INTERNAL SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)

MEDICINE
02/19/2022
FEBRUARY 2022

OUTLINE Eyes: (-) Blurring of vision

I. CASE PRESENTATION Ears: (-) Hearing loss, (-) Ear pain or discharge
II. CASE DISCUSSION Nose: (-) Nasal congestion, (-) Nasal discharge
Throat/Mouth: (-) Dysphagia
I. CASE PRESENTATION Respiratory (-) Chest pain, (-) Cough
A. GENERAL DATA Cardiovascular (-) Palpitations
 Name: DPA Gastrointestinal (-) Abdominal pain, (-) Constipation
 Age: 39 years old Musculoskeletal (-) Muscle stiffness
 Gender: Female Genitourinary (-) Polyuria, (-) Hematuria, (-) Incontinence
 Civil Status: Married Neurologic (-) Numbness, (-) Tingling sensation
 Date of Birth: January 5, 1983 Endocrine (-) Heat/cold intolerance, (-) Polydipsia,
 Address: Assasi, Baggao, Cagayan Polyphagia, (-)Tremors, (-) Profuse sweating
 Religion: Roman Catholic Hematologic (-) Easy bruising, (-) Bleeding
 Nationality: Filipino E. PAST MEDICAL HISTORY
 Date of Admission: January 28,022 Childhood Illnesses ● Unrecalled
 Time of Admission: 4: 00 PM Immunizations ● Unrecalled
B. CHIEF COMPLAINT Medical ● (+) Blood Transfusion history during
 Generalized body weakness primary school
C. HISTORY OF PRESENT ILLNESS Surgical ● No previous surgical procedures done
2019 Psychiatric ● No psychiatric history
● (+) Generalized body weakness accompanied by non-migrating joint Allergies ● No allergies to food and medications
pains in the knee, back, and elbows F. FAMILY HISTORY
● Appearance of skin rashes on her anterior chest Father Mother
● No fever, no reported grating sound on joints upon movement, no Hypertension (-) (-)
deformities on extremities or digits, no swelling, no other associated Diabetes mellitus (-) (-)
symptoms noted Heart Disease (-) (-)
● No medications taken and no consultation done Cancer (-) (-)
1 year PTA Blood Disorder (-) (-)
● (+) Diffuse thinning of hair and hair loss Renal Disease (-) (-)
● (+) Appearance of skin rashes on her face and neck after sometime Asthma or other pulmonary Disease (-) (-)
during sunlight exposure G. PERSONAL AND SOCIAL HISTORY
○ Occasionally painful, pruritic, and erythematous lesions
● No fever, chills, nausea, vomiting, lymphadenopathy, vesicles or ● The patient is married and a housewife.
bullae noted ● Currently residing in a semi-concrete house consisting of 2 rooms,
● No medications taken; no consultation done with her family. Their bathroom has a pail-flush type of toilet
1 month PTA ● The patient is a non smoker and non alcoholic drinker.
● (+) Complaint of difficulty sleeping ● The patient eats three times a day which usually consists of rice,
● (+) Generalized body weakness meat and vegetables.
● (+) Visual hallucinations ● Her hobbies include surfing the internet and watching TV shows.
● (+) Episodes of blank stares ● Their source of drinking water is mineral water
● No fever, chills, vomiting, loss of consciousness, or history of head H. PHYSICAL EXAMINATION
trauma noted. A. GENERAL SURVEY
● No medications taken and no consultation done  Awake and not in cardiopulmonary distress
3 Days PTA B. VITAL SIGNS
● (+) Chest discomfort
BP 100/70 mmHg
● Cardiac panel:

HR 98 bpm

RR 20 cpm

Temp. 36.8 deg. C

O2 Saturation 98% at room air

Few Hours PTA
● With persistence of generalized body weakness
SKIN (-) pallor, (-) jaundice
● (+) seizure episode at CVMC-ER
HEENT Anicteric sclera, pale palpebral
● RAT positive (Jan. 24); swabbed for RT-PCR --> Nightward
conjunctiva
D. REVIEW OF SYSTEMS
CHEST AND LUNGS Symmetrical chest expansion, clear
Constitutional (+) Generalized body weakness
breath sounds
(-) Loss of appetite
CARDIOVASCULAR Adynamic precordium, normal rate,
(-) Fever
regular rhythm, (-) murmur
(-) Fatigue
ABDOMEN Flabby, soft, no tenderness
Integumentary (-)Discoloration
EXTREMITIES Full and equal pulses, (-) edema
(-)Rash/lesions
NEUROLOGICAL Not Assessed
HEENT Head: (-)Headache
I. SALIENT FEATURES

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 INTERNAL MEDICINE | Topic discussed
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February 2022

● 39-year-old female
● (+) generalized body weakness
● (+) non-migrating joint pains
● (+) history of rashes on anterior chest
● (+) hair loss/thinning of hair- Alopecia
● (+) rashes on face and neck
● (+) difficulty sleeping
● (+) visual hallucinations
● (+) episodes of blank stares
● (+) worsening changes in behavior
● (+) seizure
● (+) chest discomfort
● (+) COVID-19 RAT
● (+) blood transfusion history
● Low C3 level
● Unvaccinated
● (-) cough
● (-) fever
● (-) sore throat
● (-) recent known exposure to confirmed case of COVID-19
● Pale palpebral conjunctiva
● (-) peripheral edema
J. INITIAL IMPRESSION
 SLE in SEVERE FLARE t/c Neuropsychosis; COVID-19
Probable
K. DIFFERENTIAL DIAGNOSES

