Sunday, May 27, 2007

 

Predisposition to infection in patients with pemphigus

Predisposition to infection in patients with pemphigus

Presse Med. 2007 May 18

Belgnaoui FZ,
Senouci K,
Chraibi H,
Aoussar A,
Mansouri F,
Benzekri L,
Ourhroui MA,
Abouqal R,
Heid E,
Hassam B.
Service de dermatologie, Hopital Ibn Sina, Rabat, Maroc.


INTRODUCTION: The relation between pemphigus and infection is complex. The aim of this work was to determine the frequency and impact of infection as well as the factors associated with it among our patients with pemphigus.

METHODS: This retrospective case series examined records of patients with pemphigus admitted to the dermatology unit of Ibn Sina University Hospital of Rabat between 1989 and 2004. We compared the patients with and without infections as well as the patients with and without severe bacterial infections according to patient profile and outcome. The principal outcome measure was death and the secondary measure, duration of hospitalization.

RESULTS: Of the 141 patients with pemphigus included in our study, 68% developed an infection. Infections were bacterial in 52% of cases, fungal in 50%, herpetic in 19% and parasitic in 1.5%. They were associated with diabetes mellitus and immunosuppressive drugs. Severe bacterial infection was frequent in patients with diabetes and rare in those treated with corticosteroids or with pemphigus foliaceous. Death occurred significantly more often among infected subjects (p=0.01), especially those with severe bacterial infections

DISCUSSION: Our study confirms the predisposition to all types of infection among patients with pemphigus, as well as the undeniable role its treatment plays in promoting infection. Severe bacterial infections were most often contracted before hospitalization. The literature reports a wide variety of infections, with pemphigus-herpes documented most often. Prevention and management require hygienic measures as well as early diagnosis and treatment of pemphigus and infections. Preventive treatment may be considered, but studies are needed to define the patients who might benefit from it.

Masson

Pemphigus

Introduction

Pemphigus is a group of rare skin disorders that cause blisters of your skin or mucous membranes, such as in your mouth or on your genitals.

Pemphigus usually occurs in people between the ages of 30 and 60, but it also can affect children and older adults. Men and women develop pemphigus equally, and it affects all races and cultures. However, pemphigus tends to be more common in people of Middle Eastern or Jewish descent.

Usually a chronic condition, pemphigus is best controlled by early diagnosis and treatment, which may include medications or treatments similar to those used for severe burns. Left untreated, pemphigus may be fatal.

Signs and symptoms

Pemphigus is characterized by blisters on your skin and mucous membranes. The blisters rupture easily, leaving open sores, which may ooze and become infected. The signs and symptoms of the three main types of pemphigus differ depending on the type:

Pemphigus vulgaris. The most common form, pemphigus vulgaris usually begins with blisters in your mouth, which then erupt on your skin. Blisters also can break out on the mucous membranes of your genitals. The blisters typically are painful, but don't itch.

Pemphigus foliaceus. This type doesn't usually affect mucous membranes. The blisters, which usually begin on your face and scalp and later erupt on your chest and back, usually aren't painful. They tend to be crusty and itchy.

Paraneoplastic pemphigus. This form causes painful sores on your mouth and lips and in your esophagus, as well as skin lesions. This form of pemphigus also can cause lesions in your lungs, resulting in progressive lung disease and making it difficult for you to breathe (dyspnea).

Causes

The exact cause of pemphigus is unknown, but it may be an autoimmune disorder.

Normally, your immune system attacks foreign invaders, such as harmful viruses and bacteria. But in pemphigus, your immune system produces antibodies that attack healthy cells in your skin or mucous membranes, specifically proteins called desmogleins. Desmogleins bind skin cells to each other. The antibodies cause separation of the cells of the top layer of your skin (epidermis). This reaction is known as acantholysis.

Paraneoplastic pemphigus generally occurs in people who have cancer, most commonly non-Hodgkin's lymphoma and chronic lymphocytic leukemia. In cases in which the cancer hasn't yet been discovered, the appearance of pemphigus blisters may alert doctors to look for a malignancy.

