Gene/Protein Disease Symptom Drug Enzyme Compound
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We describe a case of a 10 year-old boy who had fever, weakness, anorexia, weight loss and general malaise. No other remarkable symptoms were present. He had been treated with Aspirin and Ibuprofen. Deterioration of renal function, glucosuria, proteinuria, anemia and increased erythrocyte sedimentation rate were detected. After 7 days observation with no treatment, renal function worsened, glucosuria increased and fever persisted. A renal biopsy was performed and acute tubulointerstitial nephritis was diagnosed. The most common aetiologies of this entity were excluded. An ophthalmologic study revealed bilateral anterior uveitis, therefore the patient was diagnosed as having tubulointerstitial nephritis with uveitis. The child improved on corticosteroid therapy, but uveitis relapsed when treatment was stopped.
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PMID:Tubulointerstitial nephritis and asymptomatic uveitis. 1106 42

The epidemiological and clinical observations of 240 patients with Weil's disease and 10 patients with canicola fever, and these observations in two epidemics of canicola fever, are presented. Early diagnosis is most important for the prognosis of patients with the severe form of leptospirosis. It depends on the clinical features, clinical laboratory findings, and the epidemiological situation. The most characteristic clinical signs for early diagnosis were febrile illness of sudden onset, severe general malaise, muscular pain, and conjunctival congestion. Proteinuria, leukocytosis with neutrophilia, and raised erythrocyte sedimentation rate were the most indicative clinical laboratory findings for early diagnosis. Although jaundice and hemorrhage are the most important signs of the severe form of leptospirosis, Weil's disease, these are rarely useful in early diagnosis. Of a variety of antibiotics used, penicillins and cephems had the lowest minimal inhibitory concentration against leptospires. However, it became apparent from basic studies in vitro and in vivo that streptomycin showed the best bactericidal action against leptospires and that it was the most effective anti-leptospiral antibiotic. Gentamicin, tobramycin, and isepamicin are also effective as alternatives to streptomycin. Although penicillins, cephems, tetracyclines, and macrolides are also effective for the treatment of leptospirosis, when these antibiotics with inadequate bactericidal activity are used for the treatment of the disease, long-term therapy with sufficiently large doses may be required from an early stage of the disease until the appearance of antibodies.
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PMID:Clinical observation and treatment of leptospirosis. 1145 95

We report an autopsy case of elderly-onset anticentromere antibody-positive pulmonary-renal syndrome. An 84-year-old woman was admitted to our hospital with complaints of leg edema and general malaise. Neither skin rush nor arthritis was seen. Because of hematuria, proteinuria with various casts, renal dysfunction and anemia, a clinically diagnosis of rapidly progressive glomerulonephritis was made. Slight pulmonary hypertension was observed in ultrasonic cardiography. Hypocomplementemia was not seen. Tests for MPO- and PR 3-anti-neutrophil cytoplasmic antibodies and anti-glomerular basement membrane antibody were negative, but a high titer of antinuclear antibody with a discrete speckled pattern on immunofluorescent staining was disclosed. Results for anticentromere antibody and anti-Ki antibody were positive, but for anti-Sm antibody and anti-double stranded DNA antibody were both negative. She did not present any clinical features of systemic sclerosis or CREST syndrome. Subsequently, prednisolone was administered, but pulmonary alveolar hemorrhage occurred and the patient died of acute respiratory failure caused by massive pulmonary hemorrhage. Autopsy revealed crescentic glomerulonephritis including glomerular capillaritis and pulmonary capillaritis with positive granular deposits of immunoglobulins and compliment on the glomerular and pulmonary capillary walls. Immunologically mediated crescentic glomerulonephritis and pulmonary capillaritis was then diagnosed histopathologically. The main pathological feature of the case was small-vessel vasculitis with immune-complex deposition. Although this case did not fulfill the clinical criteria for systemic lupus erythematosus (SLE), its histological features resembled those of lupus nephritis and acute lupus pneumonitis. We speculated that anticentromere antibody-positive pulmonary-renal syndrome without any other symptoms or signs of connective tissue disease, such as our case, is a clinical entity distinct from typical SLE or CREST syndrome.
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PMID:[Elderly-onset anticentromere antibody-positive pulmonary-renal syndrome: report of an autopsy case]. 1157 30

A 59-year-old male patient developed a necrotizing ulceration on the right shin. Both clinical and histopathologic examinations suggested pyoderma gangrenosum. After temporary improvement of skin symptoms under peroral glucocorticoid treatment, a hemorrhagic-purulent discharge started from the nose, he began to have fever, malaise, cough, and a chest X-ray revealed inflammation in the lung. Cerebral CT and MRI disclosed midline bone loss within the nasal septum and granulomatosus tissue masses protruding into the right orbit. The c-ANCA test was positive, serum IgA was elevated, and he had microhaematuria and proteinuria. In this severe case of Wegener's granulomatosis prolonged methylprednisone and cyclophosphamide treatment was initiated. Both the skin symptoms and the granulomatosus infiltrations resolved.
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PMID:Wegener's granulomatosis presenting as pyoderma gangrenosum. 1463 9