1. SYSTEMIC LUPUS ERYTHEMATOSUS

RULE IN RULE OUT

● 39-Year-Old Female
● (+) generalized body weakness
● (+) non-migrating joint pains
● (+) history of rashes on anterior chest
● (+) hair loss/thinning of hair
● (+) rashes on face and neck
● (+) difficulty sleeping
2. COVID-19
● (+) visual hallucinations
RULE IN RULE OUT
● (+) episodes of blank stares
● (+) worsening changes in behavior ● Generalized body weakness ● (-) fever
● (+) chest discomfort ● Joint pain ● (-) cough
● (+) seizure ● Unvaccinated ● (-) sore throat
● Low C3 level ● Chest discomfort ● (-) known recent exposure
● Pale palpebral conjunctiva ● (+) COVID-19 RAT ● Confirmatory Test: RT-PCR

3. RHEUMATOID ARTHRITIS
RULE IN RULE OUT

● Generalized body weakness ● (-) rheumatoid nodules

● Joint pains (knee, back, and ● (-) joint stiffness
elbow) ● Additional tests:
● 39 years old ● Plain X-ray
● Female ● ESR, CRP

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necrotizing granulomatous
vasculitis
● CBC ● Serum ferritin, ESR, D-dimers
● Na, K, Crea ● Oropharyngeal 7. ELECTROLYTE IMBALANCE
● AST, ALT swab/Nasopharyngeal swab- To RULE IN RULE OUT
● ABG confirm Covid-19
● CXR PA ● PT, PTT ● Generalized body weakness Can not totally rule out
● 12L ECG ● UA ● Seizure ● Request for electrolyte panel
● Procalcitonin, LDH, CRP ● ANA/ Antinuclear antibody ○ Sodium (hyponatremia)
● Cranial CT scan with contrast ○ Calcium (hypocalcemia)
● KUB ○ Magnesium (hypomagnesemia)

A. ADMITTING PLAN
● Please admit to COVID ISOLATION under the service of Dr.
Jambaro / Cannu / Bautista / Balintec / Verbo
● Secure consent for admission
● TPR q Shift
● Diet: DAT
● IVF: PNSS 1L x 12 hours
○ SLE Nephritis
○ r/o Neuropsychosis SLE
○ COVID-19 Probable

B. DIAGNOSTICS

If the patient is budget limited, What will be your priority

diagnostics? ANA/ Antinuclear antibody (screening test for SLE)
or CBC and UA (to check for proteinuria)

If the patient has money what diagnostics will be done to confirm

neuropsychosis in SLE? Antiribosomal T, antineuronal antibodies

To r/o SLE nephritis? renal biopsy, anti-dsDNA antibodies

C. TREATMENT
● Hydrocortisone 100 mg / IV q 8- mainstay of treatment
● Hydroxychloroquine 200 mg / tab, 1 tab OD
● Diazepam 5 mg / IV PRN for seizure
● Klyte tab, 1 tab TID x 3 days
● Repeat serum K, post correction
● O2 inhalation PRN
● VS and O2 sat q 2
● I and O q shift
● Refer

4. HYPOTHYROIDISM
D. COURSE IN THE WARD
RULE IN RULE OUT
HOSPITAL DAY DIAGNOSTICS THERAPEUTICS
● Generalized body weakness ● (-) Puffy face
At the ER Diagnostics: ● IVF : PNSS 1L x 12
● Seizure ● (-) Peripheral edema
JANUARY 28, 2022 ● CBC hours
● Hair loss ● (-) Bradycardia
CC: Body weakness ● Na, K, Crea ● Start Hydrocortisone
● Female ● (-) Delayed relaxation of DTR
(+) Seizure ● AST, ALT 100mg / IV q 8
● Additional tests:
SLE Nephritis ● ABG ● Hydroxychloroquine
● TSH, fT4
r/o Neuropsychosis in ● CXR PA 200 mg / tab OD
SLE ● 12L ECG ● Diazepam 5 mg / IV
5. DERMATOMYOSITIS
COVID probable ● Procalcitonin, LDH, PRN for seizure
RULE IN RULE IN
CRP Rheuma Consultation
● Generalized body weakness ● (-) Gottron papules ● Serum Ferritin, Notes
● Rashes on anterior chest ● Heliotrope rash ESR, D-dimers ● Admit as SLE
● Joint pains ● (-) dilated nailfold capillaries ● OPS / NPS Nephritis, r/o NP SLE
● Female ● UA ● Facilitate ANA,
● Pt, Ptt Cranial CT scan with
6. GRANULOMATOSIS WITH POLYANGIITIS ● ANA contrast, KUB UTZ
RULE IN RULE OUT ● Cranial CT scan ● Refer back once with
with Contrast diagnostics
● Generalized Body Weakness ● (-)Paranasal Sinus Pain ● KUB ● Refer
● 39 y/o Female ● (-)Nasal Discharge
● Arthralgia ● Diagnostics: At the ER C3 - 0.4 ● Klyte tab 1 tab TID x
● Rashes ○ Pulmonary Tissue biopsy: January 28, 2022 ICa - 1.20 3 days
Uric acid - 158.40 ● (Repeat potassium

