPPF 20th Anniversary Gala Celebration
5:30 pm – 6:00 pm Cocktail Reception
6:00 pm – 7:00 pm Dinner
7:00 pm – 7:10 pm Congressman Danny Davis Keynote (Sahana Vyas)
7:10 pm – 7:15 pm Recognizing 20 Years (Grant Anhalt)
7:15 pm – 7:20 pm TBD
7:25 pm – 7:30 pm Founder’s Award Presentation (Zrnchik/Segall)
7:30 pm – 10:00 pm Casino Night and Live DJ
10:00 pm Chip Counts and Prize Selections
10:30 pm Evening Ends

Sunday, April 27, 2014

8:00 am Morning Beverage Service
8:00 am Welcome Back and Workshop How-To (Sahana Vyas and Marc Yale)
8:05 am Patient Panel Discussion (PHCs, invited patients)
8:35 am IPPF and You (Badri Rengarajan and Will Zrnchik)
9:00 am – 11:20 am SESSION IV – WORKSHOPS (snacks/beverages available)
Workshops running concurrently; attendees SELECT ONE WORKSHOP FOR EACH BLOCK Each workshop is 40 minutes with 10 minutes between. Formats may vary (10 minutes presentation, 30 minutes Q&A; 10 minutes presentation, 20 minutes practical application, 10 minutes Q&A; 20 minutes presentation, 20 minutes Q&A; Group Discussion)
9:00 am – 9:40 am Block I

  • Diet and Nutrition (Vicky Starr)
  • Reducing Stress through Meditation (Mei Ling Moore)
  • IVIg Insurance and Reimbursement Issues (KabaFusion)
  • Caregivers and Family (Scott Oling)
9:50 am – 10:30 am Block II

  • Diet and Nutrition (Vicky Starr)
  • Oral Care and Hygiene (Sandra Boody)
  • The Science of Pemphigus at the Cellular Level (Ani Sinha)
  • P/P Awareness Focus Group (Kate Frantz)
10:40 am – 11:20 am Block III

  • Pemphigus & Pemphigoid Below the Belt (Razzaque Ahmed)
  • Ocular Concerns and Care in P/P (Ali Djalilian)
  • Reducing Stress through Hypnotherapy (Janet Segall)
  • Insurance and Reimbursement Issues (Walgreens)
11:30 am – 12:45 pm SESSION V – Ask the Experts (Moderator: Sergei Grando)
11:30 am – 12:00 pm Q&A (presubmitted questions)
12:00 pm – 12:45 pm Q&A (open mic)
12:50 pm Closing Remarks

 

In February of 1995 I noticed some eruptions on my chest which I ignored. The week after I notice them, I went to a week-long school for the Air National Guard in Virginia. While at the school, the eruptions increased on my chest, as well as in my nose, mouth, and face. I was extremely frightened; I did not know what was happening to me. I thought of going to “Sick Call” but decided not to, since the school was only for one week and I wanted to finish it. When I flew home from attending the school, my family took a look at me and begged me to go to an Emergency Room immediately. Since I was very tired from the trip, I waited until the next day.

The next day I went to the Emergency Room of one of the local hospitals. The physician in the ER admitted that he really did not know what was wrong with me. My wife suggested that he call a dermatologist at a bigger hospital which he did. The dermatologist made an appointment for me for the following Monday.

On that Monday I went to the dermatologist who diagnosed me with a disease that I never had heard of–pemphigus. He told me it was a very serious disease, one that was rare and very expensive to treat. I did not know where to turn. I did not know of anyone who had this disease or of any organization who dealt with this malady. He prescribed a mild dose of steroids and sent me home. The eruptions on my skin (which I learned were called “lesions”) increased. Despite many visits to the dermatologist and increases in the medication, the condition worsened. The dermatologist that I was going to suggested that I go to either New York City or Boston for treatment since the doctors in those cities had more experience in treating this strange disease. I opted for New York City.

After visiting a dermatologist in New York City, I was admitted to New York University Medical Center for treatment in April of 1995. The dermatologist in New York City was very aggressive in treating my disease with high doses of steroids, along with other medications and blood treatments. After a week of the aggressive treatment, the spreading of my pemphigus condition stopped. After three weeks I was sent home to recover.

