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We report a 79-year-old female with anaphylactoid purpura on her legs and unusual large annular purpura on the trunk. Histopathological characteristics of leukocytoclastic vasculitis were observed in the upper and middle dermis of both types of skin lesions. She was complicated by Sjögren's syndrome and advanced cervical cancer. The annular purpura spontaneously resolved in a week and did not recur. However, the anaphylactoid purpura relapsed more frequently and spread more widely following the elevation of her serum SCC antigen levels from the onset of purpura until her death. We consider that the characteristic annular configuration was caused by the complication of Sjögren's syndrome and that the recurrent anaphylactoid purpura indicated paraneoplastic vasculitis primarily caused by the tumor specific protein immune complexes. Complication by Sjögren's syndrome many also play a role in the development of allergic vasculitis.
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Purpura simplex manifests clinically as macular purpuric and petechial pigmented, golden, annular, or lichenoid lesions. These subtypes have been termed Schamberg's purpura, lichen aureus, Majocchi's purpura, and Gougerot-Blum purpura. Histologically, there is inflammation and hemorrhage without fibrinoid necrosis of vessels. One hundred seventy-four cases were retrospectively reviewed. In some patients, the eruption was related to medications. Treatment was usually of limited benefit. Fifty-eight of 87 patients (67%) who had follow-up data did eventually have clearing of lesions. Because of the clinical and histologic similarities among the subtypes, the inclusive term purpura simplex is favored.
Regulated intravenous doses of quinidine were given to patients with the antibody of quinidine purpura to produce controlled thrombocytopenia without clinical sequelae. The degree of thrombocytopenia and the rate at which it developed were dependent on the relative plasma concentration of quinidine and antibody. By relating in vivo changes in platelet levels to concurrent in vitro tests for antibody activity and to quantitative relationships between reactants determined in Papers I and III of this series, it was concluded that the amount of antibody which attaches to platelets when thrombocytopenia develops is insufficient to cause complement fixation or platelet agglutination. Platelets do not appear to be destroyed directly by reaction with antibody in vivo. The minimal amount of antibody which does attach to platelets in vivo appears to increase their susceptibility to the usual mechanisms of sequestration. Megakaryocytes and blood vessels do not appear to be affected directly by the antibody which causes quinidine purpura, and hemorrhagic manifestations of the disease appear to be consequent to changes in platelets alone. A safe method of performing in vivo tests for the presence of an antibody of drug purpura is described. The implications of the present work in idiopathic thrombocytopenic purpura are discussed.
Hypergammaglobulinaemic purpura, first described by Waldenstrom, is a rare skin disease. The essential features are the presence of purpura with polyclonal hypergammaglobulinaemia. We describe a case of hypergammaglobulinaemic purpura occurring in a Chinese man with reticulate purpura and haemorrhagic blisters.
Disseminated intravascular coagulation and purpura fulminans developed in association with septicemia and meningitis due to Candida tropicalis in an 18-year-old female immunosuppressed renal allograft recipient. Although systemic Candida infection was initially suspected, blood cultures showed no growth of this organism until after its identification in the dermis of a skin biopsy specimen obtained from the site of purpura fulminans. This case illustrates the association between Candida sepsis and purpura fulminans, and demonstrates the usefulness of skin biopsy of purpura fulminans in the early diagnosis of Candida sepsis.
A patient whose peculiar and painful purpura seemed to be strongly related to psychogenic factors is described. The skin bleeding pattern in this patient was consistent with the diagnosis of psychogenic purpura (autoerythrocyte sensitization). In addition, idiopathic thrombocytopenic purpura and platelet storage pool deficiency were present. These somatic conditions are considered to be of minor importance in the pathogenesis of this hemorrhagic syndrome. The association of these various types of bleeding disorders in the same patient has not been previously described.
Immune thrombocytopenic purpura (ITP) and thrombotic thrombocytopenic purpura (TTP) have each been associated with HIV infection. Sequential occurrence of these two diseases with a disease-free interval has been occasionally reported in the literature, whereas simultaneous manifestations of these two diseases have not been described. Here, we report an AIDS patient who was initially diagnosed as having TTP and showed an apparent partial response to plasmapheresis but was found to have a clinical course similar to ITP. Although precise mechanisms for the development of TTP and ITP in these patients are unclear, we offer several hypotheses. It is important to recognize that these two processes may be seen concurrently.
Autoimmune thrombocytopenic purpura (ATP) and thrombotic thrombocytopenic purpura (TTP) are each well recognized clinical syndromes which may appear as single episodes or may have chronic relapsing courses. We present four patients negative for human immunodeficiency virus (HIV) infection who appear to have both diagnoses with either concomitant or intermingled episodes, and we review seven additional patients reported in the literature with similar features. All four of our patients are female, two have underlying connective tissue disorders, and their ATP processes came to our attention because of incomplete response of the platelet count to plasma exchange therapy (PEX) during a TTP phase (Cases 1 and 2) or development of thrombocytopenia in the absence of microangiopathy on the background of prior typical TTP episodes (Cases 3 and 4). Recognition of the ATP diagnosis in each case resulted in discontinuation of PEX (Cases 1 and 2) or not instituting PEX (Cases 3 and 4). In each instance, a satisfactory rise in platelet count followed treatment for ATP. Based upon this experience, we conclude that some individuals may have a mixed immune thrombocytopenia syndrome; careful analysis of the mechanism of thrombocytopenia, especially in recurrent episodes and in patients who respond incompletely to PEX for TTP, is important when deciding whether to initiate or continue PEX, or to consider therapies appropriate for other mechanisms of thrombocytopenia.
The serum levels of thrombopoietin (TPO) were measured in 16 patients with thrombotic thrombocytopenic purpura (TTP), 12 with hemolytic uremic syndrome (HUS), 10 with aplastic anemia (AA), 10 with disseminated intravascular coagulation (DIC), and 71 with idiopathic thrombocytopenic purpura (ITP). The serum TPO levels were measured with a sensitive sandwich enzyme-linked immunosorbent assay. The serum TPO level in the ITP group (1.68 +/- 0.85 fmol/ml) were not significantly increased compared with those of the normal subjects. The TPO levels in the TTP (2.77 +/- 1.38 fmol/ml) and HUS groups (5.77 +/- 4.41 fmol/ml) were higher than those of the normal subjects. The patients with AA (12.7 +/- 8.0 fmol/ml) and those with DIC (13.3 +/- 5.7 mol/ml) had significantly higher serum TPO levels than did the normal subjects and ITP patients. The TPO levels were well correlated with the platelet counts in the TTP patients, and were negatively correlated with the platelet counts in the ITP patients. These results suggest that the serum TPO levels in some thrombocytopenic diseases are regulated not only by the platelet count and the megakaryocyte mass, but also by other factors.
Three patients were treated empirically with anti-platelet agents, prednisone, plasmapheresis, and prostacyclin for the classical clinical syndrome of thrombotic thrombocytopenic purpura (TTP). All three patients initially responded, then relapsed after one to 13 months with a clinical picture characteristic of immunogenic thrombocytopenic purpura (ITP). At relapse, all three had thrombocytopenia without microangiopathy or other causes of thrombocytopenia. All responded to splenectomy. This complication of TTP may become more common with improved survival in TTP. Recognition may prevent inappropriate therapy.