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February 2022

AST - 152 post correction) Urinary bladder wall

ALT - 297 appears
NA - 135 homogeneously
K - 3.26 echogenic.
Mg - 1.40 No mass lesions or
Ph - 3.80 lithiasis. No focal
Urea - 4.80 lesions seen
Crea - 51.20 There is an incidental
CKMB - 63 finding of increased
Platelet - 301 parenchymal
Hemoglobin - 108 echogenicity of the
Hematocrit - 0.30 liver
Wbc - 12.5 Impression:
UA: NORMAL
CHON: + ULTRASOUND OF
Blood: + THE KIDNEYS AND
Urobilinogen - ++ URINARY
WBC - 24 BLADDER.
RBC - 2 INCIDENTAL
SEROLOGY FINDING OF MILD
FERRITIN: 2000 FATTY
ng/mL (9x elevated) INFILTRATION OF
PROCALCITONIN: THE LIVER
2660 ng/mL 3RD HD: JANUARY For cbc, Na, K, Crea,
(Sepsis caused by 31, 2022 AST, ALT, For CX-
bacteria) SLE Nephritis r/o ray
HS CRP: >20.0 mg/L Neuropsychosis in
SLE
1st HD: JANUARY U/A Paracetamol 300 4TH HD: February 1, Ica - 1.31 ● To start Ceftriaxone
29, 2022 PE: mg/IV now then q 4 prn 2022 AST - 115.23 2g/IV OD
Bp: 100/70 ● Color: L/Y for fever (+) cough ALT - 136.90 ● To start Azithromycin
Temp: 38.4 ● Transparency: NA - 137.80 500mg/tab OD
RR: 20 Turbid K - 3.46
HR: 98 CA: Mg - 0.60
Spo2: 100% ● pH: 8.0 Ph - 1.20
SLE Nephritis r/o ● SG: 1.015 Urea - 3.70
Neuropsychosis in ● Protein: (-) Crea - 41.70
SLE ● Glucose: (-) Platelet - 256
COVID probable ● Ketones: (-) Hemoglobin - 78
● Blood: (-) Hematocrit - 0.25
● Bili: (-) Wbc - 14.2
● Urobili: (+)
● Nitrite: (-) 5TH HD: FEBRUARY IDS NOTES
● Leu: (-) 2, 2022 ● CLEARED FOR
URINE FLOW TRANSFER
CYTOMETRY: 6TH HD: February 3, Still for ANA Hydrocortisone 100mg
● WBC: 0-2/HPF 2022 Ffup Cranial CT w/ IV q8
● RBC: 0-1/HPF 12:20pm contrast ● Diazepam 5mg IV
● EC: 0/LPF 110/70mmHg PRN for seizure
● H. cast: 0/LPF 84 bpm official results ● Allopurinol
● Bact: 45/HPF 19 cpm 300mg/tab 1 tab OD
● Mucus Threads: 0 36.5 ● Feso4 + FA 1 tab
(+) Body weakness TID
2ND HD: JANUARY KUB UTZ IDS Consultation: (-) Seizure (-) Fever (-) ● Hydrochloroquine
30, 2022 Both kidneys are ● Complete 10 days Headache (-) 200mg/tab 1 tab OD
(-) RT-PCR within normal limits in isolation then may Dizziness (-) Chest ● Godex 1 CAP TID
SLE Nephritis size and transfer pain (-) DOB (-) Cough ● Ceftriaxone 2g/IV
r/o Neuropsychosis in configuration. Awake, coherent (+) OD (Day 3)
SLE Renal outlines are Pallor, (-) jaundice ● Azithromycin
smooth and intact. AS, PPC SCE, CBS 500mg/tab 1 tab OD
Cortical echoes are (-) Retractions AP, ● Paracetamol 500mg
homogeneous. NRRR, (-) murmur IV q4 PRN for fever
No focal lesion seen. Soft, nontender
Renal sinus is dense abdomen FEP, (-)
and centrally edema
oriented. SLE NEPHRITIS R/O
Distinct cortico- NEUROPSYCHOTIC
medullary junction SLE
noted. CAP MR
Urinary collecting COVID 19 RULED
system is not dilated.

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February 2022

OUT 8:30 am ANA

110/80 mmHg
6TH HD: February 3, Still for ANA IVF: PNSS 1L 72 bpm
2022 Ffup Cranial CT w/ Continue current 19cpm
9pm contrast medication & 36.8 C
130/80mmHg official results management 99%
80 bpm Pls secure 1u PRBC
20 cpm properly typed and 11TH HD: February Rpt CBC, Na, K, iCa, ● PNSS 1L x 24
36.5 crossmatched & 8, 2022 9:00 am Crea, Mg, Phos ● NPO temporarily
98% transfuse once Rheuma Consultant Rpt CXR ● Diazepam 5mg/IV
(-) chest pain, available Notes For cranial CT scan now then q4 PRN
dyspnea, bleeding, ● Noted latest status plain STAT ● Continue other meds
headache of patient CHEST X-RAY (AP): ● Hook to O2 @ 6
(+) joint pain ● For Cranial CT scan ● Interval progression LPM via facemask
Alert, not in ● Refer to Neuro of the air-space
cardiorespiratory (+) Seizure opacities in right mid
distress generalized tonic to lower lung
(+) Pallor, (-) jaundice clonic for 1 minute x consistent with
AS, PPC 3 episodes consolidation
SCE, CBS Vital signs: pneumonia
(-) Retractions 130/90 mmHg ● Significant clearing
AP, NRR, 105 bpm of the pneumonic
(-) murmur 23 cpm opacities in the left
Soft, nontender 36.8 C lung
abdomen 93-95% ● No significant
FEP, (-) edema change in the
previously noted right
7TH: February 4, For ANA ● Decrease PNSS 1L x sided minimal pleural
2022 ffup official result of 24h effusion while there is
1pm cranial CT ● Continue meds complete regression
(-) fever For sputum AFB x2 ● Ffup availability lf 1u in the left
(+) cough dets PRBC & transfuse ● Rest of the
(+) Hemoptysis Sputum GSCS, previous chest
(-) DOB, Chest pain GeneXpert findings remain
Awake unchanged
SCE, (+) crackles 1:30 pm ● ffuP ANA, for
bilateral lung fields RHEUMA UPCR (urine protein
AP, NRRR, (-) murmur CONSULTANT creatinine)
Slightly distended, NOTES ● For HepB profile
nontender FEP, No ● Noted re hx and
edema previous workup done
8TH HD: February 5, For CBC, Na, K, iCA, ● PNSS 1L x 24 hrs ● A: SLE (nephritis,
2022 AST, ALT post BT ● Continue meds anemia,
7am K: 2.3 ● Furosemide 40 mg mucocutaneous,
(+) cough IV POST BT immunologic,
(-) fever, hemoptysis ● KCl drip: 10 meqs + neurologic) in flare
9TH HD: February 6, 90cc NSS/ soluset to ○ SLE
2022 2am run for 1hr x 8 cycles Neuropsychosis,
● K-lyte tab 1 tab TID x seizure secondary
3 days ● Refer to IDS for
9TH HD: February 6, iCA - 1.04 ● PNSS 1L x 24 stepup of antibiotics
2022 AST - 142.9 ● Hydrocortisone (HAP)
9am ALT - 223.26 100mg IV q8 ● Refer to Neuro
(-) fever, cough, DOB, Na - 138.7 ● Hydroxychloroquine service for clearance
Chest pain, abdominal K - 2.30 200mg/tab 1 tab OD ● Refer to Behavioral
pain Crea - 49 ● Allopurinol Med
Awake s/p BT 300mg/tab OD ● For pulse therapy
SCE, (+) Crackles, (-) ● Plt - 187 ● Diazepam 5mg/IV ● Deck to ICU (Deck
wheezes ● Hgb - 112 PRN for seizure 8)
AP, NRRR ● Hct - 0.37 ● FeSO4 + FA tab TID ● Refer
Flabby, soft, non ● WBC - 2.38 ● Godex cap TID
tender Still for ANA ● Paracetamol PRN 4:30 pm Hepa B Profile ● Pip-Taz 4.5g/IV now
Decreased edema Rpt K post correction ● Cefuroxime 2g/IV (+) Fever ● Anti-HBc total: then q6 ANST
SLE NEPHRITIS Ffup cranial ct OD (Day 5) w/ seizure episode 0.290 NR ● KCl drip: 90cc PNSS
R/O Neuropsychotic ● Azithromycin ● Anti -HBe: 1.780 + 10 mEqs KCl in a
SLE 500mg/tab OD NR soluset to run for 1h x
CAP-MR ● KCl drip to continue ● Anti-HBs: 0 NR 10 cycles
COVID19 Ruled out ● K-lyte tab TID ● HBeAg: 0.357 NR ● Phenytoin 750mg
● HBsAg: 0.230 NR SIVP now w/ BP
10TH HD: February K - 3.23 post ● PNSS 1L x 24 Ica - 1.13 precautions then
7, 2022 correction Still for ● Continue meds Na - 136.80 100mgIV q8 with