Although patients with systemic lupus erythematosus (SLE), especially those with antiphospholipid antibodies, have a high incidence of arterial and venous thrombotic manifestations, renal infarction has been rarely reported in these patients and is probably underestimated. A 9-year-old boy with renal infarction, diagnosed by computed tomography and scintigraphy, is described. Initially he complained of severe flank pain; he had no urinary abnormalities and his blood pressure was normal. No evidence of systemic disease was found. He responded well to antibiotic treatment without the need for immunosuppressive therapy. In subsequent years he presented a spectrum of clinical symptoms, including fever, malaise, arterial hypertension headache, and mononeuritis multiplex, accompanied by an increased erythrocyte sedimentation rate and transitory proteinuria. This suggested vasculitis involving peripheral vessels as well as the central nervous system. Treatment with oral prednisone and azathioprine led to remission. Four years after the renal infarction, the child presented with recurrence of systemic disease. The diagnosis of SLE was established, with positive antiphospholipid antibodies. The sudden appearance of severe unexplained flank pain should alert the clinician to a possible underlying renal vessel thrombosis. Renal venous thrombosis is probably much more common; however, renal arterial thrombosis and infarction in association with SLE with positive antiphospholipid antibodies should be added to the differential diagnosis.
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PMID:Renal infarction in a child with systemic lupus erythematosus. 1506 40

Hemorrhagic fever with renal syndrome (HFRS) is caused by the Hantaviruses, a group enveloped RNA viruses transmitted through contact with infected rodent urine or feces. Although distributed widely through Europe, Asia, and the New World, infections acquired in Korea, China, and Russia tend to be among the most severe. The initial presentation of HFRS is extremely variable, but generally includes fever, malaise, headache and abdominal pain. Laboratory findings that may lead to the diagnosis include thrombocytopenia, azotemia, elevated serum creatinine, or proteinuria. We present the case of a patient that acquired hemorrhagic fever with renal syndrome in South Korea.
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PMID:Hemorrhagic fever with renal syndrome. 1554 May 21

Palpable purpura, the inflammation of blood vessels is the hallmark of vasculitis. It can be observed in a variety of settings, where vessels can be affected primarily or as a secondary event. Every patient with vasculitis should be considered to have a systemic disease unless proven otherwise. One or more systemic symptoms occur in at least 50% of patients and there is no way to predict systemic involvement. Patients may demonstrate mild systemic involvement like arthralgia and arthritis, fever and malaise or more severe symptoms such as massive proteinuria and raised creatinine leading to chronic renal failure, severe intestinal bleeding or perforation with a fatal outcome. In this article we will review the life-threatening aspects of purpura and vasculitis.
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PMID:Life-threatening purpura and vasculitis. 1589 37

A 45-year-old woman was admitted to our hospital because of high fever and malaise. She also presented abnormal urine findings including macrohematuria and proteinuria with transient renal insufficiency. Salmonella Typhi was isolated from her blood and stool culture, and then she was diagnosed as having typhoid fever. Salmonella enterica serotype typhi infection can be complicated by renal involvement, although rare. In Japan, few cases have been reported about acute nephritic syndrome in typhoid fever. Here, we report a case of endemic acquired typhoid fever associated with acute renal failure probably due to acute nephritic syndrome successfully treated with levofloxacin.
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PMID:Acute renal failure likely due to acute nephritic syndrome associated with typhoid fever. 1641 36

Acute pancreatitis (AP) rarely complicates the clinical course of systemic lupus erythematosus (SLE). AP as the initial manifestation of SLE is exceptional, but its outcome is often fatal. Corticosteroids have been suspected to play a role in the development of AP, but the therapeutic benefit seems to be far above the risk of exacerbation of pancreatic lesions. We report a 13-y-old girl presenting with arthralgia and malaise, followed by abdominal pain, generalized oedema and haemodynamic instability. Increased CRP (325 ng/ml), serum amylase (14,000 IU/l) and lipase (2500 IU/l) levels suggested AP. Acute anuric renal failure required haemodialysis. Multiorgan involvement suggested SLE, which was confirmed 3 d later by increased anti-ds-DNA levels. Three methylprednisolone pulses were administered promptly, followed by oral prednisone (1.5 mg/kg/d) and six pulses of cyclophosphamide (500 mg/1.73 m2/2 wk). Mycophenolate mofetil was introduced for long-term disease control. Amylase and lipase levels decreased over 4 wk. Renal function was normal after 3 wk and proteinuria negative after 6 wk. This case suggests that steroid pulse therapy should be promptly administered if clinical and biochemical investigations suggest SLE to be responsible for AP. Aggressive treatment may be life saving.
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PMID:Acute pancreatitis in paediatric systemic lupus erythematosus. 1637 10

We present a 5-years old boy with acquired Fanconi-de Toni-Debre syndrome being a effect of therapy for Ewing's sarcoma. At the age of 3 years, this boy was diagnosed as suffering from Ewing sarcoma of his right femur. The boy received a course of 8-month pre-surgery (6 VIDE--Vincristine, Ifosfamide, Doxorubicin, Etoposide cycles and 2 VAI--Vincristine, Actinomycin, Ifosfamide cycles) and 6-month post-surgery (6 VAI--Vincristine, Actinomycin, Ifosfamide cycles) cytostatic therapies according to EWING, EURO 99 protocol. In forth month of post-surgery cytostatic therapy, progressive malaise, polyuria, polydypsia, and recurrent vomiting occurred. The association between those symptoms and malignancy was excluded. Laboratory studies revealed hypokaliemia, hypophosphatemia, proximal tubular acidosis, proteinuria, glucosuria, aminoaciduria, hyperkaliuria and hyperphosphaturia. Acquired Fanconi-de Toni-Debre syndrome due to toxic effect of cytostatic therapy on renal proximal tubules was diagnosed. At present, two years after the time the diagnosis was made, despite constant substitution of potassium, phosphates and bicarbonates, deficit of body mass and height, and bone mineral density abnormalities are observed.
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PMID:[Acquired Fanconi-de Toni-Debre syndrome due to therapy for Ewing's sarcoma in 5-years old boy]. 1689 36


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