Pyoderma gangrenosum is a rare ulcerating skin disease with unclear etiology. Treatment is typically immunosuppression with corticosteroids or ciclosporin. Recently, anti-TNF agents like infliximab have shown effectiveness based on case reports and a small randomized controlled trial. The article reviews clinical presentation, variants, histology, differential diagnosis, and treatment approaches for pyoderma gangrenosum.
This patient, a 59-year-old man with ALL undergoing chemotherapy, presented with worsening right elbow and thigh erythema, edema and pain as well as leukocytosis. MRI showed myositis in the right upper extremity with no abscess, and a focal intramuscular abscess in the right thigh. He was diagnosed with pyomyositis, a purulent infection of skeletal muscle caused by hematogenous spread of bacteria, most commonly Staphylococcus aureus. Treatment for pyomyositis in immunocompromised patients involves drainage of abscesses along with broad-spectrum antibiotics.
1) Tinea incognito is a dermatophytic infection that presents with an atypical clinical appearance due to previous treatment with topical or systemic corticosteroids or immunomodulators like pimecrolimus and tacrolimus.
2) Tinea incognito often mimics conditions like neurodermatitis, atopic dermatitis, rosacea, and seborrheic dermatitis, making diagnosis difficult.
3) The use of topical corticosteroids is a common cause of tinea incognito by suppressing the immune response to dermatophytes and altering the clinical presentation of the infection.
Mr. Vijayakumar, a 36-year-old man with IDDM and chronic pancreatitis, was admitted with fever, body pain, and fatigue for 10-15 days. He was found to have pyomyositis with multiple muscle abscesses caused by Staphylococcus aureus. He underwent incision and drainage of the abscesses followed by treatment with cloxacillin then vancomycin. He improved with treatment and was discharged upon request to continue treatment nearer to his home.
1. The document discusses cellulitis, a bacterial skin infection causing inflammation. It defines cellulitis and describes its symptoms such as red, swollen, tender skin.
2. Common causes are bacteria like streptococcus and staphylococcus entering through breaks in the skin. Risk factors include injuries, conditions like eczema or diabetes.
3. Diagnosis involves examination of the affected area and sometimes tests. Treatment focuses on antibiotics, wound care, and rest.
1. Sweet's syndrome is an uncommon skin condition characterized by abrupt onset of tender red skin lesions and systemic symptoms. Histopathology shows a dense neutrophilic infiltrate without evidence of infection.
2. Treatment involves oral corticosteroids which provide excellent response within days to weeks. Recurrences may occur in about 30% of cases.
3. Pyoderma gangrenosum is a rare neutrophilic dermatosis presenting as painful cutaneous ulcers with undermined, irregular borders and purulent bases that may enlarge. About half of cases are associated with underlying systemic disease. Treatment focuses on controlling underlying conditions and using high-dose corticosteroids or immunosuppressants.
To understand immunologic vesiculobullous diseases, one must be aware of normal epithelium structure and autoimmune pathogenesis. Pemphigus is characterized by loss of cell-cell adhesion due to autoantibodies targeting desmoglein 3. Bullous pemphigoid involves autoantibodies targeting laminin 5 and BP180, causing subepithelial blistering. Mucous membrane pemphigoid features linear IgG and C3 deposition along the basement membrane zone.
This patient, a 59-year-old man with ALL undergoing chemotherapy, presented with worsening right elbow and thigh erythema, edema and pain as well as leukocytosis. MRI showed myositis in the right upper extremity with no abscess, and a focal intramuscular abscess in the right thigh. He was diagnosed with pyomyositis, a purulent infection of skeletal muscle caused by hematogenous spread of bacteria, most commonly Staphylococcus aureus. Treatment for pyomyositis in immunocompromised patients involves drainage of abscesses along with broad-spectrum antibiotics.
1) Tinea incognito is a dermatophytic infection that presents with an atypical clinical appearance due to previous treatment with topical or systemic corticosteroids or immunomodulators like pimecrolimus and tacrolimus.
2) Tinea incognito often mimics conditions like neurodermatitis, atopic dermatitis, rosacea, and seborrheic dermatitis, making diagnosis difficult.
3) The use of topical corticosteroids is a common cause of tinea incognito by suppressing the immune response to dermatophytes and altering the clinical presentation of the infection.
Mr. Vijayakumar, a 36-year-old man with IDDM and chronic pancreatitis, was admitted with fever, body pain, and fatigue for 10-15 days. He was found to have pyomyositis with multiple muscle abscesses caused by Staphylococcus aureus. He underwent incision and drainage of the abscesses followed by treatment with cloxacillin then vancomycin. He improved with treatment and was discharged upon request to continue treatment nearer to his home.
1. The document discusses cellulitis, a bacterial skin infection causing inflammation. It defines cellulitis and describes its symptoms such as red, swollen, tender skin.
2. Common causes are bacteria like streptococcus and staphylococcus entering through breaks in the skin. Risk factors include injuries, conditions like eczema or diabetes.
3. Diagnosis involves examination of the affected area and sometimes tests. Treatment focuses on antibiotics, wound care, and rest.
1. Sweet's syndrome is an uncommon skin condition characterized by abrupt onset of tender red skin lesions and systemic symptoms. Histopathology shows a dense neutrophilic infiltrate without evidence of infection.
2. Treatment involves oral corticosteroids which provide excellent response within days to weeks. Recurrences may occur in about 30% of cases.
3. Pyoderma gangrenosum is a rare neutrophilic dermatosis presenting as painful cutaneous ulcers with undermined, irregular borders and purulent bases that may enlarge. About half of cases are associated with underlying systemic disease. Treatment focuses on controlling underlying conditions and using high-dose corticosteroids or immunosuppressants.
To understand immunologic vesiculobullous diseases, one must be aware of normal epithelium structure and autoimmune pathogenesis. Pemphigus is characterized by loss of cell-cell adhesion due to autoantibodies targeting desmoglein 3. Bullous pemphigoid involves autoantibodies targeting laminin 5 and BP180, causing subepithelial blistering. Mucous membrane pemphigoid features linear IgG and C3 deposition along the basement membrane zone.
Erythema multiforme, Steven-Johnson syndrome and Toxic Epidermal NecrolysisBinaya Subedi
Erythema Multiforme is a common Vesiculobullous deramtological condition with mucosal manifestations trigged by Herpes virus infection and certain sulpha containing drugs.
Management of skin and soft tissue infections with ayurveda w.s.r, rasayan ch...dr.shailesh phalle
Management of skin and soft tissue infections with ayurveda w.s.r, rasayan chikitsa by dr.shailesh phalle
Thease slides are healpful for chronic skin disorders and immunity realted diseases.
Bulloous disorders (BSDs) are skin conditions characterized by blister formation between the epidermis and dermis layers of the skin. BSDs are mostly autoimmune in nature and can be caused by genetic factors, physical trauma, inflammation, the immune system, or drug reactions. The main types are genetic blistering diseases like epidermolysis bullosa, and immunobullous diseases like pemphigus and pemphigoid which involve antibody-mediated blistering between skin layers. Pemphigus is an intraepidermal immunobullous disease affecting the skin and mucous membranes, while bullous pemphigoid is a subepidermal immunobullous condition commonly affecting
Dermatitis herpetiformis (DH) is a chronic, recurrent skin rash characterized by tiny blisters and itchy bumps that are symmetrically located on the elbows, knees, buttocks, and back. It is associated with celiac disease and gluten sensitivity. A skin biopsy shows IgA antibody deposits that help diagnose DH. Treatment involves medication like dapsone or sulfasalazine to relieve symptoms, along with maintaining a lifelong gluten-free diet to prevent flare-ups.