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February 2022

K - 2.34 crystallization No active seizure for ● Follow up ANA result

Crea - 58.8 precaution 24 ● RF - established if
Hgb - 105 hours there is really history of
Hct - 0.25 No headache SLE
WBC - 3.67 No nausea ● Noted change in
Plt - 160 No vomiting anti-seizure meds
Cl - 90.8 No chest pain ● Noted normal level t4
Mg - 0.67 No palpitation and tsh
Phosphorus - 1.50 No changes in ● Refer if there is any
FT4: 0.99 ng/dL sensorium impairment
For 12L ECG now, Decrease rashes ● May start with
then rpt ECG after 11AM Risperidone ½ tab OD
pulse therapy HS
6pm ● Check thyroid ● After LD of Continue active
Rheuma Consultant function antibiotics, start pulse medication
Notes therapy as follows: VS q2hrs and record
● Updated patient methylprednisolone Maintain O2
status 500mg + 250cc D5W WOF untoward s/sx
● Agree w/ meds to run for 4hrs OD x 3 14TH HD: February Clinical Chemistry ● Pulse therapy (D2)
● Hook to cardiac days 11, 2022 ● SGOT/AST: 96 u/L ● continue active meds
monitor if available ● Hold hydrocortisone 1AM ● SGPT/ALT: 130 u/L ● Maintain O2
● Monitor patient prior to start of pulse (-) Fever Culture and ● VS Q2 and record
closely therapy (-) seizure sensitivity (right arm): ● WOF untoward s/sx
● Refer (-) DOB No growth after 24 IM NEURO NOTE:
(-) chest pain hours of incubation ● Do repeat AST, ALT
12TH HD: February ● TSH: 0.80 uIU/mL PNSS 1L x 24hrs 10:07 AM 12 Lead ECG: Non- ● Continue active
09, 2022 Culture and Resume Diet: DAT + 1 No seizure episode specific ST changes medications
10AM sensitivity banana each meal SLE ● May discontinue
(-) fever ● Blood, L and R arm TX Activity Phenytoin, continue
(-) DOB ○ No growth after 5 ● D1 Pulse Therapy: ● Anemia Levetiracetam 500mg
(-) chest pain days of incubation methylprednisolone ● Nephritis, resolved BID
(-) pain ● Rpt potassium after 500mg + D5W 250 cc ● Neuropsychosis, ● Refer
(-) seizure; correction to run for 4 hours OD seizure resolved
(-) hallucinations, H/V ● For blood CS for 3 days HAP
PE ● Repeat 12 lead ● Phenytoin 100mg IV
PPC, (+) rashes face ECG after pulse q8hrs 15TH HD: February ● PNSS 1L to run for
& neck, (+) crackles therapy ● Diazepam 5mg IV 12, 2022 24hrs
BLF q4hrs prn for seizure 4PM ● DAT & 1 banana
Vital signs: WNL ● Hydroxychloroquine (-) fever each meal
SLE in flare 200mg/tab PD (-) DOB ● DX: D3 Pulse
SLE neuropsychosis, ● Pip-Taz 4.5g IV (-) chest pain Therapy:
seizure secondary q6hrs (-) seizure ● D/C phenytoin
Electrolyte imbalance ● Hold hydrocortisone, PE ● Continue active
(Hypokalemia) allopurinol Decreased facial medication
HAP ● Klyte tab TID edema ● VS q4hrs and record
● Godex cap TID (+) crackles ● I and O qnshift
● Feso4 + FA tab TID ● WOF untoward s/sx
Maintain O2 VS and 16TH HD: February SGOT: 96 RHEUMA-IM NOTES
NVS q1 and record I 13, 2022 SGPT: 130 ● Updated regarding
and O q shift WOF 8:40 AM Sputum AFB x2 patient
untoward S/SX Patient ● Agree to continue
NOTES: M-IDS NOTES: Awake hydrocortisone
NEURO ● Thank you for this Oriented, ● Follow-up ANA result
CONSULTANT: referral Follows command ● Follow up repeat
● Hx, PE and labs ● Patient seen and No active seizure sgot, sgpt
relayed examined Decrease facial ● Continue monitoring
● Assessed patient ● Hx and PE edema and management
● Agree with meds reviewed Decrease rashes on ● refer
● May do switching of ● A: Hospital ear and neck IM NEURO NOTES
anti-seizure Acquired Pneumonia 12 PM ● Continue neuro
medications. ● P: Start Piperacillin- (-) seizure meds
● Start levetiracetam tazobactam 4.5gIV q 9PM PNSS 1L x 24hrs
500 mg/tab 1 tab BID 6H (-) fever DAT
● For blood CS (-) cough TX: resume
● Updated regarding (-) DOB hydrocortisone 250g IV
the patient (-) chest pain now then 100g IV q8
● Refer Furosemide 40mg IV
now
13TH HD: February IM-RHEUMA NOTES Start NAC 600mg
10, 2022 ● Follow up referral to ODHS
8AM behavioral medicine Give after meals

