Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 42-year-old female was admitted to our hospital on October 1, 1990 because of one week history of back pain, weakness of her right lower extremity and sensory disturbance of her left lower extremity. Physical examination revealed swollen hands, Raynaud's phenomenon, sclerodactyly and heliotrope rash. The body temperature was 37.0 degrees C. Neurological findings included weakness in the right lower extremity, left hypalgesia and thermohypesthesia below Th4, hyperreflexia on the right lower extremity and right extensive plantar response. Laboratory data showed leucopenia (3,700/mm3) and hypergammaglobulinemia. Serological examination revealed antinuclear antibodies with a titer of 1:5120 (speckled pattern) and anti-RNP antibody with a titer of 1:32. Neither anti-DNA antibody nor anti-Sm antibody were detected. Serum C3 and C4 were normal. The cerebrospinal fluid (CSF) contained mononuclear cells of 5/mm3, protein 29 mg/dl and glucose 56 mg/dl. Queckenstedt test was negative. Treatment with prednisolone 60 mg daily was started. On the 8th day of therapy, she complained of a burning sensation in the back, then paraplegia and urinary retention developed. MRI examination showed a high intensity area of the spinal cord at the right Th4 on T2-weighted images. Next day the treatment with 1000-mg intravenous daily pulse of methylprednisolone for 3 days was started, followed by prednisolone 40 mg daily. After this pulse therapy, the CSF contained mononuclear cells of 52/mm3, protein 34 mg/dl, glucose 67 mg/dl and IgG 7.6 mg/dl. Her neurological manifestation gradually improved and at six weeks after the pulse therapy neurological examination revealed no abnormality except for painful tonic spasm. Prednisolone was slowly tapered to 15 mg daily.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of mixed connective tissue disease (MCTD) associated with transverse myelitis responding to pulse therapy]. 181 87

A 25-year-old woman with a 2 years history of painful enlargement of the left calf visited our clinic because of ache in the left calf which became severe enough to interfere her walk. She had no history of trauma to the calf, and family history was negative for muscle disease. Physical examination showed an enlarged left calf muscle with pain which was evoked by stretching of the Achilles tendon. There was no muscle weakness or neurological abnormality. Laboratory tests were all within normal limits, including erythrocyte sedimentation rate and serum enzymes such as creatine kinase and aldolase. The CT scan revealed an isolated round-shaped low density area in the left calf muscle, which showed up as a markedly high signal intensity on T2 weighted images of MRI. The lesion was confirmed to be the lateral head of the gastrocnemius muscle. The specimen obtained from the affected muscle demonstrated degenerative and inflammatory changes together with excess fibrosis. There was no sarcoid lesion or malignancy. From the above results, the present case was thought to have isolated focal myositis. Prednisolone 80 mg (40 mg, twice, at 4-day intervals) was given to the left femoral artery without any trouble. Thereafter the patient became free from pain and difficulty in walking, and the lesion demonstrated by CT scan disappeared in 15 days. However, the high signal intensity on T2 weighted images faintly remained until the 54th day after the treatment. In summary, MRI is more sensitive than CT scan for detection of isolated focal myositis, which might be successfully treated by arterial injection of prednisolone within a short period than any other conventional methods.
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PMID:[A case of isolated focal myositis successfully treated by arterial injection of prednisolone--its findings by CT scan and MRI]. 208 34

A case of polymyositis associated with chronic active hepatitis was reported. A 53-year-old man, who had no previous history of blood transfusion nor hepatitis, noticed proximal dominant muscle weakness on January 29, 1985. He was admitted to Kyoto National Hospital on February 7, and laboratory studies disclosed the elevation of serum enzyme levels; creatine kinase (CK) 9845 IU/L (normal 54-263), glutamate oxaloacetate transaminase (GOT) 834 IU/L (9-31), glutamate pyruvate transaminase (GPT) 491 IU/L (4-34), lactate dehydrogenase (LDH) 2135 IU/L (248-464). Also serum gamma globulin was high (1.8 g/dl) and LE-like cell was found. The diagnosis of polymyositis was made and prednisolone therapy (60 mg/day) was started on February 23. The elevated serum enzymes decreased gradually, but severe muscle weakness persisted for about one month. On April 3, he was admitted to our hospital. Physical examination revealed moderate proximal dominant muscle weakness without skin eruption, jaundice or hepatosplenomegaly. The serum enzymes were still high; CK 1826, GOT 173, GPT 232 (GOT less than GPT), LDH 1548. However, alkaline phosphatase (ALP) and bilirubin were normal. Hepatitis B surface antigen (HBsAg) was not detected. Antinuclear antibody was positive. The electromyogram study showed myopathic change, and the muscle biopsy demonstrated myopathic change and cell infiltration, compatible with polymyositis. These results suggested liver dysfunction associated with polymyositis. Prednisolone therapy was continued and muscle weakness decreased. From December, 1985, serum enzymes (CK, GOT, GPT, LDH) elevated again and muscle weakness also slightly increased. Anti-smooth muscle antibody was positive. It was suggested that both polymyositis and liver dysfunction deteriorated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of polymyositis associated with chronic active hepatitis]. 218 64

