Uncommon causes of ulceration.
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Drug Eruptions↗
Biomedical subjects
Girish K Patel
Publications and source records attributed to Girish K Patel.
Imiquimod 5% cream monotherapy for cutaneous squamous cell carcinoma in situ (Bowen's disease): a randomized, double-blind, placebo-controlled trial.
BACKGROUND: We conducted a double-blind, placebo-controlled, randomized trial to evaluate the preliminary efficacy and safety of imiquimod 5% cream treatment for cutaneous squamous cell carcinoma (SCC) in situ. METHODS: In all, 31 patients with biopsy-proven cutaneous SCC in situ were randomly assigned to placebo (vehicle) (n = 16) or imiquimod 5% cream (n = 15) daily for 16 weeks. Patients were assessed at week 28 for the primary end point, resolution of cutaneous SCC in situ. RESULTS: Of the 31 patients enrolled, 3 dropped out. Intention-to-treat analysis revealed 11 of the 15 patients (73%) in the imiquimod group achieved resolution of cutaneous SCC in situ, with no relapse during the 9-month follow-up period; none in the placebo group achieved resolution (P < .001). Imiquimod 5% cream was generally well tolerated and there were no serious adverse events. LIMITATIONS: Topical imiquimod 5% cream has proven to be an effective treatment for cutaneous SCC in situ. However, studies to define the ideal dosing regimen and cost-effectiveness are required before it can be accepted as a recognized therapy. CONCLUSIONS: In this controlled trial, patients with cutaneous SCC in situ receiving topical imiquimod 5% cream as monotherapy experienced a high degree of clinical benefit compared with placebo.
Aged↗
Numerous keratinocyte subtypes involved in wound re-epithelialization.
The expression of different keratin intermediate filaments has been used to define keratinocyte maturation and different phenotypic subtypes involved in acute wound (AW) healing. Immunohistochemistry with specific anti-keratin monoclonal and polyclonal antibodies was used to examine AW in normal healthy volunteers (n = 16). In all wounds examined, basal keratinocytes and cells at the leading edge of the wound expressed keratins K5 and K14. However, suprabasal cells had a more complex pattern of keratin expression, which was dependent on their position relative to the wound and location within the suprabasal compartment of the epidermis. In general, K10 was expressed in suprabasal keratinocytes at the wound edge, but not in keratinocytes covering the wound center, which expressed K6, K16, and K17 in a complex fashion. Ki67 expression, a marker of cell proliferation, was restricted to basal and immediate suprabasal layers at the wound edge. Keratinocytes populated the wound bed below the scab by migration, which was supported by keratinocyte proliferation in the surrounding epidermis both at and adjacent to the wound edge.
Cell Differentiation↗
Nocturnal sedation in a child with facial ulceration.
Mostly, herpes zoster affects adults and therefore childhood presentation can represent a diagnostic challenge. Childhood herpes zoster, when it occurs, can also be associated with peripheral nerve complications, as illustrated by this case. A 3-year-old child who had herpes zoster developed a nasolabial scar resulting in a shallow non-healing ulcer from being repeatedly picked. Healing was only achieved after nocturnal sedation, with chloral hydrate.
Acyclovir↗
Generalised cutaneous necrosis: a complication of low-molecular-weight heparin.
Subcutaneous low-molecular-weight heparin (LMWH) injections have a predictable dose-dependent anticoagulant effect and have therefore become popular for the prevention and management of thromboembolic diseases. It was initially hoped that use of the smaller molecule and better dose titration would reduce the incidence of side-effects associated with conventional heparin therapy. However, case reports such as this have demonstrated that LMWHs still have the capacity to cause heparin-induced thrombocytopaenia and heparin-induced thrombocytopaenia with thrombosis, as well as heparin necrosis. To our knowledge, this is the first-ever-reported case of heparin necrosis associated with tinazaparin. Heparin necrosis is characterised by widespread life-threatening cutaneous necrosis and systemic thrombosis, in which fatal progression of disease can only be halted by stopping heparin therapy. As heparin necrosis is an uncommon disorder, in this report we focus on the clinical clues that may help woundcare professionals consider and confirm the diagnosis.
Aged↗
The role of nutrition in the management of lower extremity wounds.
