Category Archives: Treatment and Medication

Time for the Infusion

As the treatment drew near, I had a lot of questions for Dr. Williams. She felt an oncologist was better equipped to answer them, so she scheduled a consult with one. That was a great move. The oncologist answered all my questions. He said prescribing and administering Rituxamab is an everyday occurrence for the infusion room. He said they give this treatment to leukemia and lymphoma patients who are in very poor health. Since I was in relatively good health, his concerns of complications for me were minimal. That was reassuring.

I had to do a lot of lab tests, which is common for intravenous treatments affecting the immune system. I was tested for several types of hepatitis, HIV, TB, and other infectious ailments. You can see from my “before” picture how bad my skin was.

I was treated using the Rheumatoid Arthritis Protocol (1,000 mg intravenously on days 1 and 15). My first dose was administered on June 17, 2014 and lasted 6 hours; the second on July 1, 2014, lasted 4 hours. I was relieved that other than a little jitteriness caused by a steroid drip, I had absolutely no side effects or reactions. It literally felt like I was getting a routine saline solution infusion.

Jack Sherman 4 Jack Sherman 3

When I went in for my second infusion, there was no change in my disease activity. I didn’t expect to see any changes for at least a month. To my surprise, as you can see by this photograph comparison, I was seeing signs of improvement a week after my second infusion! I was still taking 250 milligrams of azathioprine and 25 milligrams of prednisone every other day.

Jack Sherman 6 Jack Sherman 5

Stay tuned for next week’s conclusion of Jack Sherman’s Road to Rituximab Story…

Part One
Part Three

Background  Hailey-Hailey disease (HHD) or familial benign chronic pemphigus is a rare autosomal dominant inherited skin disorder, characterized by flaccid vesicles and erosions on the intertriginous areas. Current treatments are not particularly effective. We report 6 cases dramatically improving with doxycycline.

Case reports  6 patients, aged from 33 to 77 years old, presented with a variable 4 to 40 year history of severe treatment-resistant HHD. All 6 patients were then treated successfully with doxycycline 100 mg per day for at least 3 months.

Discussion  An improvement was observed in all 6 patients from 1 week to 3 months after the beginning of treatment. Relapses were observed after various periods. Maintenance half-dose therapy seemed to be beneficial in patients experiencing recurrence. Only one patient developed gastro-intestinal intolerance. No other side effects were reported. Currently, 2 patients have improved and present a decreased number of exacerbations, 2 others are in complete remission after more than 5 years of follow-up. Treatment efficiency is difficult to evaluate in HHD as it is a rare condition. No controlled studies have been published. Local treatments may improve inflammation but do not treat the underlying cause, targeted systemic therapies exist but there is little evidence supporting their use, physical treatments are cumbersome. Besides their antibiotic potential, tetracycline antibiotics also have anti-inflammatory properties and anticollagenase activity via inhibition of matrix metalloproteinases.

Conclusions  Doxycycline appears to be an interesting therapeutic option in Hailey-Hailey disease.

Full article available at:;jsessionid=8314ECF44FF542D304546752C44E6B24.d02t03

Inflammation is a key component of immune responses to infection, but when uncontrolled can lead to autoimmune diseases like Crohn’s disease, rheumatoid arthritis, type I diabetes, ankylosing spondylitis, lupus, psoriasis and multiple sclerosis. In these diseases inflammation is mediated by molecules of the immune system called cytokines and cells that respond to these cytokines called T cells. Autophagy is an ubiquitous process whereby cells degrade their own internal components, either to release valuable nutrients in times of starvation, or to remove damaged or noxious intracellular components. The work by Dr Harris and colleagues showed that autophagy also control release of the inflammatory cytokines and cells that have been implicated in the pathology of autoimmune diseases. The findings suggest that autophagy represents a potent target for new anti-inflammatory therapies, which could be beneficial in a range of autoimmune disorders. The group, in combination with Professor Kingston Mills, now hopes to apply these findings to specific models of autoimmune disease. The work is funded by Science Foundation Ireland as part of a Strategic Research Cluster (SRC) award based in The Trinity Biomedical Sciences Institute. “Autophagy is a common cellular process that is important for the maintenance of normal cell functions. Our work has shown that this process is important in the control of inflammation and, as such, could represent a particularly efficacious target for new drugs against inflammatory conditions. There are over 80 different autoimmune diseases, most of which are chronic and debilitating and can be difficult and expensive to treat. Any research which helps us to better understand the underlying mechanisms behind the control of inflammation will ultimately lead to better treatments,” explained Dr James Harris.