Risk factors

Pemphigus isn't contagious, and there's no way to predict who'll get it. However, your risk increases if:

You're between the ages of 30 and 60.
You're of Mediterranean or Jewish descent.
You have another autoimmune condition, particularly myasthenia gravis, a chronic disorder characterized by muscle weakness and fatigue, or thymoma, a tumor of the thymus. The thymus is an organ that produces white blood cells known as lymphocytes, an important part of your immune system.

When to seek medical advice

See your doctor if you develop blisters inside your mouth or on your skin. If you've been treated for pemphigus, see your doctor if you develop any of the following:

New blisters or sores
A rapid spread in the number of sores
Fever
Chills
Achy muscles or joints
A general sense of feeling ill (malaise)


Screening and diagnosis

Because it's uncommon, pemphigus may be difficult to diagnose. Blisters are common to a number of conditions, so besides taking a medical history and visually examining your skin and mouth, your doctor may lightly rub unblistered skin with a cotton swab or finger. With pemphigus, the top layers of your skin are likely to separate easily from the lower layers (positive for Nikolsky's sign). Other tests may include:

Skin biopsy. In this test, a piece of tissue from a blister is removed and examined under a microscope. Examination of the biopsy tissue may also involve a process called direct immunofluorescence (DIF). DIF entails staining the tissue with fluorescent dye to make the antibodies "light up" under a special microscope so they can be identified.
Blood tests. The purpose of these tests is to detect and identify antibodies (anti-desmogleins) in your blood.


Complications

The most common complications of pemphigus are infection of your skin and spread of infection through your bloodstream (sepsis). Systemic infection can be fatal.
Complications of paraneoplastic pemphigus include respiratory problems. The mortality rate for this type of pemphigus is estimated to be 90 percent, independent of the underlying cancer.
Other complications are the possible side effects of the medications used to treat pemphigus, particularly corticosteroids.


Treatment

Treatment, which aims at reducing signs and symptoms and preventing complications, is most effective when it begins as early as possible. The less widespread pemphigus is, the easier it may be to control. Specific treatment methods depend on the severity of the disease.

Mild pemphigusIf your pemphigus isn't too widespread, you may be able to remain at home for treatment. The mainstay of treatment is usually corticosteroids, such as prednisone. However, using corticosteroids over an extended time or in high doses may cause serious side effects, including:

Weight gain
Mood swings
Elevated blood sugar (diabetes)
Osteoporosis
Redistribution of body fat, leading to a round face (moon face)
Hair loss


Increased chance of infection because of suppression of the immune system
Corticosteroids may be combined with other medications, including:


Immunosuppressants. These medications, such as azathioprine (Imuran) or methotrexate (Rheumatrex), help keep your immune system from attacking healthy tissue. These drugs have serious side effects, including increased risk of infection.

Antibiotics and antifungal medications. These may be prescribed to control or prevent infections.

Severe pemphigusWidespread pemphigus may require you to stay in the hospital, where you may receive treatment similar to treatment for severe burns. The open sores make you highly vulnerable to infection, which if it spreads to your bloodstream, may be fatal. Besides the medications listed above, you may be given:

Fluids. Because you may have lost bodily fluids due to oozing of the sores, you may receive fluids through a vein (intravenously), as well as electrolytes — minerals such as sodium, potassium and calcium that maintain the balance of fluids in your body — and proteins.

Intravenous feeding. This may be necessary if mouth sores make it painful for you to eat.

Anesthetic mouth lozenges. These can help control pain of mild to moderate mouth sores.
Therapeutic plasmapheresis. In this process, the fluid part of your blood, called plasma, is removed from blood cells by a device known as a cell separator. The purpose is to get rid of the antibodies that are attacking your skin. The plasma is replaced with donated plasma or intravenous fluids.



Self-care

Pemphigus and some of the drugs used to treat it render your skin fragile and prone to infection. Here are some things you can do:

Minimize trauma to your skin. Avoid situations in which your skin could be touched or bumped, such as contact sports.