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VS q2hrs and record ○ Renal involvement: 21-65% at diagnosis; 40-82% over

I and O time
Maintain 02 with Nasal ○ Leading causes of death: infections, active SLE,
cannula cardiovascular involvement
WOF untoward s/sx ● Philippines
17TH DAY: CBC ● VS q4 and record ○ Age at onset: 26.7 y/o
FEBRUARY 14, ● Hgb - 105 g/L ● WOF untoward s/sx ○ Age at diagnosis: 28.5 y/o
2022 ● Hct - 0.35 ○ W>M
2pm ● Erythrocytes - C. PREDISPOSING FACTORS
3.46/L
● Platelet count -
403/L
● MCV - 100
● MCH - 30
● MCHC - 303
● WBC - 12.6
DIFFERENTIAL
COUNT
● Neutrophils - 87.1
● Lymphocytes - 8.6
● Monocytes - 4.3
● Eosinophil - 0
● Basophil - 0
Clinical Chemistry
● Ionized Calcium -
1.30
● Sodium - 136.90
● Potassium - 3.43
● Creatinine - 87.20

18TH DAY: AFB Stain PNSS 1L x 24hrs

FEBRUARY 15, 2022 ● 1st determination DAT
7PM (Salivary) TX: pip-taz 4.5gIV q6
(-) fever ● AFB = 0 Hydroxychloroquine
(-) cough Repeat CXR 200mg OD D. PATHOPHYSIOLOGY
(-) DOB Hydrocortisone 100g
(-) Chest pain IV q8
(-) seizure Levetiracetam
(-) hallucinations 500mg/tab BID
VS Godex cap TID
BP: 120/90 Feso4 + FA tab TID
HR: 72 Risperidone ½ tab
RR :11 ODHS
Temp: 36.5 NAC 600mg tab ODHS
O2 sat: 99% Maintain 02
VS q4 and record
Input and output
monitor
WOF untoward s/sx

E. WORKING IMPRESSION
1. SLE in FLARE
a. Nephritis Resolved
b. Anemia Secondary
c. Transaminitis
d. Neuropsychosis, seizure resolved
2. HAP

II. CASE DISCUSSION

A. DEFINITION
 an autoimmune disease in which organs and cells undergo
damage initially mediated by tissue-binding autoantibodies and
immune complexes.
B. EPIDEMIOLOGY
● 90% - women of child-bearing years
● All genders, ages, and ethnic groups are susceptible.
● US Prevalence: 20–150 per 100,000 women
● Asia-Pacific
○ Overall crude prevalence rate: 4.3-45.3 per 100,000

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E. CLINICAL MANIFESTATIONS

CUTANEOUS MANIFESTATIONS
● Discoid Lupus Erythematosus (DLE)
○ Most common chronic dermatitis in lupus
○ Lesions: Roughly circular with slightly raised, scaly
hyperpigmented erythematous rims and depigmented,
atrophic centers
○ Only 5% of people with DLE have SLE, however, among
individuals with SLE, as many as 20% have DLE
○ Treatment: Topical or locally injected glucocorticoids and
systemic antimalarials

● Acute SLE
○ Most common rash: Photosensitive, slightly raised
erythema, occasionally scaly
MUSCULOSKELETAL MANIFESTATIONS ■ Locations:
● Intermittent polyarthritis ● Face (particularly the cheeks and nose — the
○ Characterized by soft tissue swelling and tenderness in “butterfly” rash)
joints and/or tendons, most commonly in hands, wrists, and ● Ears
knees ● Chin
● Joint deformities - develop in 10% of patients with SLE ● V region of the neck and chest
● Erosions on joint x-rays - 10–50% of patients ● Upper back
● “Rhupus” ● Extensor surfaces of the arms
○ Patients with rheumatoid-like arthritis with erosions and ○ Worsening of this rash often accompanies flare of systemic
fulfill criteria for both RA and SLE disease
● Joint pain
○ Most common reason that patients increase their dose of
glucocorticoids

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VASCULAR OCCLUSIONS INCLUDING STROKE AND

● Subacute Cutaneous Lupus Erythematosus (SCLE) MYOCARDIAL INFARCTIONS
○ Scaly red patches similar to psoriasis, or circular flat red- ● TIA, Strokes, and MI
rimmed lesions (exquisitely photosensitive) ○ increased in patients with SLE
○ Most have antibodies to Ro (SS-A) ● MI (3-10 fold increased)
● Other SLE Rashes ○ Manifestations of accelerated atherosclerosis
○ Recurring urticaria ○ Highest in women aged <49 years
○ Lichen planus-like dermatitis ● Statin therapies show significant reduction of cardiac events in SLE
○ Bullae patients
○ Panniculitis (“lupus profundus”)

CARDIOPULMONARY MANIFESTATIONS (60%)