This document provides guidelines for the management of Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) from an Indian perspective. It summarizes 104 sources on managing SJS/TEN and makes recommendations. Key points include promptly withdrawing the culprit drug, providing supportive care, and initiating moderate to high doses of oral or parenteral corticosteroids or cyclosporine within 72 hours. A multidisciplinary approach is recommended due to the systemic nature of SJS/TEN.
This case report describes a rare complication of breast reduction surgery - pyoderma gangrenosum (PG). A 61-year-old woman underwent right breast reduction surgery and initially presented with wound dehiscence and erythema, treated as infection. However, the wound rapidly progressed despite antibiotics. After debridement, the patient developed systemic inflammatory response syndrome. Pathology found no infection. High-dose steroids halted progression and healed the wound. Topical tacrolimus additionally treated the wound and steroid dose was tapered. At 8 months, the wounds were healed with no further issues, demonstrating PG following breast surgery can be treated successfully with steroids and topical tacrolimus.
This document discusses pemphigus, a group of immunologically-mediated mucocutaneous blistering disorders. Pemphigus vulgaris is the most common variant seen in oral medicine, characterized by intra-epithelial blister formation and anti-desmoglein antibodies. Clinical presentation includes widespread ulceration/blistering, rapid progression, and positive Nikolsky's sign. Histology shows intra-epithelial blisters and Tzank cells. Treatment involves systemic corticosteroids and immunosuppressants to control symptoms and progression. The role of dentists is in early diagnosis and monitoring of pemphigus patients.
Bullous pemphigoid , dermatitis herpitiformis and cbdcNavya Suresh
This document provides information on bullous skin disorders including bullous pemphigoid, chronic bullous disease of childhood, and dermatitis herpetiformis. It discusses the pathophysiology of blister formation, describing how autoantibodies can bind to proteins in the basement membrane zone and cause inflammation. For bullous pemphigoid specifically, it outlines the antigens, pathogenic antibodies, clinical features, variants, associations, differential diagnosis, investigations including direct immunofluorescence findings, and treatment approaches. It also briefly summarizes the history, epidemiology, pathogenesis involving HLA genes, and clinical presentation of dermatitis herpetiformis.
Stevens-Johnson syndrome is a severe mucocutaneous reaction typically caused by drugs involving skin and mucous membranes. It begins with flu-like symptoms followed by distinctive target lesions. Complications can include blindness, infections, and death. Treatment focuses on stopping the causative agent, supportive care, corticosteroids, IVIG, and antibiotics for secondary infections.
Pemphigus is a group of chronic autoimmune bullous diseases characterized by the presence of autoantibodies against desmosomal proteins. The main types are pemphigus vulgaris, pemphigus foliaceus, and pemphigus erythematosus. Pemphigus vulgaris presents with flaccid blisters and erosions especially in the oral cavity and skin folds. Pemphigus foliaceus presents with fragile superficial blisters that leave moist erosions and crusts mainly on the face and scalp. Diagnosis involves clinical features and detection of autoantibodies through laboratory tests. Nikolsky's sign, elicited by applying pressure to separate
Mucormycosis is a serious fungal infection caused by mucormycetes molds commonly found in soil and decaying organic matter. It can infect humans through inhalation, ingestion or skin contact. Those at highest risk include diabetics, especially those with ketoacidosis, as well as those with organ transplants, cancer, HIV/AIDS or prolonged corticosteroid use. Common symptoms depend on the infected area but may include sinus congestion, eye swelling, coughing or abdominal pain. Diagnosis involves imaging, biopsy and identifying fungal elements microscopically. Treatment requires controlling underlying conditions, antifungal drugs like amphotericin B and aggressive surgery to remove infected tissues
This document discusses several types of palisaded granulomatous dermatoses including granuloma annulare (GA), annular elastolytic giant cell granuloma, and actinic granuloma. It provides information on the presentation, associations, and treatments for localized and generalized GA. It also includes photographs and descriptions of GA lesions on the hands. Treatment options discussed include topical steroids for localized GA and tetracycline combined with nicotinamide or PUVA for generalized GA.
Pemphigus - intra epidermal blistering disordersPreethi
This document summarizes several intra-epidermal blistering disorders including pemphigus vulgaris, pemphigus foliaceus, and paraneoplastic pemphigus. Pemphigus vulgaris is characterized by suprabasal acantholysis and antibodies against desmoglein 3. Pemphigus foliaceus involves subcorneal acantholysis and antibodies against desmoglein 1. Paraneoplastic pemphigus is associated with an underlying neoplasm and antibodies against both desmogleins and plakins. Treatment for these disorders involves high dose corticosteroids along with immunosuppressive agents.
This document describes the case of a 48-year-old woman who presented with joint pain and was found to have an elevated ASO level and was diagnosed with rheumatic fever. She later developed fever, breathlessness, and a skin rash. A skin biopsy showed features of Sweet's syndrome. Her condition improved with treatment but she later had recurrent fever and joint swelling. She was ultimately diagnosed with Sweet's syndrome.
This document summarizes a study on using maggot debridement therapy (MDT) to treat necrotizing fasciitis. It found that among 15 patients treated with surgery, antibiotics, and MDT: 1) MDT reduced the number of surgical debridements needed, especially when started within 9 days of diagnosis; and 2) the wounds eventually healed in all patients except two who died from unrelated causes. It also describes in detail one patient's case of necrotizing fasciitis that was successfully treated with multiple debridements and 19 days of MDT.
The document discusses infections of the skin and subcutaneous tissue. It introduces a variety of skin and soft tissue infections (SSTIs), ranging from simple cellulitis to necrotizing fasciitis. Common causes include Staphylococcus aureus, Streptococcus pyogenes, and site-specific organisms. Infections are classified as uncomplicated SSTI, nonnecrotizing complicated SSTI, or necrotizing fasciitis. The document also defines several types of skin infections and provides ICD-10-CM codes to identify infectious agents and conditions.
Dermatomyositis is a chronic inflammatory disorder of the skin and muscles that is characterized by an autoimmune pathogenesis. It commonly presents with characteristic rashes like Gottron's papules and heliotrope rash as well as proximal muscle weakness. Dermatomyositis can also involve internal organs like the lungs, esophagus and heart. Diagnosis involves assessing clinical features, muscle enzymes, electromyography, muscle/skin biopsies and identifying myositis-specific antibodies. Prognosis depends on the severity and organ involvement, with risks of residual weakness, contractures and death from respiratory or cardiac complications.
Necrotizing fasciitis is a rapidly progressive soft tissue infection that causes necrosis of subcutaneous tissue and fascia. It can be polymicrobial or monomicrobial. Streptococcus pyogenes is a common cause and is frequently associated with toxic shock syndrome. Necrotizing fasciitis has distinct clinical stages from early erythema and swelling to late stage necrosis, crepitus, and anesthesia. Aggressive management is required including intravenous antibiotics, surgical debridement, and supportive care due to high morbidity and mortality rates.