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A new study in mice where researchers replicated a rare type of immune cell in the lab and then infused it back into the body, is raising hope for a new treatment for severe autoimmune diseases such as multiple sclerosis and rheumatoid arthritis.

The researchers, from Duke University Medical Center in the US, write about their work on a type of B cell, in a paper that was published online in Nature at the weekend.

B Cells

B cells are immune cells that create antibodies to attack unwanted pathogens like bacteria and viruses.

The type that the researchers on this study focused on are known as regulatory B cells or B10, after interleukin-10 (IL-10), a cell-signalling protein that the cells use.

B10 cells help control immune response and limit autoimmunity, which is where the immune system attacks the body’s own healthy tissue as if it were an unwanted pathogen.

Although there aren’t many of them, B10 cells play a key role in controlling inflammation: they limit normal immune response during inflammation, thus averting damage to healthy tissue.

Regulating Immune Response Is a Highly Controlled Process

Study author Thomas F. Tedder is a professor of immunology at Duke. He says in a statement that we are only just beginning to understand these recently discovered B10 cells.

He says these regulatory B cells are important because they “make sure an immune response doesn’t get carried away, resulting in autoimmunity or pathology”.

“This study shows for the first time that there is a highly controlled process that determines when and where these cells produce IL-10,” he adds.

What they Did

For their study, Tedder and colleagues used mice to study how B10 cells produce IL-10. For IL-10 production to start, the B10 cells have to interact with T cells, which are involved in switching on the immune system.

They found B10 cells only react to certain antigens. They found that binding to these antigens makes the B10 cells turn off some of the T cells (when they come across the same antigen). This stops the immune system from harming healthy tissue.

This was a new insight into the function of B10 cells that spurred the researchers to see if they could take this further: what if it were possible to use this cellular control mechanism to regulate immune responses, particularly in respect of autoimmunity?

Replicating Large Numbers Outside the Body

B10 cells however are not common, they are extremely rare. So Tedder and colleagues had to find a way to make a ready supply of them outside the body.

They found a way to isolate the B10 cells without damaging their ability to control the immune responses. And they found a way to replicate them in large numbers, as Tedder explains:

“Normal B cells usually die quickly when cultured, but we have learned how to expand their numbers by about 25,000-fold.”

“However, the rare B10 cells in the cultures expand their numbers by four-million-fold, which is remarkable. Now, we can take the B10 cells from one mouse and increase them in culture over nine days to where we can effectively treat 8,000 mice with autoimmune disease,” he adds.

Influencing Autoimmunity

The next stage was to try out the new B10 cells: could they influence autoimmunity sufficiently to affect disease symptoms?

They found when they introduced a small number of B10 cells into mice bred to have a disease similar to multiple sclerosis, their symptoms lessened significantly.

“B10 cells will only shut off what they are programmed to shut off,” explains Tedder.

If you have rheumatoid arthritis, you would want cells that would only go after your rheumatoid arthritis,” he adds.


He and his colleagues suggest their work shows there is potential to remove regulatory cells, replicate them in their millions, and put them back in the body of a person with an autoimmune disease and it will effectively “shut down the disease”, as Tedder describes it:

“This may also treat transplanted organ rejection,” he adds.