● Pleuritis - Most common pulmonary manifestation
○ Mild - Respond to treatment with NSAids
○ Severe - brief course of glucocorticoid therapy
● Life-threatening pulmonary manifestations:
○ Interstitial inflammation leading to fibrosis
○ Shrinking lung syndrome
○ Intraalveolar hemorrhage
● Pericarditis - most frequent cardiac manifestation
○ More serious cardiac manifestations: Myocarditis and
RENAL MANIFESTATIONS Fibrinous endocarditis of Libman-Sacks
● Nephritis
○ Most serious manifestation of SLE
○ Asymptomatic in most lupus patients
○ Renal biopsy is recommended for every SLE patient with
any clinical evidence of nephritis
● Patients with ISN III and IV
○ Microscopic hematuria and proteinuria (>500 mg per 24 h)
○ One-half develop nephrotic syndrome
○ Most develop hypertension
● Patients with DPGN
○ If inadequately treated, patients will develop ESRD within 2
years of Diagnosis

HEMATOLOGIC MANIFESTATIONS (80%)

● Anemia - most frequent manifestation of SLE
○ normochromic normocytic
● Leukopenia
NERVOUS SYSTEM MANIFESTATIONS
● Thrombocytopenia
● Diffuse CNS lupus
○ If platelet counts are >40,000/μL and abnormal bleeding is
○ Cognitive dysfunction
absent, therapy may not be required.
○ Headaches
● Seizures
○ Treatment: Antiseizure and immunosuppressive therapies
● Psychosis
○ Can be the dominant manifestation of SLE
○ Must be distinguished from glucocorticoid-induced
psychosis
○ Glucocorticoid-induced psychosis: Usually occurs in
the first weeks of glucocorticoid therapy, at daily doses of
≥40 mg of prednisone or equivalent and resolves over
several days after glucocorticoids are decreased or stopped

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● Renal biopsy read as systemic lupus qualifies for classification as

SLE if any lupus autoantibodies are present, even if total criteria are
fewer than 4.

GASTROINTESTINAL MANIFESTATIONS (40%)

● Nausea, vomiting, and diarrhea
○ Manifestations of an SLE flare
● Diffuse abdominal pain
● Increase AST and ALT
● Vasculitis
● Aggressive immunosuppressive therapy with high-dose
glucocorticoids is recommended for short-term control

2019 EULAR/ACR classification Criteria

● Entry criterion :POSITIVE ANA
● Classification threshold score : ≥ 10
● Sensitivity of 96.1%
OCULAR MANIFESTATIONS (15%) ● Specificity of 93.4%

● Sicca syndrome and nonspecific conjunctivitis

○ Common in SLE and rarely threaten vision
● Retinal vasculitis and optic neuritis
○ Serious manifestations
○ Blindness can develop over days to weeks.

DIAGNOSIS

SLEDAI SCORE

SLICC CRITERIA
● Presence of any FOUR criteria (must have at least 1 in each
category) qualifies patient as having SLE with 93% specificity and 92%
sensitivity

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Staining Patterns of Autoantibodies

LABORATORY EXAMINATIONS B. CBC

A. AUTOANTIBODIES  Decreased Hgb (< 124g/L or <12.4g/dL)
 Decreased Hct; erythrocytopenia
 Leukopenia (<4000/ uL)
 Lymphopenia (<1000/uL)
 Thrombocytopenia (<100,000/uL)

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 Most frequent hematologic manifestation of SLE:

NORMOCHROMIC, NORMOCYTIC ANEMIA
C. HEMATOLOGY AND IMMUNOLOGY
 C3, C4: low serum complement
 ESR, CRP: high ESR, low CRP
 Coomb’s test: Positive direct Coomb’s test in the absence of
hemolytic anemia
 Reticulocyte count: increased
D. BLOOD CHEMISTRY
 FBS, Lipid Profile: elevated in lupus nephritis
 ALT, AST: increased when SLE is active
 Serum creatinine: increased (>124 umol/L or >1.4 mg/dL)
 LDH: increased
E. URINALYSIS
 Hematuria
 Proteinuria
 RBC casts
 Protein-creatinine ratio >/= 0.5
o 24-hour urine protein excretion: >2.6 g
F. ECG
 Most frequent cardiac manifestation: PERICARDITIS
o Stage 1: widespread elevation of ST segments, often with
upward concavity involving 2 o3 standard limb leads and V2-
V6, with reciprocal depressions only in aVR and sometimes
V1
o Stage 2: ST segment normalizes
o Stage 3: T wave inversions
o Stage 4: ECG returns to normal
G. CXR
 Most common pulmonary finding in SLE: PLEURITIS WITH OR
WITHOUT PLEURAL EFFUSION

H. RENAL BIOPSY CLASS I: MINIMAL MESANGIAL LN

 Light microscopy: Normal glomeruli
 Immunofluorescence: Mesangial immune Deposits

CLASS II: MESANGIAL PROLIFERATIVE LN

 Light microscopy: Purely mesangial hypercellularity of any
degree or mesangial matrix expansion with mesangial immune

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deposits Immunofluorescence/ Electron Microscopy: isolated

subepithelial or subendothelial deposits

CLASS VI: ADVANCED SCLEROTIC LN

 ≥ 90% of glomeruli globally sclerosed without residual activity
CLASS III: FOCAL LN
 Active or inactive focal segmental or global endo or extracapillary
involving </=50%

