Academic literature on the topic 'Migratory oedema'

Purpose: We attempt to describe the unique diagnostic features of dirofilariasis affecting the eye, a rare disease caused by the nematode dirofilaria repens. Case report: The cohort includes 5 adult cases of ocular dirofilariasis. Migratory oedema was present in all but one case. The occurrence of the lesions near the medial canthus in all the cases including subconjunctival mass suggests predictable pattern of migration of the worm. Absence of systemic eosinophila and lack of marked eosinophilic infiltration around the parasitic granuloma in histopathology indicates alternative immune response against the parasite. Persistence of live worm despite antihelminthic drugs can be accounted by the presence of a thick capsule which protects the filaria against adulticidal and larvicidal drugs. Surgical exicision was curative in all cases.Conclusion: Our case series points to the importance of having high index of suspicion and early detection of ocular dirofilariasis as it is amenable to simple and effective treatment.

An investigation was carried out on incidence and pathology of fascioliasis in deer of Chittagong Zoo and some houses of Chittagong city during the period from January 2001 to June 2004. A total of 57 domesticated deer of various types were examined to diagnose the fascioliasis in Chittagong zoo and some house deer of Chittagong city. By faecal examination out of 44 cases 34 (77.3%) were positive for fascioliasis, of which, 15 (34.1%) cases were recorded in Chittra deer, 12 (27.3%) in Maya deer, 05 (11.4%) in Shambar deer and 02 (4.5%) in Nathrini deer. In post mortem examination, fascioliasis found in 13 (100%) cases, of which, 08 (61.5%) from Chittra deer and 05 (38.5%) from Maya deer. The overall incidence of fascioliasis in deer was 82.5%. In relation to sex the fasciolasis was significantly (p < 0.05) higher in female (82.6%) than male (71.4%) deer. The incidence of fascioliasis in various types of deer in relation to age was significantly (p < 0.05) higher in age group of above 2 years old than in age group below 2 years old. The gross examination revealed enlarged livers with round edges and thickened capsule with numerous haemorrhagic spots on the parietal surface (subacute form). In chronic form, the livers were cirrhotic and reduced in size. The affected intra-hepatic bile ducts were protruded and were engorged with flukes. Microscopically the migratory tracts were represented by the presence of haemorrhagic, oedema and infiltration with numerous eosinophils mixed with few lymphocytes. The wall of the bile ducts was thickened with fibrous tissue proliferation and the lining epithelium showed hyperplastic changes.

Abstract Background Fibroblast Ggrowth factor-23 (FGF-23) is a phosphate regulator primarily expressed by osteocytes. Excess FGF-23 leads to decreased hydroxylation of 25-hydroxyvitamin D and poor renal phosphate reabsorption. This leads to hypophosphataemia and represents a rare cause of osteomalacia, resulting in bone oedema and stress fractures. Methods A 57-year-old man with known skin psoriasis presented with a two-year history of left foot and ankle pain. On examination, he had chronic dactylitis of the left, big toe associated with skin psoriasis and nail pitting. Serum inflammatory markers were normal, and autoimmune screens for RF, anti-CCP and HLA-B27 were negative. Bilateral foot and ankle X-rays showed no bony abnormality. This was diagnosed as likely psoriatic arthritis and MRI showed talar bone oedema, felt to be related to the inflammatory arthritis. Symptoms settled well on non-steroidal anti-inflammatories. However, he presented two months later with focal distal tibial pain and swelling. There was no history of trauma. Repeat MRI showed proximal migration of bone oedema with stress fractures of the left posterior talus and distal tibial metaphysis. Results Blood tests showed low phosphate, elevated PTH, normal adjusted calcium, raised ALP and low 25-hydroxyvitamin D. DEXA scan confirmed osteoporosis of the hip. The patient was commenced on intravenous three-monthly pamidronate and colecalciferol (vitamin D3) supplements. Despite this, the patient continued to have migratory joint pain affecting the ankle, hip and sacroiliac joints. Methotrexate was prescribed to improve his psoriasis, but whilst his skin improved his legs remained painful. A repeat MRI showed new insufficiency fractures to the left talus and right neck of femur. Although taking colecalciferol supplementation, his serum