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 40-year-old woman with clinical and laboratory features of myasthenia gravis, hyperthyroidism, and polymyositis responded to treatment with prednisone alone. Symptoms of myasthenia gravis appeared first followed by hyperthyroid symptoms. Triiodothyronine, thyroxine, and thyroid uptake were elevated as were serum levels of CPK, SGOT, SGPT, and LDH. Muscle biopsy specimen showed mild type II fiber atrophy and a small focus of inflammatory cells. Two weeks after initiation of prednisone, 100 mg every other day, the ESR declined from 44 to 12 mm/hr, serum enzyme values became normal, and the weakness improved. Over the ensuing four months, the thyroid function values returned to normal and the patient no longer needed any anticholinesterase drug. At present, she is functionally normal except for mild defects in eye movement and she takes no medication. Physicians should consider treating patients who have several concurrent autoimmune diseases with prednisone to see if all conditions can be brought under control with one simple therapy.
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PMID:Prednisone use in concurrent autoimmune diseases. 42 Jun 18

Seven patients of temporal arteritis with eye involvement have been presented. These cases represent a spectrum of disease from intermittent diplopia with minimal 6th nerve weakness through mild retinal ischemia with recovery to permanent bilateral blindness. Temporal arteritis should be suspected when any form of ocular ischemia is suspected by history or found on examination of an elderly person. An early diagnosis may protect the vision in both eyes if vision is normal at the time of diagnosis. If vision in one eye is decreased because of ischemia, the vision in the other eye can usually be retained if proper therapy is instituted. Furthermore, adequate therapy may even result in improvement in vision in the involved eye. Patients with biopsy proven temporal arteritis should be continued on steroid therapy until the active disease is quiescent. Inactivity should be determined by carefully monitoring the ESR while steroids are being tapered. If the ESR rises, it is indicative of continued inflammation and if steroids are not continued, the eyes remain at risk as seen in Case 5. If the ESR remains elevated for a year or more despite continuation of high steroid levels, consideration should be given to repeating the temporal artery biopsy. Temporal arteritis should be considered in the differential diagnosis of any multisystem disease in older patients. Even central nervous system involvement may occur concomitantly, since the intracranial vessels are not immune from the disease process. Tuberculosis, systemic syphilis and more recently the collagen vascular diseases have been dubbed the "great imitators" and "the protean diseases." We suggest that the same terminology can be applied to temporal arteritis. Temporal arteritis can affect any organ. Moreover, there is a wide spectrum of variation in the degree of involvement of any particular tissue as illustrated by these 7 cases of ocular involvement.
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PMID:Temporal arteritis: a spectrum of ophthalmic complications. 118 Apr 60

A 69-year-old-female with a history of rheumatoid arthritis since 1975 had suffered from dysesthesia of extremities since October 1989. Radiating pain and weakness occurred when she tried to stand up on Dec. 25 in 1989. She was admitted to our hospital in October 1990. Physical examination showed emaciation, hypesthesia of extremities, hypesthesia over the right chest and back, impaired vibration and position sense, and hyperreflexia. Laboratory findings revealed that the erythrocyte sedimentation rate was elevated to 46mm/hr, rheumatoid factor (RF) to 83.1IU/ml and CRP to 3.7mg/dl. Her blood sugar was high and she was diagnosed as having diabetes mellitus. Cervical X ray film showed atlanto-axial subluxation. A pseudotumor around the odontoid process bulging into the spinal canal and compression of the upper cervical cord was observed by MRI. In spite of administration of bucillamine (100mg/day), the size of pseudotumor did not change. Methotrexate (MTX) at a dose of 5mg/week was started in February 1991 and the pseudotumor decreased in size with a concurrent reduction of ESR, RF and CRP. However, the high intensity lesion by T2 weighed image did not change and dysesthesia persisted. The pseudotumor was thought to be due to pannus and it was revealed that MTX was effective for reduction. The persistent dysesthesia was probably due to the degeneration of the upper cervical cord, although diabetic neuropathy may also have played a role.
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PMID:[A case of rheumatoid arthritis complicated with pseudotumor around odontoid process successfully treated by methotrexate]. 144 85