DETAILED DISCUSSION OF NECROTIZING FASCIITIS.
A SOFT TISSUE INFECTION. USUALLY CALLED AS FLESH EATING BACTERIAL INFECTION. CAUSED BY BACTERIA. AFFECTS THE SOFT SKIN TISSUES
Hoàn thiện công tác kế toán tập hợp chi phí sản xuất và tính giá thành sản ph...NOT
Giá 10k/5 lượt download Liên hệ page để mua: https://www.facebook.com/garmentspace Xin chào, Nếu bạn cần mua tài liệu xin vui lòng liên hệ facebook: https://www.facebook.com/garmentspace Tại sao tài liệu lại có phí ??? Tài liệu một phần do mình bỏ thời gian sưu tầm trên Internet, một số do mình bỏ tiền mua từ các website bán tài liệu, với chi phí chỉ 10k cho 5 lượt download tài liệu bất kỳ bạn sẽ không tìm ra nơi nào cung cấp tài liệu với mức phí như thế, xin hãy ủng hộ Garment Space nhé, đừng ném đá. Xin cảm ơn rất nhiều
This document contains the resume of Milind Dattaram Shirke. It summarizes his professional experience working as a Team Leader for Accounts Payable at Tata Consultancy Services and as a Back Office Executive in the finance department of HDFC Bank. It also lists his educational qualifications and technical skills. His roles included monitoring invoice processing, conducting audits and process improvements, and verifying payments and resolving discrepancies. He received several awards for his performance and helped improve on-time payment rates.
Erythema multiforme, Steven-Johnson syndrome and Toxic Epidermal NecrolysisBinaya Subedi
Erythema Multiforme is a common Vesiculobullous deramtological condition with mucosal manifestations trigged by Herpes virus infection and certain sulpha containing drugs.
Management of skin and soft tissue infections with ayurveda w.s.r, rasayan ch...dr.shailesh phalle
Management of skin and soft tissue infections with ayurveda w.s.r, rasayan chikitsa by dr.shailesh phalle
Thease slides are healpful for chronic skin disorders and immunity realted diseases.
Bulloous disorders (BSDs) are skin conditions characterized by blister formation between the epidermis and dermis layers of the skin. BSDs are mostly autoimmune in nature and can be caused by genetic factors, physical trauma, inflammation, the immune system, or drug reactions. The main types are genetic blistering diseases like epidermolysis bullosa, and immunobullous diseases like pemphigus and pemphigoid which involve antibody-mediated blistering between skin layers. Pemphigus is an intraepidermal immunobullous disease affecting the skin and mucous membranes, while bullous pemphigoid is a subepidermal immunobullous condition commonly affecting
Dermatitis herpetiformis (DH) is a chronic, recurrent skin rash characterized by tiny blisters and itchy bumps that are symmetrically located on the elbows, knees, buttocks, and back. It is associated with celiac disease and gluten sensitivity. A skin biopsy shows IgA antibody deposits that help diagnose DH. Treatment involves medication like dapsone or sulfasalazine to relieve symptoms, along with maintaining a lifelong gluten-free diet to prevent flare-ups.
This document provides guidelines for the management of Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) from an Indian perspective. It summarizes 104 sources on managing SJS/TEN and makes recommendations. Key points include promptly withdrawing the culprit drug, providing supportive care, and initiating moderate to high doses of oral or parenteral corticosteroids or cyclosporine within 72 hours. A multidisciplinary approach is recommended due to the systemic nature of SJS/TEN.
This case report describes a rare complication of breast reduction surgery - pyoderma gangrenosum (PG). A 61-year-old woman underwent right breast reduction surgery and initially presented with wound dehiscence and erythema, treated as infection. However, the wound rapidly progressed despite antibiotics. After debridement, the patient developed systemic inflammatory response syndrome. Pathology found no infection. High-dose steroids halted progression and healed the wound. Topical tacrolimus additionally treated the wound and steroid dose was tapered. At 8 months, the wounds were healed with no further issues, demonstrating PG following breast surgery can be treated successfully with steroids and topical tacrolimus.
This document discusses pemphigus, a group of immunologically-mediated mucocutaneous blistering disorders. Pemphigus vulgaris is the most common variant seen in oral medicine, characterized by intra-epithelial blister formation and anti-desmoglein antibodies. Clinical presentation includes widespread ulceration/blistering, rapid progression, and positive Nikolsky's sign. Histology shows intra-epithelial blisters and Tzank cells. Treatment involves systemic corticosteroids and immunosuppressants to control symptoms and progression. The role of dentists is in early diagnosis and monitoring of pemphigus patients.
Bullous pemphigoid , dermatitis herpitiformis and cbdcNavya Suresh
This document provides information on bullous skin disorders including bullous pemphigoid, chronic bullous disease of childhood, and dermatitis herpetiformis. It discusses the pathophysiology of blister formation, describing how autoantibodies can bind to proteins in the basement membrane zone and cause inflammation. For bullous pemphigoid specifically, it outlines the antigens, pathogenic antibodies, clinical features, variants, associations, differential diagnosis, investigations including direct immunofluorescence findings, and treatment approaches. It also briefly summarizes the history, epidemiology, pathogenesis involving HLA genes, and clinical presentation of dermatitis herpetiformis.
Stevens-Johnson syndrome is a severe mucocutaneous reaction typically caused by drugs involving skin and mucous membranes. It begins with flu-like symptoms followed by distinctive target lesions. Complications can include blindness, infections, and death. Treatment focuses on stopping the causative agent, supportive care, corticosteroids, IVIG, and antibiotics for secondary infections.
Pemphigus is a group of chronic autoimmune bullous diseases characterized by the presence of autoantibodies against desmosomal proteins. The main types are pemphigus vulgaris, pemphigus foliaceus, and pemphigus erythematosus. Pemphigus vulgaris presents with flaccid blisters and erosions especially in the oral cavity and skin folds. Pemphigus foliaceus presents with fragile superficial blisters that leave moist erosions and crusts mainly on the face and scalp. Diagnosis involves clinical features and detection of autoantibodies through laboratory tests. Nikolsky's sign, elicited by applying pressure to separate
Mucormycosis is a serious fungal infection caused by mucormycetes molds commonly found in soil and decaying organic matter. It can infect humans through inhalation, ingestion or skin contact. Those at highest risk include diabetics, especially those with ketoacidosis, as well as those with organ transplants, cancer, HIV/AIDS or prolonged corticosteroid use. Common symptoms depend on the infected area but may include sinus congestion, eye swelling, coughing or abdominal pain. Diagnosis involves imaging, biopsy and identifying fungal elements microscopically. Treatment requires controlling underlying conditions, antifungal drugs like amphotericin B and aggressive surgery to remove infected tissues
This document discusses several types of palisaded granulomatous dermatoses including granuloma annulare (GA), annular elastolytic giant cell granuloma, and actinic granuloma. It provides information on the presentation, associations, and treatments for localized and generalized GA. It also includes photographs and descriptions of GA lesions on the hands. Treatment options discussed include topical steroids for localized GA and tetracycline combined with nicotinamide or PUVA for generalized GA.