Slowly I was weaned off of my medications in order to determine what my “maintenance level” was. By May of 1996 I was completely off all medications and have not seen a reocrurrence of pemphigus.

What is cicatricial pemphigoid?

Cicatricial pemphigoid is an autoimmune disease that is characterised by blistering lesions on mucous membranes. It is also called benign mucous membrane pemphigoid or oral pemphigoid. Areas commonly involved are the oral mucosa (lining of the mouth) and conjunctiva (mucous membrane that coats the inner surface of the eyelids and the outer surface of the eye). Other areas that may be affected include the nostrils, oesophagus, trachea and genitals. Sometimes the skin may also be involved where blistering lesions can be found on the face, neck and scalp.

Brunsting Perry cicatricial pemphigoid is a rare variant in which localised crops of recurrent blisters arise within urticarial plaques, usually on the head and neck. The blisters may burst resulting in blood-crusted plaques and scars.

Who gets cicatricial pemphigoid?

Cicatricial pemphigoid is predominantly a disease of the elderly with a peak incidence at around 70 years. However, childhood cases have been reported. It appears to be twice as common in women than men.

What are the signs and symptoms of cicatricial pemphigoid?

Site Features
Eye
  • Sensation of grittiness or pain
  • Conjunctivitis
  • Lesions form, erode and heal to leave scar tissue
  • May lead to impaired vision or blindness
Mouth
  • Blisters form first on the gums near the teeth
  • Palate, tongue, lips, buccal mucosa, floor of the mouth and throat may be affected
  • Painful and make it difficult to eat
  • Lesions occurring in the throat (oesophagus, trachea and larynx) can become life-threatening
Skin
  • Blisters on the skin develop in 25-30% of patients
  • May be itchy
  • Bleeding may occur if traumatised
Nose
  • Nose bleeds after blowing the nose
  • Crusting causing discomfort
Genitals
  • Painful blisters and erosions on the clitoris, labia, shaft of the penis, perianal area

What causes cicatricial pemphigoid?

Cicatricial pemphigoid is an autoimmune blistering disease, which basically means that an individual’s immune systems starts reacting against his or her own tissue. In this particular instance autoantibodies react with proteins found in mucous membranes and skin tissue resulting in blistering lesions. The binding site appears to be within the anchoring filaments that help the epidermis (outside layer of skin) stick to the dermis (inner layer of skin).

Full article from DermNet NZ

http://www.dermnetnz.org/immune/cicatricial-pemphigoid.html

 

The relationship between bullous pemphigoid (BP) and neurological disease has been the subject of numerous recent studies and BP antigens and their isoforms have been identified in the central nervous system (CNS). Whilst epidemiological data support this association, little is known about the pathomechanism behind this link and the immunological characteristics of patients with BP and neurological disease, other than multiple sclerosis (MS), has not been studied. We aimed to compare the cutaneous immune response in BP patients with and without neurological disease, to investigate whether or not there is a distinctive immunopathological profile in patients with concomitant BP and neurological disease. Seventy-two patients with BP were included and divided into two groups; those with neurological disease (BP+N, n = 43) and those without (BP−N, n = 29).

Patients in BP+N group had a confirmed neurological disease by a hospital physician, neurologist or psychiatrist with positive neurological imaging where appropriate, or a Karnofsky score of 50 or less due to mental impairment. All sera were analysed with indirect immunofluorescence (IIF) using serial dilutions up to 1:120000, immunoblotting (IB) and Enzyme-linked immunosorbent assay (ELISA) for BP180 and BP230. Median antibody titres by IIF were 1:1600 vs. 1:800 for BP−N and BP+N, respectively, although the difference did not reach statistic significance (P = 0.93, Mann–Whitney U-test).

ELISA values for both BP180 and BP230 did not differ significantly between the two groups. Similarly, autoantibodies to specific antigens as identified by ELISA and IB were not related to the presence of neurological disease. The results of this study indicate that patients with BP and neurological disease exhibit an immune response to both BP180 and BP230, thus the link between the CNS and the skin is not dependent on a specific antigen, but possibly both antigens or their isoforms may be exposed following a neurological insult, and play a role in generation of an immune response. 