A 68-year-old man with suspected allergic granulomatosis and angiitis is reported. He had received 10 mg of prednisolone daily since July 1988 for asthma. He abruptly developed muscle weakness of the lower extremities, followed two days later by paraplegia. Six days after the onset of the muscle weakness, he was hospitalized. He showed disturbance of recent memory, disorientation, neck rigidity, paraplegia, mild muscle fasciculation and hypesthesia. He also showed paralytic ileus. Laboratory findings showed leukocytosis (24580/mm3), eosinophilia (56% of the peripheral white blood cells and 19% of the cells in the cerebrospinal fluid), on erythrocyte sedimentation rate of 31 mm/h, and the IgE level of 1200 IU/ml. The ECG showed loss of the r-wave in V1 and V2. A granulomatous lesion anterior to the spinal cord was found on myelography and MRI. Prednisolone was given at a dose of 60 mg daily resulting in improvement of the clinical symptoms and eosinophilia. There was disappearance of the granuloma on MRI performed after prednisolone therapy. Despite the severe manifestation of allergic granulomatosis and angiitis, prednisolone therapy had a marked effect in this patient. The granulomatous lesion anterior to the spinal cord shown by MRI suggested an eosinophilic granuloma, and may have been the etiology of some of the neurological symptoms.
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PMID:[A case of suspected allergic granulomatosis and angiitis with a rapid clinical course of paraplegia]. 224 87

Chronic relapsing polyneuropathy (CRPN) is an idiopathic disorder characterized by relapsing and remitting course, elevated CSF protein, slow nerve conduction and absence of systemic disease(s). Systemic lupus erythematosus (SLE), however, has been reported to manifest clinical symptoms and signs mimicking CRPN. A few authors described CRPN as a presenting manifestation or more rarely as the only illness of SLE. In these cases diagnosis of SLE was confirmed by some laboratory tests to detect auto-antibodies which were positive in subclinical SLE. We experienced a 24-year-old female whose illness started as CRPN without any auto-antibodies and recurred with autoimmune abnormalities indicating SLE. She noticed muscle weakness in the lower extremities about ten months previous to the first admission. The weakness progressed gradually and was accompanied by urinary incontinence and sensory deficits in limbs. In another hospital lumbar puncture revealed highly elevated CSF protein and she was referred to us. Neurologic examination showed sensorimotor polyneuropathy with normal blood chemistry and negative auto-antibodies. Prednisolone therapy brought out gradual improvement. She was readmitted 2 years after the first admission because of severe motor dominant polyneuropathy. Serological examination revealed positive auto-antibodies including antinuclear (ANA), anti-DNA, anti-RNP and anti-ENA antibodies. CBC showed decreased number of white blood cells. Nerve conduction velocities were markedly reduced. Again prednisolone was administrated successfully. Thereafter, she experienced several relapsing and remitting cycles. It was characteristic that deterioration of symptomatological findings such as motor weakness was always accompanied by an elevated titer of ANA and increased CSF protein in each of the cycles.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Systemic lupus erythematosus presenting chronic relapsing polyneuropathy as the first manifestation without auto-antibodies]. 226 10

We report a 37-year-old woman who developed chronic thyroiditis, and polymyositis with rimmed vacuoles (RVs). She developed paresthesia of glove and stocking type, muscle weakness of the lower extremities, and slowness in motion. On examination, her lower legs were atrophic and weak, more prominent on the right, while proximal muscles in the upper and lower extremities were slightly affected. Deep tendon reflexes of the upper and lower extremities were normal except for the absent Achilles tendon reflexes. Serum CK was high (1,809 IU/l), and laboratory data indicated chronic thyroiditis and hypothyroidism. Muscle CT showed severe fatty changes in the gastrocnemius and soleus muscles, more marked on the right, and slight atrophy of the thigh muscles. Electromyography and nerve conduction velocity study revealed peripheral neuropathy. Muscle biopsy revealed numerous myofibers with RVs, together with myofiber necrosis, phagocytosis and lymphocyte infiltration, consistent with myositis. Nerve biopsy was indicative of slight axonal degeneration. A diagnosis of polymyositis with RVs in combination with chronic thyroiditis was made. Prednisolone combined with levothyroxine markedly improved muscle weakness though atrophy and weakness of the lower legs were barely improved. Distal-dominant asymmetric affection of the leg muscles and many myofibers with RV on the biopsied muscle are atypical and rare findings of polymyositis. Associated chronic thyroiditis and neuropathy may be related to the formation of marked rimmed-vacuolar degeneration of myofibers in the present case.
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PMID:[Polymyositis with rimmed vacuoles in a case of chronic thyroiditis]. 761 67