Pemphigus - intra epidermal blistering disordersPreethi
This document summarizes several intra-epidermal blistering disorders including pemphigus vulgaris, pemphigus foliaceus, and paraneoplastic pemphigus. Pemphigus vulgaris is characterized by suprabasal acantholysis and antibodies against desmoglein 3. Pemphigus foliaceus involves subcorneal acantholysis and antibodies against desmoglein 1. Paraneoplastic pemphigus is associated with an underlying neoplasm and antibodies against both desmogleins and plakins. Treatment for these disorders involves high dose corticosteroids along with immunosuppressive agents.
This document describes the case of a 48-year-old woman who presented with joint pain and was found to have an elevated ASO level and was diagnosed with rheumatic fever. She later developed fever, breathlessness, and a skin rash. A skin biopsy showed features of Sweet's syndrome. Her condition improved with treatment but she later had recurrent fever and joint swelling. She was ultimately diagnosed with Sweet's syndrome.
This document summarizes a study on using maggot debridement therapy (MDT) to treat necrotizing fasciitis. It found that among 15 patients treated with surgery, antibiotics, and MDT: 1) MDT reduced the number of surgical debridements needed, especially when started within 9 days of diagnosis; and 2) the wounds eventually healed in all patients except two who died from unrelated causes. It also describes in detail one patient's case of necrotizing fasciitis that was successfully treated with multiple debridements and 19 days of MDT.
The document discusses infections of the skin and subcutaneous tissue. It introduces a variety of skin and soft tissue infections (SSTIs), ranging from simple cellulitis to necrotizing fasciitis. Common causes include Staphylococcus aureus, Streptococcus pyogenes, and site-specific organisms. Infections are classified as uncomplicated SSTI, nonnecrotizing complicated SSTI, or necrotizing fasciitis. The document also defines several types of skin infections and provides ICD-10-CM codes to identify infectious agents and conditions.
Dermatomyositis is a chronic inflammatory disorder of the skin and muscles that is characterized by an autoimmune pathogenesis. It commonly presents with characteristic rashes like Gottron's papules and heliotrope rash as well as proximal muscle weakness. Dermatomyositis can also involve internal organs like the lungs, esophagus and heart. Diagnosis involves assessing clinical features, muscle enzymes, electromyography, muscle/skin biopsies and identifying myositis-specific antibodies. Prognosis depends on the severity and organ involvement, with risks of residual weakness, contractures and death from respiratory or cardiac complications.
Necrotizing fasciitis is a rapidly progressive soft tissue infection that causes necrosis of subcutaneous tissue and fascia. It can be polymicrobial or monomicrobial. Streptococcus pyogenes is a common cause and is frequently associated with toxic shock syndrome. Necrotizing fasciitis has distinct clinical stages from early erythema and swelling to late stage necrosis, crepitus, and anesthesia. Aggressive management is required including intravenous antibiotics, surgical debridement, and supportive care due to high morbidity and mortality rates.
DETAILED DISCUSSION OF NECROTIZING FASCIITIS.
A SOFT TISSUE INFECTION. USUALLY CALLED AS FLESH EATING BACTERIAL INFECTION. CAUSED BY BACTERIA. AFFECTS THE SOFT SKIN TISSUES
Hoàn thiện công tác kế toán tập hợp chi phí sản xuất và tính giá thành sản ph...NOT
Giá 10k/5 lượt download Liên hệ page để mua: https://www.facebook.com/garmentspace Xin chào, Nếu bạn cần mua tài liệu xin vui lòng liên hệ facebook: https://www.facebook.com/garmentspace Tại sao tài liệu lại có phí ??? Tài liệu một phần do mình bỏ thời gian sưu tầm trên Internet, một số do mình bỏ tiền mua từ các website bán tài liệu, với chi phí chỉ 10k cho 5 lượt download tài liệu bất kỳ bạn sẽ không tìm ra nơi nào cung cấp tài liệu với mức phí như thế, xin hãy ủng hộ Garment Space nhé, đừng ném đá. Xin cảm ơn rất nhiều
This document contains the resume of Milind Dattaram Shirke. It summarizes his professional experience working as a Team Leader for Accounts Payable at Tata Consultancy Services and as a Back Office Executive in the finance department of HDFC Bank. It also lists his educational qualifications and technical skills. His roles included monitoring invoice processing, conducting audits and process improvements, and verifying payments and resolving discrepancies. He received several awards for his performance and helped improve on-time payment rates.
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Gedion Mwangi Macharia is seeking a job that allows him to use his problem-solving, analytical, and communication skills to increase an organization's innovation and efficiency. He has a Bachelor's degree in Economics and Sociology from Egerton University. His work experience includes roles in merchant services, customer experience, and internships in banking and sales. He is proficient in Microsoft Office and has leadership experience from community service projects and university clubs.
áP dụng lean manufacturing vào trong thực tế sản xuất tại xí nghiệp may pleik...TÀI LIỆU NGÀNH MAY
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The document discusses research into passive design strategies for thermal comfort at PJ Trade Centre. It examines the effectiveness of shading devices, concrete vent blocks, and building orientation. Regarding shading devices, trees and vent blocks provide effective shading while allowing ventilation. Vent blocks improve indoor comfort and air flow. The building's orientation and materials also contribute to cooling and comfort through shading and heat absorption. Passive strategies like these provide natural ventilation and achieve thermal comfort similar to traditional Malay houses.
This document provides information on desquamative gingivitis, including its classification, diagnosis, and associated diseases. It classifies desquamative gingivitis into 7 categories including dermatosis, endocrine imbalance, aging, metabolic disturbances, abnormal response to irritation, chronic infection, and drug reactions. Key aspects of diagnosis include clinical history, examination, biopsy, and microscopic/immunofluorescence examination. Associated diseases discussed in detail include lichen planus, pemphigoid, pemphigus vulgaris, chronic ulcerative stomatitis, and linear IgA disease. Treatment varies depending on the underlying cause and severity of symptoms.
This document summarizes information about Buruli ulcer, a chronic skin disease caused by Mycobacterium ulcerans. It describes the typical presentation as painless skin lesions that slowly ulcerate. Peak incidence is in children ages 5-15 in central and western Africa near slow-moving bodies of water. While the mode of transmission is unknown, water bugs and fish are believed to carry the bacteria. Treatment involves antibiotics like rifampicin and streptomycin or clarithromycin, with surgery reserved for advanced cases to prevent deformities from scarring.
This document contains 10 multiple choice questions about common skin diseases, along with explanations for each answer. The questions cover topics like scabies, psoriasis, tinea capitis, bullous pemphigoid, hereditary haemorrhagic telangiectasia, and erythema induratum. The explanations provide details about the diagnoses, typical presentations, treatments, and pathogenic mechanisms of the various skin conditions.
This document provides an overview of necrobiotic disorders including granuloma annulare, necrobiosis lipoidica, and granuloma multiforme. It discusses the etiology, clinical features, histopathology, differential diagnosis, and treatment of each condition. Granuloma annulare commonly presents as annular or arciform plaques on the extremities of young people. Necrobiosis lipoidica typically causes yellow-brown, atrophic plaques on the pretibial area that may ulcerate. Granuloma multiforme forms firm papules aggregated into plaques or forming the edges of annular lesions, predominantly affecting sun-exposed areas.
