Cutaneous leucocytoclastic vasculitis (CLV) is a type of small vessel vasculitis, predominantly presenting with palpable purpuras and sometimes with systemic manifestations. The following report describes the case of a woman, who presented with fever, anorexia and maculopapular lesions over both lower limbs. Skin biopsy revealed CLV. CT scan demonstrated bilateral pulmonary nodules, ileocecal wall thickening and generalised lymphadenopathy. Colonoscopy guided biopsy obtained from ileocecal valve ulcer showed epitheloid cell granuloma with Langhans-type giant cells and caseous necrosis. Rapid clinical improvement was seen with anti-tubercular therapy. Among infectious causes, although rare and an uncommon presentation, Mycobacterium tuberculosis should be considered as an important cause of CLV.

We report a case of IgA vasculitis that developed during the treatment of tuberculosis. Patients with tuberculosis who are on antituberculosis treatment can be administered steroids for severe disease or complications.

Cutaneous tuberculosis is an uncommon entity with several clinical forms recognized. Histopathologically, most cases are characterized by granulomatous inflammation and caseating necrosis, although less common findings, including vasculitis, have also been described. We report a 55-year-old male with a history of recently diagnosed dermatomyositis receiving immunosuppression with mycophenolate mofetil and prednisone, who developed multifocal soft tissue abscesses and an indurated erythematous plaque on the back. Skin biopsy of the back revealed a necrotizing medium-vessel vasculitis. Mycobacterium tuberculosis was detected in the skin via acid-fast bacilli stain and confirmed by tissue culture and polymerase chain reaction. Cutaneous findings improved rapidly with antituberculosis therapy. This case illustrates an uncommon clinical and histopathologic presentation of disseminated tuberculosis.

Infection by the hepatitis C virus (HCV) is currently considered to be a global health issue, with a high worldwide prevalence and causing chronic disease in afflicted individuals. The disease largely involves the liver but it can affect other organs, including the skin. While leukocytoclastic vasculitis has been reported as one of the dermatologic manifestations of HCV infection, there are no reports of this condition as the first symptom of HCV recurrence after liver transplantation.

We report here a case of leukocytoclastic vasculitis in a liver transplant recipient on maintenance immunosuppression. The condition presented as a palpable purpura in both lower extremities. Blood and urine cultures were negative and all biochemical tests were normal, excepting evidence of anemia and hypocomplementemia. Imaging examination by computed tomography showed a small volume of ascites, diffuse thickening of bowel walls, and a small bilateral pleural effusion. Skin biopsy showed leukocytoclasia and fibrinoid necrosis. Liver biopsy was suggestive of HCV recurrence in the graft, and HCV polymerase chain reaction yielded 11460 copies/mL and identified the genotype as 1A. Treatment of the virus with a 12-wk direct-acting antiviral regimen of ribavirin, sofosbuvir and daclatasvir led to regression of the symptoms within the first 10 d and subsequent complete resolution of the symptoms.

This case highlights the difficulties of diagnosing skin lesions caused by HCV infection in immunosuppressed patients.

Tuberculosis (TB) is the commonest infectious cause of death globally. Adverse reactions to first-line tuberculosis antibiotics are common and have a major impact on the outcomes of patients as second-line antibiotics are less effective and more toxic. The present review addresses the most recent literature regarding epidemiology, investigating reactions, and reintroducing treatment in patients who have had their treatment interrupted.

Studies have demonstrated that up to 60% of patients experience adverse reactions to TB treatment; around a third of these are idiosyncratic and may relate to immune sensitization. There is an increased risk in patients with HIV. For patients with severe cutaneous reactions patch testing has an important role; however, systemic reactions to patch testing are common in patients with HIV. In-vitro testing remains limited to specialist centers but studies have identified drug-specific lymphocyte responses in patients with cutaneous and liver reactions. Desensitization of patients with severe cutaneous reactions have been demonstrated to be possible, albeit at high risk.

Management of these patients remains suboptimal. Better identification of predisposing factors, such as HLA alleles, are needed to identify patients at risk. Improved in-vitro diagnostics will reduce the need to re-expose the patient to the drug and optimized desensitization regimens will improve patient safety when drugs have to be re-introduced.

Cutaneous tuberculosis (CT) is rare in industrialized countries. Given the clinicopathological polymorphism and the difficulty of isolating the pathogen, diagnosis can be difficult. The condition may be associated with other known locations of the disease or in rare cases, it may be a tell-tale sign, as in our case, in which leg ulcers revealed paucisymptomatic disseminated tuberculosis.