Ask your doctor for wound care instructions. Taking good care of your wounds can help prevent infection and scarring.

Use talcum powder. Generously sprinkling talcum powder on your sheets may help keep oozing skin from sticking.

Use lotions or dressings. To ease discomfort, treat sores and blisters with soothing or drying lotions or wet dressings.

Coping skills

Some cases of pemphigus can be debilitating, especially before treatment starts to work. To help you cope with the disease and the effects of the drugs used for treatment, you may find it helpful to talk to others with the condition. You can find in-person or virtual support groups.

Ask your dermatologist or contact the International Pemphigus Foundation.

Mayo Clinic

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Saturday, May 19, 2007

 

Bacterial Infection-Related Morbidity and Mortality in Cirrhosis.

Bacterial Infection-Related Morbidity and Mortality in Cirrhosis.

Am J Gastroenterol. 2007 May
Christou L,
Pappas G,
Falagas ME.
Division of Internal Medicine of the Medical School at the University of Ioannina, Ioannina, Greece.


OBJECTIVES:

Bacterial infections are acknowledged causes of morbidity and mortality in cirrhotic patients; yet, apart from spontaneous bacterial peritonitis, other infection issues have been understudied. We evaluated the existing medical data on infectious risks and related preventive and treatment data for cirrhotic patients.


METHODS:

Medical literature search through MEDLINE, using a variety of keywords focused on: (a) immunodeficiency parameters of cirrhosis and attempts at therapeutic reversal, (b) relative incidence of various focal infections and implications for prevention, and (c) specific pathogens posing a risk in cirrhosis and availability of preventive strategies.

RESULTS:

Immunodeficiency in cirrhosis is multifactorial and might not be reversed by isolated interventions. Epidemiologic data on the incidence of specific infections and risk factors are scarce, only Child-Pugh stage C being a common denominator. A variety of common, such as Staphylococcus aureus, Streptococcus pneumoniae, and Mycobacterium tuberculosis, as well as uncommon pathogens possess significant risks in cirrhosis. Certain aspects of these risks remain though unrecognized.

CONCLUSIONS:

To better understand the overall burden of bacterial infections on cirrhotic patients' survival, more data on preventive efficacy of pneumococcal vaccination, on the overall burden of tuberculosis, and the relative incidence of specific infections as endocarditis are warranted.

PMID: 17509025 [PubMed - as supplied by publisher]

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Friday, May 11, 2007

 

Predictors of long term neurological outcome in bacterial meningitis.

Predictors of long term neurological outcome in bacterial meningitis.
Indian J Pediatr. 2007 Apr

Singhi P,
Bansal A,
Geeta P,
Singhi S.
Department of Pediatrics, Postgraduate Institute of Medical Education and Research, Chandigarh, India.

OBJECTIVE: To study the long-term neurological and developmental outcome and the clinical and laboratory predictors of sequelae in children with acute bacterial meningitis (ABM).

METHODS: Detailed clinical and demographic data was retrieved from the medical records of study children. Subsequently they were followed up for a minimum of 12 months after discharge for development, neurological and hearing assessment. All sequelae were identified and divided into minor or major. For analysis data was divided into 2 groups those with sequelae and without sequelae at follow-up. Statistical analysis was done using SPSS version 10.00 and Epi Info version 2000.

RESULTS: 61 boys and 19 girls, a mean age of 31.4 +/= 41.9 months at the time of ABM, were included in the study. Of these 62.5% children were infants. Mean age at follow-up was 58.6 +/= 47.2 months. Sequelae were observed in 32 (40%) children (8 (10%) minor and 24 (30%) major). Mean social quotient at follow-up was 92.8 +/= 32.6. Developmentally 22 (37.9%) children were normal and 20 (34.5%) had global delay. Seizures (P=0.015), cranial nerve palsy (P=0.0065), abnormal deep tendon reflexes (P=0.002), Glasgow coma scale score (GCS) < p =" 0.044)" p="0.001)" p="0.001)">

CONCLUSION: Neurological and audiological sequelae and global developmental delay may be seen in about one third of survivors of bacterial meningitis. GCS score <8,>

Indian Journal of Pediatrics

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Sunday, May 06, 2007

 

Treatment of hospital-acquired pneumonia caused by methicillin-resistant Staphylococcus aureus.