Fournier’s Gangrene in a 9 Yrs. Old Patient; A Rare Presentation in Paediatri...semualkaira
Necrotizing fasciitis of the perineum and external genitalia is a
life-threatening infective gangrene, primarily seen in adults but
relatively rare in children. We present a nine-year-old male child
with spinal bifida and double incontence who was admitted at our
hospital due to gangrenous right hemi-scrotal ulcer extending to
the right thigh. It was proceeded with painful swollen hemi-scrotum 2wks prior to admission. We treated him aggressively with
broad spectrum antibiotics and early surgical debridement. Being
paraplegic with double incontinence hence spending most of the
time dressed with diapers we therefore think of poor hygiene and
the diaper rash as the etiological factors. Early surgical debridement with appropriate antibiotics and aggressive supportive care
usually gave good results.
Fournier’s Gangrene in a 9 Yrs. Old Patient; A Rare Presentation in Paediatri...semualkaira
Necrotizing fasciitis of the perineum and external genitalia is a
life-threatening infective gangrene, primarily seen in adults but
relatively rare in children. We present a nine-year-old male child
with spinal bifida and double incontence who was admitted at our
hospital due to gangrenous right hemi-scrotal ulcer extending to
the right thigh. It was proceeded with painful swollen hemi-scrotum 2wks prior to admission. We treated him aggressively with
broad spectrum antibiotics and early surgical debridement. Being
paraplegic with double incontinence hence spending most of the
time dressed with diapers we therefore think of poor hygiene and
the diaper rash as the etiological factors. Early surgical debridement with appropriate antibiotics and aggressive supportive care
usually gave good results.
Glomerulonephritis refers to a group of disorders involving inflammation of the glomeruli. It can be classified based on clinical presentation, histological appearance, etiology, and other factors. Common types include post-infectious glomerulonephritis, lupus nephritis, anti-GBM disease, IgA nephropathy, and rapidly progressive glomerulonephritis. The pathogenesis involves immunological injury to the glomerular capillary wall that can lead to scarring, loss of filtration, and decreased kidney function over time if not properly treated.
ETAS_MCQ_10 manifestations of systemic diseases1Derma202
The document provides information about various systemic diseases and their cutaneous manifestations:
- Neurofibromatosis type 1 can cause kyphoscoliosis, pseudoarthrosis, lordosis, and spina bifida but not monoarticular arthropathy.
- Candida albicans causes erosio interdigitalis blastomycetica.
- Erythema gyratum repens is associated with various malignancies except gastric carcinoma.
- Eruptive xanthomas are associated with familial hyperlipidemias types I, IV and V and high triglyceride levels.
- Paraneoplastic pemphigus is associated with various tumors except lung carcinoma.
Inflammatory myopathies are rare diseases characterized by symmetric proximal muscle weakness. The main types are polymyositis, dermatomyositis, juvenile dermatomyositis, myositis associated with other conditions, and inclusion body myositis. Diagnosis involves muscle biopsy showing inflammation, elevated muscle enzymes, EMG changes, and sometimes autoantibodies. Treatment begins with glucocorticoids and may include immunosuppressants if weak response. Prognosis depends on type, with dermatomyositis having best outlook.
Dentists play an important role in the diagnosis and management of desquamative gingivitis. The importance of being able to recognise and properly diagnose this condition is accentuated by the fact that a serious and life threatening disease may initially manifest as desquamative gingivitis.
Zygomycosis is a rare fungal infection caused by bread mold fungi called mucormycetes. It most commonly affects people with weakened immune systems from conditions like diabetes, cancer, or organ transplant. The fungi are found in soil and decaying matter. Symptoms depend on the infected area but can include sinus pain, coughing blood, or skin lesions. Risk factors are diabetes, cancer treatments, corticosteroids, or skin injuries. Diagnosis involves tissue samples analyzed microscopically or in culture. Treatment requires antifungal medications like amphotericin B and sometimes surgery to remove infected tissue. Prevention focuses on controlling underlying illnesses that weaken the immune system.
Zygomycosis is a rare fungal infection caused by bread mold fungi called mucormycetes. It most commonly affects people with weakened immune systems due to conditions like diabetes, cancer, or organ transplant. The infection can start in the lungs, sinuses, skin, or gastrointestinal tract and cause symptoms like cough, fever, or skin lesions. Risk factors include uncontrolled diabetes, cancer treatments, corticosteroid use, and skin injuries. While it is not contagious, prevention focuses on controlling underlying illnesses. Diagnosis involves tissue samples and imaging tests. Treatment requires antifungal medications like amphotericin B as well as sometimes surgery to remove infected tissue.
This document discusses adjuvant medications in the treatment of pemphigus vulgaris. It begins with definitions and epidemiology of pemphigus vulgaris. It then discusses diagnostic features such as clinical manifestations involving mucous membranes and skin. Management is focused on using corticosteroids as the primary treatment along with immunosuppressive drugs as adjuvants to reduce steroid dosage and side effects. Newer treatments discussed include rituximab and mycophenolate mofetil. Prognosis is generally good with treatment but mucosal lesions can be recalcitrant.
Mooren's ulcer is a rare autoimmune condition characterized by a chronic, painful peripheral corneal ulcer. It is more common in males and older individuals. Treatment involves a stepwise approach starting with topical steroids, then conjunctival resection to remove inflammatory cells, followed by systemic immunosuppressants if needed. Later stages may require additional surgeries like lamellar keratectomy or keratoplasty to promote healing and rehabilitation of the cornea. The goals are to arrest the destructive process and promote reepithelialization of the corneal surface.
Rheumatology MCQs Practice questions with explanationDr. Almas A
Topic: Rheumatology
Exam type: MCQs Practice questions
Q. A 26-year-old female presented to ER with dry cough and shortness of breath and often complains of chest pain. Chest x-ray shows bilateral hilar lymphadenopathy. Which of the following will indicate that the patient suffers from sarcoidosis?
Q: A 50-year-old female presents to ER with dyspnea on exertion and orthopnea, red painful eyes. She complains of chronic dull pain in the gluteal region for the last 5 years and stiffness in the lower back that wakes her up in the morning. X-ray spine reveals squaring of vertebrae with bone spur formation. On MRI sacroiliitis is seen. Which of the following is the most likely diagnosis?
Q: A 60-year-old female presents in OPD with knee joint stiffness in the morning and increases with activity and decreases on rest. She also complains about a crackling noise on joint movement. X-ray shows narrowing of the joint space and osteophytes. Which of the following treatments is recommended in this patient?
Q: A 70-year-old female presented to ER with swelling of knee joint and severe pain. Arthrocentesis revealed rhomboid-shaped crystals that stained deeply blue with H&E stain, and show weak positive birefringence on light microscopy. X-ray reveals chondrocalcinosis. Which of the following statements is true?
Q: A 40-year-old female comes to OPD with dry eyes and dyspareunia for the last 6 months. She also complains of cough and fatigue with joint pains. On examination, her parotid gland was enlarged and laboratory tests revealed anti-Ro antibodies are positive. Which of the following tests is recommended to this patient?