We reported the first case of Rothmann-Makai syndrome associated with mononeuropathy in a 31-year-old woman. In June 1989, she noticed several small subcutaneous nodules in the bilateral upper arms. On July 2, she woke up because of severe pain below the knee in the right leg which lasted 15 hours. On admission, subcutaneous nodules were recognized on bilateral upper arms, abdomen, gluteal regions and thighs. None of these nodules were associated with local heat or pain. Muscle weakness and dysesthesia were observed in the right foot, but deep tendon reflexes were normal. Electrophysiological studies revealed a decrease of the amplitude of action potential and of the conduction velocity in the right tibial nerve. Microscopic examination of skin biopsy showed lipolysis and diffuse lymphocyte infiltration (panniculitis) and perivascular lymphocyte infiltration was also observed. Routine laboratory data including peripheral blood, ESR, blood chemistry, and CRP were in the normal range and antinuclear antibodies and LE cells were not detected. By those findings, she was diagnosed as Rothmann-Makai syndrome associated with mononeuropathy. Steroid treatment was effective on both skin lesions and mononeuropathy. Steroid treatment was effective on both skin lesions and mononeuropathy. We concluded that this mononeuropathy may be induced by a ischemic change which may be caused by panniculitis.
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PMID:[A case of Rothmann-Makai syndrome associated with mononeuropathy]. 166 45

A rare case of mixed connective tissue disease (MCTD) with subacute transverse myelopathy and various neurological signs was reported. The patient, a 53 year-old woman, was admitted to our hospital with subacute progressive muscle weakness of left lower limb and sensory disturbance of bilateral lower extremities. At the age of 40, she suffered from sensory disturbance of her face, which improved in about three years. She had a high fever, Raynaud phenomenon, dyshydrosis on right side of her face at the age of 43. On the admission, physical examination revealed swollen fingers and telangiectasia of her face. Neurologically, she had transverse myelopathy at the level of Th6, bilateral trigeminal neuropathy, tonic, pupils, polyneuropathy and dyshydrosis. Laboratory examination showed positive antinuclear antibody, a high titer of antibody to RNase-sensitive components of extractable nuclear antigen, positive antinuclear RNP antibody and negative anti-Sm antibody. Her myelopathy improved with corticosteroid therapy, and ESR and the level of immunoglobulin were normalized. But, other neurological signs showed no improvement.
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PMID:[A case of mixed connective tissue disease with subacute transverse myelopathy]. 180 65

A case study is given of a 25-year old woman with rhabdomyolysis associated with HIV infection. The presenting symptoms were a 1-week history of backache, gross swelling of both hands and feet, and weakness and marked pain in most muscle groups; 3 days before admission the urine was black and she was unable to walk. Multiple, firm 1-2 cm lymph nodes were revealed during examination. White blood cell count (WBC) was 22,000/microliter with 12 pc lymphocytes, 7.3 pc monocytes, and 80.5 pc polymorphonuclear leukocytes. Hemoglobin concentration was 15.8 g/deciliter; platelet count was 124,000/microliter with a Westergren ESR of 109 mm/h. An antinuclear antibody test was negative. Serum concentration of urea was 3.8 mmol/liter, creatinine 42 microliter/liter, sodium 128 mmol/liter, and potassium 5.9 mmol/liter. Microscopic examination of urine revealed WBC 100/HPF, red blood cells 20/HBF, and granular casts. The dipstick test showed blood land protein in the urine. Electromyography showed inflammatory myopathy. Creatine Kinase (CK) concentration was 2359 IU/liter and lactate dehydrogenase concentration 1000 IU/liter. Hemolysis was present from clinical or laboratory signs. The patient tested HIV positive by ELISA (Abbott) and Western blot (Dupont). Treatment consisted of administration of 60 mg/day of prednisolone orally. Over 2 weeks, swelling of limbs was reduced and CK concentration was reduced to 931 IU/liter. The patient was discharged and did not keep a follow-up appointment. The patient did not have a history of other predisposing conditions, only HIV infection and persistent muscle weakness and inflammatory myopathy. There is evidence from other patient studies of myopathy associated with HIV infection and polymyositislike illness. In this case study, the patient may have had a acute form of polymyositis, or acute viral myositis such as occurs with echo, influenza, coxsackie, and other viral infections. A detailed viral investigation was not performed. HIV infection may have directly infected myocytes or immunosuppression predisposing to acute myositis by other pathogens. HIV-related muscle disease should include rhabdomyolysis.
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PMID:Rhabdomyolysis associated with human immunodeficiency virus (HIV) infection. 180 50