MANAGEMENT
○ No cure for SLE
○ Aim for low-level disease activity
○ Therapeutic choice depends on:
CLASS IV: DIFFUSE LN ■ Whether disease manifestations are life-
 Active or inactive diffuse segmental or global endo or threatening or likely to cause organ damage
extracapillary glomerulonephritis involving >/= 50% of glumeruli ■ Whether manifestations are potentially reversible
■ The best approaches to preventing
complications of disease and its treatment
CONSERVATIVE THERAPIES FOR MANAGEMENT OF NON-LIFE-
THREATENING DISEASE
● Analgesics and Antimalarials- mainstay
○ NSAIDS
■ Analgesic and anti-inflammatory
■ Increased risk of NSAID-induced aseptic
meningitis, elevated transaminases, hypertension,
and renal dysfunction
○ COX-2 inhibitors
■ Increased risk for MI
○ Acetaminophen
■ Good strategy
● Antimalarials - Reduce dermatitis, arthritis and fatigue
○ Hydroxychloroquine
■ Reduces accrual tissue damage
■ >/= 750 ng/mL
■ Potential retinal toxicity
CLASS V: MEMBRANOUS LN ● Belimumab
 Global or segmental subepithelial immune deposits; occur ○ Monoclonal antibodies
combination with Class III or IV; may show advanced sclerosis ○ Fatigue, rash, and/or arthritis (50%)
○ Expensive
○ Effective in patients with SLEDAI score of >/= 10, positive
anti-DNA, and low complement serum
LIFE-THREATENING SLE: PROLIFERATIVE FORMS OF LUPUS
NEPHRITIS
● Systemic glucocorticoids
○ Mainstay treatment

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○ (0.5-1 mg/kg/day PO or Methylprednisolone sodium
succinate IV 500-1000 mg daily for 3 days followed by 0,5-1
mg/kg/day prednisone or equivalent)
○ Increased survival rate in DPGN (40-60 mg of prednisone
daily for 4-6 months)
○ Tapered with maintenance dose of 5-10 mg/day
● Pulse therapy
○ administration of suprapharmacologic doses of drugs in an
intermittent manner to enhance the therapeutic effect and
reduce the side effects
● Aim of pulse therapy: getting quicker and stronger efficacy and
decreasing the need for long-term use of steroids
● Methylprednisolone (MP)- most commonly used for corticosteroid
pulse therapy
○ an intermediate acting
○ Potent anti inflammatory agent
○ With a low tendency to induce sodium and water retention
● INTRAVENOUS (IV) pulses of methylprednisolone (MEP) are
commonly used to treat the severe manifestations of systemic lupus
erythematosus (SLE).
o Dosage: 20-30 mg/kg (500-1000 mg/m2) per pulse; up
to a maximum dose of 1 g.
o Preparation: dissolved in 150-200 ml of 5% dextrose
and infused intravenously, slowly over 2-3 hours.
○ Repeat pulses are given at intervals of 24-48 hours
● Effects of high dose intravenous/pulse steroids:
○ Downregulation of activation of immune cells and
proinflammatory cytokine production, leading to reduced
expression of adhesion molecules and reduced movement of
neutrophils into sites of inflammation.
● Contraindication:
○ Systemic infections
○ Uncontrolled hypertension
○ Hypersensitivity to the steroid preparation
● Cytotoxic / Immunosuppressive Agents
○ Cyclophosphamide
■ Alkylating agent
■ ISN grade III or IV diseases, combination with
glucocorticoids reduces progression to ESRD and
death
■ Toxicity: Amenorrhea, leukopenia, nausea
■ Late responses begin 3-16 weeks after
treatment is initiated
■ Teratogenic
● Cyclophosphamide
○ 2 different regimens for IV preparation:
■ Low dose: 500 mg every 2 weeks for six total
doses, followed by azathioprine or mycophenolate
maintenance
 As standard high doses, with less toxicity
● Cyclophosphamide
○ 2 different regimens for IV preparation:
■ High dose cyclophosphamide: 500–1000 mg/m2
body surface area given monthly IV for 6 months, followed
by azathioprine or mycophenolate maintenance an
acceptable approach for patients with severe nephritis
● Ovarian Failure (gonadotropin releasing hormone)
 Cytotoxic / Immunosuppressive Agents
○ Mycophenolate mofetil
■ relatively lymphocyte-specific inhibitor of inosine
monophosphatase
■ Toxicity: diarrhea
■ Superior to azathioprine in maintaining renal
function
■ Teratogenic
○ Azathioprine
■ a purine analogue and cycle-specific
antimetabolite)
■ may be effective but is associated with more
flares
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■ Similar in efficacy and toxicity in with
mycophenolate for maintenance therapy
■ Can be used if necessary to control active SLE
during pregnancy
■ Prescreen patients for homozygous deficiency of
the TMPT enzyme
o Methotrexate
 Folinic acid antagonist
 Treatment for arthritis and dermatitis
o Cyclosporine and Tacrolimus
 Inhibit calcium influx
 Inhibit production of IL-2 and T lymphocyte
functions
 Used in patients with steroid-resistant
cytopenias of SLE
o ACE inhibitors / ARBs
 For patients with proteinuria > 500 mg daily
 Reduce the chance of ESRD
o Belimumab
 Approved for use with SLE w/o active renal
disease
SPECIAL CONDITIONS IN SLE
CRESCENTIC LUPUS NEPHRITIS
● The presence of cellular or fibrotic crescents in glomeruli with
proliferative glomerulonephritis indicates a worse prognosis.
● High-dose cyclophosphamide as the induction therapy of choice
● Mycophenolate mophetil is equally effective
MEMBRANOUS LUPUS NEPHRITIS
● Immunosuppression is not recommended unless proteinuria is in the
nephrotic range
● Alternate-day glucocorticoids plus cyclophosphamide or
mycophenolate mofetil or cyclosporine are all effective in reducing
Proteinuria
PREGNANCY AND LUPUS
● Fetal loss is increased (2-3x) in women with SLE
● Controlled with hydroxychloroquine and if necessary
prednisone/prednisolone at thelowest effective doses for the shortest
time required.
● Patients with antiphospholipid antibodies and prior fetal losses,
treatment with heparin (usually low-molecular-weight) plus low dose
aspirin.
● Presence of antibodies to Ro, associated with neonatal lupus.
○ Rash
○ Congenital heart block
○ With or without cardiomyopathy
● Treatment is with Hydroxychloroquine of an anti-Ro-positive mother
reduces the chance that subsequent fetuses will develop heart block.
LUPUS AND ANTIPHOSPHOLIPID SYNDROME
● Patients with SLE who have venous or arterial clotting and/or
repeated fetal losses and at least two positive tests for antiphospholipid
antibodies have APS
● Managed with long-term anticoagulation: warfarin
● INR of 2.0–2.5 for patients with one episode of venous clotting.
● INR of 3.0–3.5 for patients with recurring clots or arterial clotting
MICROVASCULAR THROMBOTIC CRISIS (Thrombotic
Thrombocytopenic Purpura, Hemolytic-Uremic Syndrome)
● Syndrome of hemolysis, thrombocytopenia, and microvascular
thrombosis in kidneys, brain, and other tissues
● High mortality rate
● Occurs most commonly in young individuals with lupus nephritis.
● Plasma exchange or extensive plasmapheresis is usually life-saving
and concomitant glucocorticoid therapy.
LUPUS DERMATITIS
● Minimize exposure to ultraviolet light.
● Topical glucocorticoids and anti-malarials (hydroxychloroquine) are
effective in reducing lesion severity.
15 of 17