phosphate remained low (0.5mmol/L). On further investigation, Myeloma screen and FDG PET were normal but he was noted to have an increased fractional urinary phosphate excretion indicating poor renal phosphate reabsorption. Serum FGF-23 assay was elevated at 131 mIU/L (normal <100mIU/L). The patient underwent 68-Gallium DOTATATE PET imaging, utilising a tracer specific for somatostatin receptors found on neuroendocrine tumours, which showed a T9 pedicle lesion. CT-guided biopsy confirmed a mesenchymal tumour as the cause of FGF-23 secretion, resulting in transient bone marrow oedema and insufficiency fractures. The patient has become asymptomatic on calcitriol (1,25-dihydroxyvitamin D) and phosphate supplementation, and is being considered for radiofrequency ablation therapy. Conclusion This case illustrates the need for thorough investigation of symptomatic, treatment-refractory hypophosphataemia. Although mild hypophosphatemia could indicate adult onset rickets, rarer causes such as FGF-23 secreting tumours should be considered. These tumours are notoriously difficult to locate; 68-Gallium DOTATATE PET may offer superior specificity to other imaging modalities, including FDG-PET, in detecting these mesenchymal tumours. FGF-23 decreases hydroxylation of vitamin D3 and renal phosphate reabsorption, and calcitriol alongside phosphate supplementation is advisable for symptomatic management until definitive treatment. Disclosures K. Fisher None. S. Melath None. S. Patel None.

Abstract Background Fibroblast growth factor-23 (FGF-23) is a phosphate regulator primarily expressed by osteocytes. Excess FGF-23 leads to decreased hydroxylation of 25-hydroxyvitamin D and poor renal phosphate reabsorption. This leads to hypophosphatemia and represents a rare cause of osteomalacia, resulting in bone oedema and stress fractures. Methods A 57-year-old man with known skin psoriasis presented with a two-year history of left foot and ankle pain. On examination, he had chronic dactylitis of the big toe and extra-articular features included skin psoriasis on the scalp, elbows, knees, and nail pitting. Serum inflammatory markers were normal, and autoimmune screens for RF, anti-CCP and HLA-B27 were negative. Bilateral foot and ankle X-rays showed no bony abnormality. This was diagnosed as likely psoriatic arthritis and MRI showed talar bone oedema, felt to be related to inflammatory arthritis. Symptoms settled well on non-steroidal anti-inflammatories. However, he presented with focal distal tibial swelling and pain, two months later. There was no history of trauma, Repeat MRI2 showed proximal migration of bone oedema with stress fractures of the left posterior talus and distal tibial metaphysis. Bloods tests showed low phosphate, elevated PTH, normal adjusted calcium, raised ALP and low 25-OH vitamin D. DEXA scan confirmed osteoporosis of the hip. The patient was commenced on bisphosphonate with 25-hydroxyvitamin D and phosphate supplementation. Despite this, the patient continued to have migratory joint pain affecting the ankle, hip and sacroiliac joints. Methotrexate was started for psoriasis and whilst his skin improved, his pain remained and further MRI showed left talar and right neck of femur insufficiency fractures. Results Although taking vitamin D3 supplementation, he remained hypophosphateamic 0.5mmol/L. Myeloma screen and PET FDG were normal. However, he was noted to have an increased fractional urinary phosphate excretion indicating poor renal phosphate reabsorption. One possible cause of this is elevated FGF-23, which was confirmed with FGF-23 assay (include levels and normal range). The patient underwent PET Ga-DOTATE imaging, utilising a tracer specific for somatostatin receptors found on neuroendocrine tumours. This showed a T9 pedicle lesion and a CT-guided biopsy confirmed a mesenchymal tumour as the cause of FGF-23 secretion, resulting in TBMO and insufficiency fractures. The patient has become asymptomatic on calcitriol and phosphate supplementation. He is now being considered for radiofrequency ablation therapy. Conclusion This case illustrates the need for a thorough investigation of symptomatic, treatment-refractory hypophosphataemia. Although mild hypophosphatemia could indicate adult-onset rickets, rarer causes such as FGF-23 secreting tumours should be considered. These tumours are notoriously difficult to locate; Ga-DOTATE PET is probably superior to other imaging modalities including FDG-PET in isolating mesenchymal tumours. Disclosures K. Fisher None. S. Melath None. S. Patel None.

