Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the pharmacokinetics and effects of intravenous foscarnet, 13 relatively healthy male patients with human immunodeficiency virus infection and a mean CD4+ lymphocyte value of 0.45 x 10(-9) cells per liter were given a continuous intravenous infusion of foscarnet (0.14 to 0.19 mg/kg per min) for 8 to 21 days. Blood and urine samples were taken during and after drug administration to monitor foscarnet concentrations. Lumbar puncture was performed during the infusion in five patients. The concentrations in plasma showed large variations both within and between patients. The disposition of foscarnet could be explained by a triexponential equation (t1/2 lambda 1, 0.40 to 2.52 h; t1/2 lambda 2, 3.20 to 16.7 h; t1/2 lambda 3, 36 to 196 h). Renal clearance accounted for most of the plasma clearance, the difference probably reflecting the passage of foscarnet into bone. Up to 20% of the cumulative dose may have been deposited in bone 7 days postinfusion. Foscarnet was distributed to the cerebrospinal fluid in a concentration varying from 13 to 68% of the simultaneous concentration in plasma. Polyuria and polydipsia were recorded in all patients. There appears to be an association between the degree of malaise, including symptoms such as nausea, vomiting, fatigue, and headache, and concentrations in plasma above 350 mumol/liter.
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PMID:Pharmacokinetics of foscarnet and distribution to cerebrospinal fluid after intravenous infusion in patients with human immunodeficiency virus infection. 252 39

Tenofovir disopril fumarate, a new nucleotide analogue against human immunodeficiency virus-1 (HIV-1), can induce hypophosphataemia, the mechanism of which is unclear. Moreover, a renal tubulopathy can occur in long-term treated patients, as observed in 2 HIV-1-infected patients after 12 months of tenofovir therapy, with polyuria-polydipsia, proteinuria, glycosuria and amino-aciduria, which resolved after discontinuation of tenofovir. The risk of renal tubulopathy symptoms in patients on long-term tenofovir therapy should be noted.
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PMID:Tubulopathy consecutive to tenofovir-containing antiretroviral therapy in two patients infected with human immunodeficiency virus-1. 1530 94

Primary CNS lymphomas (PCNSLs) constitute 3% of all intracranial neoplasms. From these, primary pituitary lymphomas (PPLs) represent extremely rare clinical entity. Nearly all of PCNSLs are non-Hodgkin diffuse large B-cell lymphomas. We present a 60-year-old female with right-sided third cranial nerve palsy, mild bitemporal visual field deficit, severe cephalea, and polyuria-polydipsia. Hypopituitarism with hyperprolactinemia was confirmed; brain imaging revealed a 16 mm-diameter sellar mass with suprasellar extension. A presumptive diagnosis of pituitary adenoma was established. The patient underwent a neurosurgical intervention. Histopathological examination and immunophenotyping (cytokeratin, CD45+, CD79+, bcl-2-) verified high-grade B-cell non-Hodgkin lymphoma of the Burkitt type. Systemic work-up showed no other foci of lymphoma, the patient's HIV status was negative, Epstein-Barr virus status was not disclosed. Although PPL can be undistinguishable from pituitary adenoma at imaging, one should consider lymphoma when evaluating an invasive sellar mass that is iso- to hypointense on T2-weighted magnetic resonance images, particularly when the patient is immunocompromised or old and presents with diabetes insipidus, cranial nerve palsy and fever of unknown origin in addition to the expected finding of hypopituitarism.
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PMID:Primary B-cell pituitary lymphoma of the Burkitt type: case report of the rare clinic entity with typical clinical presentation. 1909 61

We report 3 cases of patients with HIV/AIDS in whom Fanconi syndrome and nephrogenic diabetes insipidus developed secondary to use of an antiretroviral regimen containing tenofovir disoproxil fumarate and didanosine. These patients presented with a history of polydipsia, polyuria, weight loss, anorexia, and wasting. Interestingly, 1 patient was not taking protease inhibitors. This response is a well-documented yet uncommon complication of tenofovir use in the HIV population. We recommend continued monitoring for renal toxicity when using NRTI combination of tenofovir and didanosine.
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PMID:Proximal tubular dysfunction associated with tenofovir and didanosine causing Fanconi syndrome and diabetes insipidus: a report of 3 cases. 1933 29

