Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1832526 (PCC)
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Polymyalgia rheumatica (PMR) is an inflammatory disease of unknown etiology affecting elderly patients and characterized by muscle pain and morning stiffness in proximal areas (pelvic and shoulder girdles and neck). It is sometimes difficult to distinguish PMR from rheumatoid arthritis (RA), or vasculitis. In the present study, we examined the clinical characteristics of the patients diagnosed with PMR in our hospital retrospectively. There were 44 patients with the median age of 71s. Eighty percent of the patients were in their 60s or 70s, and 3 patients (6.8%) were in there 50s or younger. There was no sex preponderance in frequency. Fifteen patients (34%) presented with both proximal and distal muscle pain. Arthritis occurred in 16 patients (36%), the half of which was monarthritis or oligoarthritis, and was more involved in wrist or knee joint. Only 3 patients had temporal arteritis (TA) complicated with PMR. Mean of maximum serum CRP was 8.18 mg/dl, and rheumatoid factor and anti-CCP antibodies were positive in 2 patients and a patient, respectively. There was no patient positive for ANCA. Serum MMP-3 levels tended to be higher in female patients. Median of maximum prednisolone (PSL) dose used for the treatment was 0.195 mg/kg of body weight daily. No patient needed any immunosuppressants. In the 26 patients we had a chance to follow, there were no patients who developed RA 6 months after the initial diagnosis. Progression from PMR to RA was reported, and mean period between the diagnosis of PMR and RA was one to 5 years.
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PMID:[Clinical features in patients with polymyalgia rheumatica]. 1972 49

The various types of glomerulonephritis, including many forms of vasculitis, are responsible for about 15% of cases of end-stage renal disease (ESRD). Arterial hypertension represents a frequent finding in patients suffering from glomerulonephritis or vasculitis and hypertension also serves as an indicator for these severe types of diseases. In addition, there are symptoms and signs like hematuria, proteinuria and renal failure. Especially, rapidly progressive glomerulonephritis (RPGN) constitutes a medical emergency and must not be missed by treating physicians. This disease can either occur limited to the kidneys or in the context of a systemic inflammatory disorder, like a vasculitis. If left untreated, RPGN can lead to a necrotizing destruction of glomeruli causing irreversible kidney damage within several months or even weeks. With respect to the immunologically caused vasculitis, there are - depending upon the severity and type of organ involved - many clinical warning signs to be recognized, such as arterial hypertension, hemoptysis, arthalgias, muscle pain, palpable purpura, hematuria, proteinuria and renal failure. In addition, constitutional signs, such as fever and loss of body weight may occur concurrently. Investigations of glomerulonephritis or vasculitis must contain a careful and complete examination of family history and medications used by the respective patient. Thereafter, a thorough clinical examination must follow, including skin, joints and measurement of arterial blood pressure. In addition, a spectrum of laboratory analyses is required in blood, such as full blood screen, erythrocyte sedimentation rate, CRP, creatinine, urea and glucose, and in urine, including urinalysis looking for hematuria, red cell casts and proteinuria. Importantly, proteinuria needs to be quantified by the utilization of a random urine sample. Proteinuria > 3g/d is diagnostic for a glomerular damage. These basic tests are usually followed by more specialized analyses, such as a screening for infections, including search for HIV, hepatitis B or C and various bacteria, and for systemic inflammatory diseases, including tests for antibodies, such as ANA, anti-dsDNA, ANCA, anti-GBM and anti-CCP. In cases of membranous nephropathy, antibodies against phospholipase-A2-receptor need to be looked for. Depending upon the given clinical circumstances and the type of disease, a reasonable tumor screening must be performed, especially in cases of membranous and minimal-change nephropathy. Finally, radiological examinations will complete the initial work-up. In most cases, at least an ultrasound of the kidney is mandatory. Thereafter, in most cases a renal biopsy is required to establish a firm diagnosis to define all treatment options and their chance of success. The elimination of a specific cause for a given glomerulonephritis or vasculitis, such as an infection, a malignancy or a drug-related side-effect, remains the key principle in the management of these diseases. ACE-inhibitors, angiotensin receptor-blockers, aldosteron antagonists and renin-inhibitors remain the mainstay in the therapy of arterial hypertension with proteinuria. Only in cases of persistently high proteinuria, ACE-inhibitors and angiotensin receptor blockers can be prescribed in combination. Certain types of glomerulonephritis and essentially all forms of vasculitis require some form of more specific anti-inflammatory therapy. Respective immunosuppressive drug regimens contain traditionally medications, such as glucocorticoids (e. g. prednisone), cyclosporine A, mycophenolate mofetil, cyclophosphamide, and azathioprine. With respect to more severe forms of glomerulonephritis and vasculitis, the antibody rituximab represents a new and less toxic alternative to cyclophosphamide. Finally, in certain special cases, like Goodpasture's syndrome or severe ANCA-positive vasculitis, a plasma exchange will be useful and even required.
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PMID:[Glomerulonephritis and vasculitis as causes of arterial hypertension]. 2254 60

A 50-year-old female patient presented with severe myalgia involving her proximal muscles for 3-4 weeks. She also reported mild thyrotoxic symptoms over the same time period. Examination revealed mild thyrotoxicosis, a moderate diffuse goiter and no eye signs. The clinical picture was dominated by muscle pain and tenderness involving mainly her proximal arms and legs, her calves and her fingers, requiring opiate analgesia. Muscle power and tendon reflexes were normal. Laboratory evaluation revealed undetectable serum thyroid stimulating hormone (TSH) with raised FT4, FT3 and positive TSH receptor antibodies. Treatment with carbimazole was started. Additional laboratory investigations were negative (inflammatory markers, creatine kinase and antibodies to antinuclear antibodies, gastric parietal cell, smooth muscle, mitochondrial, dsDNA, centromere, extractable nuclear antigen (ENA) ribonucleoprotein, ENA Sm, ENA Ro, ENA Anti-La, ENA Scl70, ENA Jo-1, anti-CCP and rheumatoid factor). Further assessment in the rheumatology clinic confirmed there was no small joint tenderness or loss of range of movement of her limbs, but widespread and profound muscle tenderness of the common extensors of the forearms, biceps, trapezius, calves and thighs. She was treated symptomatically with analgesic medication and continued on carbimazole. A month later she was euthyroid and her myalgia had resolved. Hyperthyroidism has a profound effect on skeletal muscle and often leads to myopathy. Severe myalgia in association with Graves' disease is rare and resolves with the restoration of euthyroidism.
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PMID:An unusual presenting symptom of graves' disease: myalgia. 2478 30

A patient with polymyalgia rheumatica(PMR)had increasing thrombocytosis. CRP levels, the ESR, and serum interleukin (IL)-6 levels were slightly elevated, and the patient tested negative for RF and anti CCP antibodies. Muscle pain was ameliorated with the administration of corticosteroids. Genetic analysis of the peripheral white blood cells demonstrated the presence of a JAK2V617F mutation. The muscle pain experienced by the patient was considered to be due to essential thrombocythemia( ET)of myeloproliferative neoplasms(MPNs)along with an inflammatory reaction. Unfortunately, the patient died suddenly because of cerebral infarction.
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PMID:[A Case of Essential Thrombocythemia with a JAK2V617F Mutation andPolymyalgia Rheumatica]. 3002 32