A 67-year-old man was referred for rapidly extensive ulcers of the right leg contiguous to debilitating arthritis of the knee of unknown aetiology for 18 months. Earlier investigations revealed thymoma and a pulmonary nodule considered to be sarcoidosis. A skin biopsy showed a granulomatous eosinophilic-rich infiltrate and vasculitis of the small vessels. Screening of the skin sample and gastric aspirate for Koch Bacillus (BK) was negative. A diagnosis of sarcoidosis was made. A positive QuantiFERON test eventually led to the correct diagnosis. On further testing of bronchoalveolar fluid and a synovial biopsy, culture for Mycobacterium tuberculosis (MT) was positive. The PET scan showed high metabolism in the prostate, bone, spleen, liver, nodes and heart. The quad- and then dual-antibiotic antitubercular therapies produced a rapid improvement but treatment was continued over 12 months, given the persistence of high metabolism on PET-CT scan and the low blood rifampicin concentration.

A CT should be considered in the presence of giant-cell granulomas, even in the absence of caseous necrosis, and where both direct examination and culture for the skin are negative. Our case also underlines the importance of an extensive workup to rule out disseminated disease even if the patient is not symptomatic.

Leukocytoclastic vasculitis (LCV), a disease characterized by inflammation of the small vessels, presents with palpable purpura, especially in the lower extremities. Its etiology is known to include drugs, infection, collagen tissue disease, and malignancy, but LCV caused by anti-tuberculosis drugs is very rarely seen. This report describes the case of a 12-year-old girl who developed LCV with rifampicin and ethambutol while undergoing anti-tuberculosis treatment due to extensive pulmonary involvement.

Anti-tuberculosis drugs frequently result in cutaneous adverse reactions but Isoniazid is known to have least toxic potential for cutaneous reactions. We report a rare case of Isoniazid induced cutaneous leucocytoclastic vasculitis. A 64-year-old male was diagnosed to have Pott's spine with multiple vertebral body involvement (D8-12 vertebrae). Subsequently, he was treated with first line anti-TB drugs i.e., Isoniazid, Rifampicin, Pyrazinamide and Ethambutol. On the fourth day of treatment with Anti Tuberculosis Treatment (ATT), the patient developed an erythematosus rash over right upper limb not associated with itching or pain, non-blanchable macules and papules over bilateral shins on lower limbs, petechiae on both forearms and hyper pigmented, scaly rash over right axilla and buttocks. The skin biopsy report was consistent with cutaneous leukocytoclastic vasculitis. Although rare, Isoniazid among anti-tuberculosis drugs should be considered as potential cause of drug-induced cutaneous leukocytoclastic vasculitis in the differential diagnosis of erythematosus rash with petechiae.

Antituberculosis therapy-associated cutaneous leukocytoclastic vasculitis (CLV) has been rarely reported. We describe a case of CLV induced by rifampicin and pyrazinamide. A 14-year-old male diagnosed with disseminated tuberculosis developed purpuric lesions after 1.5 months of treatment. Histopathology was consistent with leukocytoclastic vasculitis. Skin lesion improved after cessation of the two drugs and treatment with corticosteroids.

Cutaneous leukocytoclastic vasculitis (CLV) is an inflammatory vascular disorder rarely reported to be associated with tuberculosis. The following report describes the case of a young man with multifocal tuberculosis revealed by CLV. Diagnosis was confirmed by the presence of tuberculoid granuloma with caseous necrosis on pleural and perianal biopsy, and a rapid improvement in anti-tuberculous quadritherapy. Although rarely seen, Mycobacterium tuberculosis should be considered as a potential cause of CLV.

Peripheral gangrene, characterized by distal ischemia of the extremities, is a rare complication in patients with tuberculosis (TB). We diagnosed a female patient with gangrene of her left toe caused by TB infection. She presented with fever, lymphadenectasis, and peripheral gangrene of the left toe. Lymph node biopsy confirmed tuberculous lymphadenitis and the computer tomography angiography showed vasculitis. The patient underwent antituberculous therapy and her condition was gradually improved. Although it is rare, TB should be considered as a possible cause of peripheral gangrene.

Anti-tuberculosis drugs frequently result in cutaneous adverse reactions, including pruritus, maculopapular exanthems, and urticaria. However, anti-tuberculosis drug-associated cutaneous leukocytoclastic vasculitis (CLV) has been rarely reported. We describe a case of CLV induced by rifampin and pyrazinamide. A 38-year-old male had been diagnosed with pulmonary tuberculosis two months ago and then he started standard anti-tuberculosis therapy with isoniazid, rifampin, ethambutol, and pyrazinamide. Purpuric lesions developed in the extremities after 1.5 months of anti-tuberculosis medication; the lesions progressively spread over the entire body. Histopathology of the purpuric skin lesion was consistent with leukocytoclastic vasculitis. The skin lesion improved after cessation of anti-tuberculosis medications and treatment with oral corticosteroids and antihistamines. Anti-tuberculosis drugs were rechallenged one at a time over 3 days. Purpura recurred on the right forearm and forehead after taking 300 mg of rifampin. The skin lesion disappeared after taking oral prednisolone. Finally, 1,500 mg of pyrazinamide was readministrated, and then purpuric lesions recurred on both forearms. This report describes a case of leukocytoclastic vasculitis secondary to rifampin and pyrazinamide therapy.