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Granulomatous Diseases
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Albert Alhatem, Robert A. Schwartz, Muriel W. Lambert, W. Clark Lambert
Overview: Purpuric eruptions are subdivided into two types: non-thrombocytopenic (normal platelet) and thrombocytopenic (low platelet). Purpura may result from compromising the vessel walls (trauma, infection, vasculitis, collagen disorders) or due to hemostatic pathology (thrombocytopenia, abnormal platelet function, clotting factor deficiency, or abnormal clotting factor function). Other conditions may be associated with petechiae, including septicemia, immune thrombocytopenia (ITP), hemolytic uremic syndrome, leukemia, and coagulopathies (e.g., hemophilia). Non-thrombocytopenic purpura may result from coagulation disorders, connective tissue disorders, scurvy, or vasculitis. Thrombocytopenic purpura may be due to medications, immune disorders, septicemia, Rocky Mountain spotted fever, or systemic lupus erythematous.
Haematology and oncology
Published in Jagdish M. Gupta, John Beveridge, MCQs in Paediatrics, 2020
Jagdish M. Gupta, John Beveridge
9.20. A boy aged 6 years has a history of severe bruising and petechiae of several days' duration. He is not anaemic. There is no enlargement of liver or spleen. Which of the following statements is/are true of this patient?The most likely diagnosis is idiopathic thrombocytopenic purpura.Bone marrow examination will show numerous megakaryocytes.Complete recovery would be expected in 3-8 weeks in more than 70% of cases.Bleeding in joints is a likely complication,Splenectomy is recommended if the disease is still active after 3-4 months.
Gastroenterology
Published in Stephan Strobel, Lewis Spitz, Stephen D. Marks, Great Ormond Street Handbook of Paediatrics, 2019
There are at least four different mechanisms of virulence (see Aetiology above), each of which presents in a different way. ETEC – ‘traveller’s diarrhoea’, nausea, vomiting, cramping abdominal pain and watery diarrhoea.Enteroadherent (EPEC) E coli infection presents with a fever and a more prolonged illness, which can persist for many weeks in children, with the same symptoms as ETEC.EIEC presents with fever and bloody diarrhoea that is clinically indistinguishable from Shigella (Fig. 9.41).EHEC causes bloody diarrhoea with haemolytic uraemic syndrome often developing about 1 week after the onset, particularly in young children (Fig. 9.42). Thrombocytopenic purpura may also develop.
A case of pulmonary arterial hypertension complicated by anti-neutrophil cytoplasmic antibody-associated vasculitis and systemic sclerosis
Published in Immunological Medicine, 2021
Hajime Yoshifuji, Sumika Kagebayashi, Hideyuki Kinoshita, Takao Fujii, Yoshiaki Okano, Masao Katsushima, Tsuneyo Mimori
The patient was classified with SSc according to 2013 American College of Rheumatology/European League Against Rheumatism classification criteria for SSc [11] and Sjögren syndrome (SS) according to the diagnostic criteria of Japanese Ministry of Health, Labour and Welfare [12]. Because of positive MPO-ANCA, elevated CRP, proteinuria, and microhematuria, he was suspected of having ANCA-associated glomerulonephritis. Although we performed a renal biopsy, we could not evaluate his renal lesion because the sample contained only two glomeruli. After the biopsy, subcapsular hematoma emerged; therefore, re-examination was not performed. According to Watt’s algorithm [13], he was classified as having microscopic polyangiitis (MPA). We excluded SLE because (1) malar rash, photosensitivity, serositis, and polyarthritis were not observed, and (2) although ANA was positive, it showed a discrete speckled pattern specific to SSc. We excluded thrombotic thrombocytopenic purpura, because no hemolysis or thrombocytopenia was observed. We excluded anti-glomerular basement membrane (GBM) disease, since anti-GBM antibody was negative. Next, according to 2015 ESC/ERS guidelines for the diagnosis and treatment of pulmonary hypertension [14], he was diagnosed as having group I pulmonary hypertension (PH) (i.e., PAH), after groups II, III, and IV PH were excluded because of low PAWP, normal lung CT findings, and normal pulmonary perfusion scintigraphy results.
Cortical vein thrombosis in a case of idiopathic thrombocytopenic purpura
Published in Platelets, 2015
Kamal Kant Sahu, Subhash Chander Varma
A 16-year-old boy with history of epistaxis and petechial spots over body for last 2 years was evaluated and found to have low platelet counts of 10 × 103/µl. Bone marrow examination suggested megakaryocytic thrombocytopenia. Other benign causes were ruled out and final diagnosis of idiopathic thrombocytopenic purpura was made. He was started on prednisolone 1 mg/kg once a day to which he responded over period of next 4–6 weeks and platelet counts rose up to maximum value of 75000/µL. However, as steroid doses were tapered down, his platelet counts started worsening. Hence he required alternative drugs – danazol and azathioprine, to which he again responded dramatically and his average platelet counts varied between 75 and 100 × 103/µl. Unfortunately, he did not turned up for next 6 months and finally presented to emergency services with the complaints of focal, involuntary movement of right upper limb. Initial clinical possibility of intracranial bleed was kept in view of past history of thrombocytopenic disorder. However, radiological investigations including magnetic resonance and venography showed venous thrombosis of left transverse and sigmoid sinus (Figure 1a and b). His platelet count was 90 × 103/µl. Therapeutic anticoagulation with injectable low-molecular weight heparin followed by oral warfarin was started. Later on, he was continued with azathioprine for his basic disease with threshold of platelet count being maintained ∼50–75 × 103/µl.
Decreased vision as a presenting symptom of acquired thrombotic thrombocytopenic purpura relapse
Published in Clinical and Experimental Optometry, 2021
Thrombotic thrombocytopenic purpura is a diagnostic challenge due to non‐specific signs and symptoms such as confusion, malaise, fatigue, weakness, fever, bruising, and abdominal pain.2,5 It is important to note that not all patients with TTP present as critically ill.6 The known ophthalmic complications of TTP include: bilateral serous macular detachments, Purtscher‐like retinopathy, choroidal haemorrhaging, papilledema, central retinal artery occlusions, central retinal vein occlusions, and cortical infarcts resulting in visual symptoms.3