Dear Editor, Granuloma annulare (GA) is an asymptomatic, chronic, and relatively common granulomatous skin condition which presents with annular papules usually slowly progressing into plaques on the extremities and the trunk. It usually presents with non-scaly, erythematous, annular plaques on the distal extremity (1,2). The pathogenesis of GA is still unknown, although a variety of possible factors contributing the disease have been reported, including drugs (3), insect bites, sun exposure, trauma, vaccinations, and viral infections (e.g. hepatitis B, hepatitis C, HIV, Epstein-Barr virus) (1). Several cases in which GA developed on residual skin changes from herpes zoster have also been reported (4). A 47-year-old woman presented with erythematous-livid plaques on the dorsa of her hands and linear and circular lesions on her neck, gradually spreading for the last 4 months prior to admission at our Department (Figure 1a and Figure 1b). She reported excessive thirst and sweating in the last 30 days, but did not consider it significant since it was summer. The patient was otherwise healthy and was not taking any medications. Mycological swabs taken from the dorsal parts of both hands and the neck were negative. Biopsy of the skin changes was consistent with GA, showing palisading granulomatous inflammation which surrounded degenerated collagen within the dermis. A routine laboratory check revealed increased levels of glucose (23 mmol/L) and HgbA1C, while lipid and thyroid hormone levels were normal. Fasting blood sugar lever was 17 mmol/L. Therapy with topical corticosteroid (betamethasone cream) for skin lesions was initiated and applied two times daily for 2 weeks. The patient was immediately referred to an endocrinologist and insulin therapy was initiated due to diabetes mellitus. Complete remission of the skin changes was observed on the follow-up visit after 3 months. There are many clinical variants of GA such as localized, generalized, disseminated, subcutaneous, arcuate dermal erythema, and perforating GA (1). The localized form of GA is most common with annular plaques on the distal extremities. In addition to the typical lesions on the dorsal side of both hands, our patient also presented with atypical, circular lesions around her neck. The relationship between GA and systemic diseases such as diabetes mellitus, thyroid disorders, dyslipidemia, and malignancies remains unclear (5). It is also uncertain whether genetic factors influence susceptibility to GA. Familial cases have been documented, but studies investigating the association between the disease and human leukocyte antigen (HLA) genes have yielded inconsistent results (6). Increased frequency of HLA-B35 in patients with the generalized form has been reported in a few studies (7). GA mostly affects children and young adults, mostly women. Many cases of GA resolve spontaneously within 2 years, but relapses occur in many patients. Treatment is divided into localized skin therapies and systemic therapies (1). High potency topical corticosteroids along with intralesional corticosteroids are the most common localized treatments (8). Systemic therapy includes corticosteroids, chloroquine, dapsone, and isotretinoin (1,9). Cryotherapy and UV-therapy can also be used, although with limited efficacy (10). GA is a common idiopathic disorder of the dermis and subcutaneous tissue that can be associated with a variety of underlying conditions such as diabetes mellitus. The relationship between GA and diabetes mellitus is still unknown. Since skin lesions preceded the diagnosis of DM in our patient and complete remission of skin changes occurred with induction of insulin therapy, it is important to perform routine laboratory test in every patient.
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PMID:Unusual Case of Granuloma Annulare Associated with Diabetes Mellitus. 3265 Aug 53

Immune checkpoint inhibitor-associated diabetes mellitus (ICI-DM) is a known immune-related adverse event (irAE) following treatment with programmed cell death protein 1 (PD-1), with a reported 0.9% incidence. We hereby present the first case, to our knowledge, of ICI-DM following ICI use in a human immunodeficiency virus (HIV) patient. In this case, a 48-year-old man with HIV stable on highly active antiretroviral therapy (HAART) was diagnosed with Hodgkin lymphoma and initiated treatment with the PD-1 inhibitor nivolumab. His lymphoma achieved complete response after 5 months. However, at month 8, he reported sudden polydipsia and polyuria. Labs revealed a glucose level of 764 mg/dL and glycated hemoglobin A1c (HbA1c) of 7.1%. Low C-peptide and elevated glutamic acid decarboxylase 65 (GAD65) antibody levels confirmed autoimmune DM, and he was started on insulin. Major histocompatibility complex class II genetic analysis revealed homozygous HLA DRB1*03-DQA1*0501-DQB1*02 (DR3-DQ2), which is a known primary driver of genetic susceptibility to type 1 DM. Autoimmune DM has been reported as an ICI-associated irAE. However, patients with immunocompromising conditions such as HIV are usually excluded from ICI trials. Therefore, little is known about such irAEs in this population. In this case, risk of ICI-DM as an irAE was likely increased by several factors including family history, a high-risk genetic profile, islet-related immunologic abnormalities, active lymphoma, and HIV infection with a possible immune reconstitution event. Clinicians should maintain a high index of suspicion for development of irAEs associated with ICI, particularly as use of these therapies broadens. Thorough investigation for presence of higher-risk features should be conducted and may warrant inclusion of pre-therapy genetic and/or autoantibody screening.
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PMID:Checking the Checkpoint Inhibitors: A Case of Autoimmune Diabetes After PD-1 Inhibition in a Patient with HIV. 3322 97