Bullous diseases involve the formation of blisters or vesicles in the epidermis or dermis. There are several types of bullous disorders of immunological origin where autoantibodies damage skin molecules. Pemphigus is an autoimmune disease where antibodies form against desmoglein proteins, causing blistering of the skin and mucous membranes. Pemphigoid also involves autoantibodies targeting basement membrane zone proteins, resulting in tense subepidermal blisters mainly affecting the elderly. Dermatitis herpetiformis is associated with celiac disease and granular IgA deposits in the skin, causing extremely itchy grouped vesicles.
gyanaecology.endometriosis and adenomyosis.(dr.salama)student
The document summarizes endometriosis and adenomyosis. Endometriosis occurs when endometrial tissue grows outside the uterus, most commonly on the ovaries, uterine ligaments and pelvis. It causes pain and infertility. Adenomyosis involves endometrial tissue in the uterine wall. Both can be diagnosed by laparoscopy and treated through drugs or surgery, with hysterectomy providing definitive treatment for severe adenomyosis.
Dermatomyositis is an inflammatory myopathy that affects the skin and muscles. It is characterized by progressive proximal muscle weakness, elevated muscle enzymes, abnormal electromyography and muscle biopsy findings. The cause is unknown but genetic, immunological, infectious and environmental factors may play a role. Treatment involves sun protection, immunosuppressants like hydroxychloroquine and methotrexate, and corticosteroids like prednisone to control muscle and skin symptoms.
Crohn's disease is a chronic inflammatory bowel disease that can involve any part of the gastrointestinal tract. Metastatic Crohn's disease (MCD) is a rare cutaneous manifestation where noncaseating granulomatous skin lesions occur at sites separate from the GI tract in patients with Crohn's. MCD most often presents as papules, plaques or nodules on the arms, legs, genitalia and face. Histopathology of MCD shows granulomatous inflammation in the dermis. Treatment options include steroids, antibiotics, immunosuppressants, infliximab and surgery.
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Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
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Top Effective Soaps for Fungal Skin Infections in India
Bmj33300181
1. Clinical review
Diagnosis and treatment of pyoderma gangrenosum
Trevor Brooklyn, Giles Dunnill, Chris Probert
Pyoderma gangrenosum is a rare but serious
ulcerating skin disease, the treatment of which is
mostly empirical. Pyoderma can present to a variety of
health professionals and several variants exist that may
not be recognised immediately. This can delay the
diagnosis and have serious clinical consequences.1
The
mainstay of treatment is long term immunosuppres-
sion, often with high doses of corticosteroids or low
doses of ciclosporin. Recently, good outcomes have
been reported for treatments based on anti-tumour
necrosis factor , and infliximab proved effective in a
randomised controlled trial. This article reviews the
presentation of pyoderma gangrenosum and the
therapeutic options available.
Methods
We used the keyword “pyoderma gangrenosum” to
search Medline. We also searched the Cochrane
database but found no Cochrane review on this disease.
How can pyoderma be recognised?
Several variants exist, but the most common one is
classic pyoderma gangrenosum. This presents as a
deep ulcer with a well defined border, which is usually
violet or blue. The ulcer edge is often undermined
(worn and damaged) and the surrounding skin is ery-
thematous and indurated (fig 1). The ulcer often starts
as a small papule or collection of papules, which break
down to form small ulcers with a “cat’s paw”
appearance. These coalesce and the central area then
undergoes necrosis to form a single ulcer.
Classic pyoderma gangrenosum can occur on any
skin surface, but is most commonly seen on the legs.
Patients are often systemically unwell with symptoms
such as fever, malaise, arthralgia, and myalgia. Lesions
are usually painful and the pain can be severe. When
the lesions heal the scars are often cribriform. Early
diagnosis and prompt treatment reduce the risk of
scars, and disfigurement may occur if the diagnosis is
missed.1
Pathergy occurs in 25-50% of cases—lesions
develop at the site of minor trauma, so surgery or
debridement are contraindicated.2
Peristomal pyoderma gangrenosum
Peristomal pyoderma, which occurs close to abdominal
stomas, comprises about 15% of all cases of pyoderma.
Most of these patients have inflammatory bowel disease,
but peristomal pyoderma can occur in patients who
have had an ileostomy or colostomy for malignancy or
diverticular disease.3
A large questionnaire based study
found a 0.6% incidence of peristomal pyoderma among
patients with abdominal stomas.4
The ulcers in these
patients have a similar morphology to classic pyoderma
gangrenosum, but bridges of normal epithelium may
traverse the ulcer base (fig 2). The lesions are painful and
often interfere with the stoma bag adhering to the
abdominal wall, which can cause the contents of the bag
to irritate the skin more than usual.5
Summary points
Pyoderma gangrenosum presents in a variety of
guises and is easy to misdiagnose
A biopsy is needed only to exclude other diagnoses
Most treatments are empirical and based on small
series or local experience
Infliximab was more effective than placebo in a
small randomised controlled trial
Fig 1 Classic pyoderma gangrenosum
Cheltenham
General Hospital,
Cheltenham
GL53 7AN
Trevor Brooklyn
consultant
gastroenterologist
Bristol Royal
Infirmary, Bristol
BS2 8HW
Giles Dunnill
consultant
dermatologist
Chris Probert
reader in medicine
Correspondence to:
T Brooklyn
trevor.brooklyn@
glos.nhs.uk
BMJ 2006;333:181–4
181BMJ VOLUME 333 22 JULY 2006 bmj.com
2. Pustular pyoderma gangrenosum
Pustular pyoderma is a rare superficial variant of the
disease. Pyoderma often begins as a pustule or group
of pustules that later coalesce and ulcerate. This
process stops at the pustular stage in pustular
pyoderma, and the patient has a painful pustular lesion
that may persist for months (fig 3). Pustular pyoderma
seems to be confined to patients with inflammatory
bowel disease and tends to occur on the trunk and
extensor surfaces of the limbs.6–8
Bullous pyoderma gangrenosum
Bullous pyoderma is a superficial variant that affects the
upper limbs and face more than the lower limbs. It is
associated mostly with haematological conditions. This
form of the disease presents as concentric bullous areas
that spread rapidly in a concentric pattern. They may
break down to form more superficial ulcers than those
seen in classic pyoderma, although they still have the
blue undermined edge. Prognosis is often poor because
of the underlying haematological malignancy.8 9
Vegetative pyoderma gangrenosum
Vegetative pyoderma is a superficial form of disease
that seems to be less aggressive than other varieties (fig
4). It usually occurs as a single lesion in patients who
are otherwise well and may respond to local treatment
more readily than other forms of the disease.8 10
What is the histopathology of pyoderma?
The histopathology of pyoderma gangrenosum
depends on the timing and site of the biopsy.11
Biopsies
taken early in the disease and from the advancing, ery-
thematous border tend to show an infiltrate of chronic
inflammatory cells confined to the dermis (fig 5). They
often have features suggestive of vasculitis at the edge
of the ulcer, with a perivascular lymphocytic infiltrate
and fibrinoid necrosis of the dermal vessel wall. Occa-
sionally, extravasation of red blood cells and areas of
thrombosis are also seen. Ulceration of the epidermis
tends to be secondary to the dermal inflammation.