Hypoderma tarandi causes myiasis in reindeer and caribou (Rangifer tarandus spp.) in most northern hemisphere regions where these animals live. We report a series of 39 human myiasis cases caused by H. tarandi in Norway from 2011 to 2016. Thirty-two were residents of Finnmark, the northernmost county of Norway, one a visitor to Finnmark, and six lived in other counties of Norway where reindeer live. Clinical manifestations involved migratory dermal swellings of the face and head, enlargement of regional lymph nodes, and periorbital oedema, with or without eosinophilia. Most cases of human myiasis are seen in tropical and subtropical countries, and in tourists returning from such areas. Our findings demonstrate that myiasis caused by H. tarandi is more common than previously thought. Healthcare professionals in regions where there is a likelihood of human infestation with H. tarandi (regions populated by reindeer), or treating returning travellers, should be aware of the condition. All clinicians are advised to obtain a detailed travel history when assessing patients with migratory dermal swellings. On clinical suspicion, ivermectin should be given to prevent larval invasion of the eye (ophthalmomyiasis). Since H. tarandi oviposits on hair, we suggest wearing a hat as a prevention measure.

Abstract Autoimmune constrictive pericarditis constitutes a conundrum to modern cardiology with much uncertainty surrounding both pathophysiology and optimal treatment strategies. We hereby describe the case of a 35-year-old woman of Nigerian origin with severe right heart failure secondary to calcific constrictive pericarditis. Her past medical history included coagulation factor XI deficiency, leukopenia, 2nd trimester miscarriage and premature labour due to placenta previa with fibrin deposition. Further investigations revealed atrial fibrillation, severe biatrial enlargement, moderate tricuspid and mitral regurgitation, pericardial thickening, post-capillary pulmonary hypertension and right ventricular dip-and-plateau pattern, compatible with severe constrictive pericarditis. Extensive screening for infectious and autoimmune causes only revealed borderline positive ANA (1:80). Thereafter, the patient underwent complete surgical pericardiectomy with pericardial biopsies revealing fibrous thickening, diffuse calcification and lymphocyte/macrophage infiltrates, in the absence of giant multinucleated cells or granulomas. The patient was later discharged but soon experienced relapse of exertional dyspnoea presenting with right-sided haemo-pneumothorax (requiring pleural drainage), diffuse alveolar haemorrhage, large right-sided basal and infrascissural pleural effusion, and ascites. She was treated with high dose iv furosemide, oral ibuprofen and colchicine, suspension of rate control medications, achieving initial reduction in pulmonary oedema and ascites, relapsing however after attempts to switch to oral diuretic therapy. Due to the finding of persistent lymphopenia, further immunological tests were conducted, revealing raised IgG1 levels as well as altered peripheral lymphocyte populations (raised CD4+/CD8+ ratio and CD8+ central memory, reduced CD8 effector memory). This finding in conjunction with the history of factor XI deficiency, 2nd trimester miscarriage and placental fibrin deposition as well as the observation of painful cutaneous nodules at sites of venepuncture, suggestive of Koebner’s phenomenon, veered the diagnostic focus to a potential autoimmune aetiology and in particular to systemic lupus erythematosus (>10 ACR-EULAR score points with case reports describing all the above as potential disease manifestations). Furthermore, revision of thoracic CT scans, demonstrated bilateral migratory peribronchovascular nodules with ground-glass halo. CT- guided biopsies thereof were performed revealing focal alveolar damage with capillaritis and alveolar haemorrhage, further corroborating the clinical suspicion of autoimmune disease and justifying the introduction of high-dose oral corticosteroid therapy. In liaison with our tertiary rheumatology centre, the patient was later switched to mycophenolate with gradual weaning from corticosteroid. Concurrent cardiological follow-up revealed persistence of good haemodynamic status (NYHA class II, absence of pulmonary oedema and ascites) with oral diuretic therapy, regression of cutaneous symptoms and echocardiography demonstrating consistent reduction in both mitral and tricuspid regurgitation. This constitutes to our knowledge the first report of autoimmune calcific constrictive pericarditis with significant haemodynamic response to immunosuppressive therapy. Despite the relative rarity of this disease entity, early recognition and instatement of immunosuppressive treatment may prove fundamental to halt and potentially reverse the haemodynamic progression of this highly morbid condition.