Treatment of hospital-acquired pneumonia caused by methicillin-resistant Staphylococcus aureus.
Int J Antimicrob Agents. 2007 Apr 30
Ferrara AM.
Department of Haematological, Pneumological, Cardiovascular and Surgical Sciences, University of Pavia, Fondazione IRCCS Policlinico San Matteo, Viale Taramelli 5, 27100 Pavia, Italy.


Nosocomial pneumonia and ventilator-assisted pneumonia may be polymicrobial and can be caused by a wide spectrum of pathogens. Potentially multidrug-resistant microorganisms often represent the 'core' pathogens of the most severe infections. Among Gram-positive pathogens, methicillin-resistant Staphylococcus aureus (MRSA) plays a key role, mainly in mechanically ventilated patients or in patients with specific risk factors. The mainstay of treatment for MRSA pneumonia has been glycopeptide antibiotics, i.e. vancomycin and, to a lesser extent, teicoplanin. However, owing to its insufficient penetration into lung compartments, vancomycin may result in therapeutic failure or slow clinical responses. Moreover, vancomycin serum levels must be monitored in order to minimise nephrotoxicity and to maximise the concentration in the lung. Finally, the emergence of staphylococci isolates with reduced susceptibility to vancomycin suggests that glycopeptides should no longer be considered as first-line antibacterial agents for Gram-positive lung infections. Among new therapeutic options, linezolid may be an appropriate choice for MRSA pulmonary infections owing to its good pharmacokinetic profile in the lung and its acceptable tolerability, especially in patients with renal insufficiency or in those receiving other nephrotoxic agents. However, to contain the increasing emergence of drug resistance among hospitalised patients, these novel antimicrobial agents should be used judiciously, restricting their use to patients not responsive to, or intolerant of, glycopeptides. Other new drugs under development appear to be promising and deserve further evaluation.

PMID: 17475449 [PubMed - as supplied by publisher]

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Tuesday, May 01, 2007

 

Mortality in patients with necrotizing fasciitis.

Mortality in patients with necrotizing fasciitis.
Plast Reconstr Surg. 2007 May

Golger A,
Ching S,
Goldsmith CH,
Pennie RA,
Bain JR.
Division of Plastic Surgery, Department of Surgery, McMaster University,Hamilton, Ontario, Canada.

BACKGROUND: The prognostic factors that determine outcome in patients with necrotizing fasciitis remain poorly understood. The aim of this study was to analyze the variables that affect the mortality and morbidity of patients with necrotizing fasciitis and to create a simple method for estimating the probability of mortality.

METHODS: The authors undertook a retrospective review of all patients with necrotizing fasciitis treated in three tertiary care hospitals in Ontario, Canada, between January of 1994 and June of 2001. Demographic, comorbid illness, and disease-specific data were collated and analyzed for associations with outcome. Using logistic regression analysis, probability estimates for the prediction of mortality were developed, based on three contributing independent factors.

RESULTS: Ninety-nine patients satisfied the inclusion criteria. Overall mortality was 20 percent. Sixteen patients suffered from amputation or organ loss. The most common comorbidities were diabetes (30 percent), immunocompromised status (17 percent), and chickenpox (11 percent). Advanced age (odds ratio, 1.04; 95 percent confidence interval, 1.01 to 1.08; p = 0.012), streptococcal toxic shock syndrome (odds ratio, 10.54; 95 percent confidence interval, 2.80 to 39.44; p < p =" 0.044)">

CONCLUSIONS: Age, streptococcal toxic shock syndrome, and immune status are significant determinants of mortality and can predict the probability of death from necrotizing fasciitis soon after admission. This objective information can guide clinicians in communication with patients and in making clinical decisions.

Lippincott Williams Wilkins

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