From 3000 BC, healers have understood the importance of nutrition in wound care and used nutritional supplements to aid healing. Many of the teachings from Hippocrates, the father of modern-day medicine, clearly state his firm belief that good health can be achieved through nutrition. In the early 1900s when advances in biochemistry were frequent, many of the essential constituents of nutrition were characterized, which formed the basis for many animal and human wound-healing experiments. This led to the discovery of vitamin C, zinc, and many other components essential for the orderly progression of healing. Modern-day research has concentrated on finding nutritional components that can enhance healing through supra-physiological doses, such as in the use of the amino acids arginine and carnitine. However, clinicians need to be aware that approximately 50% of patients admitted to the hospital are malnourished, requiring dietary supplementation; appropriate nutritional assessment and advice therefore should be an integral part of all wound management. This review provides an up-to-date commentary on the role of nutrition in wound care, with specific emphasis on lower limb wounds, from a historical perspective, and within it both the biomedical approach and current herbalist practices are considered.
Animals↗
Wound problems due to zinc deficiency.
Zinc deficiency, though uncommon, can occasionally present in current medical practice. A 4.5-year-old boy with previous gastrointestinal surgery presented with diarrhoea, disinterest and dermatitis affecting the face and perineum. The clinical diagnosis was confirmed by the presence of a low serum zinc level. Administration of parenteral zinc led to rapid improvement in diarrhoea, demeanor and dermatitis. Further surgery was then undertaken, surgery had been postponed until normalisation of zinc levels due the association between zinc deficiency and poor postoperative wound healing.
Child, Preschool↗
Treatment of staphylococcal scalded skin syndrome.
Humans are a natural reservoir for Staphylococcal aureus. Colonization begins soon after birth and predisposes to infection. S. aureus is one of the most common causes of skin infection, giving rise to folliculitis, furunculosis, carbuncles, ecthyma, impetigo, cellulitis and abscesses. In addition, S. aureus may cause a number of toxin-mediated life-threatening diseases, including staphylococcal scalded skin syndrome (SSSS). Epidermolytic toxins released by certain S. aureus strains cause SSSS by cleaving the epidermal cell adhesion molecule, desmogelin-1, resulting in superficial skin erosion. Recent experiments have revealed similarities in the pathophysiology of SSSS and pemphigus foliaceus, an autoimmune disorder that is characterized by antibodies targeting the same epidermal attachment protein. SSSS typically affects neonates and infants but may also occur in predisposed adults. It is painful and distressing for the patient and parents, although most cases respond to antibiotic treatment. Mortality is low in infants but can be as high as 67% in adults, and is dependent on the extent of skin involvement and the comorbid state. Thus, the management of adults who develop SSSS remains a major therapeutic challenge. The antibody response against the toxins neutralizes their effect and prevents recurrence or limits the effects to the area of infection, which is known as bullous impetigo.
Animals↗
Staphylococcal scalded skin syndrome: diagnosis and management.
Staphylococcal scalded skin syndrome (SSSS) is a common disorder that is usually seen in infants and children and rarely seen in adults. SSSS usually presents with a prodrome of sore throat or conjunctivitis. Extremely tender flaccid bullae, which are Nikolsky sign-positive, develop within 48 hours and commonly affect the flexures; occasionally, large areas of the skin may be involved. The bullae enlarge and rupture easily to reveal a moist erythematous base, which gives rise to the scalded appearance. SSSS in adults is a rare disorder, though there are now over 50 documented cases. Usually SSSS occurs in predisposed individuals, but not all adults have an underlying illness. Whereas mortality in childhood SSSS is approximately 4%, the mortality rate in adults is reported to be greater than 60%. SSSS is caused by an infection with a particular strain of Staphylococcus aureus, which leads to blistering of the upper layer of the skin, by the release of a circulating exotoxin. It has recently been demonstrated that the exfoliative exotoxin responsible for SSSS leads to the cleavage of desmoglein 1 complex, an important desmosomal protein. The same toxins that are responsible for causing SSSS also cause bullous impetigo. There appears to be a relationship between the disease extent, the amount of toxin produced and whether the toxin is released locally or systemically. As a result there is likely to be a spectrum of disease and there are likely to be a number of milder cases of adult SSSS that go undiagnosed. Social improvements and hygiene have led to a dramatic fall in the number of cases of SSSS. Treatment is usually straightforward, when there is no coexistent morbidity and the presentation is mild, but can be demanding if the patient is particularly ill. SSSS is still associated with mortality, particularly when it occurs in adults.
Biopsy, Needle↗
Familial confluent and reticulated papillomatosis.
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Adult↗