Abstract Case report - Introduction Chikungunya is a tropical arbovirus transmitted by female Aedes Aegypti or Aedes Abopitus mosquitos. It is not indigenous to UK but occurs in epidemics in Africa and Asia. It often presents with pyrexia, arthralgia or arthritis, myalgia and a maculopapular rash and can mimic both peripheral and axial inflammatory arthritis as well as more common forms of viral arthritis. It can also become chronic leading to disabling symptoms. The diagnosis should be considered in all patients presenting with early inflammatory arthritis who have travelled to affected areas. Case report - Case description A 57-year-old female developed sudden onset fever along with a macular rash whilst visiting South East Asia. She then developed widespread joint pains and severe inactivity stiffness, particularly affecting her ankles. The rash and fever settled after a few days, but her arthralgia persisted in her cervical spine and both small and large joints. She had a history of recurrent episcleritis and had been investigated for axial spondyloarthropathy two years previously, but MRI imaging of the spine and sacroiliac joints did not show any inflammatory changes. Examination in the rheumatology clinic confirmed right medial epicondylitis, bilateral shoulder tenderness, tenderness over the extensor tendons of the feet and painful cervical spine movement. Investigations revealed high inflammatory markers; CRP 29 (0-10 mg/L) and ESR 48 (0-15 mm/hr), a positive rheumatoid factor but negative anti CCP antibodies and a normal white cell count. Acute seronegative spondyloarthropathy was suspected but Chikungunya serology was requested at the suggestion of the patient, because of the history of a mosquito bite. IgM and IgG antibodies were positive on immunofluorescence, confirming recent infection. She was initially given intramuscular depomedrone and non-steroidal anti-inflammatory drugs (NSAIDs) with a short response but required oral prednisolone 20mg daily to suppress the inflammation in her feet. An MRI confirmed an ankle effusion and peroneal tenosynovitis. After 6 months her symptoms improved, and she was able to stop prednisolone completely and she remains well 9 months after the initial infection. Case report - Discussion Chikungunya infection causes musculoskeletal symptoms in all affected patients, but the clinical presentation can highly variable, from mild joint pain to erosive arthritis. It can be divided into three phases: incubation phase, acute phase, and chronic phase. The incubation phase varies between one to twelve days after the mosquito bite. The acute phase begins with high fever, headache, polyarthralgia/arthritis, lymphadenopathy, and anorexia. Joint involvement is often distal and symmetrical affecting the hands, wrists, shoulders, knees, ankles, and feet. A maculopapular rash is common. Dengue virus and Zika virus infection can present similarly. Treatment for acute Chikungunya fever is supportive. Analgesic, anti-pyretic and NSAIDs are used for symptom relief. During the chronic phase, infected people develop symmetrical, migratory, oligoarticular or polyarticular arthritis with morning stiffness and joint oedema, which can last from months to years. Our patient had a previous history which was consistent with seronegative spondyloarthropathy, an acute presentation of inflammatory arthritis and results and imaging which supported this diagnosis. The correct diagnosis could easily have been missed if a travel history had not been taken and the patient’s suspicions ignored. The best treatment for chronic Chikungunya arthritis is unclear. NSAIDs are often the first treatment but, as in this case systemic steroids are often necessary. Conventional synthetic DMARDs have also been reported efficacious. Biologic DMARDS have been used in resistant cases. Case report - Key learning points Chikungunya has emerged as a global disease affecting millions of people with significant musculoskeletal morbidity. Any patient has travelled to