The researchers call for more studies to learn how to replicate human B10 cells, and find out how they behave in humans.

Autoimmune diseases are complex, so making a single therapy that targets several diseases without causing immunosuppression is not easy, Tedder explains.

“Here, we’re hoping to take what Mother Nature has already created, improve on it by expanding the cells outside of the body, and then put them back in to let Mother Nature go back to work,” he says.

Grants from the National Institutes of Health, the Lymphoma Research Foundation, and the Division of Intramural Research, National Heart, Lung, and Blood Institute, NIH, helped pay for the study.

Article from:

Written by Catharine Paddock PhD
Copyright: Medical News Today

Background -  Glucocorticoids as sole therapy for pemphigus foliaceus (PF) in cats are not always successful, and it is common to need additional immunomodulating agents to manage the disease. Hypothesis/Objectives -  This retrospective study evaluated the use of modified ciclosporin as an adjuvant or sole immunomodulating drug in cats with PF and compared their response to PF cats managed with chlorambucil. Animals -  Fifteen client-owned cats diagnosed with PF that received ciclosporin and/or chlorambucil as part of their treatment and had adequate follow-up to assess treatment response were evaluated. Methods -  Records were reviewed from feline PF patients presented between the years of 1999 and 2009. Cats were divided into two treatment groups: those treated with ciclosporin and those treated with chlorambucil. Most cats in both groups also received concurrent systemic glucocorticoids. Each group contained six patients. Three cats were treated with both medications and are discussed separately. Time to disease remission, remission-inducing glucocorticoid dose, maintenance or final glucocorticoid dose, disease response and adverse effects were assessed. Results -  There was no significant difference in remission times or disease response between groups. All six patients maintained with ciclosporin for PF management were weaned off systemic glucocorticoids, while glucocorticoid therapy was stopped in only one of the six cats receiving chlorambucil. Conclusions and clinical importance -  Modified ciclosporin is effective in the management of feline pemphigus foliaceus and is glucocorticoid sparing. PMID: 22731616 [PubMed – as supplied by publisher] (Source: Veterinary Dermatology)

Managing Side Effects

Radiation therapy

Skin problems: Try not to scratch or rub the treated skin


Nausea and vomiting: Have small meals or snacks throughout the day instead of 2 or 3 large meals

RITUXAN (a targeted therapy)

Fever, chills, and shaking: The doctor may give you certain medicines before infusions to help reduce side effects. For example, it is common for you to be given acetaminophen (Tylenol®) and diphenhydramine HCI (Benadryl®) before the RITUXAN to reduce side effects

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Jennifer E. Thorne, MD, PhD(1,2)
Fasika A. Woreta, MD, MPH(1)
Douglas A. Jabs, MD, MBA(1,2,3)
Grant J. Anhalt, MD(4)

Received 5 March 2008; received in revised form 3 June 2008; accepted 1 August 2008. published online 20 October 2008


To evaluate the effectiveness of immunosuppressive drug therapy in the treatment of ocular mucous membrane pemphigoid (MMP).


Retrospective cohort study.


Ninety-four patients with biopsy-proven ocular MMP seen at the Pemphigoid Clinic at Wilmer Eye Institute from July 1984 through November 2006.


Data recorded included demographics, use and doses of immunosuppressive drugs, response to therapy, and side effects associated with drug use.

Main Outcome

Measures Outcome measures included:

  1. ocular control, defined as resolution of inflammation and cessation of cicatrization of the conjunctiva;
  2. ocular remission, defined as ocular control for 3 months or more after the cessation of immunosuppressive drug therapy; and
  3. ocular relapse, defined as the recurrence of ocular disease in either eye after a remission.


By 1 year of treatment, 82.9% of patients had complete control of the inflammation, and of these, 86.3% achieved a remission at some point during follow-up. The incidences of ocular control, remission, and relapse were 1.03 (95% confidence interval [CI], 0.78—1.33), 0.50 (95% CI, 0.37—0.67), and 0.04 (95% CI, 0.02—0.09) events per person-years (PY), respectively.

