Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 71-year-old man was admitted to the Wake Forest University/Baptist Hospital Medical Center on February 1, 1989, with pharyngitis and a cutaneous eruption that began that day. The past history was significant for a diagnosis of chronic lymphocytic leukemia (CLL) made in 1984, and for longstanding hypertension, severe coronary artery disease, and prostatic hypertrophy. The patient had required no therapy for his CLL until August, 1988, when he developed hemolytic anemia and was treated with oral chlorambucil, 4 mg/day, and a tapering course of prednisone. By December, 1988, the prednisone therapy had been discontinued, but the patient required hospital admission for pneumococcal pneumonia, which responded well to intravenous antibiotic therapy. One day prior to the current admission the patient complained of persistent fevers, sore throat, productive cough, and headache. He noted a new cutaneous eruption on the day of admission in February, 1989. The past history was positive for occasional herpes stomatitis. The patient did not know if he had previously been infected with varicella. Skin examination revealed multiple (greater than 20), single, and grouped vesicles in a generalized distribution involving the bilateral trunk, head, neck, arms, and legs. The heaviest involvement was on the right posterior auricular area and on the neck. A Tzanck preparation obtained from an early lesion was positive for multinucleated giant cells. Viral culture was negative at 24 hours and at 1 week. A skin biopsy of an early vesicular lesion was performed and revealed intraepidermal vesicles with acantholysis and giant cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Granuloma annulare and disseminated herpes zoster. 145 73

In the immunocompromised patient, even mild forms of any combination of headache, meningismus, altered mental status, or focal neurologic signs should initiate an evaluation for possible CNS infection. The limited signs and symptoms of acute CNS infection are not due to specific organisms but to pathologic changes at the neuroanatomic site of infection. The initial clinical history, examination, laboratory, and neuroradiographic data will narrow the problem to one of several groups of agents, although it may not be possible to specify a single causative agent. It should be remembered that several concurrent infections (i.e., CMV and toxoplasmosis, aspergillosis, and bacterial sepsis) may be present. Thus, the clinician should rely on broad antibiotic coverage appropriate to the suspected causative agent or agents at the site of infection. It may be necessary to offer broad-spectrum antibiotic coverage for a CSF presentation that is subsequently found to result from a viral illness or from a noninfectious cause. However, one should avoid undertreating those infections for which specific therapy can be offered, and broad-spectrum treatment usually will not be regretted. Uncertainty in diagnosis following noninvasive procedures should lead to a brain biopsy. Although many of the infections discussed in this article have a poor prognosis, some of the most common pathogens, such as Cryptococcus, Listeria, and Toxoplasma, have effective specific therapies to which the patient should have access as rapidly as possible. The clinician who has successfully treated a patient with CNS infection should remain vigilant for late sequelae or recurrence of infection. Chronic treatment of some infections, such as toxoplasmosis or aspergillosis, may be necessary. The reintroduction of steroids for the treatment of an underlying cancer may reactivate previously treated disease, such as cryptococcosis, and periodic CSF surveillance is appropriate under these circumstances. Recurrence of the symptoms should raise the suspicion of recurrent or new infection, and the patient also should be evaluated with CT or MRI for the development of hydrocephalus or for new metastatic disease. In patients who have had varicella-zoster infection, postherpetic neuralgia and delayed arteritis may develop. Seizures, hearing loss, and neuropsychologic sequelae may follow any meningoencephalitis. The patient should always be reevaluated for the possibility of infection with a different opportunistic organism. CNS infections remain a major cause of morbidity and mortality in immunosuppressed patients with malignancies. In one series, 60% of such patients died as a result of their CNS infection, many at a time when the underlying disease had an otherwise good prognosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Central nervous system infections in cancer patients. 175 29

The chronic fatigue syndrome is a poorly defined symptoms complex characterized primarily by chronic or recurrent debilitating fatigue and various combinations of other symptoms, including psychological symptoms, sore throat, lymph node pain, headache, myalgia, arthralgias. Psychological disturbances, ranging from mild depression or anxiety to severe behavioral abnormalities, are always present. Chronic fatigue syndrome is the name that more accurately describes this symptom complex of unknown cause. A viral aetiology has long been hypothesized: many viruses are potential candidates, including any of the 23 Coxsackie A or 6 Coxsackie B viruses, herpes viruses, particularly Epstein-Barr virus and varicella. These studies, though interesting, remain unconvincing because of methodological flaws such as a poor case definition and inadequate control groups. This syndrome may represent an infection by a yet unidentified virus. It is more likely due to an abnormal immune response toward different intracellular pathogens. There is no treatment to ameliorate the chronic fatigue syndrome. Epidemiological studies are essential with explicit operational case definition before progress can be made in the management of this distressing disorder.
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PMID:[The chronic fatigue syndrome. A multifactorial approach and the treatment possibilities]. 207 78

A case of severe generalised herpes simplex type 2 infection is described in an adult male who had known exposure to herpes. The patient first complained of headache, fever and neurological symptoms, and three to six days later of conjunctivitis, severe pharyngitis, arthralgia and vesicular lesions about the body. During the first 14 days of illness, including three in hospital, the patient was diagnosed as having infection with varicella virus, vesicular stomatitis virus, or hand-foot-and-mouth disease virus. The diagnosis of infection with herpesvirus was not considered until herpesvirus was visualised in vesicular fluid by electron microscopy six weeks after onset. HSV-2 was then repeatedly isolated from vesicular fluids over the next four years. Detailed serological tests on the patient's sequential serum samples demonstrated a specific and continued response to HSV-2. He possibly acquired the virus iatrogenically, either by oral droplet transmission into or finger contamination of a PPD injection site, from the nurse who administered the injection and then palpated the site.
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PMID:Herpes type 2 infection with unusual generalised manifestations and delayed diagnosis in an adult male. 687 92