endemic areas including Africa and Asia, with fever and joint pain should be screened for Chikungunya virus as well as Dengue virus, and Zika virus. Diagnosis is either by RT PCR (positive 0-7 days of infection or Immunoglobulin M (detectable after 5 – 10 day of infection and persists for few months). Treatment is supportive in acute phase, may require low doses of steroids to aid resolution of symptoms. Conventional DMARDS have shown benefit in chronic phase with ongoing synovitis/tenosynovitis. Patients may know more about rare, endemic diseases than their European doctors and their suspicions about potential diagnoses should always be considered.

Abstract Case report - Introduction Panniculitides comprise a heterogeneous group of inflammatory diseases involving the subcutaneous fat. They remain the most challenging areas for clinicians. Skin biopsy is commonly needed to confirm diagnosis. Because there are many underlying aetiologies for panniculitis, detailed history and thorough investigations are needed. We present a case of A 20-year male who was admitted with painful lumps treated initially as cellulitis/abscess but turned to be neutrophilic panniculitis on skin biopsy. Extensive workup failed to reveal underlying aetiology. Eventually Imradli (AntiTNF) was thought to be the culprit and therefore was kept on hold with no recurrence of panniculitis. Case report - Case description A 20-year-old, Asian Malawian. Moved to the UK at the age of 6. He was diagnosed with Ankylosing spondylitis in November 2016. Initially received Naproxen followed by (Humira) with good clinical response. He was switched to biosimilar Imradli in Nov 2019. He was admitted with 2–3 weeks history of progressive right hip and buttock pain, 1 week of very tender erythematous swelling of the right buttock but without fever or weight loss. He reported mild weakness of lower limbs. Physical examination revealed 5x 8 cm swelling on Right buttock, Rest of examination was unremarkable. He was reviewed by neurology team who arranged MRI spine and brain, EMG and lumbar puncture which all came back as unremarkable excluding the possibilities of myelitis and myositis. Initially thought to be abscess/cellulitis but absence of fever/inflammatory response, abnormal CT finding and no response to antibiotics made it less likely. While the Right buttock erythema/swelling started to resolve, he developed two new migratory erythematous lesions appearing around the left buttock and lower lumbar spine. Working diagnosis of panniculitis was made which was confirmed on biopsy. Due to lack of response to NSAIDs, colchicine or oral steroids, a 3rd biopsy of the freshest lesion was performed to exclude deep-seated infection. Investigations – FBC, U&ES, LFT, CRP, CK, ACE - all were unremarkable ASO titre <200, serology for Borrelia and TPHA negative. Viral, parasitic, and Autoimmune screen were unremarkable. CXR clear, MRI/CT: extensive subcutaneous inflammatory changes in the right buttock with sacral oedema. PET-CT – showed resolving inflammatory changes in the right flank, FDG intake in C6 and SI joints presumed secondary to ankylosing spondylitis and sacroiliitis. The underlying cause of panniculitis remains uncertain. Anti TNF was kept on hold and the patient was followed up with no evidence of recurrence of panniculitis Case report - Discussion Panniculitis (inflammation of subcutaneous fat) is a relatively uncommon condition. It has various aetiologies including infection, trauma, inflammation, and malignancy. Skin biopsy can give valuable information including microbiological studies if infectious panniculitis was suspected. However, clinical correlation and careful consideration of the differential diagnosis is needed in many cases. The diagnosis can be quite challenging as in this case where all investigations and skin biopsy could not point towards the underlying aetiology. Although anti-TNF inhibitors are commonly used in treating a wide range of autoimmune conditions. But their use can