Biopsies taken later in the course of ulceration usually
show a polymorphonuclear cell infiltrate with features
of ulceration, infarction, and abscess formation.11
Who gets pyoderma gangrenosum?
About half of the cases are associated with underlying
systemic conditions, such as inflammatory bowel
disease, arthritis, and haematological malignancies.2
About 30% of cases occur in patients with inflammatory
bowel disease. About 2% of patients with inflammatory
bowel disease will develop pyoderma.12
Occasionally, the
skin condition presents before the bowel disease.
Pyoderma gangrenosum was thought to be associated
only with ulcerative colitis, but both Crohn’s disease and
ulcerative colitis have a similar incidence.13
Pyoderma
gangrenosum is not related to the activity of the inflam-
matory bowel disease, and it often occurs in patients
whose bowel disease is in clinical remission.
About 25% of patients have arthritis, most often
seropositive rheumatoid arthritis, although the disease
can occur in patients with seronegative arthritis or
spondyloarthropathy. As with inflammatory bowel dis-
ease, the activity of the arthritis is not related to
pyoderma.14
Haematological malignancies are the next
most common disorders associated with pyoderma,
and these tend to be myeloid rather than lymphoid in
origin. Leukaemia is the most frequently reported
Fig 2 Peristomal pyoderma gangrenosum
Fig 3 Pustular pyoderma gangrenosum
Fig 4 Vegetative pyoderma gangrenosum
Clinical review
182 BMJ VOLUME 333 22 JULY 2006 bmj.com
3. malignancy, usually acute myeloid leukaemia and most
commonly the myelocytic or monomyelocytic type.15
What is the differential diagnosis?
The diagnosis of pyoderma gangrenosum is based
mainly on clinical findings because biopsies show no
specific diagnostic features. In many cases, however, a
biopsy can help exclude other conditions such as malig-
nancy, infections, or cutaneous vasculitis. Swabs should
be taken from the ulcer, as pyoderma is treated
differently from infection. The differential diagnosis of
pyoderma gangrenosum is wide (box). Special mention
must be made of Sweet’s syndrome, which is character-
ised by sudden onset of fever and an erythematous,
papular eruption. Patients have leucocytosis and skin
biopsy shows a dense neutrophilic infiltrate. Sweet’s syn-
drome and pyoderma can coexist in the same patient as
they are both neutrophilic dermatoses.12
How is it treated?
No single, specific treatment exists and few controlled
trials of treatment have been done.16
Most clinicians use
a stepwise approach and both topical and systemic
treatments. Immunosuppression is the mainstay of
treatment, and the most commonly used drugs are
corticosteroids and ciclosporin. Several other immuno-
suppressive agents have been used with varied results,
but treatment is largely empirical and the choice of
treatment often depends on local experience.12 16
Topical treatments
Highly potent topical corticosteroids (occasionally
underneath occlusive dressings) may be sufficient to
induce remission.2
Triamcinolone 40 mg/ml may be
injected into the ulcer edge, either alone or as an
adjunct to systemic treatment.17
Recently, topical
tacrolimus has been shown to be effective in patients
with peristomal disease. This is now available as a 0.1%
and 0.03% ointment.5
Corticosteroids
Most patients need systemic treatment to induce
remission and doctors often start patients on oral cor-
ticosteroids at an early stage. Prednisolone is the drug
of choice and is usually started at high doses (60-120
mg) (level B evidence).8 16
Patients exposed to these
doses for a long time are at risk of steroid related side
effects and may benefit from the addition of a bone
protecting agent. Minocycline 100 mg twice daily may
be of some benefit, usually as an adjunct to oral
steroids (level C evidence).18
Rapid improvement has
been reported in patients with severe disease given
intravenous methylprednisolone as pulse therapy of
1 g daily for three to five days (level B evidence), and
several series and reviews support this treatment.16 19
Ciclosporin
Other immunosuppressive agents may be used—firstly,
to reduce the dependence on corticosteroids and, sec-
ondly, because pyoderma is often resistant to
treatment. When corticosteroids fail, the most widely
used alternative is ciclosporin. Several case reports and
small case series have demonstrated a good clinical
response to low dose ciclosporin (level B evidence).
Most patients show clinical improvement within three
weeks with a dose of 3-5 mg/kg/day. Ciclosporin has
several serious side effects, including nephrotoxicity,
hypertension, and increased risk of cancer. Such side
Fig 5 A lymphocytic infiltrate within the dermis in pyoderma
gangrenosum
Differential diagnosis of pyoderma gangrenosum
Infections
Bacterial
Mycobacterial
Fungal
Viral
Parasitic
Malignancy
Squamous cell carcinoma
Cutaneous lymphoma
Vascular ulceration
Venous or arterial disease
Antiphospholipid syndrome
Systemic conditions
Systemic lupus erythematosis
Rheumatoid arthritis
Behçet’s disease
Wegner’s granulomatosis
Sweet’s syndrome
Additional educational resources
Review article in the Lancet (www.thelancet.com/journals/lancet/article/
PIIS0140673697101878/abstract)—an excellent overview of pyoderma
gangrenosum
DermAtlas (http://www.dermatlas.org/derm/result.cfm?Diagnosis =
47670916)—images of pyoderma gangrenosum with brief case histories
Information for patients
emedicine (emedicine.com/derm/topic367.htm )—detailed overview from a
leading American based e-learning website (with pictures)
Ongoing research
When is the optimal time to introduce treatments based on anti-tumour
necrosis factor ?
If remission is achieved with infliximab, should patients be placed on
maintenance infusions? If so, for how long?
How does infliximab compare with conventional treatments, such as
corticosteroids or ciclosporin?
Clinical review
183BMJ VOLUME 333 22 JULY 2006 bmj.com
4. effects have not been reported for the low doses used
to treat pyoderma.16 20
Other immunosuppressants
Azathioprine, used alone or combined with cortico-
steroids, has had variable results.16
Tacrolimus has also
been used systemically, and two centres where patients
received 0.1-0.3 mg/kg have reported sustained
responses.21
Anti-tumour necrosis factor agents
Pyoderma has been reported to respond to infliximab,
a monoclonal antibody against tumour necrosis factor
.22
More recently, pyoderma gangrenosum was
reported to resolve after treatment with etanercept, a
recombinant protein that neutralises the soluble factor.
The authors reported a single case where pyoderma
gangrenosum healed when etanercept was given in
conjunction with oral corticosteroids, although the
steroids could not be tapered completely (level C
evidence).23
In a randomised controlled trial, we found
that infliximab was superior to placebo. We ran-
domised 30 patients to infliximab 5 mg/kg or placebo.
The response rate between the groups differed by 40%
at week 2 (P = 0.025, 95% confidence interval 11% to
70%), giving a number needed to treat of 2.5.
Confidence intervals were wide because of the small
number of patients. By the end of the study, 20 of 29
patients (69%) had benefited from infliximab, includ-
ing six of 29 (21%) who were in remission.24
Two
serious adverse effects occurred in the trial. Reports on
side effects in inflammatory bowel disease are rare.25
What is our approach to treatment?
