Tuberculosis verrucosa cutis (TVC) is a common cutaneous form of paucibacillary tuberculosis in an individual with moderate to high degree of immunity to Mycobacterium tuberculosis infection. Clinical appearance of TVC is mostly very typical with well-defined warty plaques presenting mostly on hands, knees, ankle, and buttocks; however several atypical morphology of the lesions have also been described. We hereby report a case of TVC, masquerading as asymptomatic diffuse keratoderma of left foot for nine months, in an otherwise healthy individual, obstructing easy diagnosis of cutaneous tuberculosis. Diagnosis was confirmed by histopathology.
Acne vulgaris is the most common condition treated by physicians worldwide. Though most acne patients remit spontaneously, for the ones that do not or are unresponsive to conventional therapy or have obvious cutaneous signs of hyperandrogenism, hormonal therapy is the next option in the therapeutic ladder. It is not strictly indicated for only those patients who have cutaneous or biochemical evidence of hyperandrogenism, but can be used even without any evidence of hyperandrogenism, for therapy-resistant acne. It can be prescribed as monotherapy, but when used in combination with other conventional therapies, it may prove to be more beneficial. Hormonal evaluation is a prerequisite for hormonal therapy, to identify the cause behind hyperandrogenism, which may be ovarian or adrenal. This article reviews guidelines for patient selection and the various available hormonal therapeutic options, their side-effect profile, indications and contraindications, and various other practical aspects, to encourage dermatologists to become comfortable prescribing them.
Intra-hepatic cholestasis of pregnancy is a cholestatic disorder characterized by i) pruritus, with onset in the third trimester of pregnancy, without any primary skin lesions, ii) elevated fasting serum bile acids > 10 μmol/L (and elevated serum transaminases), iii) spontaneous relief of signs and symptoms within two to three weeks after delivery, and iv) absence of other disease that cause pruritus and jaundice. It is believed to be a multi-factorial disease with interplay between genetic, environmental and hormonal factors. Incidence is between 0.02% to 2.4% of all pregnancies; with wide geographical variations. Maternal prognosis is usually good but can result in adverse fetal outcomes like meconium staining of amniotic fluid, fetal bradycardia and even fetal loss. Response to anti-histaminic is poor. Of all the medical therapies that have been described for the treatment for IHCP, ursodeoxycholic acid has the best response in relieving pruritus in mother, and probably has a role in preventing even the perinatal complications. Timely diagnosis and treatment is urged in order to prevent fetal complications and an early delivery between 37 to 38 weeks should be contemplated in severe cases, especially once fetal lung maturity is attained.
Gerhard-Henrik Armauer Hansen, a Norwegian scientist, discovered Mycobacterium leprae as the causative organism for leprosy, defying the hereditary affliction theory of the disease. He was born in Bergen, Norway in 1841 in a Danish family. After acquiring his medical degree in 1866 from the University of Oslo, he joined as an assistant physician in a leprosy hospital in Bergen. In 1873, he published his report claiming leprosy to be an infectious disease with a description of the infectious material in leprous tissue. His conviction of belief and an unstinted devotion to a lifetime of scientific research changed the way leprosy was approached as a disease. It was the fruit of his untiring work that the amended act of 1885 was passed, which resulted in steady decline in leprosy burden in Norway. In February 1912 he breathed his last, leaving behind an inspirational story of a brave heart scientist who fought all odds to unveil the truth for the benefit of mankind.
Epidermolysis bullosa pruriginosa (EBP) is a subtype of dominant dystrophic epidermolysis bullosa (DDEB) and is clinically characterized by pruritic lichenified plaques or prurigo-like lesions with violaceous linear scarring. Pruritus has always been described as one of the most striking features in EBP. Mutations in COL7A gene, especially in the glycine residue, have been shown to cause this form of DDEB. In this report, we describe a north Indian familial clustering of three cases of EBP, spread across two generations, presenting with hypertrophic lichenoid cutaneous lesions, which were completely asymptomatic. Clinical and histopathological analysis favored the diagnosis of EBP in all three cases. They are being reported for their unusual asymptomatic presentation.
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