● Systemic treatment with retinoic acid is a used in patients with
inadequate improvement on topical glucocorticoids and antimalarials.
PREVENTIVE THERAPIES
● Vaccinations (Influenza and pneumococcal)
● Calcium supplementation, Vitamin D, and either bisphosphonates or
denosumab.
● Statin therapies
PROGNOSIS
● Poor prognosis (~50% mortality in 10 years)
○ high serum creatinine levels (>124 μmol/L [>1.4 mg/dL]),
○ Hypertension
○ nephrotic syndrome (24-h urine protein excretion >2.6 g)
○ anemia (hemoglobin <124 g/L [<12.4 g/dL])
○ Hypoalbuminemia
○ hypocomplementemia
○ antiphospholipid antibodies
○ male sex
○ ethnicity (African American, Hispanic with mestizo
heritage)
○ low socioeconomic status.
PATIENT OUTCOMES AND SURVIVAL
● Renal transplants
○ twofold increase in graft rejection compared to patients
with other causes of ESRD
○ Overall patient survival 85% at 2 years
● Disability is due to chronic fatigue, arthritis, pain and renal disease.
● The leading causes of death in the first decade of disease are
systemic disease activity, renal failure, and infections; subsequently,
thromboembolic events become increasingly frequent causes of
mortality.
DRUG-INDUCED LUPUS
● syndrome of positive ANA associated with symptoms such as fever,
malaise, arthritis or intense arthralgias/myalgias, serositis, and/ or rash.
● Medications:
○ Antiarrhythmics (procainamide, disopyramide, and
propafenone)
○ the anti-hypertensive (hydralazine; several angiotensin-
converting enzyme inhibitors and beta blockers)
○ the antithyroid (propylthiouracil)
○ the antipsychotics (chlorpromazine and lithium)
○ the anticonvulsants (carbamazepine and phenytoin)
○ the antibiotics (isoniazid, minocycline, and
nitrofurantoin(Macrodantin)
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○ the antirheumatic (sulfasalazine)
○ the diuretic (hydrochlorothiazide
○ the antihyperlipidemics (lovastatin and simvastatin)
○ Biologic agents
○ Inhibitors of IFNs and TNF. In DIL, ANA usually appears
before symptoms;
● It is appropriate to test for ANA at the first hint of relevant symptoms
and to use test results to help decide whether to withdraw the suspect
agent.
References
● Anum Fayyaz, et.al (2015), Haematological Manifestations of
Lupus, .ncbi.nlm.nih.gov/pmc/articles/PMC4378375/
● Aringer M, Costenbader K, Daikh D, et al. 2019 European League
Against Rheumatism/American College of Rheumatology Classification
Criteria for Systemic Lupus Erythematosus. Arthritis Rheumatol. 2019
● Birtane, Murat. "Diagnostic role of anti-nuclear antibodies in
rheumatic diseases / romatizmal hastaliklarda antInukleer antIkorlarin
tanisal rolu." Turkish Journal of Rheumatology, vol. 27, no. 2, June
2012, pp. 79+. Gale OneFile: Health and Medicine,
link.gale.com/apps/doc/A300062185/HRCA?
u=googlescholar&sid=googleScholar&xid=3ed86576. Accessed 16
Feb.2022.
● Elkon, K., & Casali, P. (2008). Nature and functions of
autoantibodies. Nature clinical practice. Rheumatology, 4(9), 491–498.
https://doi.org/10.1038/ncprheum0895
● Kasper et al. (2018) Harrison’s Principles of Internal Medicine. 20th
Edition. McGraw-Hill Education. United States of America.
● Kumar, Y., Bhatia, A. & Minz, R.W. Antinuclear antibodies and their
detection methods in diagnosis of connective tissue diseases: a
journey revisited. Diagn Pathol 4, 1 (2009)
● Qudsiya Z, Waseem M. Dermatomyositis. [Updated 2021 Nov 7]. In:
StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022
Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK558917
● Stavroula Giannouli et. al(2005), Anemia in Systemic lupus
erythematosus: from pathophysiology to clinical assessment.
www.hindawi.com/journals/crin/2020/7869216/
● Sobia Sarwar, et. al., Neuropsychiatric Systemic Lupus
Erythematosus: A 2021 Update on Diagnosis, Management, and
Current Challenges
● Turner J, Parsi M, Badireddy M. Anemia. [Updated 2022 Jan 9]. In:
StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022
Jan-. Available from:s https://www.ncbi.nlm.nih.gov/books/NBK499994/
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Appendix A
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● You can also freely change the orientation of this section. If the table will look better in landscape orientation then go lang. If it is hard to layout you
can create a separate trans for appendices,
● THE NUMBERS OF TABLES AND FIGURES SHALL RESET HERE. Use this format: “Refer to Table A.1, refer to Table A.2, Refer to Figure B.1,
etc. etc.” on the discussion above where table should be seen

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