Two female patients developed localized scleroderma on the trunk and the thighs after oral ingestion of L-tryptophan for some years. Both patients reported acute progressive myalgia and weakness of the proximal parts of the extremities. On laboratory evaluation, the leucocyte count was approximately 20,000/mm3, with 38% blood eosinophils in one patient and 53% in the other. The ESR was slightly elevated; electrophoresis and muscle enzymes were normal. Skin and muscle biopsies revealed characteristic features of diffuse fasciitis with eosinophilia. High-dose glucocorticoid therapy resulted in a rapid normalization of the ESR and blood eosinophilia, whereas the scleroderma showed little improvement. The diffuse edema observed in one patient receded within a few days. A correlation between oral ingestion of L-tryptophan and the eosinophilia-myalgia syndrome has been reported recently, and the present case reports must be discussed in the light of this observation. Both patients developed a tryptophan-induced scleroderma-like illness resembling diffuse fasciitis with eosinophilia (Shulman's syndrome).
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PMID:[L-tryptophan-induced eosinophilia-myalgia syndrome with features of diffuse fasciitis with eosinophilia]. 225 2

A case in reported of the clinical syndrome of polymyositis in a young man. The syndrome masked pulmonary tuberculosis. Sudden appearance of pains and weakness of the muscles of the shoulder and abdominal muscles was accompanied by fever up to 40 degrees C, and macular rash on the trunk and extremities. During the disease right-sided pneumonia developed and regressed after treatment with antibiotics (tetracyclines, penicillin). Laboratory investigations showed high ESR, high leucocyte count, high levels of transaminases, CPK and LDH, and in cutaneo-muscular++ biopsy specimen scan subepidermal infiltrations were present. The patient was treated with corticosteroids with a striking improvement of the general condition. During this treatment left-sided pleural effusion developed. Bacteriological examination of the pleural fluid, including tests for acid-fast bacilli, was negative in direct examination, but these bacilli were cultured from fluid. No malignant cells were found. After antituberculous treatment the condition of the patient and the biochemical parameters became normal.
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PMID:[Polymyositis in pulmonary tuberculosis]. 262 70

A 57-year-old woman suffered from polyarthralgia for 7 years, and was treated by using NSAID with the diagnosis of RA. From Jan. 20th 1987, she complained of back pain and numbness of both hands, and from May 7th 1987, she also complained of dysphagia and dysarthria, and she was not able to button up. Soon afterwards she could eat only one custard pudding a day, so she admitted to our hospital on March 17th 1987. The neurological examination showed hyporeflexia and muscle weakness of the four extremities; and hypesthesia of the 7th to 11th intercostal nerve area and both lateral sides of the dorsum pedis. The laboratory examination showed ESR 17 mm/h, gamma-glob 1.66 g/dl, CRP(+), RAHA 80 x, CH50 24.0 U/dl, HLA-antigen; DR 4(+). Cerebrospinal fluid examination showed cell 5/mm3, protein 63 mg/dl, IgG 13 mg/dl, IgG% 20.6%. X-ray examination indicated destruction of both wrists, left elbow, right 2-5th MTP, and left 5th MTP joints. A light microscopic examination of the left sural nerve showed perivascular infiltration with lymphocyte, occasional macrophages and giant cells at the epineurium, and no demyelination or Wallerian degeneration at the nerve fiber. These histological findings were the same as type-I arteritis in nerves in RA proposed by D.L. Conn. Clinical improvement was obtained after administration of prednisolone 30-60 mg/day.
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PMID:[A case of rheumatoid arthritis associated with polyneuritis]. 266 32

A 63-year-old man presented six days after the sudden onset of horizontal double vision. His left eye became divergent two days later. On initial examination he had bilateral internuclear ophthalmoplegia with weakness of adduction and abducting nystagmus. Convergence was weak but there were no other neuro-ophthalmic signs. Constitutional signs included confusion and unsteadiness on his feet. A provisional diagnosis of arteritis was made. His ESR was 92 mm/h and a superficial temporal artery biopsy confirmed the diagnosis of giant cell arteritis. After two weeks or oral prednisolone his eye movements returned to normal. There have been no further relapses. This would appear to be a unique presentation of giant cell arteritis. The causes of internuclear ophthalmoplegia are discussed along with a review of the ocular and neuro-ophthalmic signs of giant cell arteritis.
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PMID:Bilateral internuclear ophthalmoplegia--an unusual initial presenting sign of giant cell arteritis. 276 84


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