lead to the development of secondary autoimmune diseases, such as cutaneous vasculitis, lupus-like syndrome, and interstitial lung disease, paradoxically induced by anti-TNF-α agents. Llamas-Velasco and Requena, reported the first case of panniculitis induced by etanercept injection in a 62-year-old woman with severe psoriasis who developed an erythematous, slightly painful nodule on the skin of the anterior abdominal wall. Adalimumab induced lupus panniculitis was reported in a Rhu-lupus patient. Although the lesions stopped progressing after cessation of adalimumab, they remained unchanged for two more years. The mechanism for adalimumab-induced CLE is uncertain. Although there is not enough data about autoimmunity with biosimilars, we think secondary autoimmune conditions could similarly be induced by biosimilar as illustrated in this case. Anti-TNF induced cutaneous panniculitis is considered most likely although uncertain. If anti-TNF drug-induced, this should gradually resolve but can be slow (4–6 months). Corticosteroids have been added for an anti-inflammatory response, but there was little benefit which might point to a different pathogenetic mechanism. NSAIDs has helped to keep his AS relatively stable during the COVID-19pandemic. During the last review, the patient expressed his wishes to go back on biologic. But the question remains whether he will a have a recurrence of panniculitis or not? Case report - Key learning points 1/Anti-TNF inhibitors sometimes cause secondary autoimmune conditions like cutaneous vasculitis, lupus-like syndrome, but there is not enough data regarding biosimilar induced autoimmunity. 2/This case illustrates the high importance of having a tissue diagnosis. (whenever there is an issue, the diagnosis would be in the tissue). 3/There is still uncertainty whether a recurrence of panniculitis might occur or not if the patient went again on biologics.

<p>Previous studies of an intermittent migratory oedema occurring in people living in the Central Queensland coastal areas of Woodbury, supported by skin testing and subsequent serology tests established that this problem was</p> <p>possibly a gnathostomiasis. The problem was previously reported as occurring in an area north of the coastal town of Yeppoon in Central Queensland. It was described as a rapidly moving intermittent oedema lasting for periods between one week and six months. </p> <p><br></p> <p>A study of 96 people living in the Central Queensland area was carried out from 1992 to 1995, showing that the 'Woodbury Bug' is a migrating oedema occurring at irregular intervals over all areas of the body. The phenomenon</p> <p>was not confined to people living in areas north of Yeppoon, but occurred in all areas of Central Queensland, mostly in the summer months with urticaria lasting from days to several weeks. Reoccurrence of the urticaria occurred</p> <p>again in the summer months of January to April, every year or every second year, often lasting several years.</p> <p><br></p> <p>The physical findings in the study were remarkably consistent with those found in cases of gnathostomiasis. In contrast to previous serology testing, however, all gnathostome serology tests were negative. The lack of a history of eating raw meats or fish also contradicted the previous suggestion that this was gnathostomiasis. Serology testing for Strongyloides species was also</p> <p>negative, and the physical findings eliminated Ancylostoma species as a possibility.</p> <p><br></p> <p>During the study it was established that many patients had contact with nest material of the brush turkey, Alectura lathami, a leafy material used as garden mulch. A Heterakid, found as a parasite in the brush turkey is suggested as a</p> <p>cause of the 'Woodbury Bug'. This parasite could be treated using an anthelminthic, albendazole, or the condition known as the 'Woodbury Bug' could be controlled by avoiding any accidental ingestion of parasites when working with brush turkey nest material.</p> <p><br></p>