A 43-years-old woman was admitted to the Hokkaido University Hospital because of high fever, muscle weakness and dyspnea in May 1993. She had has muscle weakness of upper extremities since December 1992. She had developed swollen hand, polyarthralgia and Raynaud's phenomenon. High fever and severe dyspnea developed in May 1993. Chest roentogenogram was normal in April 1993. Physical examination showed Velcro rales in both lower lung fields. Her laboratory data showed increased muscle enzymes, high titers of anti-nuclear-antibody (1: 1280) and anti-RNP-antibody (index 199.4 (normal < 7)). Anti-DNA, anti-Sm and anti-Jo-1-antibodies were all negative. Blood gas analysis showed severe hypoxemia. Chest roentogenogram revealed diffuse bilateral interstitial infiltrates prominent in the bases. Diagnosis of mixed connective tissue disease with acute interstitial pneumonitis was made. She was treated with steroid pulse therapy (methylprednisolone 1 g x 3 days) followed by high dose oral prednisolone (60 mg/day), and diffuse interstitial infiltrates disappeared within one week. Prednisolone could be tapered to 17.5 mg/day without relapse. Acute interstitial pneumonitis is a rare complication of mixed connective tissue disease, but may be life threatening. In such cases, high dose steroid therapy should be started without delay.
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PMID:[A case of mixed connective tissue disease with acute interstitial pneumonitis]. 767 Nov 32

The authors present a case report of a 62-year old woman, with hypertension for many years. She suffered from weakness, anorexia and weight loss in the last 6 months. On admission, anemia, elevated ESR, haematuria, proteinuria and renal failure were present. Renal biopsy was compatible with chronic glomerulonephritis. The clinical picture and positivity for P-ANCA suggested systemic vasculitis. Later evidence of maxillary sinusitis and nasal mucosae ulcers as well as pneumonitis, although biopsy did not reveal granulomas, suggested the diagnosis of Wegener Vasculitis. Medicated with Cyclophosphamide and Prednisolone, for a year, with improvement. The authors make a brief discussion of the clinical criteria for classification of ANCA-associated systemic vasculitis.
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PMID:[Vasculitis associated with ANCA]. 794 37

This is the report with muscle disorder associated carbamazepine (CBZ)-induced lupus. A 39-year-old female had been treated with CBZ 400 mg per day for 2 years because of complex partial seizure. In November, 1992 laboratory studies showed elevation of serum CK, IgG and titers of antinuclear antibody. Physical examination on admission revealed muscle weakness of neck flexors and iliopsoas but no rash or arthralgia. The electromyography showed myogenic change in the right biceps. CBZ was discontinued and replaced by zonisamide. Prednisolone 40 mg daily was started and the patient steadily improved. In the literature, there have been a few cases with muscle symptoms in CBZ-induced lupus, but muscle involvement with highly elevated CK associated with CBZ-induced lupus has not been reported.
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PMID:[A case of carbamazepine-induced lupus with myositis]. 829 14

A 65-year-old woman was given a diagnosis of polymyositis in April 1991. She was treated with prednisolone until December 1993, at which time muscle strength had increased and high blood pressure had developed. In May 1994 she was hospitalized for muscle weakness and mild liver dysfunction. Prednisolone was given and the levels of hepatobiliary enzymes decreased. Immunological examination revealed strongly positive results for anti-mitochondria antibody and M-2 antibody, which lead to the diagnosis of primary biliary cirrhosis. administration of ursodeoxycholic acid in addition to prednisolone was followed by normalization of liver function and a decrease in the production of the autoantibodies. Although polymyositis can be complicated by autoimmune diseases, reports of complication by primary biliary cirrhosis are rare, here we report that treatment with the combination of ursodeoxycholic acid and prednisolone was successful in a patient with liver dysfunction and primary biliary cirrhosis.
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PMID:[Primary biliary cirrhosis with polymyositis successfully treated with prednisolone and ursodeoxycholic acid]. 895 42


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