Science Alerts Social Network

The oral cavity can be affected by a wide variety of disorders characterized by inflammation of the gingiva and/or oral mucosa. In dogs and cats, differential diagnoses for generalized oral inflammatory disorders include plaque-reactive mucositis, chronic gingivostomatitis, eosinophilic granuloma complex, pemphigus and pemphigoid disorders, erythema multiforme, and systemic lupus erythematosus. In addition, endodontic or periodontal abscesses, infectious conditions, reactive lesions, and neoplastic conditions may initially present with localized or generalized inflammation of the oral mucosa. Determination of the underlying cause of an oral inflammatory condition relies on a thorough history, complete physical and oral examination, and incisional biopsy and histopathologic examination of lesions.

Article: http://www.vetsmall.theclinics.com/article/S0195-5616(13)00009-0/abstract

Pictures: http://www.sciencedirect.com/science/article/pii/S0195561613000090

Background: Pemphigus vulgaris was almost fatal before the advent of glucocorticoids. Unfortunately, the high doses and prolonged administration of glucocorticoids, which often needed to control the disease, result in numerous adverse effects many of which are serious.

Aims: To evaluate the patients with pemphigus vulgaris on treatment in respect of osteoporosis and to compare the frequency of osteoporosis in these patients with the healthy ones.

Methods: The study consisted of 40 patients with pemphigus vulgaris and 34 healthy controls. Bone mineral density measurements were obtained by dual- energy X-ray absorptiometry. Blood serum, bone parameters, and biochemical hormonal measurements were examined in both groups.

Results: When the bone mineral density values of patients with pemphigus vulgaris were compared with those of the control group, there was no significant difference between hip bone mineral density values, while lumbar region T and Z scores were found significantly low in the patient group (p = 0.034 and p = 0.006, respectively). Osteoporosis, osteopenia, and normal dual-energy X-ray absorptiometry rates in the patient group were found to be 32.5%, 32.5%, and 35%, respectively. These rates were found to be 18%, 23%, and 59% in control group, respectively. There were more fractures in the patient group and the difference was statistically significant (p = 0.004). 

Conclusion: An increase in osteoporosis frequency and secondary fracture to osteoporosis in the patients with pemphigus vulgaris was detected.

Full acticle can be viewed at: Indian Journal of Dermatology

IMPORTANCE A rare variant of mucous membrane pemphigoid (MMP) is characterized by circulating anti-laminin 332 (Lam332) autoantibodies and seems to be associated with concurrent malignant neoplasms.

OBJECTIVE To determine the prevalence and clinical significance of anti-Lam332 autoantibody detection from a large series of patients with MMP. DESIGN Multicenter retrospective study.

SETTING Four French national centers for autoimmune bullous diseases.

PARTICIPANTS One hundred fifty-four patients with MMP and 89 individuals serving as controls were included.

INTERVENTIONS Serum samples were analyzed by a new Lam332 enzyme-linked immunosorbent assay (ELISA); clinical and immunopathologic data were obtained from the patients’ medical records.

MAIN OUTCOME MEASURES The Lam332 ELISA scores were evaluated with respect to clinical characteristics, standard and salt-split indirect immunofluorescence, and bullous pemphigoid (BP) 230 and BP180-NC16A ELISAs.

RESULTS The Lam332 ELISA score was positive (≥9 U/mL) in 20.1% of serum samples from patients with MMP, 1 of 50 patients with bullous pemphigoid (BP), none of 7 with pemphigus, and 3 of 32 other controls. No relationship was evidenced between a positive ELISA Lam332 score and age; sex ratio; oral, ocular, genital, skin, or esophageal/laryngeal involvement; internal malignant neoplasm; or BP180 ELISA score. Salt-split skin indirect immunofluorescence and ELISA BP230 results were more frequently positive when Lam332 ELISA results were positive (P = .04 and .02, respectively). Patients with a positive Lam332 ELISA score frequently had more severe MMP (67.8% vs 47.2%; P = .04).

CONCLUSIONS AND RELEVANCE Results of this novel ELISA showed that serum anti-Lam332 autoantibodies are detected in 20.1% of patients with MMP. Anti-Lam332 autoantibodies are mainly detected in patients with severe MMP but not preferentially in those with a malignant neoplasm. The association between anti-Lam332 and anti-BP230 autoantibodies might arise from an epitope-spreading phenomenon.

JAMA dermatology (Chicago, Ill.)