Morbidity and potential for rapid progression are high
in most patients, so once suspected we advise an urgent
referral to the dermatology department. We recom-
mend oral corticosteroids (with or without mino-
cycline) as first line treatment. If patients do not
respond promptly, we then use infliximab as this has
fewer recognised side effects than ciclosporin and has
been used widely in inflammatory bowel disease and
rheumatoid arthritis.25
We recommend an induction
dose regimen of 5 mg/kg at weeks 0, 2, and 6, followed
by further treatments as necessary, depending on
response. Another immunosuppressant, such as
azathioprine, should be given at the same time as
infliximab. This approach is not strictly evidence based
but is now accepted practice in other inflammatory
conditions, such as Crohn’s disease.25
Contributors: CP had the idea for this review. TB searched the
literature and wrote the first draft, which was edited by CP and
GD. TB is guarantor.
Funding: None.
Competing interests: The authors took part in a trial of
infliximab for treating pyoderma gangrenosum, supported by a
grant from Schering-Plough Ltd. The company played no part
in study design; collection, analysis, and interpretation of data;
writing of the paper; or the decision to submit the paper for
publication.
1 Harris AJ, Regan P, Burge S. Early diagnosis of pyoderma gangrenosum
is important to prevent disfigurement. BMJ 1998;316:52-3.
2 Bennett ML, Jackson JM, Jorizzo JL, Fleischer AB Jr, White WL, Callen JP.
Pyoderma gangrenosum. A comparison of typical and atypical forms
with an emphasis on time to remission. Case review of 86 patients from 2
institutions. Medicine (Baltimore) 2000;79:37-46.
3 Lyon CC, Smith AJ, Beck MH, Wong GA, Griffiths CE. Parastomal
pyoderma gangrenosum: clinical features and management. J Am Acad
Dermatol 2000;42:992-1002.
4 Lyon CC, Smith AJ, Griffiths CE, Beck MH. The spectrum of skin disor-
ders in abdominal stoma patients. Br J Dermatol 2000;143:1248-60.
5 Lyon CC, Stapleton M, Smith AJ, Mendelsohn S, Beck MH, Griffiths CE.
Topical tacrolimus in the management of peristomal pyoderma
gangrenosum. J Dermatol Treat 2001;12:13-7.
6 Fenske NA, Gern JE, Pierce D, Vasey FB. Vesiculopustular eruption of
ulcerative colitis. Arch Dermatol 1983;119:664-9.
7 Callen JP, Woo TY. Vesiculopustular eruption in a patient with ulcerative
colitis. Pyoderma gangrenosum. Arch Dermatol 1985;121:399, 402.
8 Powell FC, Collins S. Pyoderma gangrenosum. Clin Dermatol 2000;
18:283-93.
9 Hay CR, Messenger AG, Cotton DW, Bleehen SS, Winfield DA. Atypical
bullous pyoderma gangrenosum associated with myeloid malignancies. J
Clin Pathol 1987;40:387-92.
10 Wilson-Jones E, Winkelmann RK. Superficial granulomatous pyoderma:
a localized vegetative form of pyoderma gangrenosum. J Am Acad
Dermatol 1988;18:511-21.
11 Su WP, Schroeter AL, Perry HO, Powell FC. Histopathologic and immu-
nopathologic study of pyoderma gangrenosum. J Cutan Pathol 1986;
13:323-30.
12 Callen JP. Pyoderma gangrenosum. Lancet 1998;351:581-5.
13 Thornton JR, Teague RH, Low-Beer TS, Read AE. Pyoderma gangreno-
sum and ulcerative colitis. Gut 1980;21:247-8.
14 Von den Driesch P. Pyoderma gangrenosum: a report of 44 cases with
follow-up. Br J Dermatol 1997;137:1000-5.
15 Duguid CM, Powell FC. Pyoderma gangrenosum. Clin Dermatol 1993;
11:129-33.
16 Reichrath J, Bens G, Bonowitz A, Tilgen W. Treatment recommendations
for pyoderma gangrenosum: an evidence-based review of the literature
based on more than 350 patients. J Am Acad Dermatol 2005;53:273-83.
17 Hughes AP, Jackson JM, Callen JP. Clinical features and treatment of
peristomal pyoderma gangrenosum. JAMA 2000;284:1546-8.
18 Berth-Jones J, Tan SV, Graham-Brown RAC, Pembroke AC. The success-
ful use of minocycline in pyoderma gangrenosum—a report of seven
cases and review of the literature. J Dermatol Treat 1989;1:23-5.
19 Johnson RB, Lazarus GS. Pulse therapy. Therapeutic efficacy in the treat-
ment of pyoderma gangrenosum. Arch Dermatol 1982;118:76-84.
20 Friedman S, Marion JF, Scherl E, Rubin PH, Present DH. Intravenous
cyclosporine in refractory pyoderma gangrenosum complicating inflam-
matory bowel disease. Inflamm Bowel Dis 2001;7:1-7.
21 Lyon CC, Kirby B, Griffiths CE. Recalcitrant pyoderma gangrenosum
treated with systemic tacrolimus. Br J Dermatol 1999;140:562-4.
22 Regueiro M, Valentine J, Plevy S, Fleisher MR, Lichtenstein GR.
Infliximab for treatment of pyoderma gangrenosum associated with
inflammatory bowel disease. Am J Gastroenterol 2003;98:1821-6.
23 McGowan JW, Johnson CA, Lynn A. Treatment of pyoderma gangreno-
sum with etanercept. J Drugs Dermatol 2004;3:441-4.
24 Brooklyn TN, Dunnill MG, Shetty A, Bowden JJ, Williams JD, Griffiths CE,
et al. Infliximab for the treatment of pyoderma gangrenosum: a
randomised, double blind, placebo controlled trial. Gut 2006;55:505-9.
25 Hanauer SB, Feagan BG, Lichtenstein GR, Mayer LF, Schreiber S,
Colombel JF, et al. Maintenance infliximab for Crohn’s disease: the
ACCENT I randomised trial. Lancet 2002;359:1541-9.
(Accepted 20 June 2006)
GP tips
Pyoderma gangrenosum can occur on any skin surface and should be
considered in any ulcer or surgical wound that does not heal
Pyoderma usually develops rapidly and can progress from a pimple to a
crater in 24-48 hours
Pyoderma is usually painful and patients may have systemic features such as
fever
If pyoderma is suspected, the patient should be referred urgently for a
specialist opinion
A patient’s story
I first came across pyoderma about a month after having an ileostomy in
December 2001. It started out as a small but sore spot rather like an insect
bite, just under the stoma. Over the next 24-48 hours the spot took on a life
of its own, growing and erupting into an ulcer with blue and red edges. I
occasionally needed morphine for the pain.
I was admitted to hospital where I was introduced to a doctor conducting
a trial of infliximab, a new treatment for pyoderma. I decided to take up the
offer of a place on the trial—I felt I had nothing to lose. The drug was given
by infusion and the pyoderma was brought under control within 48 hours.
Four years later I am on a maintenance regimen of infusions every eight
weeks. I contracted pyoderma on my leg about two years ago, which flared up
while I was not being treated with infliximab (during a six month break in
treatment). Since being on the maintenance dose I have had no problems.
Clinical review
184 BMJ VOLUME 333 22 JULY 2006 bmj.com