Among patients initially treated with prednisone and cyclophosphamide (n = 44), 91% of patients achieved a remission within 2 years after the initiation of immunosuppressive drug therapy. Characteristics at presentation associated with failing to achieve remission in the univariate analysis were trichiasis (relative risk [RR], 0.28; 95% CI, 0.08—097), prior eyelid surgery (RR, 0.11; 95% CI, 0.02—0.78), and esophageal involvement (RR, 0.29; 95% CI, 0.10—0.83).

After adjusting for confounding, an initial treatment regimen containing cyclophosphamide and prednisone was associated with a greater likelihood of achieving ocular remission (RR, 8.53; 95% CI, 2.53—28.86; P = 0.001) when compared with other initial treatment regimens. Infections, hematuria, and anemia were the most common side effects observed in patients receiving cyclophosphamide therapy.

The rate of discontinuing cyclophosphamide resulting from side effects was 0.20/PY; however, 74% of these patients still achieved remission despite early discontinuation of cyclophosphamide.


In patients with ocular MMP, most achieved ocular disease control with immunosuppressive drug therapy. Treatment with cyclophosphamide and prednisone was strongly associated with the development of ocular remission. Financial Disclosure(s) The author(s) have no proprietary or commercial interest in any materials discussed in this article.

Available online: October 18, 2008.

1 Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, Maryland
2 Department of Epidemiology, Center for Clinical Trials, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland
3 Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland
4 Department of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland

Correspondence: Jennifer E. Thorne, MD, PhD, Wilmer Eye Institute, 550 North Broadway, Suite 700, Baltimore, MD 21205 Manuscript no. 2008-290.

Dr Jabs is now at the Department of Ophthalmology, Mount Sinai School of Medicine, New York, New York. Supported by the National Eye Institute, Baltimore, Maryland (grant nos.: EY-13707 [JET] and EY-00405 [DAJ]); and the Mildred Weiner Ocular MMP Research Fund, Baltimore, Maryland (JET).

Dr Thorne is the recipient of a Research to Prevent Blindness Harrington Special Scholars Award.

Financial Disclosure(s): The author(s) have no proprietary or commercial interest in any materials discussed in this article. PII: S0161-6420(08)00740-9 doi:10.1016/j.ophtha.2008.08.002

© 2008 American Academy of Ophthalmology. Published by Elsevier Inc. All rights reserved.

The costs of medication are high and many people have trouble paying for them if they don’t have medical insurance. You need to take your medication exactly as your doctor wants you to. Skipping doses or reducing doses on your own can have serious consequences.

One common way to reduce the cost is by switching to a generic brand. Check with your doctor or pharmacist. If you are a veteran, check with the Veteran's Administration. Perhaps you can join an organization which offers members a discount on medication, such as The American Association of Retired Persons (AARP Website or AARP MedicareRx Plans Website).

Check to see if buying more at one time, or buying smaller amounts of medication more often can save you money. You can also check with your county health department to see if you are eligible to get medical treatment at reduced rates. Another organization that may help is the National Council on the Aging. Finally, most drug manufacturers have a plan where patients can get medication at reduced prices or even free. This is not usually easy and sometimes your doctor has to make the effort, but it certainly worth checking into.

The area around a wound must be kept clean and reasonably moist. When the dressings are dirty, they need to be replaced promptly. Leaving bandages on too long can slow the healing process and encourage infection. Replace any dressing when fluids soak through. This is called bleed-through and ideally, bandages should be changed before this occurs. Bleed-through increases the danger that a bandage will adhere to the wound. When this happens, soak the dressings and coax it off gently. The frequency of dressing changes depends on the wounds and the dressings applied. Talk with your doctor or nurse to familiarize yourself with the correct treatment protocols.