Two previously healthy men, aged 54 and 41 years, fell ill with headaches and increased fatiguability, one also with vomiting, the other with fever, transitory visual disturbances and slight weakness of the left hand. Both of them had a stiff neck and clouded consciousness. The EEG had moderate to severe dysrhythmia, predominantly over the temporal area, CSF showed an increased cell count of 1000/3, predominantly lymphocytes, and increased protein. The younger patient also had global aphasia and the computed tomography indicated an area of decreased density in the left temporal region. In the CSF there were locally produced IgG. The clinical findings were similar to those of herpes encephalitis, but were milder and regressed more quickly. Severe months later only a few minor organic behavioural changes were present. Antibody findings in CSF and serum suggest varicella-zoster virus as the causative agent, although in both instances no rash was observed throughout the entire period of observation.
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PMID:[Zoster encephalitis without rash: report of two cases (author's transl)]. 707 5

Rickettsialpox is a mild illness characterized by the appearance of a primary eschar at the site of a mite bite followed by fever, headache, and a papulovesicular rash. It can be confused with a variety of illnesses including several other rickettsial diseases and chickenpox. R. akari, the etiologic agent, is a rickettsia belonging to the spotted fever group (SFG) of rickettsial illnesses. In spite of significant serologic cross-reactivity with other SFG agents, there is no convincing evidence of cross-immunity to these agents after recovery from rickettsialpox. Tetracyclinie is the drug of choice in the treatment of this disease.
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PMID:Rickettsialpox: report of an outbreak and a contemporary review. 727 20

The atypical measles syndrome is a relatively new disease that was first recognized 15 years ago. Initially, it occurred in children who were exposed to wild measles virus several years after they were immunized with killed measles vaccine. It was characterized by a two- to three-day prodrome of high fever, cough, headache, and myalgia followed by a rash that resembled Rocky Mountain spotted fever, scarlet fever, or varicella and associated with roentgenographic evidence of pneumonia with or without pleural effusion. This report highlights three unusual manifestations of this syndrome: 1) transient hepatitis, 2) persistence of pulmonary lesions for several years, and 3) occurrence of excessively high measles hemagglutination-inhibition antibody titers. Today, this syndrome occurs predominantly in adolescents and young adults.
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PMID:Atypical measles syndrome: unusual hepatic, pulmonary, and immunologic aspects. 746 41

We report here our findings in two Japanese siblings who experienced recurrent bacterial and viral infections since early infancy. Recent symptoms included diarrhoea, conjunctivitis, rashes, headache, sore throat, joint pain, vomiting and vertigo, all similar to those seen in toxic shock syndrome, except for shock. These symptoms improved following gammaglobulin treatment. Staphylococcus aureus with coagulase type IV was continuously isolated from nasal smears producing toxic shock syndrome toxin-1 (TSST-1). Serum antibodies did not or only poorly responded to TSST-1, diphtheria toxoid, varicella virus and rubella virus, whereas total and subclass levels of serum immunoglobulin and in vitro DNA synthesis of lymphocytes stimulated by TSST-1, Staph. aureus, varicella vaccine and mitogens were normal. In the family, ten other members in three generations (five males: five females) including the mother had similar clinical symptoms. Thus, the disease may be inherited in an autosomal dominant fashion.
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PMID:A family of selective immunodeficiency with normal immunoglobulins: possible autosomal dominant inheritance. 803 20

Varicella is an infrequent but potentially severe infection in adult HIV-infected patients. We reviewed five cases of varicella in HIV-seropositive men; two were complicated by severe headache and meningismus, and one of these patients also had hepatitis and thrombocytopenia. All five patients responded well to acyclovir therapy, but one patient had dermatomal zoster 2 years later, and another failed to have detectable antibody after infection. We also performed a serosurvey on 181 consecutive HIV-infected patients presenting themselves for evaluation. A total of 95% of these patients had demonstrable antibody to varicella-zoster virus. Immune status to varicella did not correlate with the declining CD4 count, which was well preserved even in patients with fewer than 200 CD4 cells/mm3.
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PMID:Varicella immunity and clinical disease in HIV-infected adults. 828 23

Oka/Merck varicella vaccine has been studied in this institution since 1981. Persistence of antibody for 6 to 8 years has been demonstrated; however, cases of chickenpox have been seen in immunized children. The severity of chickenpox in healthy children who have received Oka/Merck varicella vaccine since 1981 is described. All vaccinees who developed chickenpox-like rashes more than 6 weeks postimmunization were examined. Of 2163 vaccinees, 164 were examined, of whom 114 had rashes consistent with chickenpox. When sera were available (46%), antibody studies uniformly confirmed varicella-zoster virus infection. Chickenpox occurred 2 to 96 months (median of 44 months) postimmunization. The range for the number of skin lesions was 1 to 285 (median 18) in seroconverters. Symptoms included itching in 39%, fever in 9%, headaches in 7%, lymphadenopathy in 3%, and malaise in 2%; 54% were asymptomatic, except for the rash. The median time to total healing was 5 days. The median time lost from school was 2 days. Thirteen of the children in whom infections developed had failed to seroconvert after immunization. Their infections were similar in severity to those of children who had seroconverted originally. When varicella was introduced into families as a result of chickenpox in an immunized family member (index case), the rate of secondary chickenpox among immunized siblings was 12.2%. Eleven such secondary cases were similar in severity to the 9 index cases. It is concluded that chickenpox is generally mild in previously immunized children.
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PMID:Modified chickenpox in children immunized with the Oka/Merck varicella vaccine. 841 99


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